Cutis

Historically, a variety of tools have been used to alter one’s appearance for cultural or religious purposes or to conform to standards of beauty. As a defining feature of the face, the lips provide a unique opportunity for facial aesthetic enhancement. There has been a paradigm shift in medicine favoring preventative health and a desire to slow and even reverse the aging process.¹ Acknowledging that product technology, skill sets, and cultural ideals continually evolve, this article highlights perioral anatomy, explains aging of the lower face, and reviews techniques to achieve perioral rejuvenation through volume restoration and muscle control.

Perioral Anatomy

The layers of the lips include the epidermis, subcutaneous tissue, orbicularis oris muscle fibers, and mucosa. The upper lip extends from the base of the nose to the mucosa inferiorly and to the nasolabial folds laterally. The curvilinear lower lip extends from the mucosa to the mandible inferiorly and to the oral commissures laterally.² Circumferential at the vermilion-cutaneous junction, a raised area of pale skin known as the white roll accentuates the vermilion border and provides an important landmark during lip augmentation.³ At the upper lip, this elevation of the vermilion joins at a V-shaped depression centrally to form the Cupid’s bow. The cutaneous upper lip has 2 raised vertical pillars known as the philtral columns, which are formed from decussating fibers of the orbicularis oris muscle.² The resultant midline depression is the philtrum. These defining features of the upper lip are to be preserved during augmentation procedures (Figure 1).⁴

The superior and inferior labial arteries, both branches of the facial artery, supply the upper and lower lip, respectively. The anastomotic arch of the superior labial artery is susceptible to injury from deep injection of the upper lip between the muscle layer and mucosa; therefore, caution must be exercised in this area.⁵ Injections into the vermilion and lower lip can be safely performed with less concern for vascular compromise. The vermilion derives its red color from the translucency of capillaries in the superficial papillae.² The capillary plexus at the papillae and rich sensory nerve network render the lip a highly vascular and sensitive structure.

Aging of the Lower Face

Subcutaneous fat atrophy, loss of elasticity, gravitational forces, and remodeling of the skeletal foundation all contribute to aging of the lower face. Starting as early as the third decade of life, intrinsic factors including hormonal changes and genetically determined processes produce alterations in skin quality and structure. Similarly, extrinsic aging through environmental influences, namely exposure to UV radiation and smoking, accelerate the loss of skin integrity.⁶

The decreased laxity of the skin in combination with repeated contraction of the orbicularis oris muscle results in perioral rhytides.⁷ For women in particular, vertically oriented perioral rhytides develop above the vermilion; terminal hair follicles, thicker skin, and a greater density of subcutaneous fat are presumptive protective factors for males.⁸ With time, the cutaneous portion of the upper lip lengthens and there is redistribution of volume with effacement of the upper lip vermilion.⁹ Additionally, the demarcation of the vermilion becomes blurred secondary to pallor, flattening of the philtral columns, and loss of projection of the Cupid’s bow.¹⁰

Downturning of the oral commissures is observed secondary to a combination of gravity, bone resorption, and soft tissue volume loss. Hyperactivity of the depressor anguli oris muscle exacerbates the mesolabial folds, producing marionette lines and a saddened expression.⁷ With ongoing volume loss and ligament laxity, tissue redistributes near the jaws and chin, giving rise to jowls. Similarly, perioral volume loss and descent of the malar fat-pad deepen the nasolabial folds in the aging midface.⁶

The main objective of perioral rejuvenation is to reinstate a harmonious refreshed look to the lower face; however, aesthetic analysis should occur within the context of the face as a whole, as the lips should complement the surrounding perioral cosmetic unit and overall skeletal foundation of the face. To accomplish this goal, the dermatologist’s armamentarium contains a broad variety of approaches including restriction of muscle movement, volume restoration, and surface contouring.

