The American Journal of Orthopedics

Differences in bone size are established early in life, before puberty and perhaps even in utero.¹ Bone begins to form when mesenchymal cells form condensations—clusters of cells that adhere through expression of adhesion molecules² (Figure 1). Bone must be stiff, flexible enough to change shape to absorb energy, and light enough to allow mobility.^1,3 Longitudinal bone growth is detrimental to bone stability, but this effect is counteracted by concomitant bone growth in width.⁴ Bone growth in width has not been studied as extensively, despite its paramount role in skeletal development.⁵

Bone growth and development are products of the complex interactions of genetic and environmental factors, including diet, hormones, and mechanical stimuli.^6-9 Longitudinal bone growth is controlled by systemic and local hormones and local mechanical factors. Two models for control of bone growth in width have been suggested—the mechanostat theory (mechanical requirements regulate periosteal apposition) and the sizostat hypothesis (a master gene or set of genes regulates bone growth in width so bone reaches a preprogrammed size, independent of mechanical requirements).⁵

In this article, we review the most recent data regarding bone growth from the embryonic age and analyze the factors that control bone growth. An understanding of this complex system is important in identifying metabolic and developmental bone diseases¹⁰ and fracture risk.^11,12

Growth Plate

The growth plate consists mainly of collagen fibrils, proteoglycans, and water, arranged to form a sort of sponge with very small pores.¹³ The growth plate is located between epiphyseal and metaphyseal bone at the distal end of long bones¹⁴ and is strain-rate–dependent,^15,16 which means it is hard when squeezed rapidly but soft when deformed slowly. The growth plate becomes ossified after puberty and epiphyseal fusion.¹⁷

Histologically, the growth plate consists of horizontal zones of chondrocytes at different stages of differentiation.⁴ The germinal zone, at the epiphyseal end of the growth plate, contains resting chondrocytes, which seem crucial in orienting the underlying columns of chondrocytes and, therefore, in unidirectional bone growth, probably by secretion of a growth plate–orienting factor.^14,18 Next is the proliferative zone, a matrix-rich zone in which flattened chondrocytes undergo longitudinal cell division and orient themselves in typical column-wise fashion. At some point, proliferating chondrocytes lose their capacity to divide; they start to differentiate and become prehypertrophic, coinciding with a size increase.⁴ Proliferating chondrocytes are located in the transition (maturation or prehypertrophic) zone. In the hypertrophic zone, round chondrocytes secrete matrix proteins in large amounts.¹⁴ This stage is characterized by an increase in intracellular calcium concentration, which is essential in the production of matrix vesicles. These vesicles, small membrane-enclosed particles, are released from chondrocytes^19,20 and secrete calcium phosphates, hydroxyapatite, and matrix metalloproteinases, resulting in mineralization of the vesicles and their surrounding matrix.⁴ The chondrocytes in this mineralized zone eventually undergo programmed cell death (apoptosis), leaving a scaffold for new bone formation.

Longitudinal Bone Growth

Generally, bones increase in length as long as new material is being squeezed between the reserve zone of the growth plate and the zone of provisional calcification.⁴

Postnatal linear growth occurs in 3 phases. Phase 1 is characterized by a high rate of growth at the beginning of fetal life, and then rapid deceleration up to about 3 years; phase 2, by a lower, slowly decelerating growth rate up to puberty; and phase 3, by an increased rate of longitudinal growth until a peak is reached.^14,21,22

In 1964, Park²³ proposed that the structure of the epiphyseal cartilage may determine the pattern of the growing bone shaft. The changes within the hypertrophic zone are directly related to matrix mineralization, vascular invasion, and subsequent development.²⁴ Intracellular calcium concentration increases in the hypertrophic chondrocytes in the hypertrophic zone of growth plate cartilage; at some point, these chondrocytes begin to mineralize the longitudinal septa in the surrounding matrix²⁵ (Figure 2). At the growth cartilage junction, mononuclear cells of undetermined origin resorb the unmineralized horizontal septa of the growth cartilage. These cells are called septoclasts or chondroclasts.^25,26 Blood vessels invade the area and pave the way for bone cell precursors.²⁷ Eighty percent of the longitudinal septa of the growth cartilage is rapidly resorbed in the metaphyseal zone immediately behind the invading blood vessels, paving the way for bone cell precursors.²⁸ Fazzalari and colleagues²⁸ reported that about 40% of mineralized septa serves as scaffold for the formation of primary bone trabeculae; the other 60% is absorbed by chondroclasts (osteoclasts) near the vascular invasion front.

Regulation of Longitudinal Bone Growth

Longitudinal bone growth is regulated by genetic, hormonal, growth, and environment factors^17,29-31 (Table). It must be controlled on at least 3 different levels.⁴ Level 1 is systemic control by factors such as growth hormone (GH), sex hormones, and glucocorticoids. The major systemic hormones that control longitudinal bone growth during childhood are GH, insulin-like growth factor 1 (IGF-1), the thyroid hormones triiodothyronine (T₃) and thyroxine (T₄), and glucocorticoids; during puberty, the sex steroids play the most significant role.¹⁴ Level 2 is local control by factors such as Indian hedgehog (Inh), parathyroid hormone–related peptide (PTHrP), and fibroblast growth factors (FGFs).^14,31 Level 3 is mechanical control.⁴

Systemic Regulation. After birth, GH becomes an important modulator of longitudinal growth and appears to be, together with IGF-1, the central player in the hypothalamus–pituitary–growth plate axis.¹⁴ According to the original somatomedin hypothesis,³² GH stimulates hepatic production of IGF-1, which in turn promotes growth directly at the epiphyseal plate.¹⁷ GH acts on resting zone chondrocytes and is responsible for local IGF-1 production, which stimulates clonal expansion of proliferating chondrocytes in an autocrine/paracrine manner.³³ Infusion of GH or IGF-1 shortens stem- and proliferating-cell cycle times in the growth plate of hypophysectomized rats and decreases the duration of the hypertrophic differentiation phase, with GH being more effective.¹⁷ According to the experimental study of Hunziker and colleagues,³⁴ GH or IGF-1 treatment restores mean cell volume and height, but the growth rate is not normalized by either hormone.

Thyroid hormones also play a vital role in bone growth. T₃ and, to a lesser extent, T₄ are crucial in normal bone maturation.^30,35 Childhood hypothyroidism causes growth failure; growth failure may develop insidiously, but, once established, it is severe.¹⁷ On the other hand, hyperthyroidism increases the growth rate in children but also leads to premature growth plate fusion and short stature.^36,37 T₃ seems to stimulate recruitment of cells from the germinal zone to the proliferating zone and facilitates differentiation of growth plate chondrocytes.^38-40 Its precursor, T₄, increases the number of [³H]methylthymidine-labeled chondrocyte nuclei and [³⁵S]incorporation in Snell dwarf mice growth plates, suggesting a stimulatory role in chondrocyte proliferation and differentiation.⁴¹

Glucocorticoids suppress growth by modifying the GH/IGF-1 pathway at different levels.¹⁷ Silvestrini and colleagues⁴² localized the glucocorticoid receptor in rat bone cells, including chondrocytes. The glucocorticoid receptor was also localized by Abu and colleagues⁴³ in human growth plates, especially in hypertrophic chondrocytes, suggesting direct effects of glucocorticoids on the growth plate. An excess of glucocorticoids enhances bone resorption, inhibits osteoblast activity, and reduces bone matrix production to retard growth in children.^44,45 Excess glucocorticoids also induce apoptosis of osteoblasts and osteocytes in rabbit trabecular bone⁴⁶ and osteoblasts in rat long bones,⁴⁷ resulting in an almost complete absence of new bone formation.¹⁷ In addition, glucocorticoids induce sex hormone deficiency and alter vitamin D metabolism, leading to deleterious effects on growth and skeletal integrity.⁴⁸ Excess glucocorticoids modify the GH/IGF-1 pathway at different levels, suppressing growth.¹⁷ In contrast, low levels of glucocorticoids, as in familial glucocorticoid deficiency, are associated with tall stature.⁴⁹

Longitudinal bone growth is also based on sex hormones, especially during puberty.¹⁷ In rats, estrogen depletion stimulates longitudinal growth, whereas estrogen administration inhibits longitudinal growth.^50-52 Nilsson and colleagues⁵³ studied ovariectomized immature rabbits treated with either estrogen or the selective estrogen receptor modulator raloxifene and found reduced chondrocyte proliferation and growth plate height as well as accelerated growth plate senescence. Many experimental studies have concluded that estrogen can inhibit longitudinal growth in the absence of GH.^51,54,55

Androgens can directly influence growth plate function and may account for some skeletal differences between males and females.^56-58 Unlike estrogens, androgens stimulate longitudinal growth, as shown in several studies that assessed the effect of administering nonaromatizable androgens on longitudinal growth in boys with constitutionally delayed growth.^59,60

Local Regulation. Inh, a master regulator of bone development, coordinates chondrocyte proliferation, chondrocyte differentiation, and osteoblast differentiation.³¹ Inh belongs to the hedgehog protein family, which plays a crucial role in embryonic patterning and development.⁴ The proliferative effect of Inh is likely to be direct action on chondrocytes.³¹ In 1996, Vortkamp and colleagues⁶¹ reported that misexpression of Inh in chicken long bones blocked chondrocyte differentiation. More recently, St-Jacques and colleagues⁶² studied Inh-null mutant mice and found failure of both chondrocyte differentiation and osteoblast development. Inh is now thought to coordinate endochondral ossification, regulating chondrocyte proliferation and differentiation and osteoblast differentiation and coupling chondrogenesis and osteogenesis.^62,63

PTHrP acts primarily to keep proliferating chondrocytes in the proliferative pool.³¹ Mice that did not express PTHrP showed accelerated chondrocyte differentiation leading to dwarfism.⁶⁴ On the other hand, ectopic expression of PTHrP in the growth plate inhibited chondrocyte differentiation, resulting in a smaller cartilaginous skeleton compared with wild-type mice.⁶⁵ PTHrP appears to regulate the rate of programmed chondrocyte differentiation in developing endochondral bone and at the level of the growth plate.^64,66-69

The family of FGFs, which are major regulators of embryonic bone development, has at least 22 members.^70,71 Achondroplasia, the most common type of dwarfism, is caused by an activating mutation in FGF receptor 3 (FGFR3).^72-74 FGF18 deficiency also leads to delayed ossification and decreased expression of osteogenic markers.⁷⁵

Bone morphogenetic proteins (BMPs) are recognized as important regulators of growth, differentiation, and morphogenesis during embryology.⁷⁶ In 2001, Minina and colleagues⁷⁷ showed that normal chondrocyte proliferation requires parallel signaling of both Inh and BMPs and that BMPs can inhibit chondrocyte differentiation independently of the Inh/PTHrP pathway.

Vascular endothelial growth factor (VEGF), a chemoattractant for endothelial cells, is one of the most important growth factors for endothelial cells.⁷⁸ VEGF is a key player in the actions that occur during the end stage of endochondral bone formation; these actions include terminal differentiation of chondrocytes, vascular invasion, chondrocyte apoptosis, and replacement of chondrocytes with bone.^27,79,80 When Gerber and colleagues²⁷ inactivated VEGF in 24-day-old mice, they noticed suppressed blood vessel invasion and trabecular bone formation concomitant with an increased width of the hypertrophic zone.

Mechanical Regulation. Mechanical forces influence bone formation and adaptation.⁸¹ Growth rates from early infancy through late adolescence were found to be strongly correlated between an appropriate measure of mechanical loading (body size, or body weight–bone length) and bone strength (assessed by section modulus).⁸² The observation that compression inhibits bone growth was well known to the ancient Romans.⁸³ In the 19th century, the Hueter-Volkmann law was proclaimed. This law is well known to pediatric orthopedic surgeons and is the basis of growth modulation for correcting angular deformities of the lower extremities and spinal deformities.^4,84

If compression always inhibited bone growth, as it was believed, growth plates would be extremely unstable, as any slight deviation from the straight alignment of the long bones of the lower extremities would induce a vicious circle of positive feedback and result in catastrophic deformities.⁴ Mild compression leads to increased, not decreased, growth. Nevertheless, when compression on one side of the growth plate exceeds a certain level, growth is indeed suppressed, and the lesion begins to worsen.⁴

In 1997, Frost⁸⁵ proposed using a single graph that combines the clinical observation of mechanical forces affecting longitudinal bone growth. Both mild tension and mild compression induce bone growth, whereas heavy compression inhibits growth (Figure 3).

Three rules describe bone adaptation in mathematical terms. First, bone adaptation is driven by dynamic, not static, loading. Second, only a short period of mechanical loading is needed to initiate an adaptive response (extending the loading period has a diminishing effect on further bone adaptation). Third, bone cells accommodate to a customary mechanical loading environment, making them less responsive to routine loading signals.⁸¹

Also playing a significant role in bone physiology is the nervous system, with leptin-dependent central control of bone formation via the sympathetic system.⁸⁶ Several investigators have tried to determine the effect of muscle activity on bone growth in length.⁸⁷ Pottorf⁸⁸ in 1916 and Allison and Brooks⁸⁹ in 1921 were among the first to study this correlation; they concluded that long bones grow less after denervation. On the other hand, Ring⁹⁰ in 1961 reported that, despite innervation, longitudinal bone growth was increased. Investigators in more recent studies have advanced the idea that the nervous system plays a negative role in bone physiology. Dysart and colleagues⁸⁷ showed that muscle pull affects periosteal tension and, consequently, bone form and growth in length. In a clinical study involving 32 children with neonatal brachial plexus injury,⁹¹ the ratio of skewness between the affected humeral head and the contralateral normal head was calculated. Skewness was determined by dividing the anterior area of the humeral head by the posterior area. There was a significant preoperative difference between the 2 sides, but the skewness ratio was significantly improved after surgery.

Bone Growth in Width

Bone growth in width has not received as much attention as longitudinal bone growth. Several studies have indicated that body mass and muscle strength have important influences on long bone strength in children and adolescents.^92-97 As bone width changes only slowly after the growth period, bone growth in width is one of the most important determinants of bone strength throughout life.⁴ It is clear that, if bones grew in length without increasing in width, they would become unstable and break.⁴

Histologically, osteoblasts add mineralized tissue to the outer (periosteal) bone surface. This process is periosteal apposition.⁹⁸ The periosteum has an outer layer, composed mainly of fibrous tissue, and an inner layer, the cambium, which harbors osteogenic cells.⁴ In children, bone formation is continuous, which is the hallmark of modeling^99,100; in adults, periosteal bone may undergo cyclical resorption and formation, which are characteristic of remodeling.^101,102

Macroscopically, bone grows rapidly during early life; then, growth continuously slows down until reaching a nadir during early school age.⁴ It is clear that wider bones must have higher midshaft periosteal apposition rates, as this is how they become wider.^4,103

Regulation of Bone Growth in Width (Table)

Systemic Regulation. Periosteal apposition at diaphyseal bone sites is stimulated by androgen and GH and inhibited by estrogens.^104-106 In an experimental study, Turner and colleagues¹⁰⁴ found that androgen treatment stimulated bone formation in orchiectomized rats and suppressed bone formation in ovariectomized rats. A large dose of diethylstilbestrol also suppressed bone formation in ovariectomized rats. Parathyroid hormone is associated with faster periosteal expansion in adults, according to Parfitt.¹⁰⁷ In addition, nutrition with high calcium intake has the same effects on children, especially those with high levels of physical activity.¹⁰⁸

Local Regulation. Given that periosteal bone development is site-specific, whereas systemic hormones and nutrition are blind to structure,⁴ it is clear that local regulation is key to bone growth in width. Genetic heritage seems to have an overwhelming effect on periosteal bone development. Volkman and colleagues,¹⁰⁹ who experimented with various genetic markers in rats, concluded that genetic control of cortical bone geometry is complex and that femoral size and shape may be influenced by different but overlapping groups of polymorphic loci.

Mechanical Regulation. Mechanical forces seem to be very important in determining bone width. For example, the difference in width between femur and humerus can be explained by the different mechanical forces acting on each bone. This perspective is supported by Ruff,⁸² who showed that the correlation of body size (body weight–bone length) and bone strength is stronger in the femur than in the humerus.

The vital role of mechanical forces in bone growth in width is also supported by results of a study by Goodship and colleagues,¹¹⁰ who overloaded the radius of young pigs by partially removing the ulna. They showed that the radius was strengthened by rapid periosteal apposition. This effect has also been noticed in the clinical setting, when the tibia is replaced with the fibula, which quickly hypertrophies in order to resemble the tibia.¹¹¹

Conclusion

Longitudinal bone growth has been extensively studied. Systemic and local hormonal pathways control bone growth in a complicated regulation system. Mechanical loading is also strongly correlated with longitudinal bone growth. Bone growth in width has received less attention. Despite its importance in bone stability, periosteal development—and periosteal apposition and resorption more specifically—has not received enough attention. Researchers need to clarify the role of genetic factors affecting periosteal development.

Differences in bone size are established early in life, before puberty and perhaps even in utero.¹ Bone begins to form when mesenchymal cells form condensations—clusters of cells that adhere through expression of adhesion molecules² (Figure 1). Bone must be stiff, flexible enough to change shape to absorb energy, and light enough to allow mobility.^1,3 Longitudinal bone growth is detrimental to bone stability, but this effect is counteracted by concomitant bone growth in width.⁴ Bone growth in width has not been studied as extensively, despite its paramount role in skeletal development.⁵

Bone growth and development are products of the complex interactions of genetic and environmental factors, including diet, hormones, and mechanical stimuli.^6-9 Longitudinal bone growth is controlled by systemic and local hormones and local mechanical factors. Two models for control of bone growth in width have been suggested—the mechanostat theory (mechanical requirements regulate periosteal apposition) and the sizostat hypothesis (a master gene or set of genes regulates bone growth in width so bone reaches a preprogrammed size, independent of mechanical requirements).⁵

In this article, we review the most recent data regarding bone growth from the embryonic age and analyze the factors that control bone growth. An understanding of this complex system is important in identifying metabolic and developmental bone diseases¹⁰ and fracture risk.^11,12

Growth Plate

The growth plate consists mainly of collagen fibrils, proteoglycans, and water, arranged to form a sort of sponge with very small pores.¹³ The growth plate is located between epiphyseal and metaphyseal bone at the distal end of long bones¹⁴ and is strain-rate–dependent,^15,16 which means it is hard when squeezed rapidly but soft when deformed slowly. The growth plate becomes ossified after puberty and epiphyseal fusion.¹⁷

Histologically, the growth plate consists of horizontal zones of chondrocytes at different stages of differentiation.⁴ The germinal zone, at the epiphyseal end of the growth plate, contains resting chondrocytes, which seem crucial in orienting the underlying columns of chondrocytes and, therefore, in unidirectional bone growth, probably by secretion of a growth plate–orienting factor.^14,18 Next is the proliferative zone, a matrix-rich zone in which flattened chondrocytes undergo longitudinal cell division and orient themselves in typical column-wise fashion. At some point, proliferating chondrocytes lose their capacity to divide; they start to differentiate and become prehypertrophic, coinciding with a size increase.⁴ Proliferating chondrocytes are located in the transition (maturation or prehypertrophic) zone. In the hypertrophic zone, round chondrocytes secrete matrix proteins in large amounts.¹⁴ This stage is characterized by an increase in intracellular calcium concentration, which is essential in the production of matrix vesicles. These vesicles, small membrane-enclosed particles, are released from chondrocytes^19,20 and secrete calcium phosphates, hydroxyapatite, and matrix metalloproteinases, resulting in mineralization of the vesicles and their surrounding matrix.⁴ The chondrocytes in this mineralized zone eventually undergo programmed cell death (apoptosis), leaving a scaffold for new bone formation.

Longitudinal Bone Growth

Generally, bones increase in length as long as new material is being squeezed between the reserve zone of the growth plate and the zone of provisional calcification.⁴

Postnatal linear growth occurs in 3 phases. Phase 1 is characterized by a high rate of growth at the beginning of fetal life, and then rapid deceleration up to about 3 years; phase 2, by a lower, slowly decelerating growth rate up to puberty; and phase 3, by an increased rate of longitudinal growth until a peak is reached.^14,21,22

In 1964, Park²³ proposed that the structure of the epiphyseal cartilage may determine the pattern of the growing bone shaft. The changes within the hypertrophic zone are directly related to matrix mineralization, vascular invasion, and subsequent development.²⁴ Intracellular calcium concentration increases in the hypertrophic chondrocytes in the hypertrophic zone of growth plate cartilage; at some point, these chondrocytes begin to mineralize the longitudinal septa in the surrounding matrix²⁵ (Figure 2). At the growth cartilage junction, mononuclear cells of undetermined origin resorb the unmineralized horizontal septa of the growth cartilage. These cells are called septoclasts or chondroclasts.^25,26 Blood vessels invade the area and pave the way for bone cell precursors.²⁷ Eighty percent of the longitudinal septa of the growth cartilage is rapidly resorbed in the metaphyseal zone immediately behind the invading blood vessels, paving the way for bone cell precursors.²⁸ Fazzalari and colleagues²⁸ reported that about 40% of mineralized septa serves as scaffold for the formation of primary bone trabeculae; the other 60% is absorbed by chondroclasts (osteoclasts) near the vascular invasion front.

Regulation of Longitudinal Bone Growth

Longitudinal bone growth is regulated by genetic, hormonal, growth, and environment factors^17,29-31 (Table). It must be controlled on at least 3 different levels.⁴ Level 1 is systemic control by factors such as growth hormone (GH), sex hormones, and glucocorticoids. The major systemic hormones that control longitudinal bone growth during childhood are GH, insulin-like growth factor 1 (IGF-1), the thyroid hormones triiodothyronine (T₃) and thyroxine (T₄), and glucocorticoids; during puberty, the sex steroids play the most significant role.¹⁴ Level 2 is local control by factors such as Indian hedgehog (Inh), parathyroid hormone–related peptide (PTHrP), and fibroblast growth factors (FGFs).^14,31 Level 3 is mechanical control.⁴

Systemic Regulation. After birth, GH becomes an important modulator of longitudinal growth and appears to be, together with IGF-1, the central player in the hypothalamus–pituitary–growth plate axis.¹⁴ According to the original somatomedin hypothesis,³² GH stimulates hepatic production of IGF-1, which in turn promotes growth directly at the epiphyseal plate.¹⁷ GH acts on resting zone chondrocytes and is responsible for local IGF-1 production, which stimulates clonal expansion of proliferating chondrocytes in an autocrine/paracrine manner.³³ Infusion of GH or IGF-1 shortens stem- and proliferating-cell cycle times in the growth plate of hypophysectomized rats and decreases the duration of the hypertrophic differentiation phase, with GH being more effective.¹⁷ According to the experimental study of Hunziker and colleagues,³⁴ GH or IGF-1 treatment restores mean cell volume and height, but the growth rate is not normalized by either hormone.

Thyroid hormones also play a vital role in bone growth. T₃ and, to a lesser extent, T₄ are crucial in normal bone maturation.^30,35 Childhood hypothyroidism causes growth failure; growth failure may develop insidiously, but, once established, it is severe.¹⁷ On the other hand, hyperthyroidism increases the growth rate in children but also leads to premature growth plate fusion and short stature.^36,37 T₃ seems to stimulate recruitment of cells from the germinal zone to the proliferating zone and facilitates differentiation of growth plate chondrocytes.^38-40 Its precursor, T₄, increases the number of [³H]methylthymidine-labeled chondrocyte nuclei and [³⁵S]incorporation in Snell dwarf mice growth plates, suggesting a stimulatory role in chondrocyte proliferation and differentiation.⁴¹

Glucocorticoids suppress growth by modifying the GH/IGF-1 pathway at different levels.¹⁷ Silvestrini and colleagues⁴² localized the glucocorticoid receptor in rat bone cells, including chondrocytes. The glucocorticoid receptor was also localized by Abu and colleagues⁴³ in human growth plates, especially in hypertrophic chondrocytes, suggesting direct effects of glucocorticoids on the growth plate. An excess of glucocorticoids enhances bone resorption, inhibits osteoblast activity, and reduces bone matrix production to retard growth in children.^44,45 Excess glucocorticoids also induce apoptosis of osteoblasts and osteocytes in rabbit trabecular bone⁴⁶ and osteoblasts in rat long bones,⁴⁷ resulting in an almost complete absence of new bone formation.¹⁷ In addition, glucocorticoids induce sex hormone deficiency and alter vitamin D metabolism, leading to deleterious effects on growth and skeletal integrity.⁴⁸ Excess glucocorticoids modify the GH/IGF-1 pathway at different levels, suppressing growth.¹⁷ In contrast, low levels of glucocorticoids, as in familial glucocorticoid deficiency, are associated with tall stature.⁴⁹

Longitudinal bone growth is also based on sex hormones, especially during puberty.¹⁷ In rats, estrogen depletion stimulates longitudinal growth, whereas estrogen administration inhibits longitudinal growth.^50-52 Nilsson and colleagues⁵³ studied ovariectomized immature rabbits treated with either estrogen or the selective estrogen receptor modulator raloxifene and found reduced chondrocyte proliferation and growth plate height as well as accelerated growth plate senescence. Many experimental studies have concluded that estrogen can inhibit longitudinal growth in the absence of GH.^51,54,55

Androgens can directly influence growth plate function and may account for some skeletal differences between males and females.^56-58 Unlike estrogens, androgens stimulate longitudinal growth, as shown in several studies that assessed the effect of administering nonaromatizable androgens on longitudinal growth in boys with constitutionally delayed growth.^59,60

Local Regulation. Inh, a master regulator of bone development, coordinates chondrocyte proliferation, chondrocyte differentiation, and osteoblast differentiation.³¹ Inh belongs to the hedgehog protein family, which plays a crucial role in embryonic patterning and development.⁴ The proliferative effect of Inh is likely to be direct action on chondrocytes.³¹ In 1996, Vortkamp and colleagues⁶¹ reported that misexpression of Inh in chicken long bones blocked chondrocyte differentiation. More recently, St-Jacques and colleagues⁶² studied Inh-null mutant mice and found failure of both chondrocyte differentiation and osteoblast development. Inh is now thought to coordinate endochondral ossification, regulating chondrocyte proliferation and differentiation and osteoblast differentiation and coupling chondrogenesis and osteogenesis.^62,63

PTHrP acts primarily to keep proliferating chondrocytes in the proliferative pool.³¹ Mice that did not express PTHrP showed accelerated chondrocyte differentiation leading to dwarfism.⁶⁴ On the other hand, ectopic expression of PTHrP in the growth plate inhibited chondrocyte differentiation, resulting in a smaller cartilaginous skeleton compared with wild-type mice.⁶⁵ PTHrP appears to regulate the rate of programmed chondrocyte differentiation in developing endochondral bone and at the level of the growth plate.^64,66-69

The family of FGFs, which are major regulators of embryonic bone development, has at least 22 members.^70,71 Achondroplasia, the most common type of dwarfism, is caused by an activating mutation in FGF receptor 3 (FGFR3).^72-74 FGF18 deficiency also leads to delayed ossification and decreased expression of osteogenic markers.⁷⁵

Bone morphogenetic proteins (BMPs) are recognized as important regulators of growth, differentiation, and morphogenesis during embryology.⁷⁶ In 2001, Minina and colleagues⁷⁷ showed that normal chondrocyte proliferation requires parallel signaling of both Inh and BMPs and that BMPs can inhibit chondrocyte differentiation independently of the Inh/PTHrP pathway.