Volume Restoration

Treatment Options

In 2015, hyaluronic acid (HA) fillers constituted 80% of all injectable soft-tissue fillers, an 8% increase from 2014.¹¹ Hyaluronic acid has achieved immense popularity as a temporary dermal filler given its biocompatibility, longevity, and reversibility via hyaluronidase.¹²

Hyaluronic acid is a naturally occurring glycosaminoglycan that comprises the connective tissue matrix. The molecular composition affords HA its hydrophilic property, which augments dermal volume.⁷ Endogenous HA has a short half-life, and chemical modification by a cross-linking process extends longevity by 6 to 12 months. The various HA fillers are distinguished by method of purification, size of molecules, concentration and degree of cross-linking, and viscosity.^7,13,14 These differences dictate overall clinical performance such as flow properties, longevity, and stability. As a general rule, a high-viscosity product is more appropriate for deeper augmentation; fillers with low viscosity are more appropriate for correction of shallow defects.¹ Table 1 lists the HA fillers that are currently approved by the US Food and Drug Administration for lip augmentation and/or perioral rhytides in adults 21 years and older.^15-17

Randomized controlled trials comparing the efficacy, longevity, and tolerability of different HA products are lacking in the literature and, where present, have strong industry influence.^18,19 The advent of assessment scales has provided an objective evaluation of perioral and lip augmentation, facilitating comparisons between products in both clinical research and practice.²⁰

Semipermanent biostimulatory dermal fillers such as calcium hydroxylapatite and poly-L-lactic acid are not recommended for lip augmentation due to an increased incidence of submucosal nodule formation.^6,14,21 Likewise, permanent fillers are not recommended given their irreversibility and risk of nodule formation around the lips.^14,22 Nonetheless, liquid silicone (purified polydimethylsiloxane) administered via a microdroplet technique (0.01 mL of silicone at a time, no more than 1 cc per lip per session) has been used off label as a permanent filling agent for lip augmentation with limited complications.²³ Regardless, trepidations about its use with respect to reported risks continue to limit its application.²²

Similarly, surgical lip implants such as expanded polytetrafluoroethylene is an option for a subset of patients desiring permanent enhancement but are less commonly utilized given the side-effect profile, irreversibility, and relatively invasive nature of the procedure.²² Lastly, autologous fat transfer has been used in correction of the nasolabial and mesolabial folds as well as in lip augmentation; however, irregular surface contours and unpredictable longevity secondary to postinjection resorption (20%–90%) has limited its popularity.^3,14,21

HA Injection Technique

With respect to HA fillers in the perioral area, numerous approaches have been described.^10,22 The techniques in Table 2 provide a foundation for lip rejuvenation.

Several injection techniques exist, including serial puncture, linear threading, cross-hatching, and fanning in a retrograde or anterograde manner.²⁴ A blunt microcannula (27 gauge, 38 mm) may be used in place of sharp needles and offers the benefit of increased patient comfort, reduced edema and ecchymosis, and shortened recovery period.^25,26 Gentle massage of the product after injection can assist with an even contour. Lastly, a key determinant of successful outcomes is using an adequate volume of HA filler (1–2 mL for shaping the vermilion border and volumizing the lips).²⁷ Figure 2 highlights a clinical example of HA filler for lip augmentation.

Fortunately, most complications encountered with HA lip augmentation are mild and transient. The most commonly observed side effects include injection-site reactions such as pain, erythema, and edema. Similarly, most adverse effects are related to injection technique. All HA fillers are prone to the Tyndall effect, a consequence of too superficial an injection plane. Patients with history of recurrent herpes simplex virus infections should receive prophylactic antiviral therapy.¹²

Muscle Control

An emerging concept in rejuvenation of the lower face recognizes not only restoration of volume but also control of muscle movement. Local injection of botulinum toxin type A induces relaxation of hyperfunctional facial muscles through temporary inhibition of neurotransmitter release.⁶ The potential for paralysis of the oral cavity may limit the application of botulinum toxin type A in that region.⁷ Nonetheless, the off-label potential of botulinum toxin type A has expanded to include several targets in the lower face. The orbicularis oris muscle is targeted to soften perioral rhytides. Conservative dosing (1–2 U per lip quadrant or approximately 5 U total) and superficial injection is emphasized in this area.²⁷ Similarly, the depressor anguli oris muscle is targeted by injection of 4 U bilaterally to soften the marionette lines. In the chin area, the mentalis muscle can be targeted by injection of 2 U deep into each belly of the muscle to reduce the mental crease and dimpling.²⁸ Combination treatment with dermal filler and neurotoxin demonstrates effects that last longer than either modality alone without additional adverse events.²⁹ With combination therapy, guidelines suggest treating with filler first.²⁷

Conclusion

A greater understanding of the extrinsic and intrinsic factors that contribute to the structural and surface changes of the aging face coupled with a preference for minimally invasive procedures has revolutionized the dermatologist’s approach to perioral rejuvenation. Serving as a focal point of the face, the lips and perioral skin are well poised to benefit from this paradigm shift. A multifaceted approach utilizing dermal fillers and neurotoxins may be most appropriate and has demonstrated optimal outcomes in facial aesthetics.

Historically, a variety of tools have been used to alter one’s appearance for cultural or religious purposes or to conform to standards of beauty. As a defining feature of the face, the lips provide a unique opportunity for facial aesthetic enhancement. There has been a paradigm shift in medicine favoring preventative health and a desire to slow and even reverse the aging process.¹ Acknowledging that product technology, skill sets, and cultural ideals continually evolve, this article highlights perioral anatomy, explains aging of the lower face, and reviews techniques to achieve perioral rejuvenation through volume restoration and muscle control.

Perioral Anatomy

The layers of the lips include the epidermis, subcutaneous tissue, orbicularis oris muscle fibers, and mucosa. The upper lip extends from the base of the nose to the mucosa inferiorly and to the nasolabial folds laterally. The curvilinear lower lip extends from the mucosa to the mandible inferiorly and to the oral commissures laterally.² Circumferential at the vermilion-cutaneous junction, a raised area of pale skin known as the white roll accentuates the vermilion border and provides an important landmark during lip augmentation.³ At the upper lip, this elevation of the vermilion joins at a V-shaped depression centrally to form the Cupid’s bow. The cutaneous upper lip has 2 raised vertical pillars known as the philtral columns, which are formed from decussating fibers of the orbicularis oris muscle.² The resultant midline depression is the philtrum. These defining features of the upper lip are to be preserved during augmentation procedures (Figure 1).⁴

The superior and inferior labial arteries, both branches of the facial artery, supply the upper and lower lip, respectively. The anastomotic arch of the superior labial artery is susceptible to injury from deep injection of the upper lip between the muscle layer and mucosa; therefore, caution must be exercised in this area.⁵ Injections into the vermilion and lower lip can be safely performed with less concern for vascular compromise. The vermilion derives its red color from the translucency of capillaries in the superficial papillae.² The capillary plexus at the papillae and rich sensory nerve network render the lip a highly vascular and sensitive structure.

Aging of the Lower Face

Subcutaneous fat atrophy, loss of elasticity, gravitational forces, and remodeling of the skeletal foundation all contribute to aging of the lower face. Starting as early as the third decade of life, intrinsic factors including hormonal changes and genetically determined processes produce alterations in skin quality and structure. Similarly, extrinsic aging through environmental influences, namely exposure to UV radiation and smoking, accelerate the loss of skin integrity.⁶

The decreased laxity of the skin in combination with repeated contraction of the orbicularis oris muscle results in perioral rhytides.⁷ For women in particular, vertically oriented perioral rhytides develop above the vermilion; terminal hair follicles, thicker skin, and a greater density of subcutaneous fat are presumptive protective factors for males.⁸ With time, the cutaneous portion of the upper lip lengthens and there is redistribution of volume with effacement of the upper lip vermilion.⁹ Additionally, the demarcation of the vermilion becomes blurred secondary to pallor, flattening of the philtral columns, and loss of projection of the Cupid’s bow.¹⁰