Vascular endothelial growth factor (VEGF), a chemoattractant for endothelial cells, is one of the most important growth factors for endothelial cells.⁷⁸ VEGF is a key player in the actions that occur during the end stage of endochondral bone formation; these actions include terminal differentiation of chondrocytes, vascular invasion, chondrocyte apoptosis, and replacement of chondrocytes with bone.^27,79,80 When Gerber and colleagues²⁷ inactivated VEGF in 24-day-old mice, they noticed suppressed blood vessel invasion and trabecular bone formation concomitant with an increased width of the hypertrophic zone.

Mechanical Regulation. Mechanical forces influence bone formation and adaptation.⁸¹ Growth rates from early infancy through late adolescence were found to be strongly correlated between an appropriate measure of mechanical loading (body size, or body weight–bone length) and bone strength (assessed by section modulus).⁸² The observation that compression inhibits bone growth was well known to the ancient Romans.⁸³ In the 19th century, the Hueter-Volkmann law was proclaimed. This law is well known to pediatric orthopedic surgeons and is the basis of growth modulation for correcting angular deformities of the lower extremities and spinal deformities.^4,84

If compression always inhibited bone growth, as it was believed, growth plates would be extremely unstable, as any slight deviation from the straight alignment of the long bones of the lower extremities would induce a vicious circle of positive feedback and result in catastrophic deformities.⁴ Mild compression leads to increased, not decreased, growth. Nevertheless, when compression on one side of the growth plate exceeds a certain level, growth is indeed suppressed, and the lesion begins to worsen.⁴

In 1997, Frost⁸⁵ proposed using a single graph that combines the clinical observation of mechanical forces affecting longitudinal bone growth. Both mild tension and mild compression induce bone growth, whereas heavy compression inhibits growth (Figure 3).

Three rules describe bone adaptation in mathematical terms. First, bone adaptation is driven by dynamic, not static, loading. Second, only a short period of mechanical loading is needed to initiate an adaptive response (extending the loading period has a diminishing effect on further bone adaptation). Third, bone cells accommodate to a customary mechanical loading environment, making them less responsive to routine loading signals.⁸¹

Also playing a significant role in bone physiology is the nervous system, with leptin-dependent central control of bone formation via the sympathetic system.⁸⁶ Several investigators have tried to determine the effect of muscle activity on bone growth in length.⁸⁷ Pottorf⁸⁸ in 1916 and Allison and Brooks⁸⁹ in 1921 were among the first to study this correlation; they concluded that long bones grow less after denervation. On the other hand, Ring⁹⁰ in 1961 reported that, despite innervation, longitudinal bone growth was increased. Investigators in more recent studies have advanced the idea that the nervous system plays a negative role in bone physiology. Dysart and colleagues⁸⁷ showed that muscle pull affects periosteal tension and, consequently, bone form and growth in length. In a clinical study involving 32 children with neonatal brachial plexus injury,⁹¹ the ratio of skewness between the affected humeral head and the contralateral normal head was calculated. Skewness was determined by dividing the anterior area of the humeral head by the posterior area. There was a significant preoperative difference between the 2 sides, but the skewness ratio was significantly improved after surgery.

Bone Growth in Width

Bone growth in width has not received as much attention as longitudinal bone growth. Several studies have indicated that body mass and muscle strength have important influences on long bone strength in children and adolescents.^92-97 As bone width changes only slowly after the growth period, bone growth in width is one of the most important determinants of bone strength throughout life.⁴ It is clear that, if bones grew in length without increasing in width, they would become unstable and break.⁴

Histologically, osteoblasts add mineralized tissue to the outer (periosteal) bone surface. This process is periosteal apposition.⁹⁸ The periosteum has an outer layer, composed mainly of fibrous tissue, and an inner layer, the cambium, which harbors osteogenic cells.⁴ In children, bone formation is continuous, which is the hallmark of modeling^99,100; in adults, periosteal bone may undergo cyclical resorption and formation, which are characteristic of remodeling.^101,102

Macroscopically, bone grows rapidly during early life; then, growth continuously slows down until reaching a nadir during early school age.⁴ It is clear that wider bones must have higher midshaft periosteal apposition rates, as this is how they become wider.^4,103

Regulation of Bone Growth in Width (Table)

Systemic Regulation. Periosteal apposition at diaphyseal bone sites is stimulated by androgen and GH and inhibited by estrogens.^104-106 In an experimental study, Turner and colleagues¹⁰⁴ found that androgen treatment stimulated bone formation in orchiectomized rats and suppressed bone formation in ovariectomized rats. A large dose of diethylstilbestrol also suppressed bone formation in ovariectomized rats. Parathyroid hormone is associated with faster periosteal expansion in adults, according to Parfitt.¹⁰⁷ In addition, nutrition with high calcium intake has the same effects on children, especially those with high levels of physical activity.¹⁰⁸

Local Regulation. Given that periosteal bone development is site-specific, whereas systemic hormones and nutrition are blind to structure,⁴ it is clear that local regulation is key to bone growth in width. Genetic heritage seems to have an overwhelming effect on periosteal bone development. Volkman and colleagues,¹⁰⁹ who experimented with various genetic markers in rats, concluded that genetic control of cortical bone geometry is complex and that femoral size and shape may be influenced by different but overlapping groups of polymorphic loci.

Mechanical Regulation. Mechanical forces seem to be very important in determining bone width. For example, the difference in width between femur and humerus can be explained by the different mechanical forces acting on each bone. This perspective is supported by Ruff,⁸² who showed that the correlation of body size (body weight–bone length) and bone strength is stronger in the femur than in the humerus.

The vital role of mechanical forces in bone growth in width is also supported by results of a study by Goodship and colleagues,¹¹⁰ who overloaded the radius of young pigs by partially removing the ulna. They showed that the radius was strengthened by rapid periosteal apposition. This effect has also been noticed in the clinical setting, when the tibia is replaced with the fibula, which quickly hypertrophies in order to resemble the tibia.¹¹¹

Conclusion

Longitudinal bone growth has been extensively studied. Systemic and local hormonal pathways control bone growth in a complicated regulation system. Mechanical loading is also strongly correlated with longitudinal bone growth. Bone growth in width has received less attention. Despite its importance in bone stability, periosteal development—and periosteal apposition and resorption more specifically—has not received enough attention. Researchers need to clarify the role of genetic factors affecting periosteal development.

Differences in bone size are established early in life, before puberty and perhaps even in utero.¹ Bone begins to form when mesenchymal cells form condensations—clusters of cells that adhere through expression of adhesion molecules² (Figure 1). Bone must be stiff, flexible enough to change shape to absorb energy, and light enough to allow mobility.^1,3 Longitudinal bone growth is detrimental to bone stability, but this effect is counteracted by concomitant bone growth in width.⁴ Bone growth in width has not been studied as extensively, despite its paramount role in skeletal development.⁵

Bone growth and development are products of the complex interactions of genetic and environmental factors, including diet, hormones, and mechanical stimuli.^6-9 Longitudinal bone growth is controlled by systemic and local hormones and local mechanical factors. Two models for control of bone growth in width have been suggested—the mechanostat theory (mechanical requirements regulate periosteal apposition) and the sizostat hypothesis (a master gene or set of genes regulates bone growth in width so bone reaches a preprogrammed size, independent of mechanical requirements).⁵

In this article, we review the most recent data regarding bone growth from the embryonic age and analyze the factors that control bone growth. An understanding of this complex system is important in identifying metabolic and developmental bone diseases¹⁰ and fracture risk.^11,12

Growth Plate

The growth plate consists mainly of collagen fibrils, proteoglycans, and water, arranged to form a sort of sponge with very small pores.¹³ The growth plate is located between epiphyseal and metaphyseal bone at the distal end of long bones¹⁴ and is strain-rate–dependent,^15,16 which means it is hard when squeezed rapidly but soft when deformed slowly. The growth plate becomes ossified after puberty and epiphyseal fusion.¹⁷

Histologically, the growth plate consists of horizontal zones of chondrocytes at different stages of differentiation.⁴ The germinal zone, at the epiphyseal end of the growth plate, contains resting chondrocytes, which seem crucial in orienting the underlying columns of chondrocytes and, therefore, in unidirectional bone growth, probably by secretion of a growth plate–orienting factor.^14,18 Next is the proliferative zone, a matrix-rich zone in which flattened chondrocytes undergo longitudinal cell division and orient themselves in typical column-wise fashion. At some point, proliferating chondrocytes lose their capacity to divide; they start to differentiate and become prehypertrophic, coinciding with a size increase.⁴ Proliferating chondrocytes are located in the transition (maturation or prehypertrophic) zone. In the hypertrophic zone, round chondrocytes secrete matrix proteins in large amounts.¹⁴ This stage is characterized by an increase in intracellular calcium concentration, which is essential in the production of matrix vesicles. These vesicles, small membrane-enclosed particles, are released from chondrocytes^19,20 and secrete calcium phosphates, hydroxyapatite, and matrix metalloproteinases, resulting in mineralization of the vesicles and their surrounding matrix.⁴ The chondrocytes in this mineralized zone eventually undergo programmed cell death (apoptosis), leaving a scaffold for new bone formation.

Longitudinal Bone Growth

Generally, bones increase in length as long as new material is being squeezed between the reserve zone of the growth plate and the zone of provisional calcification.⁴

Postnatal linear growth occurs in 3 phases. Phase 1 is characterized by a high rate of growth at the beginning of fetal life, and then rapid deceleration up to about 3 years; phase 2, by a lower, slowly decelerating growth rate up to puberty; and phase 3, by an increased rate of longitudinal growth until a peak is reached.^14,21,22

In 1964, Park²³ proposed that the structure of the epiphyseal cartilage may determine the pattern of the growing bone shaft. The changes within the hypertrophic zone are directly related to matrix mineralization, vascular invasion, and subsequent development.²⁴ Intracellular calcium concentration increases in the hypertrophic chondrocytes in the hypertrophic zone of growth plate cartilage; at some point, these chondrocytes begin to mineralize the longitudinal septa in the surrounding matrix²⁵ (Figure 2). At the growth cartilage junction, mononuclear cells of undetermined origin resorb the unmineralized horizontal septa of the growth cartilage. These cells are called septoclasts or chondroclasts.^25,26 Blood vessels invade the area and pave the way for bone cell precursors.²⁷ Eighty percent of the longitudinal septa of the growth cartilage is rapidly resorbed in the metaphyseal zone immediately behind the invading blood vessels, paving the way for bone cell precursors.²⁸ Fazzalari and colleagues²⁸ reported that about 40% of mineralized septa serves as scaffold for the formation of primary bone trabeculae; the other 60% is absorbed by chondroclasts (osteoclasts) near the vascular invasion front.

Regulation of Longitudinal Bone Growth

Longitudinal bone growth is regulated by genetic, hormonal, growth, and environment factors^17,29-31 (Table). It must be controlled on at least 3 different levels.⁴ Level 1 is systemic control by factors such as growth hormone (GH), sex hormones, and glucocorticoids. The major systemic hormones that control longitudinal bone growth during childhood are GH, insulin-like growth factor 1 (IGF-1), the thyroid hormones triiodothyronine (T₃) and thyroxine (T₄), and glucocorticoids; during puberty, the sex steroids play the most significant role.¹⁴ Level 2 is local control by factors such as Indian hedgehog (Inh), parathyroid hormone–related peptide (PTHrP), and fibroblast growth factors (FGFs).^14,31 Level 3 is mechanical control.⁴

Systemic Regulation. After birth, GH becomes an important modulator of longitudinal growth and appears to be, together with IGF-1, the central player in the hypothalamus–pituitary–growth plate axis.¹⁴ According to the original somatomedin hypothesis,³² GH stimulates hepatic production of IGF-1, which in turn promotes growth directly at the epiphyseal plate.¹⁷ GH acts on resting zone chondrocytes and is responsible for local IGF-1 production, which stimulates clonal expansion of proliferating chondrocytes in an autocrine/paracrine manner.³³ Infusion of GH or IGF-1 shortens stem- and proliferating-cell cycle times in the growth plate of hypophysectomized rats and decreases the duration of the hypertrophic differentiation phase, with GH being more effective.¹⁷ According to the experimental study of Hunziker and colleagues,³⁴ GH or IGF-1 treatment restores mean cell volume and height, but the growth rate is not normalized by either hormone.

Thyroid hormones also play a vital role in bone growth. T₃ and, to a lesser extent, T₄ are crucial in normal bone maturation.^30,35 Childhood hypothyroidism causes growth failure; growth failure may develop insidiously, but, once established, it is severe.¹⁷ On the other hand, hyperthyroidism increases the growth rate in children but also leads to premature growth plate fusion and short stature.^36,37 T₃ seems to stimulate recruitment of cells from the germinal zone to the proliferating zone and facilitates differentiation of growth plate chondrocytes.^38-40 Its precursor, T₄, increases the number of [³H]methylthymidine-labeled chondrocyte nuclei and [³⁵S]incorporation in Snell dwarf mice growth plates, suggesting a stimulatory role in chondrocyte proliferation and differentiation.⁴¹

Glucocorticoids suppress growth by modifying the GH/IGF-1 pathway at different levels.¹⁷ Silvestrini and colleagues⁴² localized the glucocorticoid receptor in rat bone cells, including chondrocytes. The glucocorticoid receptor was also localized by Abu and colleagues⁴³ in human growth plates, especially in hypertrophic chondrocytes, suggesting direct effects of glucocorticoids on the growth plate. An excess of glucocorticoids enhances bone resorption, inhibits osteoblast activity, and reduces bone matrix production to retard growth in children.^44,45 Excess glucocorticoids also induce apoptosis of osteoblasts and osteocytes in rabbit trabecular bone⁴⁶ and osteoblasts in rat long bones,⁴⁷ resulting in an almost complete absence of new bone formation.¹⁷ In addition, glucocorticoids induce sex hormone deficiency and alter vitamin D metabolism, leading to deleterious effects on growth and skeletal integrity.⁴⁸ Excess glucocorticoids modify the GH/IGF-1 pathway at different levels, suppressing growth.¹⁷ In contrast, low levels of glucocorticoids, as in familial glucocorticoid deficiency, are associated with tall stature.⁴⁹

Longitudinal bone growth is also based on sex hormones, especially during puberty.¹⁷ In rats, estrogen depletion stimulates longitudinal growth, whereas estrogen administration inhibits longitudinal growth.^50-52 Nilsson and colleagues⁵³ studied ovariectomized immature rabbits treated with either estrogen or the selective estrogen receptor modulator raloxifene and found reduced chondrocyte proliferation and growth plate height as well as accelerated growth plate senescence. Many experimental studies have concluded that estrogen can inhibit longitudinal growth in the absence of GH.^51,54,55

Androgens can directly influence growth plate function and may account for some skeletal differences between males and females.^56-58 Unlike estrogens, androgens stimulate longitudinal growth, as shown in several studies that assessed the effect of administering nonaromatizable androgens on longitudinal growth in boys with constitutionally delayed growth.^59,60

Local Regulation. Inh, a master regulator of bone development, coordinates chondrocyte proliferation, chondrocyte differentiation, and osteoblast differentiation.³¹ Inh belongs to the hedgehog protein family, which plays a crucial role in embryonic patterning and development.⁴ The proliferative effect of Inh is likely to be direct action on chondrocytes.³¹ In 1996, Vortkamp and colleagues⁶¹ reported that misexpression of Inh in chicken long bones blocked chondrocyte differentiation. More recently, St-Jacques and colleagues⁶² studied Inh-null mutant mice and found failure of both chondrocyte differentiation and osteoblast development. Inh is now thought to coordinate endochondral ossification, regulating chondrocyte proliferation and differentiation and osteoblast differentiation and coupling chondrogenesis and osteogenesis.^62,63

PTHrP acts primarily to keep proliferating chondrocytes in the proliferative pool.³¹ Mice that did not express PTHrP showed accelerated chondrocyte differentiation leading to dwarfism.⁶⁴ On the other hand, ectopic expression of PTHrP in the growth plate inhibited chondrocyte differentiation, resulting in a smaller cartilaginous skeleton compared with wild-type mice.⁶⁵ PTHrP appears to regulate the rate of programmed chondrocyte differentiation in developing endochondral bone and at the level of the growth plate.^64,66-69

The family of FGFs, which are major regulators of embryonic bone development, has at least 22 members.^70,71 Achondroplasia, the most common type of dwarfism, is caused by an activating mutation in FGF receptor 3 (FGFR3).^72-74 FGF18 deficiency also leads to delayed ossification and decreased expression of osteogenic markers.⁷⁵

Bone morphogenetic proteins (BMPs) are recognized as important regulators of growth, differentiation, and morphogenesis during embryology.⁷⁶ In 2001, Minina and colleagues⁷⁷ showed that normal chondrocyte proliferation requires parallel signaling of both Inh and BMPs and that BMPs can inhibit chondrocyte differentiation independently of the Inh/PTHrP pathway.

Vascular endothelial growth factor (VEGF), a chemoattractant for endothelial cells, is one of the most important growth factors for endothelial cells.⁷⁸ VEGF is a key player in the actions that occur during the end stage of endochondral bone formation; these actions include terminal differentiation of chondrocytes, vascular invasion, chondrocyte apoptosis, and replacement of chondrocytes with bone.^27,79,80 When Gerber and colleagues²⁷ inactivated VEGF in 24-day-old mice, they noticed suppressed blood vessel invasion and trabecular bone formation concomitant with an increased width of the hypertrophic zone.

Mechanical Regulation. Mechanical forces influence bone formation and adaptation.⁸¹ Growth rates from early infancy through late adolescence were found to be strongly correlated between an appropriate measure of mechanical loading (body size, or body weight–bone length) and bone strength (assessed by section modulus).⁸² The observation that compression inhibits bone growth was well known to the ancient Romans.⁸³ In the 19th century, the Hueter-Volkmann law was proclaimed. This law is well known to pediatric orthopedic surgeons and is the basis of growth modulation for correcting angular deformities of the lower extremities and spinal deformities.^4,84

If compression always inhibited bone growth, as it was believed, growth plates would be extremely unstable, as any slight deviation from the straight alignment of the long bones of the lower extremities would induce a vicious circle of positive feedback and result in catastrophic deformities.⁴ Mild compression leads to increased, not decreased, growth. Nevertheless, when compression on one side of the growth plate exceeds a certain level, growth is indeed suppressed, and the lesion begins to worsen.⁴

In 1997, Frost⁸⁵ proposed using a single graph that combines the clinical observation of mechanical forces affecting longitudinal bone growth. Both mild tension and mild compression induce bone growth, whereas heavy compression inhibits growth (Figure 3).

Three rules describe bone adaptation in mathematical terms. First, bone adaptation is driven by dynamic, not static, loading. Second, only a short period of mechanical loading is needed to initiate an adaptive response (extending the loading period has a diminishing effect on further bone adaptation). Third, bone cells accommodate to a customary mechanical loading environment, making them less responsive to routine loading signals.⁸¹

Also playing a significant role in bone physiology is the nervous system, with leptin-dependent central control of bone formation via the sympathetic system.⁸⁶ Several investigators have tried to determine the effect of muscle activity on bone growth in length.⁸⁷ Pottorf⁸⁸ in 1916 and Allison and Brooks⁸⁹ in 1921 were among the first to study this correlation; they concluded that long bones grow less after denervation. On the other hand, Ring⁹⁰ in 1961 reported that, despite innervation, longitudinal bone growth was increased. Investigators in more recent studies have advanced the idea that the nervous system plays a negative role in bone physiology. Dysart and colleagues⁸⁷ showed that muscle pull affects periosteal tension and, consequently, bone form and growth in length. In a clinical study involving 32 children with neonatal brachial plexus injury,⁹¹ the ratio of skewness between the affected humeral head and the contralateral normal head was calculated. Skewness was determined by dividing the anterior area of the humeral head by the posterior area. There was a significant preoperative difference between the 2 sides, but the skewness ratio was significantly improved after surgery.

Bone Growth in Width

Bone growth in width has not received as much attention as longitudinal bone growth. Several studies have indicated that body mass and muscle strength have important influences on long bone strength in children and adolescents.^92-97 As bone width changes only slowly after the growth period, bone growth in width is one of the most important determinants of bone strength throughout life.⁴ It is clear that, if bones grew in length without increasing in width, they would become unstable and break.⁴

Histologically, osteoblasts add mineralized tissue to the outer (periosteal) bone surface. This process is periosteal apposition.⁹⁸ The periosteum has an outer layer, composed mainly of fibrous tissue, and an inner layer, the cambium, which harbors osteogenic cells.⁴ In children, bone formation is continuous, which is the hallmark of modeling^99,100; in adults, periosteal bone may undergo cyclical resorption and formation, which are characteristic of remodeling.^101,102

Macroscopically, bone grows rapidly during early life; then, growth continuously slows down until reaching a nadir during early school age.⁴ It is clear that wider bones must have higher midshaft periosteal apposition rates, as this is how they become wider.^4,103

Regulation of Bone Growth in Width (Table)

Systemic Regulation. Periosteal apposition at diaphyseal bone sites is stimulated by androgen and GH and inhibited by estrogens.^104-106 In an experimental study, Turner and colleagues¹⁰⁴ found that androgen treatment stimulated bone formation in orchiectomized rats and suppressed bone formation in ovariectomized rats. A large dose of diethylstilbestrol also suppressed bone formation in ovariectomized rats. Parathyroid hormone is associated with faster periosteal expansion in adults, according to Parfitt.¹⁰⁷ In addition, nutrition with high calcium intake has the same effects on children, especially those with high levels of physical activity.¹⁰⁸

Local Regulation. Given that periosteal bone development is site-specific, whereas systemic hormones and nutrition are blind to structure,⁴ it is clear that local regulation is key to bone growth in width. Genetic heritage seems to have an overwhelming effect on periosteal bone development. Volkman and colleagues,¹⁰⁹ who experimented with various genetic markers in rats, concluded that genetic control of cortical bone geometry is complex and that femoral size and shape may be influenced by different but overlapping groups of polymorphic loci.

Mechanical Regulation. Mechanical forces seem to be very important in determining bone width. For example, the difference in width between femur and humerus can be explained by the different mechanical forces acting on each bone. This perspective is supported by Ruff,⁸² who showed that the correlation of body size (body weight–bone length) and bone strength is stronger in the femur than in the humerus.

The vital role of mechanical forces in bone growth in width is also supported by results of a study by Goodship and colleagues,¹¹⁰ who overloaded the radius of young pigs by partially removing the ulna. They showed that the radius was strengthened by rapid periosteal apposition. This effect has also been noticed in the clinical setting, when the tibia is replaced with the fibula, which quickly hypertrophies in order to resemble the tibia.¹¹¹

Conclusion

Longitudinal bone growth has been extensively studied. Systemic and local hormonal pathways control bone growth in a complicated regulation system. Mechanical loading is also strongly correlated with longitudinal bone growth. Bone growth in width has received less attention. Despite its importance in bone stability, periosteal development—and periosteal apposition and resorption more specifically—has not received enough attention. Researchers need to clarify the role of genetic factors affecting periosteal development.

The orthopedic community continues to be concerned about venous thromboembolism (VTE) after orthopedic procedures. There is currently no consensus on the optimal strategy for prevention of VTE after knee and hip arthroplasty. In North America, the American Association of Orthopaedic Surgeons (AAOS) and the American College of Chest Physicians (ACCP) have both been involved in putting forth guidelines that are intended to minimize this complication after orthopedic procedures.^1-2

Both of these guidelines have evaluated the available literature, whenever present, to reach their recommendations. Although the AAOS guidelines do not mention aspirin specifically, they do endorse any form of anticoagulation as acceptable after total hip and knee arthroplasty. The ACCP, on the other hand, gives their highest endorsement (1B) to aspirin as an effective prophylactic agent for prevention of VTE after total joint arthroplasty (TJA).¹ In the analysis, surgeon choice of VTE prophylaxis should be based on a balance between safety and efficacy of a particular anticoagulant, with risk stratification used to identify patients at standard risk (the vast majority) or high risk of VTE or bleeding.

Recent studies have helped to dispel the age-old misconception that aspirin is an effective modality for prevention of clots in the high-pressure (arterial) system but not in the low-pressure (venous) system. The ASPIRE study evaluated 822 patients and detected that the incidence of VTE was 4.8% in patients who received aspirin versus 6.5% in patients who did not receive aspirin.³ Although the difference in the incidence of VTE in the given sample size did not reach statistical significance, the difference did reach statistical significance when other major vascular issues were taken into account.³ Another study (WARFASA), evaluating 402 patients with prior VTE, detected 42% reduction in the incidence of recurrent VTE in patients that received aspirin, confirming the fact that aspirin does indeed act on the venous low-pressure system.⁴

The prevailing evidence over the last decade supports the notion that aspirin is an effective agent for prevention of VTE with a lower risk of imparting many of the harms that other aggressive anticoagulant agents are likely to cause, such as wound drainage, bleeding, increased incidence of readmission, reoperation, periprosthetic infection, and even mortality.^5-7

With the increasing scrutiny and penalties imposed on surgeons and health care systems by the regulatory bodies in the United States for a variety of “quality metric” considerations related to readmission and reoperation, including VTE prevention and its complications, the notion of using anticoagulant agents that are not only effective but also less harmful is gaining momentum and greater endorsement. Visiting the US Food and Drug Administration website reveals that among all drugs in the medical community, aggressive anticoagulants are associated with the highest number of adverse effects, including mortality.⁸

The medical community also needs to recognize that there have been immense changes in the practice of orthopedics, particularly in the realm of knee and hip arthroplasty. The majority of patients undergoing TJA receive regional anesthesia, using expeditious surgical techniques, and are mobilized immediately in the postoperative period—all of these elements have contributed to a declining incidence of VTE after TJA. Furthermore, patients are often discharged from the hospital within a day or two, making compliance with outpatient anticoagulant therapy more of a challenge. Thus, the historical protocols related to TJA—when patients stayed in bed for days before beginning a delayed and limited physical therapy program and a lengthy hospital stay—are behind us. These major changes in surgical and anesthesia techniques as well as accelerated postoperative protocols highlight the fact that any literature from the far past needs to be examined with caution as it may not be applicable to modern-day surgical patients.

Moving forward, while we strongly endorse risk stratification for VTE prophylaxis, in our opinion aspirin will become the mainstay of prevention of VTE for the majority of patients after TJA. The challenge that lies ahead is to determine which patients are at increased risk of VTE and in need of more aggressive anticoagulants. There has been a recent development on this front that aims to provide some guidance for selection of high-risk patients.⁹ It appears that over 90% of patients undergoing TJA can safely receive aspirin as an anticoagulation prophylaxis, while a validated risk profile can be used to detect those at higher risk for VTE and in need of more aggressive agents.⁹

Thanks to the diligent work of the ACCP and AAOS workgroups and many other scholars in the field, the science of VTE prophylaxis after TJA has truly evolved. The adaptation of the recent ACCP guidelines by the Surgical Care Improvement Project (SCIP), which accepts aspirin as an effective anticoagulation modality, is yet another step in the direction of optimizing outcomes for our patients, by preventing the feared VTE while also limiting untoward bleeding complications that can occur with administration of aggressive anticoagulants.¹⁰

The orthopedic community continues to be concerned about venous thromboembolism (VTE) after orthopedic procedures. There is currently no consensus on the optimal strategy for prevention of VTE after knee and hip arthroplasty. In North America, the American Association of Orthopaedic Surgeons (AAOS) and the American College of Chest Physicians (ACCP) have both been involved in putting forth guidelines that are intended to minimize this complication after orthopedic procedures.^1-2

Both of these guidelines have evaluated the available literature, whenever present, to reach their recommendations. Although the AAOS guidelines do not mention aspirin specifically, they do endorse any form of anticoagulation as acceptable after total hip and knee arthroplasty. The ACCP, on the other hand, gives their highest endorsement (1B) to aspirin as an effective prophylactic agent for prevention of VTE after total joint arthroplasty (TJA).¹ In the analysis, surgeon choice of VTE prophylaxis should be based on a balance between safety and efficacy of a particular anticoagulant, with risk stratification used to identify patients at standard risk (the vast majority) or high risk of VTE or bleeding.

Recent studies have helped to dispel the age-old misconception that aspirin is an effective modality for prevention of clots in the high-pressure (arterial) system but not in the low-pressure (venous) system. The ASPIRE study evaluated 822 patients and detected that the incidence of VTE was 4.8% in patients who received aspirin versus 6.5% in patients who did not receive aspirin.³ Although the difference in the incidence of VTE in the given sample size did not reach statistical significance, the difference did reach statistical significance when other major vascular issues were taken into account.³ Another study (WARFASA), evaluating 402 patients with prior VTE, detected 42% reduction in the incidence of recurrent VTE in patients that received aspirin, confirming the fact that aspirin does indeed act on the venous low-pressure system.⁴

The prevailing evidence over the last decade supports the notion that aspirin is an effective agent for prevention of VTE with a lower risk of imparting many of the harms that other aggressive anticoagulant agents are likely to cause, such as wound drainage, bleeding, increased incidence of readmission, reoperation, periprosthetic infection, and even mortality.^5-7

With the increasing scrutiny and penalties imposed on surgeons and health care systems by the regulatory bodies in the United States for a variety of “quality metric” considerations related to readmission and reoperation, including VTE prevention and its complications, the notion of using anticoagulant agents that are not only effective but also less harmful is gaining momentum and greater endorsement. Visiting the US Food and Drug Administration website reveals that among all drugs in the medical community, aggressive anticoagulants are associated with the highest number of adverse effects, including mortality.⁸

The medical community also needs to recognize that there have been immense changes in the practice of orthopedics, particularly in the realm of knee and hip arthroplasty. The majority of patients undergoing TJA receive regional anesthesia, using expeditious surgical techniques, and are mobilized immediately in the postoperative period—all of these elements have contributed to a declining incidence of VTE after TJA. Furthermore, patients are often discharged from the hospital within a day or two, making compliance with outpatient anticoagulant therapy more of a challenge. Thus, the historical protocols related to TJA—when patients stayed in bed for days before beginning a delayed and limited physical therapy program and a lengthy hospital stay—are behind us. These major changes in surgical and anesthesia techniques as well as accelerated postoperative protocols highlight the fact that any literature from the far past needs to be examined with caution as it may not be applicable to modern-day surgical patients.

Moving forward, while we strongly endorse risk stratification for VTE prophylaxis, in our opinion aspirin will become the mainstay of prevention of VTE for the majority of patients after TJA. The challenge that lies ahead is to determine which patients are at increased risk of VTE and in need of more aggressive anticoagulants. There has been a recent development on this front that aims to provide some guidance for selection of high-risk patients.⁹ It appears that over 90% of patients undergoing TJA can safely receive aspirin as an anticoagulation prophylaxis, while a validated risk profile can be used to detect those at higher risk for VTE and in need of more aggressive agents.⁹

Thanks to the diligent work of the ACCP and AAOS workgroups and many other scholars in the field, the science of VTE prophylaxis after TJA has truly evolved. The adaptation of the recent ACCP guidelines by the Surgical Care Improvement Project (SCIP), which accepts aspirin as an effective anticoagulation modality, is yet another step in the direction of optimizing outcomes for our patients, by preventing the feared VTE while also limiting untoward bleeding complications that can occur with administration of aggressive anticoagulants.¹⁰

The orthopedic community continues to be concerned about venous thromboembolism (VTE) after orthopedic procedures. There is currently no consensus on the optimal strategy for prevention of VTE after knee and hip arthroplasty. In North America, the American Association of Orthopaedic Surgeons (AAOS) and the American College of Chest Physicians (ACCP) have both been involved in putting forth guidelines that are intended to minimize this complication after orthopedic procedures.^1-2

Both of these guidelines have evaluated the available literature, whenever present, to reach their recommendations. Although the AAOS guidelines do not mention aspirin specifically, they do endorse any form of anticoagulation as acceptable after total hip and knee arthroplasty. The ACCP, on the other hand, gives their highest endorsement (1B) to aspirin as an effective prophylactic agent for prevention of VTE after total joint arthroplasty (TJA).¹ In the analysis, surgeon choice of VTE prophylaxis should be based on a balance between safety and efficacy of a particular anticoagulant, with risk stratification used to identify patients at standard risk (the vast majority) or high risk of VTE or bleeding.

Recent studies have helped to dispel the age-old misconception that aspirin is an effective modality for prevention of clots in the high-pressure (arterial) system but not in the low-pressure (venous) system. The ASPIRE study evaluated 822 patients and detected that the incidence of VTE was 4.8% in patients who received aspirin versus 6.5% in patients who did not receive aspirin.³ Although the difference in the incidence of VTE in the given sample size did not reach statistical significance, the difference did reach statistical significance when other major vascular issues were taken into account.³ Another study (WARFASA), evaluating 402 patients with prior VTE, detected 42% reduction in the incidence of recurrent VTE in patients that received aspirin, confirming the fact that aspirin does indeed act on the venous low-pressure system.⁴

The prevailing evidence over the last decade supports the notion that aspirin is an effective agent for prevention of VTE with a lower risk of imparting many of the harms that other aggressive anticoagulant agents are likely to cause, such as wound drainage, bleeding, increased incidence of readmission, reoperation, periprosthetic infection, and even mortality.^5-7

With the increasing scrutiny and penalties imposed on surgeons and health care systems by the regulatory bodies in the United States for a variety of “quality metric” considerations related to readmission and reoperation, including VTE prevention and its complications, the notion of using anticoagulant agents that are not only effective but also less harmful is gaining momentum and greater endorsement. Visiting the US Food and Drug Administration website reveals that among all drugs in the medical community, aggressive anticoagulants are associated with the highest number of adverse effects, including mortality.⁸

The medical community also needs to recognize that there have been immense changes in the practice of orthopedics, particularly in the realm of knee and hip arthroplasty. The majority of patients undergoing TJA receive regional anesthesia, using expeditious surgical techniques, and are mobilized immediately in the postoperative period—all of these elements have contributed to a declining incidence of VTE after TJA. Furthermore, patients are often discharged from the hospital within a day or two, making compliance with outpatient anticoagulant therapy more of a challenge. Thus, the historical protocols related to TJA—when patients stayed in bed for days before beginning a delayed and limited physical therapy program and a lengthy hospital stay—are behind us. These major changes in surgical and anesthesia techniques as well as accelerated postoperative protocols highlight the fact that any literature from the far past needs to be examined with caution as it may not be applicable to modern-day surgical patients.

Moving forward, while we strongly endorse risk stratification for VTE prophylaxis, in our opinion aspirin will become the mainstay of prevention of VTE for the majority of patients after TJA. The challenge that lies ahead is to determine which patients are at increased risk of VTE and in need of more aggressive anticoagulants. There has been a recent development on this front that aims to provide some guidance for selection of high-risk patients.⁹ It appears that over 90% of patients undergoing TJA can safely receive aspirin as an anticoagulation prophylaxis, while a validated risk profile can be used to detect those at higher risk for VTE and in need of more aggressive agents.⁹

Thanks to the diligent work of the ACCP and AAOS workgroups and many other scholars in the field, the science of VTE prophylaxis after TJA has truly evolved. The adaptation of the recent ACCP guidelines by the Surgical Care Improvement Project (SCIP), which accepts aspirin as an effective anticoagulation modality, is yet another step in the direction of optimizing outcomes for our patients, by preventing the feared VTE while also limiting untoward bleeding complications that can occur with administration of aggressive anticoagulants.¹⁰

Proximal humerus fractures (PHFs), AO/OTA (Ar­ beitsgemeinschaft für Osteosynthesefragen/Orthopaedic Trauma Association) type 11,¹ are common, representing 4% to 5% of all fractures in adults.² However, there is no consensus as to optimal management of these injuries, with some reports supporting and others rejecting the various fixation methods,³ and there are no evidence-based practice guidelines informing treatment decisions.⁴ Not surprisingly, orthopedic surgeons do not agree on ideal treatment for PHFs^5,6 and differ by region in their rates of surgical management.² In addition, analyses of national databases have found variation in choice of surgical treatment for PHFs between surgeons and between hospitals of different patient volumes.⁴ Few studies have assessed surgeon agreement on treatment decisions. Findings from these limited investigations indicate there is little agreement on treatment choices, but training may have some impact.^5-7 In 3 studies,^5-7 shoulder and trauma fellowship–trained surgeons differed in their management of PHFs both in terms of rates of operative treatment^5,7 and specific operative management choices.^5,6 No study has assessed surgeon agreement on radiographic outcomes.

We conducted a study to compare expert shoulder and trauma surgeons’ treatment decision-making and agreement on final radiographic outcomes of surgically treated PHFs. We hypothesized there would be poor agreement on treatment decisions and better agreement on radiographic outcomes, with a difference between shoulder and trauma fellowship–trained surgeons.

Materials and Methods

After receiving institutional review board approval for this study, we collected data on 100 consecutive PHFs (AO/OTA type 11¹) surgically treated at 2 affiliated level I trauma centers between January 2004 and July 2008. None of the cases in the series was managed by any of the surgeons participating in this study.

We created a PowerPoint (Microsoft, Redmond, Washington) survey that included radiographs (preoperative, immediate postoperative, final postoperative) and, if available, a computed tomography image. This survey was sent to 4 orthopedic surgeons: Drs. Gardner, Gerber, Lorich, and Walch. Two of these authors are fellowship-trained in shoulder surgery, the other 2 in orthopedic traumatology with specialization in treating PHFs. All are internationally renowned in PHF management. Using the survey images and a 4-point Likert scale ranging from disagree strongly to agree strongly, the examiners rated their agreement with treatment decisions (arthroplasty vs fixation). They also rated (very poor to very good) immediate postoperative reduction or arthroplasty placement, immediate postoperative fixation methods for fractures treated with open reduction and internal fixation (ORIF), and final radiographic outcomes.

Interobserver agreement was calculated using the intraclass correlation coefficient (ICC),^8,9 with scores of <0.2 (poor), 0.21 to 0.4 (fair), 0.41 to 0.6 (moderate), 0.61 to 0.8 (good), and >0.8 (excellent) used to indicate agreement among observers. ICC scores were determined by treating the 4 examiners as independent entities. Subgroup analyses were also performed to determine ICC scores comparing the 2 shoulder surgeons, comparing the 2 trauma surgeons, and comparing the shoulder surgeons and trauma surgeons as 2 separate groups. ICC scores were used instead of κ coefficients to assess agreement because ICC scores treat ratings as continuous variables, allow for comparison of 2 or more raters, and allow for assessment of correlation among raters, whereas κ coefficients treat data as categorical variables and assume the ratings have no natural ordering. ICC scores were generated by SAS 9.1.3 software (SAS Institute, Cary, North Carolina).

Results

The 4 surgeons’ overall ICC scores for agreement with the rating of immediate reduction or arthroplasty placement and the rating of final radiographic outcome indicated moderate levels of agreement (Table 1). Regarding treatment decision-making and ratings of fixation, the surgeons demonstrated poor and fair levels of agreement, respectively.

The ICC scores comparing the shoulder and trauma surgeons revealed similar levels of agreement (Table 2): moderate levels of agreement for ratings of both immediate postoperative reduction or arthroplasty placement and final radiographic outcomes, but poor and fair levels of agreement regarding treatment decision-making and the rating of immediate postoperative fixation methods for fractures treated with ORIF, respectively.

Subgroup analysis revealed that the 2 shoulder surgeons had poor and fair levels of agreement for treatment decisions and rating of immediate postoperative fixation, respectively, though they moderately agreed on rating of immediate postoperative reduction or arthroplasty placement and rating of final radiographic outcome (Table 3). When the 2 trauma surgeons were compared with each other, ICC scores revealed higher levels of agreement overall (Table 4). In other words, the 2 trauma surgeons agreed with each other more than the 2 shoulder surgeons agreed with each other.

Discussion

This study had 3 major findings: (1) Surgeons do not agree on treatment decisions, including fixation methods, regarding PHFs; (2) regardless of their opinions on ideal treatment, they moderately agree on reductions and final radiographic outcomes; (3) expert trauma surgeons may agree more on treatment decisions than expert shoulder surgeons do. In other words, surgeons do not agree on the best treatment, but they radiographically recognize when a procedure has been performed technically well or poorly. These results support our hypothesis and the limited current literature.

An analysis of Medicare databases showed marked regional variation in rates of operative treatment of PHFs.² Similarly, a Nationwide Inpatient Sample analysis revealed nationwide variation in operative management of PHFs.⁴ Both findings are consistent with our results of poor agreement about treatment decisions and ratings of postoperative fixation of PHFs. In 2010, Petit and colleagues⁶ reported that surgeons do not agree on PHF management. In 2011, Foroohar and colleagues¹⁰ similarly reported low interobserver agreement for treatment recommendations made by 4 upper extremity orthopedic specialists, 4 general orthopedic surgeons, 4 senior residents, and 4 junior residents, for a series of 16 PHFs—also consistent with our findings.

The lack of agreement about PHF treatment may reflect a difference in training, particularly in light of the recent expansion of shoulder and elbow fellowships.² Three separate studies performed at 2 affiliated level I trauma centers demonstrated significant differences in treatment decision-making between shoulder and trauma fellowship–trained surgeons.^5-7 Our results are consistent with the hypothesis that training affects treatment decision-making, as we found poor agreement between shoulder and trauma fellowship–trained surgeons regarding treatment decision for PHFs. Subanalyses revealed that expert trauma surgeons agreed with each other on treatment decisions more than expert shoulder surgeons agreed with each other, further suggesting that training may affect how surgeons manage PHFs. Differences in fellowship training even within the same specialty may account for the observed lesser levels of agreement between the shoulder surgeons, even among experts in the field.

The evidence for optimal treatment historically has been poor,^4,6 with few high-quality prospective, randomized controlled studies on the topic up until the past few years. The most recent Cochrane Review on optimal PHF treatment concluded that there is insufficient evidence to make an evidence-based recommendation and that the long-term benefit of surgery is unclear.¹¹ However, at least 5 controlled trials on the topic have been published within the past 5 years.^12-16 The evidence is striking and generally supports nonoperative treatment for most PHFs, including some displaced fractures—contrary to general orthopedic practice in many parts of the United States,² which hitherto had been based mainly on individual surgeon experience and the limited literature. Without strong evidence to support one treatment option over another, surgeons are left with no objective, scientific way of coming to agreement.

Related to the poor status quo of evidence for PHF treatments is new technology (eg, locking plates, reverse total shoulder arthroplasty) that has expanded surgical indications.^2,17 Although such developments have the potential to improve surgical treatments, they may also exacerbate the disagreement between surgeons regarding optimal operative treatment of PHFs. This potential consequence of new technology may be reflected in our finding of disagreement among surgeons on immediate postoperative fixation methods. Precisely because they are new, such technological innovations have limited evidence supporting their use. This leaves surgeons with little to nothing to inform their decisions to use these devices, other than familiarity with and impressions of the new technology.

Our study had several limitations. First is the small sample size, of surgeons who are leaders in the field. Our sample therefore may not be generalizable to the general population of shoulder and trauma surgeons. Second, we did not calculate intraobserver variability. Third, inherent to studies of interobserver agreement is the uncertainty of their clinical relevance. In the clinical setting, a surgeon has much more information at hand (eg, patient history, physical examination findings, colleague consultations), thus raising the possibility of underestimations of interobserver agreements.¹⁸ Fourth, our comparison of surgeons’ ratings of outcomes was purely radiographic, which may or may not represent or be indicative of clinical outcomes (eg, pain relief, function, range of motion, patient satisfaction). The conclusions we may draw are accordingly limited, as we did not directly evaluate clinical outcome parameters.

Our study had several strengths as well. First, to our knowledge this is the first study to assess interobserver variability in surgeons’ ratings of radiographic outcomes. Its findings may provide further insight into the reasons for poor agreement among orthopedic surgeons on both classification and treatment of PHFs. Second, our surveying of internationally renowned expert surgeons from 4 different institutions may have helped reduce single-institution bias, and it presents the highest level of expertise in the treatment of PHFs.

Although the surgeons in our study moderately agreed on final radiographic outcomes of PHFs, such levels of agreement may still be clinically unacceptable.¹⁹ The overall disagreement on treatment decisions highlights the need for better evidence for optimal treatment of PHFs in order to improve consensus, particularly with anticipated increases in age and comorbidities in the population in coming years.⁴ Subgroup analysis suggested trauma fellowships may contribute to better treatment agreement, though this idea requires further study, perhaps by surveying shoulder and trauma fellowship directors and their curricula for variability in teaching treatment decision-making. The surgeons in our study agreed more on what they consider acceptable final radiographic outcomes, which is encouraging. However, treatment consensus is the primary goal. The recent publication of prospective, randomized studies is helping with this issue, but more studies are needed. It is encouraging that several are planned or under way.^20-22

Conclusion

The surgeons surveyed in this study did not agree on ideal treatment for PHFs but moderately agreed on quality of radiographic outcomes. These differences may reflect a difference in training. We conducted this study to compare experienced shoulder and trauma fellowship–trained surgeons’ treatment decision-making and ratings of radiographic outcomes of PHFs when presented with the same group of patients managed at 2 level I trauma centers. We hypothesized there would be little agreement on treatment decisions, better agreement on final radiographic outcome, and a difference between decision-making and ratings of radiographic outcomes between expert shoulder and trauma surgeons. Our results showed that surgeons do not agree on the best treatment for PHFs but radiographically recognize when an operative treatment has been performed well or poorly. Regarding treatment decisions, our results also showed that expert trauma surgeons may agree more with each other than shoulder surgeons agree with each other. These results support our hypothesis and the limited current literature. The overall disagreement among the surgeons in our study and an aging population that grows sicker each year highlight the need for better evidence for the optimal treatment of PHFs in order to improve consensus.

Proximal humerus fractures (PHFs), AO/OTA (Ar­ beitsgemeinschaft für Osteosynthesefragen/Orthopaedic Trauma Association) type 11,¹ are common, representing 4% to 5% of all fractures in adults.² However, there is no consensus as to optimal management of these injuries, with some reports supporting and others rejecting the various fixation methods,³ and there are no evidence-based practice guidelines informing treatment decisions.⁴ Not surprisingly, orthopedic surgeons do not agree on ideal treatment for PHFs^5,6 and differ by region in their rates of surgical management.² In addition, analyses of national databases have found variation in choice of surgical treatment for PHFs between surgeons and between hospitals of different patient volumes.⁴ Few studies have assessed surgeon agreement on treatment decisions. Findings from these limited investigations indicate there is little agreement on treatment choices, but training may have some impact.^5-7 In 3 studies,^5-7 shoulder and trauma fellowship–trained surgeons differed in their management of PHFs both in terms of rates of operative treatment^5,7 and specific operative management choices.^5,6 No study has assessed surgeon agreement on radiographic outcomes.

We conducted a study to compare expert shoulder and trauma surgeons’ treatment decision-making and agreement on final radiographic outcomes of surgically treated PHFs. We hypothesized there would be poor agreement on treatment decisions and better agreement on radiographic outcomes, with a difference between shoulder and trauma fellowship–trained surgeons.

Materials and Methods

After receiving institutional review board approval for this study, we collected data on 100 consecutive PHFs (AO/OTA type 11¹) surgically treated at 2 affiliated level I trauma centers between January 2004 and July 2008. None of the cases in the series was managed by any of the surgeons participating in this study.

We created a PowerPoint (Microsoft, Redmond, Washington) survey that included radiographs (preoperative, immediate postoperative, final postoperative) and, if available, a computed tomography image. This survey was sent to 4 orthopedic surgeons: Drs. Gardner, Gerber, Lorich, and Walch. Two of these authors are fellowship-trained in shoulder surgery, the other 2 in orthopedic traumatology with specialization in treating PHFs. All are internationally renowned in PHF management. Using the survey images and a 4-point Likert scale ranging from disagree strongly to agree strongly, the examiners rated their agreement with treatment decisions (arthroplasty vs fixation). They also rated (very poor to very good) immediate postoperative reduction or arthroplasty placement, immediate postoperative fixation methods for fractures treated with open reduction and internal fixation (ORIF), and final radiographic outcomes.

Interobserver agreement was calculated using the intraclass correlation coefficient (ICC),^8,9 with scores of <0.2 (poor), 0.21 to 0.4 (fair), 0.41 to 0.6 (moderate), 0.61 to 0.8 (good), and >0.8 (excellent) used to indicate agreement among observers. ICC scores were determined by treating the 4 examiners as independent entities. Subgroup analyses were also performed to determine ICC scores comparing the 2 shoulder surgeons, comparing the 2 trauma surgeons, and comparing the shoulder surgeons and trauma surgeons as 2 separate groups. ICC scores were used instead of κ coefficients to assess agreement because ICC scores treat ratings as continuous variables, allow for comparison of 2 or more raters, and allow for assessment of correlation among raters, whereas κ coefficients treat data as categorical variables and assume the ratings have no natural ordering. ICC scores were generated by SAS 9.1.3 software (SAS Institute, Cary, North Carolina).

Results

The 4 surgeons’ overall ICC scores for agreement with the rating of immediate reduction or arthroplasty placement and the rating of final radiographic outcome indicated moderate levels of agreement (Table 1). Regarding treatment decision-making and ratings of fixation, the surgeons demonstrated poor and fair levels of agreement, respectively.

The ICC scores comparing the shoulder and trauma surgeons revealed similar levels of agreement (Table 2): moderate levels of agreement for ratings of both immediate postoperative reduction or arthroplasty placement and final radiographic outcomes, but poor and fair levels of agreement regarding treatment decision-making and the rating of immediate postoperative fixation methods for fractures treated with ORIF, respectively.

Subgroup analysis revealed that the 2 shoulder surgeons had poor and fair levels of agreement for treatment decisions and rating of immediate postoperative fixation, respectively, though they moderately agreed on rating of immediate postoperative reduction or arthroplasty placement and rating of final radiographic outcome (Table 3). When the 2 trauma surgeons were compared with each other, ICC scores revealed higher levels of agreement overall (Table 4). In other words, the 2 trauma surgeons agreed with each other more than the 2 shoulder surgeons agreed with each other.

Discussion

This study had 3 major findings: (1) Surgeons do not agree on treatment decisions, including fixation methods, regarding PHFs; (2) regardless of their opinions on ideal treatment, they moderately agree on reductions and final radiographic outcomes; (3) expert trauma surgeons may agree more on treatment decisions than expert shoulder surgeons do. In other words, surgeons do not agree on the best treatment, but they radiographically recognize when a procedure has been performed technically well or poorly. These results support our hypothesis and the limited current literature.

An analysis of Medicare databases showed marked regional variation in rates of operative treatment of PHFs.² Similarly, a Nationwide Inpatient Sample analysis revealed nationwide variation in operative management of PHFs.⁴ Both findings are consistent with our results of poor agreement about treatment decisions and ratings of postoperative fixation of PHFs. In 2010, Petit and colleagues⁶ reported that surgeons do not agree on PHF management. In 2011, Foroohar and colleagues¹⁰ similarly reported low interobserver agreement for treatment recommendations made by 4 upper extremity orthopedic specialists, 4 general orthopedic surgeons, 4 senior residents, and 4 junior residents, for a series of 16 PHFs—also consistent with our findings.

The lack of agreement about PHF treatment may reflect a difference in training, particularly in light of the recent expansion of shoulder and elbow fellowships.² Three separate studies performed at 2 affiliated level I trauma centers demonstrated significant differences in treatment decision-making between shoulder and trauma fellowship–trained surgeons.^5-7 Our results are consistent with the hypothesis that training affects treatment decision-making, as we found poor agreement between shoulder and trauma fellowship–trained surgeons regarding treatment decision for PHFs. Subanalyses revealed that expert trauma surgeons agreed with each other on treatment decisions more than expert shoulder surgeons agreed with each other, further suggesting that training may affect how surgeons manage PHFs. Differences in fellowship training even within the same specialty may account for the observed lesser levels of agreement between the shoulder surgeons, even among experts in the field.

The evidence for optimal treatment historically has been poor,^4,6 with few high-quality prospective, randomized controlled studies on the topic up until the past few years. The most recent Cochrane Review on optimal PHF treatment concluded that there is insufficient evidence to make an evidence-based recommendation and that the long-term benefit of surgery is unclear.¹¹ However, at least 5 controlled trials on the topic have been published within the past 5 years.^12-16 The evidence is striking and generally supports nonoperative treatment for most PHFs, including some displaced fractures—contrary to general orthopedic practice in many parts of the United States,² which hitherto had been based mainly on individual surgeon experience and the limited literature. Without strong evidence to support one treatment option over another, surgeons are left with no objective, scientific way of coming to agreement.