Downturning of the oral commissures is observed secondary to a combination of gravity, bone resorption, and soft tissue volume loss. Hyperactivity of the depressor anguli oris muscle exacerbates the mesolabial folds, producing marionette lines and a saddened expression.⁷ With ongoing volume loss and ligament laxity, tissue redistributes near the jaws and chin, giving rise to jowls. Similarly, perioral volume loss and descent of the malar fat-pad deepen the nasolabial folds in the aging midface.⁶

The main objective of perioral rejuvenation is to reinstate a harmonious refreshed look to the lower face; however, aesthetic analysis should occur within the context of the face as a whole, as the lips should complement the surrounding perioral cosmetic unit and overall skeletal foundation of the face. To accomplish this goal, the dermatologist’s armamentarium contains a broad variety of approaches including restriction of muscle movement, volume restoration, and surface contouring.

Volume Restoration

Treatment Options

In 2015, hyaluronic acid (HA) fillers constituted 80% of all injectable soft-tissue fillers, an 8% increase from 2014.¹¹ Hyaluronic acid has achieved immense popularity as a temporary dermal filler given its biocompatibility, longevity, and reversibility via hyaluronidase.¹²

Hyaluronic acid is a naturally occurring glycosaminoglycan that comprises the connective tissue matrix. The molecular composition affords HA its hydrophilic property, which augments dermal volume.⁷ Endogenous HA has a short half-life, and chemical modification by a cross-linking process extends longevity by 6 to 12 months. The various HA fillers are distinguished by method of purification, size of molecules, concentration and degree of cross-linking, and viscosity.^7,13,14 These differences dictate overall clinical performance such as flow properties, longevity, and stability. As a general rule, a high-viscosity product is more appropriate for deeper augmentation; fillers with low viscosity are more appropriate for correction of shallow defects.¹ Table 1 lists the HA fillers that are currently approved by the US Food and Drug Administration for lip augmentation and/or perioral rhytides in adults 21 years and older.^15-17

Randomized controlled trials comparing the efficacy, longevity, and tolerability of different HA products are lacking in the literature and, where present, have strong industry influence.^18,19 The advent of assessment scales has provided an objective evaluation of perioral and lip augmentation, facilitating comparisons between products in both clinical research and practice.²⁰

Semipermanent biostimulatory dermal fillers such as calcium hydroxylapatite and poly-L-lactic acid are not recommended for lip augmentation due to an increased incidence of submucosal nodule formation.^6,14,21 Likewise, permanent fillers are not recommended given their irreversibility and risk of nodule formation around the lips.^14,22 Nonetheless, liquid silicone (purified polydimethylsiloxane) administered via a microdroplet technique (0.01 mL of silicone at a time, no more than 1 cc per lip per session) has been used off label as a permanent filling agent for lip augmentation with limited complications.²³ Regardless, trepidations about its use with respect to reported risks continue to limit its application.²²

Similarly, surgical lip implants such as expanded polytetrafluoroethylene is an option for a subset of patients desiring permanent enhancement but are less commonly utilized given the side-effect profile, irreversibility, and relatively invasive nature of the procedure.²² Lastly, autologous fat transfer has been used in correction of the nasolabial and mesolabial folds as well as in lip augmentation; however, irregular surface contours and unpredictable longevity secondary to postinjection resorption (20%–90%) has limited its popularity.^3,14,21

HA Injection Technique

With respect to HA fillers in the perioral area, numerous approaches have been described.^10,22 The techniques in Table 2 provide a foundation for lip rejuvenation.