Related to the poor status quo of evidence for PHF treatments is new technology (eg, locking plates, reverse total shoulder arthroplasty) that has expanded surgical indications.^2,17 Although such developments have the potential to improve surgical treatments, they may also exacerbate the disagreement between surgeons regarding optimal operative treatment of PHFs. This potential consequence of new technology may be reflected in our finding of disagreement among surgeons on immediate postoperative fixation methods. Precisely because they are new, such technological innovations have limited evidence supporting their use. This leaves surgeons with little to nothing to inform their decisions to use these devices, other than familiarity with and impressions of the new technology.

Our study had several limitations. First is the small sample size, of surgeons who are leaders in the field. Our sample therefore may not be generalizable to the general population of shoulder and trauma surgeons. Second, we did not calculate intraobserver variability. Third, inherent to studies of interobserver agreement is the uncertainty of their clinical relevance. In the clinical setting, a surgeon has much more information at hand (eg, patient history, physical examination findings, colleague consultations), thus raising the possibility of underestimations of interobserver agreements.¹⁸ Fourth, our comparison of surgeons’ ratings of outcomes was purely radiographic, which may or may not represent or be indicative of clinical outcomes (eg, pain relief, function, range of motion, patient satisfaction). The conclusions we may draw are accordingly limited, as we did not directly evaluate clinical outcome parameters.

Our study had several strengths as well. First, to our knowledge this is the first study to assess interobserver variability in surgeons’ ratings of radiographic outcomes. Its findings may provide further insight into the reasons for poor agreement among orthopedic surgeons on both classification and treatment of PHFs. Second, our surveying of internationally renowned expert surgeons from 4 different institutions may have helped reduce single-institution bias, and it presents the highest level of expertise in the treatment of PHFs.

Although the surgeons in our study moderately agreed on final radiographic outcomes of PHFs, such levels of agreement may still be clinically unacceptable.¹⁹ The overall disagreement on treatment decisions highlights the need for better evidence for optimal treatment of PHFs in order to improve consensus, particularly with anticipated increases in age and comorbidities in the population in coming years.⁴ Subgroup analysis suggested trauma fellowships may contribute to better treatment agreement, though this idea requires further study, perhaps by surveying shoulder and trauma fellowship directors and their curricula for variability in teaching treatment decision-making. The surgeons in our study agreed more on what they consider acceptable final radiographic outcomes, which is encouraging. However, treatment consensus is the primary goal. The recent publication of prospective, randomized studies is helping with this issue, but more studies are needed. It is encouraging that several are planned or under way.^20-22

Conclusion

The surgeons surveyed in this study did not agree on ideal treatment for PHFs but moderately agreed on quality of radiographic outcomes. These differences may reflect a difference in training. We conducted this study to compare experienced shoulder and trauma fellowship–trained surgeons’ treatment decision-making and ratings of radiographic outcomes of PHFs when presented with the same group of patients managed at 2 level I trauma centers. We hypothesized there would be little agreement on treatment decisions, better agreement on final radiographic outcome, and a difference between decision-making and ratings of radiographic outcomes between expert shoulder and trauma surgeons. Our results showed that surgeons do not agree on the best treatment for PHFs but radiographically recognize when an operative treatment has been performed well or poorly. Regarding treatment decisions, our results also showed that expert trauma surgeons may agree more with each other than shoulder surgeons agree with each other. These results support our hypothesis and the limited current literature. The overall disagreement among the surgeons in our study and an aging population that grows sicker each year highlight the need for better evidence for the optimal treatment of PHFs in order to improve consensus.

Proximal humerus fractures (PHFs), AO/OTA (Ar­ beitsgemeinschaft für Osteosynthesefragen/Orthopaedic Trauma Association) type 11,¹ are common, representing 4% to 5% of all fractures in adults.² However, there is no consensus as to optimal management of these injuries, with some reports supporting and others rejecting the various fixation methods,³ and there are no evidence-based practice guidelines informing treatment decisions.⁴ Not surprisingly, orthopedic surgeons do not agree on ideal treatment for PHFs^5,6 and differ by region in their rates of surgical management.² In addition, analyses of national databases have found variation in choice of surgical treatment for PHFs between surgeons and between hospitals of different patient volumes.⁴ Few studies have assessed surgeon agreement on treatment decisions. Findings from these limited investigations indicate there is little agreement on treatment choices, but training may have some impact.^5-7 In 3 studies,^5-7 shoulder and trauma fellowship–trained surgeons differed in their management of PHFs both in terms of rates of operative treatment^5,7 and specific operative management choices.^5,6 No study has assessed surgeon agreement on radiographic outcomes.

We conducted a study to compare expert shoulder and trauma surgeons’ treatment decision-making and agreement on final radiographic outcomes of surgically treated PHFs. We hypothesized there would be poor agreement on treatment decisions and better agreement on radiographic outcomes, with a difference between shoulder and trauma fellowship–trained surgeons.

Materials and Methods

After receiving institutional review board approval for this study, we collected data on 100 consecutive PHFs (AO/OTA type 11¹) surgically treated at 2 affiliated level I trauma centers between January 2004 and July 2008. None of the cases in the series was managed by any of the surgeons participating in this study.

We created a PowerPoint (Microsoft, Redmond, Washington) survey that included radiographs (preoperative, immediate postoperative, final postoperative) and, if available, a computed tomography image. This survey was sent to 4 orthopedic surgeons: Drs. Gardner, Gerber, Lorich, and Walch. Two of these authors are fellowship-trained in shoulder surgery, the other 2 in orthopedic traumatology with specialization in treating PHFs. All are internationally renowned in PHF management. Using the survey images and a 4-point Likert scale ranging from disagree strongly to agree strongly, the examiners rated their agreement with treatment decisions (arthroplasty vs fixation). They also rated (very poor to very good) immediate postoperative reduction or arthroplasty placement, immediate postoperative fixation methods for fractures treated with open reduction and internal fixation (ORIF), and final radiographic outcomes.

Interobserver agreement was calculated using the intraclass correlation coefficient (ICC),^8,9 with scores of <0.2 (poor), 0.21 to 0.4 (fair), 0.41 to 0.6 (moderate), 0.61 to 0.8 (good), and >0.8 (excellent) used to indicate agreement among observers. ICC scores were determined by treating the 4 examiners as independent entities. Subgroup analyses were also performed to determine ICC scores comparing the 2 shoulder surgeons, comparing the 2 trauma surgeons, and comparing the shoulder surgeons and trauma surgeons as 2 separate groups. ICC scores were used instead of κ coefficients to assess agreement because ICC scores treat ratings as continuous variables, allow for comparison of 2 or more raters, and allow for assessment of correlation among raters, whereas κ coefficients treat data as categorical variables and assume the ratings have no natural ordering. ICC scores were generated by SAS 9.1.3 software (SAS Institute, Cary, North Carolina).

Results

The 4 surgeons’ overall ICC scores for agreement with the rating of immediate reduction or arthroplasty placement and the rating of final radiographic outcome indicated moderate levels of agreement (Table 1). Regarding treatment decision-making and ratings of fixation, the surgeons demonstrated poor and fair levels of agreement, respectively.

The ICC scores comparing the shoulder and trauma surgeons revealed similar levels of agreement (Table 2): moderate levels of agreement for ratings of both immediate postoperative reduction or arthroplasty placement and final radiographic outcomes, but poor and fair levels of agreement regarding treatment decision-making and the rating of immediate postoperative fixation methods for fractures treated with ORIF, respectively.

Subgroup analysis revealed that the 2 shoulder surgeons had poor and fair levels of agreement for treatment decisions and rating of immediate postoperative fixation, respectively, though they moderately agreed on rating of immediate postoperative reduction or arthroplasty placement and rating of final radiographic outcome (Table 3). When the 2 trauma surgeons were compared with each other, ICC scores revealed higher levels of agreement overall (Table 4). In other words, the 2 trauma surgeons agreed with each other more than the 2 shoulder surgeons agreed with each other.

Discussion

This study had 3 major findings: (1) Surgeons do not agree on treatment decisions, including fixation methods, regarding PHFs; (2) regardless of their opinions on ideal treatment, they moderately agree on reductions and final radiographic outcomes; (3) expert trauma surgeons may agree more on treatment decisions than expert shoulder surgeons do. In other words, surgeons do not agree on the best treatment, but they radiographically recognize when a procedure has been performed technically well or poorly. These results support our hypothesis and the limited current literature.

An analysis of Medicare databases showed marked regional variation in rates of operative treatment of PHFs.² Similarly, a Nationwide Inpatient Sample analysis revealed nationwide variation in operative management of PHFs.⁴ Both findings are consistent with our results of poor agreement about treatment decisions and ratings of postoperative fixation of PHFs. In 2010, Petit and colleagues⁶ reported that surgeons do not agree on PHF management. In 2011, Foroohar and colleagues¹⁰ similarly reported low interobserver agreement for treatment recommendations made by 4 upper extremity orthopedic specialists, 4 general orthopedic surgeons, 4 senior residents, and 4 junior residents, for a series of 16 PHFs—also consistent with our findings.

The lack of agreement about PHF treatment may reflect a difference in training, particularly in light of the recent expansion of shoulder and elbow fellowships.² Three separate studies performed at 2 affiliated level I trauma centers demonstrated significant differences in treatment decision-making between shoulder and trauma fellowship–trained surgeons.^5-7 Our results are consistent with the hypothesis that training affects treatment decision-making, as we found poor agreement between shoulder and trauma fellowship–trained surgeons regarding treatment decision for PHFs. Subanalyses revealed that expert trauma surgeons agreed with each other on treatment decisions more than expert shoulder surgeons agreed with each other, further suggesting that training may affect how surgeons manage PHFs. Differences in fellowship training even within the same specialty may account for the observed lesser levels of agreement between the shoulder surgeons, even among experts in the field.

The evidence for optimal treatment historically has been poor,^4,6 with few high-quality prospective, randomized controlled studies on the topic up until the past few years. The most recent Cochrane Review on optimal PHF treatment concluded that there is insufficient evidence to make an evidence-based recommendation and that the long-term benefit of surgery is unclear.¹¹ However, at least 5 controlled trials on the topic have been published within the past 5 years.^12-16 The evidence is striking and generally supports nonoperative treatment for most PHFs, including some displaced fractures—contrary to general orthopedic practice in many parts of the United States,² which hitherto had been based mainly on individual surgeon experience and the limited literature. Without strong evidence to support one treatment option over another, surgeons are left with no objective, scientific way of coming to agreement.

Related to the poor status quo of evidence for PHF treatments is new technology (eg, locking plates, reverse total shoulder arthroplasty) that has expanded surgical indications.^2,17 Although such developments have the potential to improve surgical treatments, they may also exacerbate the disagreement between surgeons regarding optimal operative treatment of PHFs. This potential consequence of new technology may be reflected in our finding of disagreement among surgeons on immediate postoperative fixation methods. Precisely because they are new, such technological innovations have limited evidence supporting their use. This leaves surgeons with little to nothing to inform their decisions to use these devices, other than familiarity with and impressions of the new technology.

Our study had several limitations. First is the small sample size, of surgeons who are leaders in the field. Our sample therefore may not be generalizable to the general population of shoulder and trauma surgeons. Second, we did not calculate intraobserver variability. Third, inherent to studies of interobserver agreement is the uncertainty of their clinical relevance. In the clinical setting, a surgeon has much more information at hand (eg, patient history, physical examination findings, colleague consultations), thus raising the possibility of underestimations of interobserver agreements.¹⁸ Fourth, our comparison of surgeons’ ratings of outcomes was purely radiographic, which may or may not represent or be indicative of clinical outcomes (eg, pain relief, function, range of motion, patient satisfaction). The conclusions we may draw are accordingly limited, as we did not directly evaluate clinical outcome parameters.

Our study had several strengths as well. First, to our knowledge this is the first study to assess interobserver variability in surgeons’ ratings of radiographic outcomes. Its findings may provide further insight into the reasons for poor agreement among orthopedic surgeons on both classification and treatment of PHFs. Second, our surveying of internationally renowned expert surgeons from 4 different institutions may have helped reduce single-institution bias, and it presents the highest level of expertise in the treatment of PHFs.

Although the surgeons in our study moderately agreed on final radiographic outcomes of PHFs, such levels of agreement may still be clinically unacceptable.¹⁹ The overall disagreement on treatment decisions highlights the need for better evidence for optimal treatment of PHFs in order to improve consensus, particularly with anticipated increases in age and comorbidities in the population in coming years.⁴ Subgroup analysis suggested trauma fellowships may contribute to better treatment agreement, though this idea requires further study, perhaps by surveying shoulder and trauma fellowship directors and their curricula for variability in teaching treatment decision-making. The surgeons in our study agreed more on what they consider acceptable final radiographic outcomes, which is encouraging. However, treatment consensus is the primary goal. The recent publication of prospective, randomized studies is helping with this issue, but more studies are needed. It is encouraging that several are planned or under way.^20-22

Conclusion

The surgeons surveyed in this study did not agree on ideal treatment for PHFs but moderately agreed on quality of radiographic outcomes. These differences may reflect a difference in training. We conducted this study to compare experienced shoulder and trauma fellowship–trained surgeons’ treatment decision-making and ratings of radiographic outcomes of PHFs when presented with the same group of patients managed at 2 level I trauma centers. We hypothesized there would be little agreement on treatment decisions, better agreement on final radiographic outcome, and a difference between decision-making and ratings of radiographic outcomes between expert shoulder and trauma surgeons. Our results showed that surgeons do not agree on the best treatment for PHFs but radiographically recognize when an operative treatment has been performed well or poorly. Regarding treatment decisions, our results also showed that expert trauma surgeons may agree more with each other than shoulder surgeons agree with each other. These results support our hypothesis and the limited current literature. The overall disagreement among the surgeons in our study and an aging population that grows sicker each year highlight the need for better evidence for the optimal treatment of PHFs in order to improve consensus.

Elbow motion is crucial for activities of daily living and full function of the upper extremity.¹ Measuring the elbow flexion arc accurately and consistently is an important part of the physical examination of patients with elbow pathology. Orthopedic surgeons rely on these measurements to follow patients over time, and they often base their treatment decisions on the range and progression/regression of motion arc.

In the clinical setting, elbow range of motion (ROM) is commonly measured with a handheld goniometer.^2,3 The literature also suggests that goniometric measurements are highly reliable in the clinical setting and that intrarater reliability of elbow ROM measurements is high.^2-4 Despite the routine use and clinical importance of flexion arc assessment, there is no universal recommendation regarding optimal measurement position. Textbooks and journal articles commonly do not specify arm position at time of elbow ROM measurements,^5-8 and a literature review found no studies directly addressing this issue.

From a biomechanical standpoint, humeral rotation is often affected by forearm pronosupination position. Although forearm pronosupination is a product of the motion at the radioulnar joints, forearm position during elbow flexion arc measurement can influence the relationship of the distal humeral intercondylar axis to the plane of measurement. Full forearm supination rotates the distal humeral intercondylar axis externally to a position parallel to the floor and in line with the plane of measurement. Humeral rotation with the forearm in neutral pronosupination places the humeral condyles internally rotated relative to the floor. Therefore, for the purposes of this study, we defined full humeral external rotation and true plane of ulnohumeral motion as full forearm supination, and relative humeral and ulnohumeral joint internal rotation as neutral pronosupination.

Because of the potential for elbow ROM measurement changes caused by differences in the motion plane in which measurements are taken, some have advocated taking flexion arc measurements with the arm in full supination to allow measurements to be taken in the true plane of motion. We hypothesized that elbow flexion arc measurements taken with the forearm in neutral rotation would underestimate the extent of elbow flexion contractures compared with measurements taken in full supination.

Materials and Methods

This study received institutional review board approval. Eighty-four patients who presented with elbow dysfunction to a single shoulder and elbow orthopedic surgeon enrolled in the study. Skeletally immature patients and patients with a fracture or other disorder that prohibited elbow ROM were excluded. A standard goniometer was used to measure elbow flexion and extension with the humerus in 2 positions: full external rotation and neutral rotation.

All goniometer measurements were made by the same surgeon (to eliminate interobserver reliability error) using a standardized technique with the patient sitting upright. The goniometer was positioned laterally with its center of rotation over the lateral epicondyle, aligned proximally with the humeral head and distally with the center of the wrist. Measurements were obtained sequentially with the hand in both positions. For external rotation measurements, the patient’s arm was fully supinated to bring the humeral condyles parallel to the floor. For neutral positioning, the patient’s arm was placed in the “thumb-up” position with the hand perpendicular to the horizontal axis of the floor (Figures 1A–1C).

Data collected included demographics, diagnosis, hand dominance, affected side, and elbow ROM measurements with the hand in the 2 positions. These data were compiled and analyzed for all patients and then stratified into 3 groups by extent of elbow flexion contracture in the supinated position (group 1, hyperextension; group 2, 0°-29° elbow extension; group 3, ≥30° flexion contracture).

Statistically, paired t tests were used to identify differences between the 2 elbow ROM measurement methods. P < .05 was considered significant.

Results

Eighty-four (44 male, 40 female) consecutive patients (85 elbows) met the inclusion and exclusion criteria. Mean age was 51 years (range, 19-84 years). Seventy-six patients were right-handed, 7 were left-handed, and dominance was unknown in 1 patient. The right elbow was affected in 45 patients, the left in 38, and both in 1 patient. There were 25 different diagnoses, the most common of which was lateral epicondylitis; 7 patients had multiple disorders (Table).

The first set of data, elbow ROM measurements, was taken with all 84 patients analyzed as a single group. In neutral humeral rotation, mean elbow extension was 14° (range, 10°-72°), and mean elbow flexion was 134° (range, 72°-145°). In external rotation, mean elbow extension was 20° (range, 12°-87°), and mean elbow flexion was 134° (range, 72°-145°). For the group, mean absolute difference in elbow extension was 8° (range, 0°-30°; P < .0001); there was no difference between external rotation and neutral rotation in flexion (Figure 2).

The data were reanalyzed after being stratified into 3 groups based on extent of elbow flexion contracture measured in supination.

The 9 elbows in group 1 (hyperextension) had mean extension of –2° (range, 10°-2°) and mean flexion of 141° (range, 130°-145°) in the neutral position. In external rotation, mean extension was –9° (range, –12° to –1°), and mean flexion was 141° (range, 130°-145°). When the 2 measurement positions were compared, group 1 had mean elbow ROM differences of –6° (range, –14° to 0°; P = .0033) for elbow extension and 0° for elbow flexion (Figure 3A).

The 50 elbows in group 2 (0°-29° flexion contracture) had mean extension of 7° (range, 0°-20°) and mean flexion of 138° (range, 100°-145°) in the neutral position. In external rotation, mean extension was 13° (range, 0°-26°), and mean flexion was 138° (range, 100°-145°). Mean difference between neutral and external rotation measurements was 6° (range, 0°-20°; P < .0001) in extension and 0° in flexion (Figure 3B).

 The 26 elbows in group 3 (≥30° flexion contracture) had mean extension of 33° (range, 0°-72°) and mean flexion of 124° (range, 72°-145°) in the neutral position. In external rotation, mean extension was 45° (range, 30°-87°), and mean flexion was 124° (range, 72°-145°). Mean difference between neutral and external rotation measurements was 12° (range, 0°-30°; P < .0001) in extension and 0° in flexion (Figure 3C).

Discussion

Elbow flexion arc measurements are crucial for patient outcomes and activities of daily living. Commonly cited as functional ROM, the 30°-to-130° flexion arc often is used to guide clinical decisions in patients with elbow disorders.¹ However, our data indicate that humeral position can alter elbow ROM measurements. Specifically, because of neutral forearm pronosupination, measurements made with the humerus in neutral rotation underestimate both the extent of elbow hyperextension and the degree of flexion contracture (Figures 4A, 4B). The more severe the flexion contracture, the more values are altered by measurements taken in this position. The same does not apply for elbow flexion measurements, as varying humeral rotation did not significantly affect those values.

Our results indicate that patients evaluated with the arm in neutral humeral rotation had flexion contractures underestimated by a mean of 8°, while there was a negligible difference in flexion measurements. Stratifying our data into 3 groups, we found that neutral humeral rotation kept elbow extension measurements closer to 0° for patients with both hyperextension and contractures. With increasing severity of flexion contractures in groups 2 and 3, the measurement errors were magnified. The differences in extension measurement values between these 2 groups based on humeral rotation increased more than 4°—an indication that, as flexion contracture severity increases, so does the degree of measurement error when elbow extension is measured with the humerus in neutral rotation rather than external rotation.

Our literature review found no studies on ROM value differences based on position of humeral rotation. Most texts, in their descriptions of elbow ROM and biomechanics, make no reference to position of pronosupination at time of flexion arc measurement.^5-8 Although many elbow authorities recommend taking elbow ROM measurements in full external rotation, we found no corroborating evidence.

Other investigators have evaluated the reliability of goniometer measurements.^2,3 Rothstein and colleagues³ concluded that elbow and knee goniometric measurements are highly reliable in the clinical setting when taken by the same person. In particular, intratester reliability for elbow extension measurements was high. Armstrong and colleagues² specifically examined intratester, intertester, and interdevice reliability and found that intratester reliability was much higher than intertester reliability for universal goniometry. In our study, all patients were measured with the same technique by the same orthopedic surgeon to eliminate any intertester reliability error. Armstrong and colleagues² also found that intratester changes vis-a-vis extension measurements are meaningful when goniometric differences are more than 7°. In our study, the difference in extension measurements between the 2 humeral positions averaged 8° overall and 12° in group 3. This suggests that the data reported here reflect a true difference dependent on humeral rotation and are not a result of goniometer intratester variability.

Other studies have examined measurement devices other than the standard universal goniometer. Cleffken and colleagues⁴ found that the electronic digital inclinometer was reliable for elbow ROM measurements. Blonna and colleagues⁹ used digital photography–based goniometry to measure patient outcomes without doctor–patient contact at tertiary-care centers and found it to be more accurate and reliable than clinical goniometry in measuring elbow flexion and extension. Chapleau and colleagues¹⁰ compared the validity of goniometric elbow measurements in radiographic methods and concluded that the maximal error of goniometric measurements in extension was 10.3°. However, they also found high intraclass correlation coefficients for goniometric measurements. With the accepted clinical reliability of universal goniometry,^2-4,10 we believe it to be the best clinical tool for this study because of its availability, minimal cost, and ease of use.

In the clinical setting, elbow flexion arc measurements are a major factor in treatment decisions and often dictate whether to proceed with operative interventions such as capsular release. In addition, ROM measurements are crucial in determining the success of treatments and the progression of disease. Erroneous elbow extension measurements can have significant consequences if they falsely indicate functional ROM when taken in neutral position. This is particularly true for patients with elbow flexion contractures of more than 30°, in whom differences in humeral rotation resulted in about 12° of variance between measured values. For instance, a patient with a true 40° flexion contracture in the externally rotated position could be determined to have functional ROM based on measurements made in the neutral position.

Limitations of this study include those involving goniometer reliability and intraobserver variability (already described) and the validity of goniometer measurements compared with radiographic measurements.

Conclusion

Because elbow goniometer extension measurements taken in neutral humeral rotation underestimate both the degree of elbow hyperextension and the degree of elbow flexion contracture, we recommend taking elbow flexion arc measurements in the true plane of motion, with the humerus externally rotated by fully supinating the forearm, such that the distal humeral condyles are parallel to the floor.

Elbow motion is crucial for activities of daily living and full function of the upper extremity.¹ Measuring the elbow flexion arc accurately and consistently is an important part of the physical examination of patients with elbow pathology. Orthopedic surgeons rely on these measurements to follow patients over time, and they often base their treatment decisions on the range and progression/regression of motion arc.

In the clinical setting, elbow range of motion (ROM) is commonly measured with a handheld goniometer.^2,3 The literature also suggests that goniometric measurements are highly reliable in the clinical setting and that intrarater reliability of elbow ROM measurements is high.^2-4 Despite the routine use and clinical importance of flexion arc assessment, there is no universal recommendation regarding optimal measurement position. Textbooks and journal articles commonly do not specify arm position at time of elbow ROM measurements,^5-8 and a literature review found no studies directly addressing this issue.

From a biomechanical standpoint, humeral rotation is often affected by forearm pronosupination position. Although forearm pronosupination is a product of the motion at the radioulnar joints, forearm position during elbow flexion arc measurement can influence the relationship of the distal humeral intercondylar axis to the plane of measurement. Full forearm supination rotates the distal humeral intercondylar axis externally to a position parallel to the floor and in line with the plane of measurement. Humeral rotation with the forearm in neutral pronosupination places the humeral condyles internally rotated relative to the floor. Therefore, for the purposes of this study, we defined full humeral external rotation and true plane of ulnohumeral motion as full forearm supination, and relative humeral and ulnohumeral joint internal rotation as neutral pronosupination.

Because of the potential for elbow ROM measurement changes caused by differences in the motion plane in which measurements are taken, some have advocated taking flexion arc measurements with the arm in full supination to allow measurements to be taken in the true plane of motion. We hypothesized that elbow flexion arc measurements taken with the forearm in neutral rotation would underestimate the extent of elbow flexion contractures compared with measurements taken in full supination.

Materials and Methods

This study received institutional review board approval. Eighty-four patients who presented with elbow dysfunction to a single shoulder and elbow orthopedic surgeon enrolled in the study. Skeletally immature patients and patients with a fracture or other disorder that prohibited elbow ROM were excluded. A standard goniometer was used to measure elbow flexion and extension with the humerus in 2 positions: full external rotation and neutral rotation.

All goniometer measurements were made by the same surgeon (to eliminate interobserver reliability error) using a standardized technique with the patient sitting upright. The goniometer was positioned laterally with its center of rotation over the lateral epicondyle, aligned proximally with the humeral head and distally with the center of the wrist. Measurements were obtained sequentially with the hand in both positions. For external rotation measurements, the patient’s arm was fully supinated to bring the humeral condyles parallel to the floor. For neutral positioning, the patient’s arm was placed in the “thumb-up” position with the hand perpendicular to the horizontal axis of the floor (Figures 1A–1C).

Data collected included demographics, diagnosis, hand dominance, affected side, and elbow ROM measurements with the hand in the 2 positions. These data were compiled and analyzed for all patients and then stratified into 3 groups by extent of elbow flexion contracture in the supinated position (group 1, hyperextension; group 2, 0°-29° elbow extension; group 3, ≥30° flexion contracture).

Statistically, paired t tests were used to identify differences between the 2 elbow ROM measurement methods. P < .05 was considered significant.