Several injection techniques exist, including serial puncture, linear threading, cross-hatching, and fanning in a retrograde or anterograde manner.²⁴ A blunt microcannula (27 gauge, 38 mm) may be used in place of sharp needles and offers the benefit of increased patient comfort, reduced edema and ecchymosis, and shortened recovery period.^25,26 Gentle massage of the product after injection can assist with an even contour. Lastly, a key determinant of successful outcomes is using an adequate volume of HA filler (1–2 mL for shaping the vermilion border and volumizing the lips).²⁷ Figure 2 highlights a clinical example of HA filler for lip augmentation.

Fortunately, most complications encountered with HA lip augmentation are mild and transient. The most commonly observed side effects include injection-site reactions such as pain, erythema, and edema. Similarly, most adverse effects are related to injection technique. All HA fillers are prone to the Tyndall effect, a consequence of too superficial an injection plane. Patients with history of recurrent herpes simplex virus infections should receive prophylactic antiviral therapy.¹²

Muscle Control

An emerging concept in rejuvenation of the lower face recognizes not only restoration of volume but also control of muscle movement. Local injection of botulinum toxin type A induces relaxation of hyperfunctional facial muscles through temporary inhibition of neurotransmitter release.⁶ The potential for paralysis of the oral cavity may limit the application of botulinum toxin type A in that region.⁷ Nonetheless, the off-label potential of botulinum toxin type A has expanded to include several targets in the lower face. The orbicularis oris muscle is targeted to soften perioral rhytides. Conservative dosing (1–2 U per lip quadrant or approximately 5 U total) and superficial injection is emphasized in this area.²⁷ Similarly, the depressor anguli oris muscle is targeted by injection of 4 U bilaterally to soften the marionette lines. In the chin area, the mentalis muscle can be targeted by injection of 2 U deep into each belly of the muscle to reduce the mental crease and dimpling.²⁸ Combination treatment with dermal filler and neurotoxin demonstrates effects that last longer than either modality alone without additional adverse events.²⁹ With combination therapy, guidelines suggest treating with filler first.²⁷

Conclusion

A greater understanding of the extrinsic and intrinsic factors that contribute to the structural and surface changes of the aging face coupled with a preference for minimally invasive procedures has revolutionized the dermatologist’s approach to perioral rejuvenation. Serving as a focal point of the face, the lips and perioral skin are well poised to benefit from this paradigm shift. A multifaceted approach utilizing dermal fillers and neurotoxins may be most appropriate and has demonstrated optimal outcomes in facial aesthetics.

Historically, a variety of tools have been used to alter one’s appearance for cultural or religious purposes or to conform to standards of beauty. As a defining feature of the face, the lips provide a unique opportunity for facial aesthetic enhancement. There has been a paradigm shift in medicine favoring preventative health and a desire to slow and even reverse the aging process.¹ Acknowledging that product technology, skill sets, and cultural ideals continually evolve, this article highlights perioral anatomy, explains aging of the lower face, and reviews techniques to achieve perioral rejuvenation through volume restoration and muscle control.

Perioral Anatomy

The layers of the lips include the epidermis, subcutaneous tissue, orbicularis oris muscle fibers, and mucosa. The upper lip extends from the base of the nose to the mucosa inferiorly and to the nasolabial folds laterally. The curvilinear lower lip extends from the mucosa to the mandible inferiorly and to the oral commissures laterally.² Circumferential at the vermilion-cutaneous junction, a raised area of pale skin known as the white roll accentuates the vermilion border and provides an important landmark during lip augmentation.³ At the upper lip, this elevation of the vermilion joins at a V-shaped depression centrally to form the Cupid’s bow. The cutaneous upper lip has 2 raised vertical pillars known as the philtral columns, which are formed from decussating fibers of the orbicularis oris muscle.² The resultant midline depression is the philtrum. These defining features of the upper lip are to be preserved during augmentation procedures (Figure 1).⁴

The superior and inferior labial arteries, both branches of the facial artery, supply the upper and lower lip, respectively. The anastomotic arch of the superior labial artery is susceptible to injury from deep injection of the upper lip between the muscle layer and mucosa; therefore, caution must be exercised in this area.⁵ Injections into the vermilion and lower lip can be safely performed with less concern for vascular compromise. The vermilion derives its red color from the translucency of capillaries in the superficial papillae.² The capillary plexus at the papillae and rich sensory nerve network render the lip a highly vascular and sensitive structure.

Aging of the Lower Face

Subcutaneous fat atrophy, loss of elasticity, gravitational forces, and remodeling of the skeletal foundation all contribute to aging of the lower face. Starting as early as the third decade of life, intrinsic factors including hormonal changes and genetically determined processes produce alterations in skin quality and structure. Similarly, extrinsic aging through environmental influences, namely exposure to UV radiation and smoking, accelerate the loss of skin integrity.⁶

The decreased laxity of the skin in combination with repeated contraction of the orbicularis oris muscle results in perioral rhytides.⁷ For women in particular, vertically oriented perioral rhytides develop above the vermilion; terminal hair follicles, thicker skin, and a greater density of subcutaneous fat are presumptive protective factors for males.⁸ With time, the cutaneous portion of the upper lip lengthens and there is redistribution of volume with effacement of the upper lip vermilion.⁹ Additionally, the demarcation of the vermilion becomes blurred secondary to pallor, flattening of the philtral columns, and loss of projection of the Cupid’s bow.¹⁰

Downturning of the oral commissures is observed secondary to a combination of gravity, bone resorption, and soft tissue volume loss. Hyperactivity of the depressor anguli oris muscle exacerbates the mesolabial folds, producing marionette lines and a saddened expression.⁷ With ongoing volume loss and ligament laxity, tissue redistributes near the jaws and chin, giving rise to jowls. Similarly, perioral volume loss and descent of the malar fat-pad deepen the nasolabial folds in the aging midface.⁶

The main objective of perioral rejuvenation is to reinstate a harmonious refreshed look to the lower face; however, aesthetic analysis should occur within the context of the face as a whole, as the lips should complement the surrounding perioral cosmetic unit and overall skeletal foundation of the face. To accomplish this goal, the dermatologist’s armamentarium contains a broad variety of approaches including restriction of muscle movement, volume restoration, and surface contouring.

Volume Restoration

Treatment Options

In 2015, hyaluronic acid (HA) fillers constituted 80% of all injectable soft-tissue fillers, an 8% increase from 2014.¹¹ Hyaluronic acid has achieved immense popularity as a temporary dermal filler given its biocompatibility, longevity, and reversibility via hyaluronidase.¹²

Hyaluronic acid is a naturally occurring glycosaminoglycan that comprises the connective tissue matrix. The molecular composition affords HA its hydrophilic property, which augments dermal volume.⁷ Endogenous HA has a short half-life, and chemical modification by a cross-linking process extends longevity by 6 to 12 months. The various HA fillers are distinguished by method of purification, size of molecules, concentration and degree of cross-linking, and viscosity.^7,13,14 These differences dictate overall clinical performance such as flow properties, longevity, and stability. As a general rule, a high-viscosity product is more appropriate for deeper augmentation; fillers with low viscosity are more appropriate for correction of shallow defects.¹ Table 1 lists the HA fillers that are currently approved by the US Food and Drug Administration for lip augmentation and/or perioral rhytides in adults 21 years and older.^15-17

Randomized controlled trials comparing the efficacy, longevity, and tolerability of different HA products are lacking in the literature and, where present, have strong industry influence.^18,19 The advent of assessment scales has provided an objective evaluation of perioral and lip augmentation, facilitating comparisons between products in both clinical research and practice.²⁰