Results

Eighty-four (44 male, 40 female) consecutive patients (85 elbows) met the inclusion and exclusion criteria. Mean age was 51 years (range, 19-84 years). Seventy-six patients were right-handed, 7 were left-handed, and dominance was unknown in 1 patient. The right elbow was affected in 45 patients, the left in 38, and both in 1 patient. There were 25 different diagnoses, the most common of which was lateral epicondylitis; 7 patients had multiple disorders (Table).

The first set of data, elbow ROM measurements, was taken with all 84 patients analyzed as a single group. In neutral humeral rotation, mean elbow extension was 14° (range, 10°-72°), and mean elbow flexion was 134° (range, 72°-145°). In external rotation, mean elbow extension was 20° (range, 12°-87°), and mean elbow flexion was 134° (range, 72°-145°). For the group, mean absolute difference in elbow extension was 8° (range, 0°-30°; P < .0001); there was no difference between external rotation and neutral rotation in flexion (Figure 2).

The data were reanalyzed after being stratified into 3 groups based on extent of elbow flexion contracture measured in supination.

The 9 elbows in group 1 (hyperextension) had mean extension of –2° (range, 10°-2°) and mean flexion of 141° (range, 130°-145°) in the neutral position. In external rotation, mean extension was –9° (range, –12° to –1°), and mean flexion was 141° (range, 130°-145°). When the 2 measurement positions were compared, group 1 had mean elbow ROM differences of –6° (range, –14° to 0°; P = .0033) for elbow extension and 0° for elbow flexion (Figure 3A).

The 50 elbows in group 2 (0°-29° flexion contracture) had mean extension of 7° (range, 0°-20°) and mean flexion of 138° (range, 100°-145°) in the neutral position. In external rotation, mean extension was 13° (range, 0°-26°), and mean flexion was 138° (range, 100°-145°). Mean difference between neutral and external rotation measurements was 6° (range, 0°-20°; P < .0001) in extension and 0° in flexion (Figure 3B).

 The 26 elbows in group 3 (≥30° flexion contracture) had mean extension of 33° (range, 0°-72°) and mean flexion of 124° (range, 72°-145°) in the neutral position. In external rotation, mean extension was 45° (range, 30°-87°), and mean flexion was 124° (range, 72°-145°). Mean difference between neutral and external rotation measurements was 12° (range, 0°-30°; P < .0001) in extension and 0° in flexion (Figure 3C).

Discussion

Elbow flexion arc measurements are crucial for patient outcomes and activities of daily living. Commonly cited as functional ROM, the 30°-to-130° flexion arc often is used to guide clinical decisions in patients with elbow disorders.¹ However, our data indicate that humeral position can alter elbow ROM measurements. Specifically, because of neutral forearm pronosupination, measurements made with the humerus in neutral rotation underestimate both the extent of elbow hyperextension and the degree of flexion contracture (Figures 4A, 4B). The more severe the flexion contracture, the more values are altered by measurements taken in this position. The same does not apply for elbow flexion measurements, as varying humeral rotation did not significantly affect those values.

Our results indicate that patients evaluated with the arm in neutral humeral rotation had flexion contractures underestimated by a mean of 8°, while there was a negligible difference in flexion measurements. Stratifying our data into 3 groups, we found that neutral humeral rotation kept elbow extension measurements closer to 0° for patients with both hyperextension and contractures. With increasing severity of flexion contractures in groups 2 and 3, the measurement errors were magnified. The differences in extension measurement values between these 2 groups based on humeral rotation increased more than 4°—an indication that, as flexion contracture severity increases, so does the degree of measurement error when elbow extension is measured with the humerus in neutral rotation rather than external rotation.

Our literature review found no studies on ROM value differences based on position of humeral rotation. Most texts, in their descriptions of elbow ROM and biomechanics, make no reference to position of pronosupination at time of flexion arc measurement.^5-8 Although many elbow authorities recommend taking elbow ROM measurements in full external rotation, we found no corroborating evidence.

Other investigators have evaluated the reliability of goniometer measurements.^2,3 Rothstein and colleagues³ concluded that elbow and knee goniometric measurements are highly reliable in the clinical setting when taken by the same person. In particular, intratester reliability for elbow extension measurements was high. Armstrong and colleagues² specifically examined intratester, intertester, and interdevice reliability and found that intratester reliability was much higher than intertester reliability for universal goniometry. In our study, all patients were measured with the same technique by the same orthopedic surgeon to eliminate any intertester reliability error. Armstrong and colleagues² also found that intratester changes vis-a-vis extension measurements are meaningful when goniometric differences are more than 7°. In our study, the difference in extension measurements between the 2 humeral positions averaged 8° overall and 12° in group 3. This suggests that the data reported here reflect a true difference dependent on humeral rotation and are not a result of goniometer intratester variability.

Other studies have examined measurement devices other than the standard universal goniometer. Cleffken and colleagues⁴ found that the electronic digital inclinometer was reliable for elbow ROM measurements. Blonna and colleagues⁹ used digital photography–based goniometry to measure patient outcomes without doctor–patient contact at tertiary-care centers and found it to be more accurate and reliable than clinical goniometry in measuring elbow flexion and extension. Chapleau and colleagues¹⁰ compared the validity of goniometric elbow measurements in radiographic methods and concluded that the maximal error of goniometric measurements in extension was 10.3°. However, they also found high intraclass correlation coefficients for goniometric measurements. With the accepted clinical reliability of universal goniometry,^2-4,10 we believe it to be the best clinical tool for this study because of its availability, minimal cost, and ease of use.

In the clinical setting, elbow flexion arc measurements are a major factor in treatment decisions and often dictate whether to proceed with operative interventions such as capsular release. In addition, ROM measurements are crucial in determining the success of treatments and the progression of disease. Erroneous elbow extension measurements can have significant consequences if they falsely indicate functional ROM when taken in neutral position. This is particularly true for patients with elbow flexion contractures of more than 30°, in whom differences in humeral rotation resulted in about 12° of variance between measured values. For instance, a patient with a true 40° flexion contracture in the externally rotated position could be determined to have functional ROM based on measurements made in the neutral position.

Limitations of this study include those involving goniometer reliability and intraobserver variability (already described) and the validity of goniometer measurements compared with radiographic measurements.

Conclusion

Because elbow goniometer extension measurements taken in neutral humeral rotation underestimate both the degree of elbow hyperextension and the degree of elbow flexion contracture, we recommend taking elbow flexion arc measurements in the true plane of motion, with the humerus externally rotated by fully supinating the forearm, such that the distal humeral condyles are parallel to the floor.

Elbow motion is crucial for activities of daily living and full function of the upper extremity.¹ Measuring the elbow flexion arc accurately and consistently is an important part of the physical examination of patients with elbow pathology. Orthopedic surgeons rely on these measurements to follow patients over time, and they often base their treatment decisions on the range and progression/regression of motion arc.

In the clinical setting, elbow range of motion (ROM) is commonly measured with a handheld goniometer.^2,3 The literature also suggests that goniometric measurements are highly reliable in the clinical setting and that intrarater reliability of elbow ROM measurements is high.^2-4 Despite the routine use and clinical importance of flexion arc assessment, there is no universal recommendation regarding optimal measurement position. Textbooks and journal articles commonly do not specify arm position at time of elbow ROM measurements,^5-8 and a literature review found no studies directly addressing this issue.

From a biomechanical standpoint, humeral rotation is often affected by forearm pronosupination position. Although forearm pronosupination is a product of the motion at the radioulnar joints, forearm position during elbow flexion arc measurement can influence the relationship of the distal humeral intercondylar axis to the plane of measurement. Full forearm supination rotates the distal humeral intercondylar axis externally to a position parallel to the floor and in line with the plane of measurement. Humeral rotation with the forearm in neutral pronosupination places the humeral condyles internally rotated relative to the floor. Therefore, for the purposes of this study, we defined full humeral external rotation and true plane of ulnohumeral motion as full forearm supination, and relative humeral and ulnohumeral joint internal rotation as neutral pronosupination.

Because of the potential for elbow ROM measurement changes caused by differences in the motion plane in which measurements are taken, some have advocated taking flexion arc measurements with the arm in full supination to allow measurements to be taken in the true plane of motion. We hypothesized that elbow flexion arc measurements taken with the forearm in neutral rotation would underestimate the extent of elbow flexion contractures compared with measurements taken in full supination.

Materials and Methods

This study received institutional review board approval. Eighty-four patients who presented with elbow dysfunction to a single shoulder and elbow orthopedic surgeon enrolled in the study. Skeletally immature patients and patients with a fracture or other disorder that prohibited elbow ROM were excluded. A standard goniometer was used to measure elbow flexion and extension with the humerus in 2 positions: full external rotation and neutral rotation.

All goniometer measurements were made by the same surgeon (to eliminate interobserver reliability error) using a standardized technique with the patient sitting upright. The goniometer was positioned laterally with its center of rotation over the lateral epicondyle, aligned proximally with the humeral head and distally with the center of the wrist. Measurements were obtained sequentially with the hand in both positions. For external rotation measurements, the patient’s arm was fully supinated to bring the humeral condyles parallel to the floor. For neutral positioning, the patient’s arm was placed in the “thumb-up” position with the hand perpendicular to the horizontal axis of the floor (Figures 1A–1C).

Data collected included demographics, diagnosis, hand dominance, affected side, and elbow ROM measurements with the hand in the 2 positions. These data were compiled and analyzed for all patients and then stratified into 3 groups by extent of elbow flexion contracture in the supinated position (group 1, hyperextension; group 2, 0°-29° elbow extension; group 3, ≥30° flexion contracture).

Statistically, paired t tests were used to identify differences between the 2 elbow ROM measurement methods. P < .05 was considered significant.

Results

Eighty-four (44 male, 40 female) consecutive patients (85 elbows) met the inclusion and exclusion criteria. Mean age was 51 years (range, 19-84 years). Seventy-six patients were right-handed, 7 were left-handed, and dominance was unknown in 1 patient. The right elbow was affected in 45 patients, the left in 38, and both in 1 patient. There were 25 different diagnoses, the most common of which was lateral epicondylitis; 7 patients had multiple disorders (Table).

The first set of data, elbow ROM measurements, was taken with all 84 patients analyzed as a single group. In neutral humeral rotation, mean elbow extension was 14° (range, 10°-72°), and mean elbow flexion was 134° (range, 72°-145°). In external rotation, mean elbow extension was 20° (range, 12°-87°), and mean elbow flexion was 134° (range, 72°-145°). For the group, mean absolute difference in elbow extension was 8° (range, 0°-30°; P < .0001); there was no difference between external rotation and neutral rotation in flexion (Figure 2).

The data were reanalyzed after being stratified into 3 groups based on extent of elbow flexion contracture measured in supination.

The 9 elbows in group 1 (hyperextension) had mean extension of –2° (range, 10°-2°) and mean flexion of 141° (range, 130°-145°) in the neutral position. In external rotation, mean extension was –9° (range, –12° to –1°), and mean flexion was 141° (range, 130°-145°). When the 2 measurement positions were compared, group 1 had mean elbow ROM differences of –6° (range, –14° to 0°; P = .0033) for elbow extension and 0° for elbow flexion (Figure 3A).

The 50 elbows in group 2 (0°-29° flexion contracture) had mean extension of 7° (range, 0°-20°) and mean flexion of 138° (range, 100°-145°) in the neutral position. In external rotation, mean extension was 13° (range, 0°-26°), and mean flexion was 138° (range, 100°-145°). Mean difference between neutral and external rotation measurements was 6° (range, 0°-20°; P < .0001) in extension and 0° in flexion (Figure 3B).

 The 26 elbows in group 3 (≥30° flexion contracture) had mean extension of 33° (range, 0°-72°) and mean flexion of 124° (range, 72°-145°) in the neutral position. In external rotation, mean extension was 45° (range, 30°-87°), and mean flexion was 124° (range, 72°-145°). Mean difference between neutral and external rotation measurements was 12° (range, 0°-30°; P < .0001) in extension and 0° in flexion (Figure 3C).

Discussion

Elbow flexion arc measurements are crucial for patient outcomes and activities of daily living. Commonly cited as functional ROM, the 30°-to-130° flexion arc often is used to guide clinical decisions in patients with elbow disorders.¹ However, our data indicate that humeral position can alter elbow ROM measurements. Specifically, because of neutral forearm pronosupination, measurements made with the humerus in neutral rotation underestimate both the extent of elbow hyperextension and the degree of flexion contracture (Figures 4A, 4B). The more severe the flexion contracture, the more values are altered by measurements taken in this position. The same does not apply for elbow flexion measurements, as varying humeral rotation did not significantly affect those values.

Our results indicate that patients evaluated with the arm in neutral humeral rotation had flexion contractures underestimated by a mean of 8°, while there was a negligible difference in flexion measurements. Stratifying our data into 3 groups, we found that neutral humeral rotation kept elbow extension measurements closer to 0° for patients with both hyperextension and contractures. With increasing severity of flexion contractures in groups 2 and 3, the measurement errors were magnified. The differences in extension measurement values between these 2 groups based on humeral rotation increased more than 4°—an indication that, as flexion contracture severity increases, so does the degree of measurement error when elbow extension is measured with the humerus in neutral rotation rather than external rotation.

Our literature review found no studies on ROM value differences based on position of humeral rotation. Most texts, in their descriptions of elbow ROM and biomechanics, make no reference to position of pronosupination at time of flexion arc measurement.^5-8 Although many elbow authorities recommend taking elbow ROM measurements in full external rotation, we found no corroborating evidence.

Other investigators have evaluated the reliability of goniometer measurements.^2,3 Rothstein and colleagues³ concluded that elbow and knee goniometric measurements are highly reliable in the clinical setting when taken by the same person. In particular, intratester reliability for elbow extension measurements was high. Armstrong and colleagues² specifically examined intratester, intertester, and interdevice reliability and found that intratester reliability was much higher than intertester reliability for universal goniometry. In our study, all patients were measured with the same technique by the same orthopedic surgeon to eliminate any intertester reliability error. Armstrong and colleagues² also found that intratester changes vis-a-vis extension measurements are meaningful when goniometric differences are more than 7°. In our study, the difference in extension measurements between the 2 humeral positions averaged 8° overall and 12° in group 3. This suggests that the data reported here reflect a true difference dependent on humeral rotation and are not a result of goniometer intratester variability.

Other studies have examined measurement devices other than the standard universal goniometer. Cleffken and colleagues⁴ found that the electronic digital inclinometer was reliable for elbow ROM measurements. Blonna and colleagues⁹ used digital photography–based goniometry to measure patient outcomes without doctor–patient contact at tertiary-care centers and found it to be more accurate and reliable than clinical goniometry in measuring elbow flexion and extension. Chapleau and colleagues¹⁰ compared the validity of goniometric elbow measurements in radiographic methods and concluded that the maximal error of goniometric measurements in extension was 10.3°. However, they also found high intraclass correlation coefficients for goniometric measurements. With the accepted clinical reliability of universal goniometry,^2-4,10 we believe it to be the best clinical tool for this study because of its availability, minimal cost, and ease of use.

In the clinical setting, elbow flexion arc measurements are a major factor in treatment decisions and often dictate whether to proceed with operative interventions such as capsular release. In addition, ROM measurements are crucial in determining the success of treatments and the progression of disease. Erroneous elbow extension measurements can have significant consequences if they falsely indicate functional ROM when taken in neutral position. This is particularly true for patients with elbow flexion contractures of more than 30°, in whom differences in humeral rotation resulted in about 12° of variance between measured values. For instance, a patient with a true 40° flexion contracture in the externally rotated position could be determined to have functional ROM based on measurements made in the neutral position.

Limitations of this study include those involving goniometer reliability and intraobserver variability (already described) and the validity of goniometer measurements compared with radiographic measurements.

Conclusion

Because elbow goniometer extension measurements taken in neutral humeral rotation underestimate both the degree of elbow hyperextension and the degree of elbow flexion contracture, we recommend taking elbow flexion arc measurements in the true plane of motion, with the humerus externally rotated by fully supinating the forearm, such that the distal humeral condyles are parallel to the floor.

The treatment of patients with severe shoulder pain and disability combined with a nonfunctional rotator cuff was a clinical challenge until the development of the reverse total shoulder arthroplasty (RTSA).^1-3 Massive rotator cuff tears can leave patients with a pseudoparalytic upper extremity and may result in advanced arthritis of the joint because of altered mechanical and nutritional factors.⁴ In this setting, simply replacing the arthritic joint with standard total shoulder arthroplasty (TSA) is not recommended because it does not address the functional deficits, and it has poor long-term outcomes.^3,5 RTSA works by changing the center of rotation of the shoulder joint so that the deltoid muscle can be used to elevate the arm.^6,7 The 4 rotator cuff muscles are not required for forward elevation or stability of this constrained implant.^6,8

Current indications for RTSA are cuff tear arthropathy, complex proximal humerus fractures, and revision from hemiarthroplasty or TSA with rotator cuff dysfunction. Patients with advanced cuff tear arthropathy have minimal forward elevation and pseudoparalysis. Previous studies have shown mean preoperative forward flexion of 55º and mean ASES (American Shoulder and Elbow Surgeons) Standardized Shoulder Assessment Form score of 34.3.⁹ Thus, minimal overhead activity is possible without RTSA. Advances in the RTSA technique have led to promising results (excellent functional improvement), but there is limited information regarding the activity levels patients can achieve after surgery.^7,9-11

We conducted a study of the types of sporting activities in which patients with RTSA could participate. We hypothesized that, relative to historic controls, patients with RTSA could return to low-intensity sporting activities with improvement in motion and ASES scores.

Materials and Methods

After this study received institutional review board approval, patients who had undergone RTSA at our institution between January 1, 2004 and December 31, 2010 were identified by the billing codes used for the procedure. Each patient who had RTSA performed during the study period was included in the study. Charts were then reviewed to extract demographic data, preoperative diagnosis, surgery date, operative side, dominant side, type of implant used, operative complications, and subsequent revisions. A questionnaire (Appendix) was designed and used to assess activity, functional status, pain, and satisfaction levels after RTSA. Patients had to be willing and able to complete this questionnaire in order to be included in the study.

The questionnaire included demographic questions; a list of 42 activities patients could choose from to describe their current activity level, activities they were able to perform before the surgery, and activities they wish they could perform; a list of reasons for any limitations; and questions about overall pain, strength, and satisfaction with the procedure. In addition, there was an open-ended question for activities that may not have been listed. The questionnaire also included a validated method for assessing shoulder range of motion (ROM) at home, where patients rated their overhead motion according to standardized physical landmarks, including the level of the shoulder, chin, eyebrows, top of head, and above head.^12-14 Also provided was the ASES Standardized Shoulder Assessment Form, which features a 100-point visual analog scale for pain plus functional ability questions, with higher scores indicating less pain and better function.^15,16 The minimal clinical significance in the ASES score is 6.4 points.^17,18 Scores were recorded and analyzed. Student t test was used to calculate statistical differences between patients who had primary RTSA performed and patients who underwent revision RTSA.

Study personnel contacted patients by telephone and direct mailing. Patients who could not be reached initially were called at least 4 more times: twice during the weekday, once during the evening, and once on the weekend. Patients who could not be contacted by telephone were then cross-referenced with the Social Security database to see if any were deceased. Response data were tabulated, and patients were stratified into high-, moderate-, and low-intensity activity.

One of the 3 senior authors (Dr. Ahmad, Dr. Bigliani, Dr. Levine) performed the 95 RTSAs: 84 Zimmer (Warsaw, Indiana), 7 DePuy (Warsaw, Indiana), 4 Tornier (Minneapolis, Minnesota). The DePuy and Tornier implants were used when a 30-mm glenoid peg was required (before Zimmer offered this length in its system). The procedure was done with a deltopectoral approach with 20° of retroversion. In revision cases, the same approach was used, the hardware or implants were removed, and the position of the humeral component was determined based on the pectoralis major insertion and the deltoid tension. In 80% of cases, the subscapularis was not repaired; in the other 20%, it was. Whether it was repaired depended on tendon viability and surgeon preference, as subscapularis repair status has been shown not to affect functional outcome.^19-21 No combined latissimus transfers were performed. Patients wore a sling the first 4 weeks after surgery (only wrist and elbow motion allowed) and then advanced to active shoulder ROM. Eight weeks after surgery, they began gentle shoulder strengthening.

Results

One hundred nine consecutive patients underwent RTSA at a single institution. Fifteen patients subsequently died, 14 could not be contacted, and 2 declined, leaving 78 patients available for clinical follow-up. Mean follow-up was 4.8 years (range 2-9 years). Mean (SD) age at surgery was 75.3 (7.5) years. Seventy-five percent of the patients were women. Sixty-one percent underwent surgery for cuff tear arthropathy, 31% for revision of previous arthroplasty or internal fixation, 7% for complex fractures, and 1% for tumor. Of the 24 revisions, 15 were for failed hemiarthroplasty, 3 were for failed TSA with rotator cuff dysfunction, 4 were for fracture with failed internal fixation, and 2 were for failed RTSA referred from other institutions. The dominant shoulder was involved 62% of the time. Preoperative active forward shoulder elevation was less than 90° in all patients. There were 10 complications: 2 dislocations that were closed-reduced and remained stable, 1 dislocation that required revision of the liner, 1 aseptic loosening in a patient who has declined revision, 2 dissociated glenosphere baseplates, 2 deep infections that required 2-stage exchanges, 1 deep infection that required a 2-stage exchange that was then complicated by dissociation of the glenosphere baseplate requiring revision, and 1 superficial infection that resolved with oral antibiotics.

After surgery, mean active forward elevation was 140°, mean active external rotation was 48°, and mean active internal rotation was to S1. Mean (SD) postoperative ASES score was 77.5 (23.4). Satisfaction level was high (mean, 8.3/10), and mean pain levels were low: 2.3 out of 10 on the visual analog scale and 44.0 (SD, 11.7) on the ASES pain component. Strength was rated a mean of good. Table 1 lists the clinical data for the primary and revision surgery patients.

Eighteen patients (23.1%) returned to 24 different high-intensity activities, such as hunting, golf, and skiing; 38 patients (48.7%) returned to moderate-intensity activities, such as swimming, bowling, and raking leaves; and 22 patients (28.2%) returned to low-intensity activities, such as riding a stationary bike, playing a musical instrument, and walking (Table 2). Four patients played golf before and after RTSA, but neither of the 2 patients who played tennis before RTSA were able to do so after. Patients reported they engaged in their favorite leisure activity a mean of 4.8 times per week and a mean of 1.5 hours each time.

A medical problem was cited by 58% of patients as the reason for limited activity. These patients reported physical decline resulting from cardiac disease, diabetes, asthma/chronic obstructive pulmonary disease, or arthritis in other joints. Reasons for activity limitation are listed in Table 3. Post-RTSA activities that patients could not do for any reason are listed in Table 4. Activity limitations that patients attributed to the RTSA are listed in Table 5.

The majority of patients (57.7%) reported no change, from before RTSA to after RTSA, in being unable to do certain desired activities (eg, softball, target shooting, horseback riding, running, traveling). Sixteen patients (20.8%) reported being unable to return to an activity (eg, tennis, swimming, baseball, kayaking) they had been able to do before surgery. Most (69%) of those patients reported being unable to return to a moderate- or high-intensity activity after RTSA, but 81.8% were able to return to different moderate- or high-intensity activities.

Revision patients, who reported lower overhead activity levels, constituted 73% of the patients who felt their shoulder mechanically limited their activity, despite the fact that revisions constituted only 25% of the cases overall. Mean active ROM was statistically lower for revision patients than for primary patients (P < .05). Mean ASES score was statistically lower for the revision group (P < .001) and represented a clinically significant difference. Mean pain level was low (3.3) and satisfaction still generally high (7.4), but pain, satisfaction, and strength were about 1 point worse on average in the revision group than in the primary group.

Discussion

In the United States and other countries, RTSA implant survivorship is good.^9,22 In this article, we have reported on post-RTSA activity levels, on the significant impact of comorbidities on this group, and on the negative effect of revisions on postoperative activity. Patients in this population reported that concomitant medical problems were the most important factor limiting their post-RTSA activity levels. Understanding and interpreting quality-of-life or functional scores in this elderly group must take into account the impact of comorbidities.²³

Patients should have realistic postoperative expectations.²⁴ In this study, some patients engaged in high-intensity overhead activities, such as golf, chopping wood, and shooting. However, the most difficulty was encountered trying to return to activities (eg, tennis, kayaking, archery, combing hair) that required external rotation in abduction.

Patients who had a previous implant (eg, hemiarthroplasty, TSA, failed internal fixation) revised to RTSA had lower activity levels and were 9 times more likely than primary patients to report having a mechanical shoulder limitation affecting their activity. Revision patients also had worse forward elevation, external rotation, pain, and satisfaction.

This study is limited in that it is retrospective. Subsequent prospective studies focused on younger patients who undergo primary RTSA may be useful if indications expand. In addition, subscapularis status and especially infraspinatus status may affect activity levels and could be analyzed in a study. Another limitation is that we did not specifically record detailed preoperative data, though all patients were known to have preoperative forward elevation of less than 90°.

In general, the primary measure of success for RTSA has been pain relief. Some studies have also reported on strength and ROM.^2,20,25,26 A recent study using similar methodology demonstrated comparable ROM and low pain after RTSA, though revisions were not included in that study.²⁶ In contrast to the present study, no patient in that study was able to play tennis or golf, but the reasons for the limited activity were not explored. In both studies, post-RTSA sports were generally of lower intensity than those played by patients after anatomical TSA.²⁷

Overall, the majority of patients were very satisfied with their low pain level after RTSA. In addition, many patients not limited by other medical conditions were able to return to their pre-RTSA moderate-intensity recreational activities.

The treatment of patients with severe shoulder pain and disability combined with a nonfunctional rotator cuff was a clinical challenge until the development of the reverse total shoulder arthroplasty (RTSA).^1-3 Massive rotator cuff tears can leave patients with a pseudoparalytic upper extremity and may result in advanced arthritis of the joint because of altered mechanical and nutritional factors.⁴ In this setting, simply replacing the arthritic joint with standard total shoulder arthroplasty (TSA) is not recommended because it does not address the functional deficits, and it has poor long-term outcomes.^3,5 RTSA works by changing the center of rotation of the shoulder joint so that the deltoid muscle can be used to elevate the arm.^6,7 The 4 rotator cuff muscles are not required for forward elevation or stability of this constrained implant.^6,8

Current indications for RTSA are cuff tear arthropathy, complex proximal humerus fractures, and revision from hemiarthroplasty or TSA with rotator cuff dysfunction. Patients with advanced cuff tear arthropathy have minimal forward elevation and pseudoparalysis. Previous studies have shown mean preoperative forward flexion of 55º and mean ASES (American Shoulder and Elbow Surgeons) Standardized Shoulder Assessment Form score of 34.3.⁹ Thus, minimal overhead activity is possible without RTSA. Advances in the RTSA technique have led to promising results (excellent functional improvement), but there is limited information regarding the activity levels patients can achieve after surgery.^7,9-11

We conducted a study of the types of sporting activities in which patients with RTSA could participate. We hypothesized that, relative to historic controls, patients with RTSA could return to low-intensity sporting activities with improvement in motion and ASES scores.

Materials and Methods

After this study received institutional review board approval, patients who had undergone RTSA at our institution between January 1, 2004 and December 31, 2010 were identified by the billing codes used for the procedure. Each patient who had RTSA performed during the study period was included in the study. Charts were then reviewed to extract demographic data, preoperative diagnosis, surgery date, operative side, dominant side, type of implant used, operative complications, and subsequent revisions. A questionnaire (Appendix) was designed and used to assess activity, functional status, pain, and satisfaction levels after RTSA. Patients had to be willing and able to complete this questionnaire in order to be included in the study.

The questionnaire included demographic questions; a list of 42 activities patients could choose from to describe their current activity level, activities they were able to perform before the surgery, and activities they wish they could perform; a list of reasons for any limitations; and questions about overall pain, strength, and satisfaction with the procedure. In addition, there was an open-ended question for activities that may not have been listed. The questionnaire also included a validated method for assessing shoulder range of motion (ROM) at home, where patients rated their overhead motion according to standardized physical landmarks, including the level of the shoulder, chin, eyebrows, top of head, and above head.^12-14 Also provided was the ASES Standardized Shoulder Assessment Form, which features a 100-point visual analog scale for pain plus functional ability questions, with higher scores indicating less pain and better function.^15,16 The minimal clinical significance in the ASES score is 6.4 points.^17,18 Scores were recorded and analyzed. Student t test was used to calculate statistical differences between patients who had primary RTSA performed and patients who underwent revision RTSA.

Study personnel contacted patients by telephone and direct mailing. Patients who could not be reached initially were called at least 4 more times: twice during the weekday, once during the evening, and once on the weekend. Patients who could not be contacted by telephone were then cross-referenced with the Social Security database to see if any were deceased. Response data were tabulated, and patients were stratified into high-, moderate-, and low-intensity activity.

One of the 3 senior authors (Dr. Ahmad, Dr. Bigliani, Dr. Levine) performed the 95 RTSAs: 84 Zimmer (Warsaw, Indiana), 7 DePuy (Warsaw, Indiana), 4 Tornier (Minneapolis, Minnesota). The DePuy and Tornier implants were used when a 30-mm glenoid peg was required (before Zimmer offered this length in its system). The procedure was done with a deltopectoral approach with 20° of retroversion. In revision cases, the same approach was used, the hardware or implants were removed, and the position of the humeral component was determined based on the pectoralis major insertion and the deltoid tension. In 80% of cases, the subscapularis was not repaired; in the other 20%, it was. Whether it was repaired depended on tendon viability and surgeon preference, as subscapularis repair status has been shown not to affect functional outcome.^19-21 No combined latissimus transfers were performed. Patients wore a sling the first 4 weeks after surgery (only wrist and elbow motion allowed) and then advanced to active shoulder ROM. Eight weeks after surgery, they began gentle shoulder strengthening.

Results

One hundred nine consecutive patients underwent RTSA at a single institution. Fifteen patients subsequently died, 14 could not be contacted, and 2 declined, leaving 78 patients available for clinical follow-up. Mean follow-up was 4.8 years (range 2-9 years). Mean (SD) age at surgery was 75.3 (7.5) years. Seventy-five percent of the patients were women. Sixty-one percent underwent surgery for cuff tear arthropathy, 31% for revision of previous arthroplasty or internal fixation, 7% for complex fractures, and 1% for tumor. Of the 24 revisions, 15 were for failed hemiarthroplasty, 3 were for failed TSA with rotator cuff dysfunction, 4 were for fracture with failed internal fixation, and 2 were for failed RTSA referred from other institutions. The dominant shoulder was involved 62% of the time. Preoperative active forward shoulder elevation was less than 90° in all patients. There were 10 complications: 2 dislocations that were closed-reduced and remained stable, 1 dislocation that required revision of the liner, 1 aseptic loosening in a patient who has declined revision, 2 dissociated glenosphere baseplates, 2 deep infections that required 2-stage exchanges, 1 deep infection that required a 2-stage exchange that was then complicated by dissociation of the glenosphere baseplate requiring revision, and 1 superficial infection that resolved with oral antibiotics.

After surgery, mean active forward elevation was 140°, mean active external rotation was 48°, and mean active internal rotation was to S1. Mean (SD) postoperative ASES score was 77.5 (23.4). Satisfaction level was high (mean, 8.3/10), and mean pain levels were low: 2.3 out of 10 on the visual analog scale and 44.0 (SD, 11.7) on the ASES pain component. Strength was rated a mean of good. Table 1 lists the clinical data for the primary and revision surgery patients.

Eighteen patients (23.1%) returned to 24 different high-intensity activities, such as hunting, golf, and skiing; 38 patients (48.7%) returned to moderate-intensity activities, such as swimming, bowling, and raking leaves; and 22 patients (28.2%) returned to low-intensity activities, such as riding a stationary bike, playing a musical instrument, and walking (Table 2). Four patients played golf before and after RTSA, but neither of the 2 patients who played tennis before RTSA were able to do so after. Patients reported they engaged in their favorite leisure activity a mean of 4.8 times per week and a mean of 1.5 hours each time.

A medical problem was cited by 58% of patients as the reason for limited activity. These patients reported physical decline resulting from cardiac disease, diabetes, asthma/chronic obstructive pulmonary disease, or arthritis in other joints. Reasons for activity limitation are listed in Table 3. Post-RTSA activities that patients could not do for any reason are listed in Table 4. Activity limitations that patients attributed to the RTSA are listed in Table 5.

The majority of patients (57.7%) reported no change, from before RTSA to after RTSA, in being unable to do certain desired activities (eg, softball, target shooting, horseback riding, running, traveling). Sixteen patients (20.8%) reported being unable to return to an activity (eg, tennis, swimming, baseball, kayaking) they had been able to do before surgery. Most (69%) of those patients reported being unable to return to a moderate- or high-intensity activity after RTSA, but 81.8% were able to return to different moderate- or high-intensity activities.

Revision patients, who reported lower overhead activity levels, constituted 73% of the patients who felt their shoulder mechanically limited their activity, despite the fact that revisions constituted only 25% of the cases overall. Mean active ROM was statistically lower for revision patients than for primary patients (P < .05). Mean ASES score was statistically lower for the revision group (P < .001) and represented a clinically significant difference. Mean pain level was low (3.3) and satisfaction still generally high (7.4), but pain, satisfaction, and strength were about 1 point worse on average in the revision group than in the primary group.

Discussion

In the United States and other countries, RTSA implant survivorship is good.^9,22 In this article, we have reported on post-RTSA activity levels, on the significant impact of comorbidities on this group, and on the negative effect of revisions on postoperative activity. Patients in this population reported that concomitant medical problems were the most important factor limiting their post-RTSA activity levels. Understanding and interpreting quality-of-life or functional scores in this elderly group must take into account the impact of comorbidities.²³

Patients should have realistic postoperative expectations.²⁴ In this study, some patients engaged in high-intensity overhead activities, such as golf, chopping wood, and shooting. However, the most difficulty was encountered trying to return to activities (eg, tennis, kayaking, archery, combing hair) that required external rotation in abduction.

Patients who had a previous implant (eg, hemiarthroplasty, TSA, failed internal fixation) revised to RTSA had lower activity levels and were 9 times more likely than primary patients to report having a mechanical shoulder limitation affecting their activity. Revision patients also had worse forward elevation, external rotation, pain, and satisfaction.

This study is limited in that it is retrospective. Subsequent prospective studies focused on younger patients who undergo primary RTSA may be useful if indications expand. In addition, subscapularis status and especially infraspinatus status may affect activity levels and could be analyzed in a study. Another limitation is that we did not specifically record detailed preoperative data, though all patients were known to have preoperative forward elevation of less than 90°.

In general, the primary measure of success for RTSA has been pain relief. Some studies have also reported on strength and ROM.^2,20,25,26 A recent study using similar methodology demonstrated comparable ROM and low pain after RTSA, though revisions were not included in that study.²⁶ In contrast to the present study, no patient in that study was able to play tennis or golf, but the reasons for the limited activity were not explored. In both studies, post-RTSA sports were generally of lower intensity than those played by patients after anatomical TSA.²⁷

Overall, the majority of patients were very satisfied with their low pain level after RTSA. In addition, many patients not limited by other medical conditions were able to return to their pre-RTSA moderate-intensity recreational activities.

The treatment of patients with severe shoulder pain and disability combined with a nonfunctional rotator cuff was a clinical challenge until the development of the reverse total shoulder arthroplasty (RTSA).^1-3 Massive rotator cuff tears can leave patients with a pseudoparalytic upper extremity and may result in advanced arthritis of the joint because of altered mechanical and nutritional factors.⁴ In this setting, simply replacing the arthritic joint with standard total shoulder arthroplasty (TSA) is not recommended because it does not address the functional deficits, and it has poor long-term outcomes.^3,5 RTSA works by changing the center of rotation of the shoulder joint so that the deltoid muscle can be used to elevate the arm.^6,7 The 4 rotator cuff muscles are not required for forward elevation or stability of this constrained implant.^6,8

Current indications for RTSA are cuff tear arthropathy, complex proximal humerus fractures, and revision from hemiarthroplasty or TSA with rotator cuff dysfunction. Patients with advanced cuff tear arthropathy have minimal forward elevation and pseudoparalysis. Previous studies have shown mean preoperative forward flexion of 55º and mean ASES (American Shoulder and Elbow Surgeons) Standardized Shoulder Assessment Form score of 34.3.⁹ Thus, minimal overhead activity is possible without RTSA. Advances in the RTSA technique have led to promising results (excellent functional improvement), but there is limited information regarding the activity levels patients can achieve after surgery.^7,9-11

We conducted a study of the types of sporting activities in which patients with RTSA could participate. We hypothesized that, relative to historic controls, patients with RTSA could return to low-intensity sporting activities with improvement in motion and ASES scores.

Materials and Methods

After this study received institutional review board approval, patients who had undergone RTSA at our institution between January 1, 2004 and December 31, 2010 were identified by the billing codes used for the procedure. Each patient who had RTSA performed during the study period was included in the study. Charts were then reviewed to extract demographic data, preoperative diagnosis, surgery date, operative side, dominant side, type of implant used, operative complications, and subsequent revisions. A questionnaire (Appendix) was designed and used to assess activity, functional status, pain, and satisfaction levels after RTSA. Patients had to be willing and able to complete this questionnaire in order to be included in the study.

The questionnaire included demographic questions; a list of 42 activities patients could choose from to describe their current activity level, activities they were able to perform before the surgery, and activities they wish they could perform; a list of reasons for any limitations; and questions about overall pain, strength, and satisfaction with the procedure. In addition, there was an open-ended question for activities that may not have been listed. The questionnaire also included a validated method for assessing shoulder range of motion (ROM) at home, where patients rated their overhead motion according to standardized physical landmarks, including the level of the shoulder, chin, eyebrows, top of head, and above head.^12-14 Also provided was the ASES Standardized Shoulder Assessment Form, which features a 100-point visual analog scale for pain plus functional ability questions, with higher scores indicating less pain and better function.^15,16 The minimal clinical significance in the ASES score is 6.4 points.^17,18 Scores were recorded and analyzed. Student t test was used to calculate statistical differences between patients who had primary RTSA performed and patients who underwent revision RTSA.

Study personnel contacted patients by telephone and direct mailing. Patients who could not be reached initially were called at least 4 more times: twice during the weekday, once during the evening, and once on the weekend. Patients who could not be contacted by telephone were then cross-referenced with the Social Security database to see if any were deceased. Response data were tabulated, and patients were stratified into high-, moderate-, and low-intensity activity.

One of the 3 senior authors (Dr. Ahmad, Dr. Bigliani, Dr. Levine) performed the 95 RTSAs: 84 Zimmer (Warsaw, Indiana), 7 DePuy (Warsaw, Indiana), 4 Tornier (Minneapolis, Minnesota). The DePuy and Tornier implants were used when a 30-mm glenoid peg was required (before Zimmer offered this length in its system). The procedure was done with a deltopectoral approach with 20° of retroversion. In revision cases, the same approach was used, the hardware or implants were removed, and the position of the humeral component was determined based on the pectoralis major insertion and the deltoid tension. In 80% of cases, the subscapularis was not repaired; in the other 20%, it was. Whether it was repaired depended on tendon viability and surgeon preference, as subscapularis repair status has been shown not to affect functional outcome.^19-21 No combined latissimus transfers were performed. Patients wore a sling the first 4 weeks after surgery (only wrist and elbow motion allowed) and then advanced to active shoulder ROM. Eight weeks after surgery, they began gentle shoulder strengthening.

Results

One hundred nine consecutive patients underwent RTSA at a single institution. Fifteen patients subsequently died, 14 could not be contacted, and 2 declined, leaving 78 patients available for clinical follow-up. Mean follow-up was 4.8 years (range 2-9 years). Mean (SD) age at surgery was 75.3 (7.5) years. Seventy-five percent of the patients were women. Sixty-one percent underwent surgery for cuff tear arthropathy, 31% for revision of previous arthroplasty or internal fixation, 7% for complex fractures, and 1% for tumor. Of the 24 revisions, 15 were for failed hemiarthroplasty, 3 were for failed TSA with rotator cuff dysfunction, 4 were for fracture with failed internal fixation, and 2 were for failed RTSA referred from other institutions. The dominant shoulder was involved 62% of the time. Preoperative active forward shoulder elevation was less than 90° in all patients. There were 10 complications: 2 dislocations that were closed-reduced and remained stable, 1 dislocation that required revision of the liner, 1 aseptic loosening in a patient who has declined revision, 2 dissociated glenosphere baseplates, 2 deep infections that required 2-stage exchanges, 1 deep infection that required a 2-stage exchange that was then complicated by dissociation of the glenosphere baseplate requiring revision, and 1 superficial infection that resolved with oral antibiotics.

After surgery, mean active forward elevation was 140°, mean active external rotation was 48°, and mean active internal rotation was to S1. Mean (SD) postoperative ASES score was 77.5 (23.4). Satisfaction level was high (mean, 8.3/10), and mean pain levels were low: 2.3 out of 10 on the visual analog scale and 44.0 (SD, 11.7) on the ASES pain component. Strength was rated a mean of good. Table 1 lists the clinical data for the primary and revision surgery patients.

Eighteen patients (23.1%) returned to 24 different high-intensity activities, such as hunting, golf, and skiing; 38 patients (48.7%) returned to moderate-intensity activities, such as swimming, bowling, and raking leaves; and 22 patients (28.2%) returned to low-intensity activities, such as riding a stationary bike, playing a musical instrument, and walking (Table 2). Four patients played golf before and after RTSA, but neither of the 2 patients who played tennis before RTSA were able to do so after. Patients reported they engaged in their favorite leisure activity a mean of 4.8 times per week and a mean of 1.5 hours each time.

A medical problem was cited by 58% of patients as the reason for limited activity. These patients reported physical decline resulting from cardiac disease, diabetes, asthma/chronic obstructive pulmonary disease, or arthritis in other joints. Reasons for activity limitation are listed in Table 3. Post-RTSA activities that patients could not do for any reason are listed in Table 4. Activity limitations that patients attributed to the RTSA are listed in Table 5.

The majority of patients (57.7%) reported no change, from before RTSA to after RTSA, in being unable to do certain desired activities (eg, softball, target shooting, horseback riding, running, traveling). Sixteen patients (20.8%) reported being unable to return to an activity (eg, tennis, swimming, baseball, kayaking) they had been able to do before surgery. Most (69%) of those patients reported being unable to return to a moderate- or high-intensity activity after RTSA, but 81.8% were able to return to different moderate- or high-intensity activities.

Revision patients, who reported lower overhead activity levels, constituted 73% of the patients who felt their shoulder mechanically limited their activity, despite the fact that revisions constituted only 25% of the cases overall. Mean active ROM was statistically lower for revision patients than for primary patients (P < .05). Mean ASES score was statistically lower for the revision group (P < .001) and represented a clinically significant difference. Mean pain level was low (3.3) and satisfaction still generally high (7.4), but pain, satisfaction, and strength were about 1 point worse on average in the revision group than in the primary group.

Discussion

In the United States and other countries, RTSA implant survivorship is good.^9,22 In this article, we have reported on post-RTSA activity levels, on the significant impact of comorbidities on this group, and on the negative effect of revisions on postoperative activity. Patients in this population reported that concomitant medical problems were the most important factor limiting their post-RTSA activity levels. Understanding and interpreting quality-of-life or functional scores in this elderly group must take into account the impact of comorbidities.²³

Patients should have realistic postoperative expectations.²⁴ In this study, some patients engaged in high-intensity overhead activities, such as golf, chopping wood, and shooting. However, the most difficulty was encountered trying to return to activities (eg, tennis, kayaking, archery, combing hair) that required external rotation in abduction.

Patients who had a previous implant (eg, hemiarthroplasty, TSA, failed internal fixation) revised to RTSA had lower activity levels and were 9 times more likely than primary patients to report having a mechanical shoulder limitation affecting their activity. Revision patients also had worse forward elevation, external rotation, pain, and satisfaction.

This study is limited in that it is retrospective. Subsequent prospective studies focused on younger patients who undergo primary RTSA may be useful if indications expand. In addition, subscapularis status and especially infraspinatus status may affect activity levels and could be analyzed in a study. Another limitation is that we did not specifically record detailed preoperative data, though all patients were known to have preoperative forward elevation of less than 90°.

In general, the primary measure of success for RTSA has been pain relief. Some studies have also reported on strength and ROM.^2,20,25,26 A recent study using similar methodology demonstrated comparable ROM and low pain after RTSA, though revisions were not included in that study.²⁶ In contrast to the present study, no patient in that study was able to play tennis or golf, but the reasons for the limited activity were not explored. In both studies, post-RTSA sports were generally of lower intensity than those played by patients after anatomical TSA.²⁷

Overall, the majority of patients were very satisfied with their low pain level after RTSA. In addition, many patients not limited by other medical conditions were able to return to their pre-RTSA moderate-intensity recreational activities.

The diagnosis of cancer is a life-changing event for the patient as well as the patient’s family, friends, and relatives. Once diagnosed, most cancer patients want more information about their prognosis, future procedures, and/or treatment options.¹ Receiving such information has been shown to reduce patient anxiety, increase patient satisfaction with care, and improve self-care.^2-6 With the evolution of the Internet, patients in general^7-9 and, specifically, cancer patients^10-17 have turned to websites and online patient education materials (PEMs) to gather more health information.

For online PEMs to convey health information, their reading level must match the health literacy of the individuals who access them. Health literacy is the ability of an individual to gather and comprehend information about their condition to make the best decisions for their health.¹⁸ According to a report by the Institute of Medicine, 90 million American adults cannot properly use the US health care system because they do not possess adequate health literacy.¹⁸ Additionally, 36% of adults in the United States have basic or less-than-basic health literacy.¹⁹ This is starkly contrasted with the 12% of US adults who have proficient health literacy. A 2012 survey showed that about 31% of individuals who look for health information on the Internet have a high school education or less.⁸ In order to address the low health literacy of adults, the National Institutes of Health (NIH) has recommended that online PEMs be written at a sixth- to seventh-grade reading level.²⁰ 

Unfortunately, many online PEMs related to certain cancer^21-25 and orthopedic conditions^26-31 do not meet NIH recommendations. Only 1 study has specifically looked at PEMs related to an orthopedic cancer condition.³² Lam and colleagues³² evaluated the readability of osteosarcoma PEMs from 56 websites using only 2 readability instruments and identified 86% of the websites as having a greater than eighth-grade reading level. No study has thoroughly assessed the readability of PEMs about bone and soft-tissue sarcomas and related conditions nor has any used 10 different readability instruments. Since each readability instrument has different variables (eg, sentence length, number of paragraphs, or number of complex words), averaging the scores of 10 of these instruments may result in less bias.

The purpose of this study was to evaluate the readability of online PEMs concerning bone and soft-tissue sarcomas and related conditions. The online PEMs came from websites that sarcoma patients may visit to obtain information about their condition. Our hypothesis was that the majority of these online PEMs will have a higher reading level than the NIH recommendations.

Materials and Methods

In May 2013, we identified online PEMs that included background, diagnosis, tests, or treatments for bone and soft-tissue sarcomas and conditions that mimic bone sarcoma. We included articles from the Tumors section of the American Academy of Orthopaedic Surgeons (AAOS) website.³³ A second source of online PEMs came from a list of academic training centers created through the American Medical Association’s Fellowship and Residency Electronic Internet Database (FREIDA) with search criteria narrowed to orthopedic surgery. If we did not find PEMs of bone and soft-tissue cancers in the orthopedic department of a given academic training center’s website, we searched its cancer center website. We chose 4 programs with PEMs relevant to bone and soft-tissue sarcomas from each region in FREIDA for a balanced representation, except for the Territory region because it had only 1 academic training center and no relevant PEMs. Specialized websites, including Bonetumor.org, Sarcoma Alliance (Sarcomaalliance.org), and Sarcoma Foundation of America (Curesarcoma.org), were also evaluated. Within the Sarcoma Specialists section of the Sarcoma Alliance website,³⁴ sarcoma specialists who were not identified from the FREIDA search for academic training centers were selected for review.

Because 8 of 10 individuals looking for health information on the Internet start their investigation at search engines, we also looked for PEMs through a Google search (Google.com) of bone cancer, and evaluated the first 10 hits for PEMs.⁸ Of these 10 hits, 8 had relevant PEMs, which we searched for additional PEMs about bone and soft-tissue cancers and related conditions. We also conducted a Google search of the most common bone sarcoma and soft-tissue sarcoma, osteosarcoma and malignant fibrous histiocytoma, respectively, and found 2 additional websites with relevant PEMs. LaCoursiere and colleagues³⁵ surveyed cancer patients who used the Internet and found that they preferred WebMD (Webmd.com) and Medscape (Medscape.com) as sources for content about their medical condition.³⁵ WebMD had been identified in the Google search, and we gathered the PEMs from Medscape also. It is worth noting that some of these websites are written for patients as well as clinicians.

Text from these PEMs were copied and pasted into separate Microsoft Word documents (Microsoft, Redmond, Washington). Advertisements, pictures, picture text, hyperlinks, copyright notices, page navigation links, paragraphs with no text, and any text that was not related to the given condition were deleted from the document to format the text for the readability software. Then, each Microsoft Word document was uploaded into the software package Readability Studio Professional (RSP) Edition Version 2012.1 for Windows (Oleander Software, Vandalia, Ohio). The 10 distinct readability instruments that were used to gauge the readability of each document were the Flesch Reading Ease score (FRE), the New Fog Count, the New Automated Readability Index, the Coleman-Liau Index (CLI), the Fry readability graph, the New Dale-Chall formula (NDC), the Gunning Frequency of Gobbledygook (Gunning FOG), the Powers-Sumner-Kearl formula, the Simple Measure of Gobbledygook (SMOG), and the Raygor Estimate Graph.

The FRE’s formula takes the average number of words per sentence and average number of syllables per word to compute a score ranging from 0 to 100 with 0 being the hardest to read.³⁶ The New Fog Count tallies the number of sentences, easy words, and hard words (polysyllables) to calculate the grade level of the document.³⁷ The New Automated Readability Index takes the average characters per word and average words per sentence to calculate a grade level for the document.³⁷ The CLI randomly samples a few hundred words from the document, averages the number of letters and sentences per sample, and calculates an estimated grade level.³⁸ The Fry readability graph selects samples of 100 words from the document, averages the number of syllables and sentences per 100 words, plots these data points on a graph, with the intersection determining the reading level.³⁹ The NDC uses a list of 3000 familiar words that most fourth-grade students know.⁴⁰ The percentage of difficult words, which are not on the list of familiar words, and the average sentence length in words are used to calculate the reading grade level of the document. The Gunning FOG uses the average sentence length in words and the percentage of hard words from a sample of at least 100 words to determine the reading grade level of the document.⁴¹ The Powers-Sumner-Kearl formula uses the average sentence length and percentage of monosyllables from a 100-word sample passage to calculate the reading grade level.⁴² The SMOG formula counts the number of polysyllabic words from 30 sentences and calculates the reading grade level of the document.⁴³ In contrast to other formulas that test for 50% to 75% comprehension, the SMOG formula tests for 100% comprehension. As a result, the SMOG formula generally assigns a reading level 2 grades higher than the Dale-Chall level. The Raygor Estimate Graph selects a 100-word passage, counts the number of sentences and number of words with 6 or more letters, and plots the 2 variables on a graph to determine the reading grade level.⁴⁴ The software package calculated the results from each reading instrument and reported the mean grade level score
for each document.

Results

We identified a total of 72 websites with relevant PEMs and included them in this study. Of these 72 websites, 36 websites were academic training centers, 10 were Google search hits, and 21 were from the Sarcoma Alliance list of sarcoma specialists. The remaining 5 websites were AAOS, Bonetumor.org, Sarcoma Alliance, Sarcoma Foundation of America, and Medscape. A list of conditions and treatments that were considered relevant PEMs is found in Appendix 1. A total of 774 articles were obtained from the 72 websites.

None of the websites had a mean readability score of 7 (seventh grade) or lower (Figures 1A, 1B). Mid-America Sarcoma Institute’s PEMs had the lowest mean readability score, 8.9. The lowest readability score was 5.3, which the New Fog Count readability instrument calculated for Vanderbilt University Medical Center’s (VUMC’s) PEMs (Appendix 2). The mean readability score of all websites was 11.4 (range, 8.9-15.5) (Appendix 2).

Seventy of 72 websites (97%) had PEMs that were fairly difficult or difficult, according to the FRE analysis (Figure 2). The American Cancer Society and Mid-America Sarcoma Institute had PEMs that were written in plain English. Sixty-nine of 72 websites (96%) had PEMs with a readability score of 10 or higher, according to the Raygor readability estimate (Figure 3). Using this instrument, the scores of the American Cancer Society and the University of Pennsylvania–Joan Karnell Cancer Center were 9; Mid-America Sarcoma Institute’s score was 8. 

Discussion

Many cancer patients have turned to websites and online PEMs to gather health information about their condition.^10-17 Basch and colleagues¹⁰ reported almost a decade ago that 44% of cancer patients, as well as 60% of their companions, used the Internet to find cancer-related information.¹⁰ When LaCoursiere and colleagues³⁵ surveyed cancer patients, they found that patients handled their condition better and had less anxiety and uncertainty after using the Internet to find health information and support.³⁵ In addition, many orthopedic patients, specifically 46% of orthopedic community outpatients,⁴⁵ consult the Internet for information about their condition and future surgical procedures.^46,47

This study comprehensively evaluated the readability of online PEMs of bone and soft-tissue sarcomas and related conditions by using 10 different readability instruments. After identifying 72 websites and 774 articles, we found that all 72 websites’ PEMs had a mean readability score that did not meet the NIH recommendation of writing PEMs at a sixth- to seventh-grade reading level. These results are consistent with studies evaluating the readability of online PEMs related to other cancer conditions^21-25 and other orthopedic conditions.^26-31

The combination of low health literacy of many US adults and high reading grade levels of the majority of online PEMs is not conducive to patients’ better understanding their condition(s). Even individuals with high reading skills prefer information that is simpler to read.⁴⁸ In many areas of medicine, there is evidence that patients’ understanding of their condition has a positive impact on health outcomes, well-being, and the patient–physician relationship.^49-61 Regarding cancer patients, Davis and colleagues⁵⁴ and Peterson and colleagues⁵⁷ showed that lower health literacy contributes to less knowledge and lower rates of breast⁵⁴ and colorectal cancer⁵⁷ screening tests. Even low health literacy of family caregivers of cancer patients can result in increased stress and lack of communication of important medical information between caregiver and physician.⁵² Among cancer patients, poor health literacy has been associated with mental distress⁶⁰ as well as decreased compliance with treatment and lower involvement in clinical trials.⁵⁵

The disparity between patients’ health literacy and the readability of online PEMs needs to be addressed by finding methods to improve patients’ understanding of their condition and to lower the readability scores of online PEMs. Better communication between patient and physician may improve patients’ comprehension of their condition and different aspects of their care.^59,62-66 Doak and colleagues⁶³ recommend giving cancer patients the most important information first; presenting information to patients in smaller doses; intermittently asking patients questions; and incorporating graphs, tables, and drawings into communication with patients.⁶³ Additionally, allowing patients to repeat information they have just received/heard to the physician is another useful tool to improve patient education.^62,64-66

Another way to address the disparity between patients’ health literacy and the readability of online PEMs is to reduce the reading grade level of existing PEMs. According to results from this study and others, the majority of online PEMs are above the reading grade level of a significant number of US adults. Many available and inexpensive readability instruments allow authors to assess their articles’ readability. Many writing guidelines also exist to help authors improve the readability of their PEMs.^20,64,67-71 Living Word Vocabulary⁷⁰ and Plain Language⁷¹ help authors replace complex words or medical terms with simpler words.²⁹ Visual aids, audio, and video help patients with low health literacy remember the information.⁶⁴

Efforts to improve PEM readability are effective. Of all the websites reviewed, VUMC was identified as having PEMs with the lowest readability score (5.3). This score was reported by the New Fog Count readability instrument, which accounts for the number of sentences, easy words, and hard words. In 2011, VUMC formed the Department of Patient Education to review and update its online and printed PEMs to make sure patients could read them.⁷² Additionally, the mean readability scores of the websites of the National Cancer Institute and MedlinePlus are in the top 50% of the websites included in this study. The NIH sponsors both sites, which follow the NIH guidelines for writing online PEMs at a reading level suitable for individuals with lower health literacy.²⁰ These materials serve as potential models to improve the readability of PEMs, and, thus, help patients to better understand their condition, medical procedures, and/or treatment options.

To illustrate ways to improve the reading grade level of PEMs, we used the article “Ewing’s Sarcoma” from the AAOS website⁷³ and followed the NIH guidelines to improve the reading grade level of the article.²⁰ We identified complex words and defined them at an eighth-grade reading level. If that word was mentioned later in the article, simpler terminology was used instead of the initial complex word. For example, Ewing’s sarcoma was defined early and then referred to as bone tumor later in the article. We also identified every word that was 3 syllables or longer and used Microsoft Word’s thesaurus to replace those words with ones that were less than 3 syllables. Lastly, all sentences longer than 15 words were rewritten to be less than 15 words. After making these 3 changes to the article, the mean reading grade level dropped from 11.2 to 7.3. 

This study has limitations. First, some readability instruments evaluate the number of syllables per word or polysyllabic words as part of their formula and, thus, can underestimate or overestimate the reading grade level of a document. Some readability formulas consider medical terms such as ulna, femur, or carpal as “easy” words because they have 2 syllables, but many laypersons may not comprehend these words. On the other hand, some readability formulas consider medical terms such as medications, diagnosis, or radiation as “hard” words because they contain 3 or more syllables, but the majority of laypersons likely comprehend these words. Second, the reading level of the patient population accessing those online sites was not assessed. Third, the readability instruments in this study did not evaluate the accuracy of the content, pictures, or tables of the PEMs. However, using 10 readability instruments allowed evaluation of many different readability aspects of the text. Fourth, because some websites identified in this study, such as Bonetumor.org, were written for patients as well as clinicians, the reading grade level of these sites may be higher than that of those sites written just for patients.

Conclusion

Because many orthopedic cancer patients rely on the Internet as a source of information, the need for online PEMs to match the reading skills of the patient population who accesses them is vital. However, this study shows that many organizations, academic training centers, and other entities need to update their online PEMs because all PEMs in this study had a mean readability grade level higher than the NIH recommendation. Further research needs to evaluate the effectiveness of other media, such as video, illustrations, and audio, to provide health information to patients. With many guidelines available that provide plans and advice to improve the readability of PEMs, research also must assess the most effective plans and advice in order to allow authors to focus their attention on 1 set of guidelines to improve the readability of their PEMs.

The diagnosis of cancer is a life-changing event for the patient as well as the patient’s family, friends, and relatives. Once diagnosed, most cancer patients want more information about their prognosis, future procedures, and/or treatment options.¹ Receiving such information has been shown to reduce patient anxiety, increase patient satisfaction with care, and improve self-care.^2-6 With the evolution of the Internet, patients in general^7-9 and, specifically, cancer patients^10-17 have turned to websites and online patient education materials (PEMs) to gather more health information.

For online PEMs to convey health information, their reading level must match the health literacy of the individuals who access them. Health literacy is the ability of an individual to gather and comprehend information about their condition to make the best decisions for their health.¹⁸ According to a report by the Institute of Medicine, 90 million American adults cannot properly use the US health care system because they do not possess adequate health literacy.¹⁸ Additionally, 36% of adults in the United States have basic or less-than-basic health literacy.¹⁹ This is starkly contrasted with the 12% of US adults who have proficient health literacy. A 2012 survey showed that about 31% of individuals who look for health information on the Internet have a high school education or less.⁸ In order to address the low health literacy of adults, the National Institutes of Health (NIH) has recommended that online PEMs be written at a sixth- to seventh-grade reading level.²⁰ 

Unfortunately, many online PEMs related to certain cancer^21-25 and orthopedic conditions^26-31 do not meet NIH recommendations. Only 1 study has specifically looked at PEMs related to an orthopedic cancer condition.³² Lam and colleagues³² evaluated the readability of osteosarcoma PEMs from 56 websites using only 2 readability instruments and identified 86% of the websites as having a greater than eighth-grade reading level. No study has thoroughly assessed the readability of PEMs about bone and soft-tissue sarcomas and related conditions nor has any used 10 different readability instruments. Since each readability instrument has different variables (eg, sentence length, number of paragraphs, or number of complex words), averaging the scores of 10 of these instruments may result in less bias.

The purpose of this study was to evaluate the readability of online PEMs concerning bone and soft-tissue sarcomas and related conditions. The online PEMs came from websites that sarcoma patients may visit to obtain information about their condition. Our hypothesis was that the majority of these online PEMs will have a higher reading level than the NIH recommendations.

Materials and Methods

In May 2013, we identified online PEMs that included background, diagnosis, tests, or treatments for bone and soft-tissue sarcomas and conditions that mimic bone sarcoma. We included articles from the Tumors section of the American Academy of Orthopaedic Surgeons (AAOS) website.³³ A second source of online PEMs came from a list of academic training centers created through the American Medical Association’s Fellowship and Residency Electronic Internet Database (FREIDA) with search criteria narrowed to orthopedic surgery. If we did not find PEMs of bone and soft-tissue cancers in the orthopedic department of a given academic training center’s website, we searched its cancer center website. We chose 4 programs with PEMs relevant to bone and soft-tissue sarcomas from each region in FREIDA for a balanced representation, except for the Territory region because it had only 1 academic training center and no relevant PEMs. Specialized websites, including Bonetumor.org, Sarcoma Alliance (Sarcomaalliance.org), and Sarcoma Foundation of America (Curesarcoma.org), were also evaluated. Within the Sarcoma Specialists section of the Sarcoma Alliance website,³⁴ sarcoma specialists who were not identified from the FREIDA search for academic training centers were selected for review.

Because 8 of 10 individuals looking for health information on the Internet start their investigation at search engines, we also looked for PEMs through a Google search (Google.com) of bone cancer, and evaluated the first 10 hits for PEMs.⁸ Of these 10 hits, 8 had relevant PEMs, which we searched for additional PEMs about bone and soft-tissue cancers and related conditions. We also conducted a Google search of the most common bone sarcoma and soft-tissue sarcoma, osteosarcoma and malignant fibrous histiocytoma, respectively, and found 2 additional websites with relevant PEMs. LaCoursiere and colleagues³⁵ surveyed cancer patients who used the Internet and found that they preferred WebMD (Webmd.com) and Medscape (Medscape.com) as sources for content about their medical condition.³⁵ WebMD had been identified in the Google search, and we gathered the PEMs from Medscape also. It is worth noting that some of these websites are written for patients as well as clinicians.

Text from these PEMs were copied and pasted into separate Microsoft Word documents (Microsoft, Redmond, Washington). Advertisements, pictures, picture text, hyperlinks, copyright notices, page navigation links, paragraphs with no text, and any text that was not related to the given condition were deleted from the document to format the text for the readability software. Then, each Microsoft Word document was uploaded into the software package Readability Studio Professional (RSP) Edition Version 2012.1 for Windows (Oleander Software, Vandalia, Ohio). The 10 distinct readability instruments that were used to gauge the readability of each document were the Flesch Reading Ease score (FRE), the New Fog Count, the New Automated Readability Index, the Coleman-Liau Index (CLI), the Fry readability graph, the New Dale-Chall formula (NDC), the Gunning Frequency of Gobbledygook (Gunning FOG), the Powers-Sumner-Kearl formula, the Simple Measure of Gobbledygook (SMOG), and the Raygor Estimate Graph.

The FRE’s formula takes the average number of words per sentence and average number of syllables per word to compute a score ranging from 0 to 100 with 0 being the hardest to read.³⁶ The New Fog Count tallies the number of sentences, easy words, and hard words (polysyllables) to calculate the grade level of the document.³⁷ The New Automated Readability Index takes the average characters per word and average words per sentence to calculate a grade level for the document.³⁷ The CLI randomly samples a few hundred words from the document, averages the number of letters and sentences per sample, and calculates an estimated grade level.³⁸ The Fry readability graph selects samples of 100 words from the document, averages the number of syllables and sentences per 100 words, plots these data points on a graph, with the intersection determining the reading level.³⁹ The NDC uses a list of 3000 familiar words that most fourth-grade students know.⁴⁰ The percentage of difficult words, which are not on the list of familiar words, and the average sentence length in words are used to calculate the reading grade level of the document. The Gunning FOG uses the average sentence length in words and the percentage of hard words from a sample of at least 100 words to determine the reading grade level of the document.⁴¹ The Powers-Sumner-Kearl formula uses the average sentence length and percentage of monosyllables from a 100-word sample passage to calculate the reading grade level.⁴² The SMOG formula counts the number of polysyllabic words from 30 sentences and calculates the reading grade level of the document.⁴³ In contrast to other formulas that test for 50% to 75% comprehension, the SMOG formula tests for 100% comprehension. As a result, the SMOG formula generally assigns a reading level 2 grades higher than the Dale-Chall level. The Raygor Estimate Graph selects a 100-word passage, counts the number of sentences and number of words with 6 or more letters, and plots the 2 variables on a graph to determine the reading grade level.⁴⁴ The software package calculated the results from each reading instrument and reported the mean grade level score
for each document.

Results

We identified a total of 72 websites with relevant PEMs and included them in this study. Of these 72 websites, 36 websites were academic training centers, 10 were Google search hits, and 21 were from the Sarcoma Alliance list of sarcoma specialists. The remaining 5 websites were AAOS, Bonetumor.org, Sarcoma Alliance, Sarcoma Foundation of America, and Medscape. A list of conditions and treatments that were considered relevant PEMs is found in Appendix 1. A total of 774 articles were obtained from the 72 websites.

None of the websites had a mean readability score of 7 (seventh grade) or lower (Figures 1A, 1B). Mid-America Sarcoma Institute’s PEMs had the lowest mean readability score, 8.9. The lowest readability score was 5.3, which the New Fog Count readability instrument calculated for Vanderbilt University Medical Center’s (VUMC’s) PEMs (Appendix 2). The mean readability score of all websites was 11.4 (range, 8.9-15.5) (Appendix 2).

Seventy of 72 websites (97%) had PEMs that were fairly difficult or difficult, according to the FRE analysis (Figure 2). The American Cancer Society and Mid-America Sarcoma Institute had PEMs that were written in plain English. Sixty-nine of 72 websites (96%) had PEMs with a readability score of 10 or higher, according to the Raygor readability estimate (Figure 3). Using this instrument, the scores of the American Cancer Society and the University of Pennsylvania–Joan Karnell Cancer Center were 9; Mid-America Sarcoma Institute’s score was 8. 

Discussion

Many cancer patients have turned to websites and online PEMs to gather health information about their condition.^10-17 Basch and colleagues¹⁰ reported almost a decade ago that 44% of cancer patients, as well as 60% of their companions, used the Internet to find cancer-related information.¹⁰ When LaCoursiere and colleagues³⁵ surveyed cancer patients, they found that patients handled their condition better and had less anxiety and uncertainty after using the Internet to find health information and support.³⁵ In addition, many orthopedic patients, specifically 46% of orthopedic community outpatients,⁴⁵ consult the Internet for information about their condition and future surgical procedures.^46,47

This study comprehensively evaluated the readability of online PEMs of bone and soft-tissue sarcomas and related conditions by using 10 different readability instruments. After identifying 72 websites and 774 articles, we found that all 72 websites’ PEMs had a mean readability score that did not meet the NIH recommendation of writing PEMs at a sixth- to seventh-grade reading level. These results are consistent with studies evaluating the readability of online PEMs related to other cancer conditions^21-25 and other orthopedic conditions.^26-31

The combination of low health literacy of many US adults and high reading grade levels of the majority of online PEMs is not conducive to patients’ better understanding their condition(s). Even individuals with high reading skills prefer information that is simpler to read.⁴⁸ In many areas of medicine, there is evidence that patients’ understanding of their condition has a positive impact on health outcomes, well-being, and the patient–physician relationship.^49-61 Regarding cancer patients, Davis and colleagues⁵⁴ and Peterson and colleagues⁵⁷ showed that lower health literacy contributes to less knowledge and lower rates of breast⁵⁴ and colorectal cancer⁵⁷ screening tests. Even low health literacy of family caregivers of cancer patients can result in increased stress and lack of communication of important medical information between caregiver and physician.⁵² Among cancer patients, poor health literacy has been associated with mental distress⁶⁰ as well as decreased compliance with treatment and lower involvement in clinical trials.⁵⁵

The disparity between patients’ health literacy and the readability of online PEMs needs to be addressed by finding methods to improve patients’ understanding of their condition and to lower the readability scores of online PEMs. Better communication between patient and physician may improve patients’ comprehension of their condition and different aspects of their care.^59,62-66 Doak and colleagues⁶³ recommend giving cancer patients the most important information first; presenting information to patients in smaller doses; intermittently asking patients questions; and incorporating graphs, tables, and drawings into communication with patients.⁶³ Additionally, allowing patients to repeat information they have just received/heard to the physician is another useful tool to improve patient education.^62,64-66

Another way to address the disparity between patients’ health literacy and the readability of online PEMs is to reduce the reading grade level of existing PEMs. According to results from this study and others, the majority of online PEMs are above the reading grade level of a significant number of US adults. Many available and inexpensive readability instruments allow authors to assess their articles’ readability. Many writing guidelines also exist to help authors improve the readability of their PEMs.^20,64,67-71 Living Word Vocabulary⁷⁰ and Plain Language⁷¹ help authors replace complex words or medical terms with simpler words.²⁹ Visual aids, audio, and video help patients with low health literacy remember the information.⁶⁴

Efforts to improve PEM readability are effective. Of all the websites reviewed, VUMC was identified as having PEMs with the lowest readability score (5.3). This score was reported by the New Fog Count readability instrument, which accounts for the number of sentences, easy words, and hard words. In 2011, VUMC formed the Department of Patient Education to review and update its online and printed PEMs to make sure patients could read them.⁷² Additionally, the mean readability scores of the websites of the National Cancer Institute and MedlinePlus are in the top 50% of the websites included in this study. The NIH sponsors both sites, which follow the NIH guidelines for writing online PEMs at a reading level suitable for individuals with lower health literacy.²⁰ These materials serve as potential models to improve the readability of PEMs, and, thus, help patients to better understand their condition, medical procedures, and/or treatment options.

To illustrate ways to improve the reading grade level of PEMs, we used the article “Ewing’s Sarcoma” from the AAOS website⁷³ and followed the NIH guidelines to improve the reading grade level of the article.²⁰ We identified complex words and defined them at an eighth-grade reading level. If that word was mentioned later in the article, simpler terminology was used instead of the initial complex word. For example, Ewing’s sarcoma was defined early and then referred to as bone tumor later in the article. We also identified every word that was 3 syllables or longer and used Microsoft Word’s thesaurus to replace those words with ones that were less than 3 syllables. Lastly, all sentences longer than 15 words were rewritten to be less than 15 words. After making these 3 changes to the article, the mean reading grade level dropped from 11.2 to 7.3. 

This study has limitations. First, some readability instruments evaluate the number of syllables per word or polysyllabic words as part of their formula and, thus, can underestimate or overestimate the reading grade level of a document. Some readability formulas consider medical terms such as ulna, femur, or carpal as “easy” words because they have 2 syllables, but many laypersons may not comprehend these words. On the other hand, some readability formulas consider medical terms such as medications, diagnosis, or radiation as “hard” words because they contain 3 or more syllables, but the majority of laypersons likely comprehend these words. Second, the reading level of the patient population accessing those online sites was not assessed. Third, the readability instruments in this study did not evaluate the accuracy of the content, pictures, or tables of the PEMs. However, using 10 readability instruments allowed evaluation of many different readability aspects of the text. Fourth, because some websites identified in this study, such as Bonetumor.org, were written for patients as well as clinicians, the reading grade level of these sites may be higher than that of those sites written just for patients.

Conclusion

Because many orthopedic cancer patients rely on the Internet as a source of information, the need for online PEMs to match the reading skills of the patient population who accesses them is vital. However, this study shows that many organizations, academic training centers, and other entities need to update their online PEMs because all PEMs in this study had a mean readability grade level higher than the NIH recommendation. Further research needs to evaluate the effectiveness of other media, such as video, illustrations, and audio, to provide health information to patients. With many guidelines available that provide plans and advice to improve the readability of PEMs, research also must assess the most effective plans and advice in order to allow authors to focus their attention on 1 set of guidelines to improve the readability of their PEMs.

The diagnosis of cancer is a life-changing event for the patient as well as the patient’s family, friends, and relatives. Once diagnosed, most cancer patients want more information about their prognosis, future procedures, and/or treatment options.¹ Receiving such information has been shown to reduce patient anxiety, increase patient satisfaction with care, and improve self-care.^2-6 With the evolution of the Internet, patients in general^7-9 and, specifically, cancer patients^10-17 have turned to websites and online patient education materials (PEMs) to gather more health information.

For online PEMs to convey health information, their reading level must match the health literacy of the individuals who access them. Health literacy is the ability of an individual to gather and comprehend information about their condition to make the best decisions for their health.¹⁸ According to a report by the Institute of Medicine, 90 million American adults cannot properly use the US health care system because they do not possess adequate health literacy.¹⁸ Additionally, 36% of adults in the United States have basic or less-than-basic health literacy.¹⁹ This is starkly contrasted with the 12% of US adults who have proficient health literacy. A 2012 survey showed that about 31% of individuals who look for health information on the Internet have a high school education or less.⁸ In order to address the low health literacy of adults, the National Institutes of Health (NIH) has recommended that online PEMs be written at a sixth- to seventh-grade reading level.²⁰ 

Unfortunately, many online PEMs related to certain cancer^21-25 and orthopedic conditions^26-31 do not meet NIH recommendations. Only 1 study has specifically looked at PEMs related to an orthopedic cancer condition.³² Lam and colleagues³² evaluated the readability of osteosarcoma PEMs from 56 websites using only 2 readability instruments and identified 86% of the websites as having a greater than eighth-grade reading level. No study has thoroughly assessed the readability of PEMs about bone and soft-tissue sarcomas and related conditions nor has any used 10 different readability instruments. Since each readability instrument has different variables (eg, sentence length, number of paragraphs, or number of complex words), averaging the scores of 10 of these instruments may result in less bias.

The purpose of this study was to evaluate the readability of online PEMs concerning bone and soft-tissue sarcomas and related conditions. The online PEMs came from websites that sarcoma patients may visit to obtain information about their condition. Our hypothesis was that the majority of these online PEMs will have a higher reading level than the NIH recommendations.

Materials and Methods

In May 2013, we identified online PEMs that included background, diagnosis, tests, or treatments for bone and soft-tissue sarcomas and conditions that mimic bone sarcoma. We included articles from the Tumors section of the American Academy of Orthopaedic Surgeons (AAOS) website.³³ A second source of online PEMs came from a list of academic training centers created through the American Medical Association’s Fellowship and Residency Electronic Internet Database (FREIDA) with search criteria narrowed to orthopedic surgery. If we did not find PEMs of bone and soft-tissue cancers in the orthopedic department of a given academic training center’s website, we searched its cancer center website. We chose 4 programs with PEMs relevant to bone and soft-tissue sarcomas from each region in FREIDA for a balanced representation, except for the Territory region because it had only 1 academic training center and no relevant PEMs. Specialized websites, including Bonetumor.org, Sarcoma Alliance (Sarcomaalliance.org), and Sarcoma Foundation of America (Curesarcoma.org), were also evaluated. Within the Sarcoma Specialists section of the Sarcoma Alliance website,³⁴ sarcoma specialists who were not identified from the FREIDA search for academic training centers were selected for review.

Because 8 of 10 individuals looking for health information on the Internet start their investigation at search engines, we also looked for PEMs through a Google search (Google.com) of bone cancer, and evaluated the first 10 hits for PEMs.⁸ Of these 10 hits, 8 had relevant PEMs, which we searched for additional PEMs about bone and soft-tissue cancers and related conditions. We also conducted a Google search of the most common bone sarcoma and soft-tissue sarcoma, osteosarcoma and malignant fibrous histiocytoma, respectively, and found 2 additional websites with relevant PEMs. LaCoursiere and colleagues³⁵ surveyed cancer patients who used the Internet and found that they preferred WebMD (Webmd.com) and Medscape (Medscape.com) as sources for content about their medical condition.³⁵ WebMD had been identified in the Google search, and we gathered the PEMs from Medscape also. It is worth noting that some of these websites are written for patients as well as clinicians.

Text from these PEMs were copied and pasted into separate Microsoft Word documents (Microsoft, Redmond, Washington). Advertisements, pictures, picture text, hyperlinks, copyright notices, page navigation links, paragraphs with no text, and any text that was not related to the given condition were deleted from the document to format the text for the readability software. Then, each Microsoft Word document was uploaded into the software package Readability Studio Professional (RSP) Edition Version 2012.1 for Windows (Oleander Software, Vandalia, Ohio). The 10 distinct readability instruments that were used to gauge the readability of each document were the Flesch Reading Ease score (FRE), the New Fog Count, the New Automated Readability Index, the Coleman-Liau Index (CLI), the Fry readability graph, the New Dale-Chall formula (NDC), the Gunning Frequency of Gobbledygook (Gunning FOG), the Powers-Sumner-Kearl formula, the Simple Measure of Gobbledygook (SMOG), and the Raygor Estimate Graph.

The FRE’s formula takes the average number of words per sentence and average number of syllables per word to compute a score ranging from 0 to 100 with 0 being the hardest to read.³⁶ The New Fog Count tallies the number of sentences, easy words, and hard words (polysyllables) to calculate the grade level of the document.³⁷ The New Automated Readability Index takes the average characters per word and average words per sentence to calculate a grade level for the document.³⁷ The CLI randomly samples a few hundred words from the document, averages the number of letters and sentences per sample, and calculates an estimated grade level.³⁸ The Fry readability graph selects samples of 100 words from the document, averages the number of syllables and sentences per 100 words, plots these data points on a graph, with the intersection determining the reading level.³⁹ The NDC uses a list of 3000 familiar words that most fourth-grade students know.⁴⁰ The percentage of difficult words, which are not on the list of familiar words, and the average sentence length in words are used to calculate the reading grade level of the document. The Gunning FOG uses the average sentence length in words and the percentage of hard words from a sample of at least 100 words to determine the reading grade level of the document.⁴¹ The Powers-Sumner-Kearl formula uses the average sentence length and percentage of monosyllables from a 100-word sample passage to calculate the reading grade level.⁴² The SMOG formula counts the number of polysyllabic words from 30 sentences and calculates the reading grade level of the document.⁴³ In contrast to other formulas that test for 50% to 75% comprehension, the SMOG formula tests for 100% comprehension. As a result, the SMOG formula generally assigns a reading level 2 grades higher than the Dale-Chall level. The Raygor Estimate Graph selects a 100-word passage, counts the number of sentences and number of words with 6 or more letters, and plots the 2 variables on a graph to determine the reading grade level.⁴⁴ The software package calculated the results from each reading instrument and reported the mean grade level score
for each document.

Results

We identified a total of 72 websites with relevant PEMs and included them in this study. Of these 72 websites, 36 websites were academic training centers, 10 were Google search hits, and 21 were from the Sarcoma Alliance list of sarcoma specialists. The remaining 5 websites were AAOS, Bonetumor.org, Sarcoma Alliance, Sarcoma Foundation of America, and Medscape. A list of conditions and treatments that were considered relevant PEMs is found in Appendix 1. A total of 774 articles were obtained from the 72 websites.

None of the websites had a mean readability score of 7 (seventh grade) or lower (Figures 1A, 1B). Mid-America Sarcoma Institute’s PEMs had the lowest mean readability score, 8.9. The lowest readability score was 5.3, which the New Fog Count readability instrument calculated for Vanderbilt University Medical Center’s (VUMC’s) PEMs (Appendix 2). The mean readability score of all websites was 11.4 (range, 8.9-15.5) (Appendix 2).

Seventy of 72 websites (97%) had PEMs that were fairly difficult or difficult, according to the FRE analysis (Figure 2). The American Cancer Society and Mid-America Sarcoma Institute had PEMs that were written in plain English. Sixty-nine of 72 websites (96%) had PEMs with a readability score of 10 or higher, according to the Raygor readability estimate (Figure 3). Using this instrument, the scores of the American Cancer Society and the University of Pennsylvania–Joan Karnell Cancer Center were 9; Mid-America Sarcoma Institute’s score was 8. 

Discussion

Many cancer patients have turned to websites and online PEMs to gather health information about their condition.^10-17 Basch and colleagues¹⁰ reported almost a decade ago that 44% of cancer patients, as well as 60% of their companions, used the Internet to find cancer-related information.¹⁰ When LaCoursiere and colleagues³⁵ surveyed cancer patients, they found that patients handled their condition better and had less anxiety and uncertainty after using the Internet to find health information and support.³⁵ In addition, many orthopedic patients, specifically 46% of orthopedic community outpatients,⁴⁵ consult the Internet for information about their condition and future surgical procedures.^46,47

This study comprehensively evaluated the readability of online PEMs of bone and soft-tissue sarcomas and related conditions by using 10 different readability instruments. After identifying 72 websites and 774 articles, we found that all 72 websites’ PEMs had a mean readability score that did not meet the NIH recommendation of writing PEMs at a sixth- to seventh-grade reading level. These results are consistent with studies evaluating the readability of online PEMs related to other cancer conditions^21-25 and other orthopedic conditions.^26-31

The combination of low health literacy of many US adults and high reading grade levels of the majority of online PEMs is not conducive to patients’ better understanding their condition(s). Even individuals with high reading skills prefer information that is simpler to read.⁴⁸ In many areas of medicine, there is evidence that patients’ understanding of their condition has a positive impact on health outcomes, well-being, and the patient–physician relationship.^49-61 Regarding cancer patients, Davis and colleagues⁵⁴ and Peterson and colleagues⁵⁷ showed that lower health literacy contributes to less knowledge and lower rates of breast⁵⁴ and colorectal cancer⁵⁷ screening tests. Even low health literacy of family caregivers of cancer patients can result in increased stress and lack of communication of important medical information between caregiver and physician.⁵² Among cancer patients, poor health literacy has been associated with mental distress⁶⁰ as well as decreased compliance with treatment and lower involvement in clinical trials.⁵⁵

The disparity between patients’ health literacy and the readability of online PEMs needs to be addressed by finding methods to improve patients’ understanding of their condition and to lower the readability scores of online PEMs. Better communication between patient and physician may improve patients’ comprehension of their condition and different aspects of their care.^59,62-66 Doak and colleagues⁶³ recommend giving cancer patients the most important information first; presenting information to patients in smaller doses; intermittently asking patients questions; and incorporating graphs, tables, and drawings into communication with patients.⁶³ Additionally, allowing patients to repeat information they have just received/heard to the physician is another useful tool to improve patient education.^62,64-66

Another way to address the disparity between patients’ health literacy and the readability of online PEMs is to reduce the reading grade level of existing PEMs. According to results from this study and others, the majority of online PEMs are above the reading grade level of a significant number of US adults. Many available and inexpensive readability instruments allow authors to assess their articles’ readability. Many writing guidelines also exist to help authors improve the readability of their PEMs.^20,64,67-71 Living Word Vocabulary⁷⁰ and Plain Language⁷¹ help authors replace complex words or medical terms with simpler words.²⁹ Visual aids, audio, and video help patients with low health literacy remember the information.⁶⁴

Efforts to improve PEM readability are effective. Of all the websites reviewed, VUMC was identified as having PEMs with the lowest readability score (5.3). This score was reported by the New Fog Count readability instrument, which accounts for the number of sentences, easy words, and hard words. In 2011, VUMC formed the Department of Patient Education to review and update its online and printed PEMs to make sure patients could read them.⁷² Additionally, the mean readability scores of the websites of the National Cancer Institute and MedlinePlus are in the top 50% of the websites included in this study. The NIH sponsors both sites, which follow the NIH guidelines for writing online PEMs at a reading level suitable for individuals with lower health literacy.²⁰ These materials serve as potential models to improve the readability of PEMs, and, thus, help patients to better understand their condition, medical procedures, and/or treatment options.

To illustrate ways to improve the reading grade level of PEMs, we used the article “Ewing’s Sarcoma” from the AAOS website⁷³ and followed the NIH guidelines to improve the reading grade level of the article.²⁰ We identified complex words and defined them at an eighth-grade reading level. If that word was mentioned later in the article, simpler terminology was used instead of the initial complex word. For example, Ewing’s sarcoma was defined early and then referred to as bone tumor later in the article. We also identified every word that was 3 syllables or longer and used Microsoft Word’s thesaurus to replace those words with ones that were less than 3 syllables. Lastly, all sentences longer than 15 words were rewritten to be less than 15 words. After making these 3 changes to the article, the mean reading grade level dropped from 11.2 to 7.3. 

This study has limitations. First, some readability instruments evaluate the number of syllables per word or polysyllabic words as part of their formula and, thus, can underestimate or overestimate the reading grade level of a document. Some readability formulas consider medical terms such as ulna, femur, or carpal as “easy” words because they have 2 syllables, but many laypersons may not comprehend these words. On the other hand, some readability formulas consider medical terms such as medications, diagnosis, or radiation as “hard” words because they contain 3 or more syllables, but the majority of laypersons likely comprehend these words. Second, the reading level of the patient population accessing those online sites was not assessed. Third, the readability instruments in this study did not evaluate the accuracy of the content, pictures, or tables of the PEMs. However, using 10 readability instruments allowed evaluation of many different readability aspects of the text. Fourth, because some websites identified in this study, such as Bonetumor.org, were written for patients as well as clinicians, the reading grade level of these sites may be higher than that of those sites written just for patients.

Conclusion

Because many orthopedic cancer patients rely on the Internet as a source of information, the need for online PEMs to match the reading skills of the patient population who accesses them is vital. However, this study shows that many organizations, academic training centers, and other entities need to update their online PEMs because all PEMs in this study had a mean readability grade level higher than the NIH recommendation. Further research needs to evaluate the effectiveness of other media, such as video, illustrations, and audio, to provide health information to patients. With many guidelines available that provide plans and advice to improve the readability of PEMs, research also must assess the most effective plans and advice in order to allow authors to focus their attention on 1 set of guidelines to improve the readability of their PEMs.

Ulnar collateral ligament (UCL) reconstruction, commonly referred to as Tommy John surgery, is a well-described surgical treatment for elite athletes with a symptomatic, deficient UCL.^{1, 2} The procedure was first performed by the late Dr. Frank Jobe in 1974, described in 1986, and has undergone several modifications over the past 30 years.³ Different graft choices, tunnel positions, graft configurations, and tunnel fixation methods are just some of the alterations that have been made to the original Jobe technique.^4-6 With time, the index procedure has become more refined, with predictable outcomes in Major League Baseball (MLB) pitchers as well as other elite overhead throwing athletes.^2,7,8 However, though this surgery was originally described for elite athletes suffering from UCL deficiency, recent times have seen an increase of over 50% in the number of UCL reconstructions performed on high school–aged and younger athletes.⁹ Furthermore, in 2000, a total of 13 MLB pitchers underwent UCL reconstruction, while in 2012 this number increased nearly threefold to 32.² This paradigm shift of performing UCL reconstructions more frequently and on younger athletes raises a very important question: what is the role of the orthopedic surgeon in this epidemic?

UCL reconstruction has become a reliable procedure for MLB pitchers and other overhead throwing athletes.^7,10,11 Recent studies have reported that MLB pitchers who undergo UCL reconstruction return to pitch in the MLB 83% of the time, whereas only 3% fail to return to pitch in either MLB or the minor league.² Furthermore, pitchers who undergo UCL reconstruction perform similarly after surgery as prior to their UCL reconstruction, with fewer innings pitched after surgery, but, more importantly, a lower earned run average (ERA) and walks plus hits per inning pitched (WHIP) after surgery. These last 2 statistics, known as sabermetrics, evaluate the pitcher’s effectiveness; the fact that these are improved after surgery is reassuring for pitchers who undergo this procedure. However, it must be recognized that these pitchers pitched fewer innings after surgery.

There has been a sharp increase in the number of MLB pitchers who have undergone UCL reconstruction in recent years, especially the past 3 seasons, in which over 60 pitchers have had Tommy John surgery.² This increase, however, is not confined to MLB pitchers. High school–aged pitchers have also been part of this drastic rise in the number of UCL reconstructions performed throughout the country. Dr. James Andrews and colleagues noted a 50% increase from 1988-1994 to 1995-2003 in the proportion of high school–aged pitchers who underwent UCL reconstruction (while the absolute number increased from 7 to 77 in high school–aged players compared with 85 to 609 in adult athletes).⁹ Given the increase in MLB pitchers over the past few years, it is likely this number has also increased among adolescent pitchers.

This data again raises the question: what is the role of the orthopedic surgeon in this epidemic? There are many plausible responses, but in my opinion, there is one answer that surpasses the others. As a trained professional, surgeons are tasked with the responsibility of looking out for the best interest of their patients, even when this conflicts with the patient’s, or the patient’s parent’s or coach’s desires. This includes injury prevention, such as instituting pitch counts and developing products that allow coaches to determine when a pitcher may be at risk for injury from fatigue, as well as injury treatment.¹² It is difficult for a patient to understand the gravity of surgery and the rehabilitation process, specifically a procedure as involved as UCL reconstruction, and especially if the patient is an adolescent who has their outlook clouded by the fact that they believe they will be the next MLB star pitcher. The reality is that the National Collegiate Athletic Association (NCAA)¹³ has released data that has demonstrated that only 6.8% of high school baseball players will play baseball in college. Furthermore, only 9.4% of college baseball players will reach the professional level. That equates to 0.5%, or 1 in 200 high school players who will eventually play professional baseball.¹³ However, the reverse of this is also true, that out of every 200 players, 1 will make it to the major leagues, and that 1 player could be the patient in question. Hence, the purpose of this data is to show parents and athletes that, while they do have a chance of playing professional, and certainly collegiate, baseball, that percentage must be weighed against the risks of surgery.

MLB pitchers who have an endless supply of rehabilitation facilities, trainers, etc, do not return to pitching competitively and consistently in the majors for more than 15 months after UCL reconstruction.² The time commitment and rehabilitation required for these patients is staggering.^14,15 Furthermore, parents of these children who are consenting for them also have a difficult time comprehending the workload they are signing their child up for. Some parents believe this surgery will help their child throw faster, longer, and more accurately—beliefs that numerous studies have shown to be flat-out inaccurate. In fact, pitchers tend to lose a slight amount of velocity and accuracy after UCL reconstruction.^11,16 Ahmad and colleagues¹⁷ administered a questionnaire to 189 players, 15 coaches, and 31 parents about the indications, risks, benefits, etc, regarding UCL reconstruction to determine the public’s perception regarding this surgery. The results demonstrated that the public, including coaches, have a significantly skewed perception of exactly how serious this surgery is. The study showed that 28% of players and 20% of coaches believed the pitcher’s performance would be improved after surgery, and, more strikingly, 26% of collegiate athletes, 30% percent of coaches, 37% of parents, and 51% of high school athletes believed UCL reconstruction should be performed as a prophylactic procedure to enhance performance in an uninjured athlete.¹⁷

Henceforth, it becomes the surgeon’s responsibility to ensure that both the patient and the parents understand what the surgery and rehabilitation process entails, to keep the expectations of the patient and his or her family realistic, and to counsel these patients on alternative options with lower risks. As Ahmad and colleagues¹⁷ demonstrated, this is not an easy task given the public’s preconceived notions. Many patients, especially patients of the younger generation, seem to be willing to jump to surgery as the first option for treatment without having truly tried any nonoperative measures, because they believe surgery to be a quick, easy, and definitive answer. This is not always the case, and a trial of nonoperative treatment, including rest, ice, physical therapy, and possibly platelet-rich plasma (PRP), should be instituted for high school–aged players who present with UCL insufficiency prior to discussing surgery.^18,19

Medial UCL reconstruction is a successful procedure for elite MLB athletes. However, UCL reconstruction is becoming a victim of its own success as younger and younger athletes who will likely never play at the major league level are undergoing this procedure at an alarming rate. This is an epidemic which must be addressed by surgeons, coaches, and parents alike to curb the beliefs that UCL reconstruction will make high school–aged pitchers more successful. This procedure should not be performed prophylactically on an athlete of any age, especially those in high school. Further studies on the effectiveness of both nonoperative rest and rehabilitation and of PRP on partial-thickness UCL tears are warranted. New technology in the form of a compression sleeve with imbedded sensors to track the biomechanics of a pitcher’s elbow has been released and will hopefully provide information to coaches about when pitchers’ elbows begin to fatigue based on several biomechanical parameters.¹² The future of UCL reconstruction is still fluid, and with proper prevention strategies, nonoperative treatment, indications, and preoperative discussions, the Tommy John epidemic can be cured. ◾

Ulnar collateral ligament (UCL) reconstruction, commonly referred to as Tommy John surgery, is a well-described surgical treatment for elite athletes with a symptomatic, deficient UCL.^{1, 2} The procedure was first performed by the late Dr. Frank Jobe in 1974, described in 1986, and has undergone several modifications over the past 30 years.³ Different graft choices, tunnel positions, graft configurations, and tunnel fixation methods are just some of the alterations that have been made to the original Jobe technique.^4-6 With time, the index procedure has become more refined, with predictable outcomes in Major League Baseball (MLB) pitchers as well as other elite overhead throwing athletes.^2,7,8 However, though this surgery was originally described for elite athletes suffering from UCL deficiency, recent times have seen an increase of over 50% in the number of UCL reconstructions performed on high school–aged and younger athletes.⁹ Furthermore, in 2000, a total of 13 MLB pitchers underwent UCL reconstruction, while in 2012 this number increased nearly threefold to 32.² This paradigm shift of performing UCL reconstructions more frequently and on younger athletes raises a very important question: what is the role of the orthopedic surgeon in this epidemic?

UCL reconstruction has become a reliable procedure for MLB pitchers and other overhead throwing athletes.^7,10,11 Recent studies have reported that MLB pitchers who undergo UCL reconstruction return to pitch in the MLB 83% of the time, whereas only 3% fail to return to pitch in either MLB or the minor league.² Furthermore, pitchers who undergo UCL reconstruction perform similarly after surgery as prior to their UCL reconstruction, with fewer innings pitched after surgery, but, more importantly, a lower earned run average (ERA) and walks plus hits per inning pitched (WHIP) after surgery. These last 2 statistics, known as sabermetrics, evaluate the pitcher’s effectiveness; the fact that these are improved after surgery is reassuring for pitchers who undergo this procedure. However, it must be recognized that these pitchers pitched fewer innings after surgery.

There has been a sharp increase in the number of MLB pitchers who have undergone UCL reconstruction in recent years, especially the past 3 seasons, in which over 60 pitchers have had Tommy John surgery.² This increase, however, is not confined to MLB pitchers. High school–aged pitchers have also been part of this drastic rise in the number of UCL reconstructions performed throughout the country. Dr. James Andrews and colleagues noted a 50% increase from 1988-1994 to 1995-2003 in the proportion of high school–aged pitchers who underwent UCL reconstruction (while the absolute number increased from 7 to 77 in high school–aged players compared with 85 to 609 in adult athletes).⁹ Given the increase in MLB pitchers over the past few years, it is likely this number has also increased among adolescent pitchers.

This data again raises the question: what is the role of the orthopedic surgeon in this epidemic? There are many plausible responses, but in my opinion, there is one answer that surpasses the others. As a trained professional, surgeons are tasked with the responsibility of looking out for the best interest of their patients, even when this conflicts with the patient’s, or the patient’s parent’s or coach’s desires. This includes injury prevention, such as instituting pitch counts and developing products that allow coaches to determine when a pitcher may be at risk for injury from fatigue, as well as injury treatment.¹² It is difficult for a patient to understand the gravity of surgery and the rehabilitation process, specifically a procedure as involved as UCL reconstruction, and especially if the patient is an adolescent who has their outlook clouded by the fact that they believe they will be the next MLB star pitcher. The reality is that the National Collegiate Athletic Association (NCAA)¹³ has released data that has demonstrated that only 6.8% of high school baseball players will play baseball in college. Furthermore, only 9.4% of college baseball players will reach the professional level. That equates to 0.5%, or 1 in 200 high school players who will eventually play professional baseball.¹³ However, the reverse of this is also true, that out of every 200 players, 1 will make it to the major leagues, and that 1 player could be the patient in question. Hence, the purpose of this data is to show parents and athletes that, while they do have a chance of playing professional, and certainly collegiate, baseball, that percentage must be weighed against the risks of surgery.

MLB pitchers who have an endless supply of rehabilitation facilities, trainers, etc, do not return to pitching competitively and consistently in the majors for more than 15 months after UCL reconstruction.² The time commitment and rehabilitation required for these patients is staggering.^14,15 Furthermore, parents of these children who are consenting for them also have a difficult time comprehending the workload they are signing their child up for. Some parents believe this surgery will help their child throw faster, longer, and more accurately—beliefs that numerous studies have shown to be flat-out inaccurate. In fact, pitchers tend to lose a slight amount of velocity and accuracy after UCL reconstruction.^11,16 Ahmad and colleagues¹⁷ administered a questionnaire to 189 players, 15 coaches, and 31 parents about the indications, risks, benefits, etc, regarding UCL reconstruction to determine the public’s perception regarding this surgery. The results demonstrated that the public, including coaches, have a significantly skewed perception of exactly how serious this surgery is. The study showed that 28% of players and 20% of coaches believed the pitcher’s performance would be improved after surgery, and, more strikingly, 26% of collegiate athletes, 30% percent of coaches, 37% of parents, and 51% of high school athletes believed UCL reconstruction should be performed as a prophylactic procedure to enhance performance in an uninjured athlete.¹⁷

Henceforth, it becomes the surgeon’s responsibility to ensure that both the patient and the parents understand what the surgery and rehabilitation process entails, to keep the expectations of the patient and his or her family realistic, and to counsel these patients on alternative options with lower risks. As Ahmad and colleagues¹⁷ demonstrated, this is not an easy task given the public’s preconceived notions. Many patients, especially patients of the younger generation, seem to be willing to jump to surgery as the first option for treatment without having truly tried any nonoperative measures, because they believe surgery to be a quick, easy, and definitive answer. This is not always the case, and a trial of nonoperative treatment, including rest, ice, physical therapy, and possibly platelet-rich plasma (PRP), should be instituted for high school–aged players who present with UCL insufficiency prior to discussing surgery.^18,19

Medial UCL reconstruction is a successful procedure for elite MLB athletes. However, UCL reconstruction is becoming a victim of its own success as younger and younger athletes who will likely never play at the major league level are undergoing this procedure at an alarming rate. This is an epidemic which must be addressed by surgeons, coaches, and parents alike to curb the beliefs that UCL reconstruction will make high school–aged pitchers more successful. This procedure should not be performed prophylactically on an athlete of any age, especially those in high school. Further studies on the effectiveness of both nonoperative rest and rehabilitation and of PRP on partial-thickness UCL tears are warranted. New technology in the form of a compression sleeve with imbedded sensors to track the biomechanics of a pitcher’s elbow has been released and will hopefully provide information to coaches about when pitchers’ elbows begin to fatigue based on several biomechanical parameters.¹² The future of UCL reconstruction is still fluid, and with proper prevention strategies, nonoperative treatment, indications, and preoperative discussions, the Tommy John epidemic can be cured. ◾

Ulnar collateral ligament (UCL) reconstruction, commonly referred to as Tommy John surgery, is a well-described surgical treatment for elite athletes with a symptomatic, deficient UCL.^{1, 2} The procedure was first performed by the late Dr. Frank Jobe in 1974, described in 1986, and has undergone several modifications over the past 30 years.³ Different graft choices, tunnel positions, graft configurations, and tunnel fixation methods are just some of the alterations that have been made to the original Jobe technique.^4-6 With time, the index procedure has become more refined, with predictable outcomes in Major League Baseball (MLB) pitchers as well as other elite overhead throwing athletes.^2,7,8 However, though this surgery was originally described for elite athletes suffering from UCL deficiency, recent times have seen an increase of over 50% in the number of UCL reconstructions performed on high school–aged and younger athletes.⁹ Furthermore, in 2000, a total of 13 MLB pitchers underwent UCL reconstruction, while in 2012 this number increased nearly threefold to 32.² This paradigm shift of performing UCL reconstructions more frequently and on younger athletes raises a very important question: what is the role of the orthopedic surgeon in this epidemic?

UCL reconstruction has become a reliable procedure for MLB pitchers and other overhead throwing athletes.^7,10,11 Recent studies have reported that MLB pitchers who undergo UCL reconstruction return to pitch in the MLB 83% of the time, whereas only 3% fail to return to pitch in either MLB or the minor league.² Furthermore, pitchers who undergo UCL reconstruction perform similarly after surgery as prior to their UCL reconstruction, with fewer innings pitched after surgery, but, more importantly, a lower earned run average (ERA) and walks plus hits per inning pitched (WHIP) after surgery. These last 2 statistics, known as sabermetrics, evaluate the pitcher’s effectiveness; the fact that these are improved after surgery is reassuring for pitchers who undergo this procedure. However, it must be recognized that these pitchers pitched fewer innings after surgery.

There has been a sharp increase in the number of MLB pitchers who have undergone UCL reconstruction in recent years, especially the past 3 seasons, in which over 60 pitchers have had Tommy John surgery.² This increase, however, is not confined to MLB pitchers. High school–aged pitchers have also been part of this drastic rise in the number of UCL reconstructions performed throughout the country. Dr. James Andrews and colleagues noted a 50% increase from 1988-1994 to 1995-2003 in the proportion of high school–aged pitchers who underwent UCL reconstruction (while the absolute number increased from 7 to 77 in high school–aged players compared with 85 to 609 in adult athletes).⁹ Given the increase in MLB pitchers over the past few years, it is likely this number has also increased among adolescent pitchers.

This data again raises the question: what is the role of the orthopedic surgeon in this epidemic? There are many plausible responses, but in my opinion, there is one answer that surpasses the others. As a trained professional, surgeons are tasked with the responsibility of looking out for the best interest of their patients, even when this conflicts with the patient’s, or the patient’s parent’s or coach’s desires. This includes injury prevention, such as instituting pitch counts and developing products that allow coaches to determine when a pitcher may be at risk for injury from fatigue, as well as injury treatment.¹² It is difficult for a patient to understand the gravity of surgery and the rehabilitation process, specifically a procedure as involved as UCL reconstruction, and especially if the patient is an adolescent who has their outlook clouded by the fact that they believe they will be the next MLB star pitcher. The reality is that the National Collegiate Athletic Association (NCAA)¹³ has released data that has demonstrated that only 6.8% of high school baseball players will play baseball in college. Furthermore, only 9.4% of college baseball players will reach the professional level. That equates to 0.5%, or 1 in 200 high school players who will eventually play professional baseball.¹³ However, the reverse of this is also true, that out of every 200 players, 1 will make it to the major leagues, and that 1 player could be the patient in question. Hence, the purpose of this data is to show parents and athletes that, while they do have a chance of playing professional, and certainly collegiate, baseball, that percentage must be weighed against the risks of surgery.

MLB pitchers who have an endless supply of rehabilitation facilities, trainers, etc, do not return to pitching competitively and consistently in the majors for more than 15 months after UCL reconstruction.² The time commitment and rehabilitation required for these patients is staggering.^14,15 Furthermore, parents of these children who are consenting for them also have a difficult time comprehending the workload they are signing their child up for. Some parents believe this surgery will help their child throw faster, longer, and more accurately—beliefs that numerous studies have shown to be flat-out inaccurate. In fact, pitchers tend to lose a slight amount of velocity and accuracy after UCL reconstruction.^11,16 Ahmad and colleagues¹⁷ administered a questionnaire to 189 players, 15 coaches, and 31 parents about the indications, risks, benefits, etc, regarding UCL reconstruction to determine the public’s perception regarding this surgery. The results demonstrated that the public, including coaches, have a significantly skewed perception of exactly how serious this surgery is. The study showed that 28% of players and 20% of coaches believed the pitcher’s performance would be improved after surgery, and, more strikingly, 26% of collegiate athletes, 30% percent of coaches, 37% of parents, and 51% of high school athletes believed UCL reconstruction should be performed as a prophylactic procedure to enhance performance in an uninjured athlete.¹⁷

Henceforth, it becomes the surgeon’s responsibility to ensure that both the patient and the parents understand what the surgery and rehabilitation process entails, to keep the expectations of the patient and his or her family realistic, and to counsel these patients on alternative options with lower risks. As Ahmad and colleagues¹⁷ demonstrated, this is not an easy task given the public’s preconceived notions. Many patients, especially patients of the younger generation, seem to be willing to jump to surgery as the first option for treatment without having truly tried any nonoperative measures, because they believe surgery to be a quick, easy, and definitive answer. This is not always the case, and a trial of nonoperative treatment, including rest, ice, physical therapy, and possibly platelet-rich plasma (PRP), should be instituted for high school–aged players who present with UCL insufficiency prior to discussing surgery.^18,19

Medial UCL reconstruction is a successful procedure for elite MLB athletes. However, UCL reconstruction is becoming a victim of its own success as younger and younger athletes who will likely never play at the major league level are undergoing this procedure at an alarming rate. This is an epidemic which must be addressed by surgeons, coaches, and parents alike to curb the beliefs that UCL reconstruction will make high school–aged pitchers more successful. This procedure should not be performed prophylactically on an athlete of any age, especially those in high school. Further studies on the effectiveness of both nonoperative rest and rehabilitation and of PRP on partial-thickness UCL tears are warranted. New technology in the form of a compression sleeve with imbedded sensors to track the biomechanics of a pitcher’s elbow has been released and will hopefully provide information to coaches about when pitchers’ elbows begin to fatigue based on several biomechanical parameters.¹² The future of UCL reconstruction is still fluid, and with proper prevention strategies, nonoperative treatment, indications, and preoperative discussions, the Tommy John epidemic can be cured. ◾