Semipermanent biostimulatory dermal fillers such as calcium hydroxylapatite and poly-L-lactic acid are not recommended for lip augmentation due to an increased incidence of submucosal nodule formation.^6,14,21 Likewise, permanent fillers are not recommended given their irreversibility and risk of nodule formation around the lips.^14,22 Nonetheless, liquid silicone (purified polydimethylsiloxane) administered via a microdroplet technique (0.01 mL of silicone at a time, no more than 1 cc per lip per session) has been used off label as a permanent filling agent for lip augmentation with limited complications.²³ Regardless, trepidations about its use with respect to reported risks continue to limit its application.²²

Similarly, surgical lip implants such as expanded polytetrafluoroethylene is an option for a subset of patients desiring permanent enhancement but are less commonly utilized given the side-effect profile, irreversibility, and relatively invasive nature of the procedure.²² Lastly, autologous fat transfer has been used in correction of the nasolabial and mesolabial folds as well as in lip augmentation; however, irregular surface contours and unpredictable longevity secondary to postinjection resorption (20%–90%) has limited its popularity.^3,14,21

HA Injection Technique

With respect to HA fillers in the perioral area, numerous approaches have been described.^10,22 The techniques in Table 2 provide a foundation for lip rejuvenation.

Several injection techniques exist, including serial puncture, linear threading, cross-hatching, and fanning in a retrograde or anterograde manner.²⁴ A blunt microcannula (27 gauge, 38 mm) may be used in place of sharp needles and offers the benefit of increased patient comfort, reduced edema and ecchymosis, and shortened recovery period.^25,26 Gentle massage of the product after injection can assist with an even contour. Lastly, a key determinant of successful outcomes is using an adequate volume of HA filler (1–2 mL for shaping the vermilion border and volumizing the lips).²⁷ Figure 2 highlights a clinical example of HA filler for lip augmentation.

Fortunately, most complications encountered with HA lip augmentation are mild and transient. The most commonly observed side effects include injection-site reactions such as pain, erythema, and edema. Similarly, most adverse effects are related to injection technique. All HA fillers are prone to the Tyndall effect, a consequence of too superficial an injection plane. Patients with history of recurrent herpes simplex virus infections should receive prophylactic antiviral therapy.¹²

Muscle Control

An emerging concept in rejuvenation of the lower face recognizes not only restoration of volume but also control of muscle movement. Local injection of botulinum toxin type A induces relaxation of hyperfunctional facial muscles through temporary inhibition of neurotransmitter release.⁶ The potential for paralysis of the oral cavity may limit the application of botulinum toxin type A in that region.⁷ Nonetheless, the off-label potential of botulinum toxin type A has expanded to include several targets in the lower face. The orbicularis oris muscle is targeted to soften perioral rhytides. Conservative dosing (1–2 U per lip quadrant or approximately 5 U total) and superficial injection is emphasized in this area.²⁷ Similarly, the depressor anguli oris muscle is targeted by injection of 4 U bilaterally to soften the marionette lines. In the chin area, the mentalis muscle can be targeted by injection of 2 U deep into each belly of the muscle to reduce the mental crease and dimpling.²⁸ Combination treatment with dermal filler and neurotoxin demonstrates effects that last longer than either modality alone without additional adverse events.²⁹ With combination therapy, guidelines suggest treating with filler first.²⁷

Conclusion

A greater understanding of the extrinsic and intrinsic factors that contribute to the structural and surface changes of the aging face coupled with a preference for minimally invasive procedures has revolutionized the dermatologist’s approach to perioral rejuvenation. Serving as a focal point of the face, the lips and perioral skin are well poised to benefit from this paradigm shift. A multifaceted approach utilizing dermal fillers and neurotoxins may be most appropriate and has demonstrated optimal outcomes in facial aesthetics.

Tattoos have been viewed as one of the most exotic forms of art for thousands of years. In ancient times, tattoos were used mainly for therapeutic and status purposes. According to British archeologist Joann Fletcher, the oldest evidence of tattoo use was found on the famous “Iceman,” a 5200-year-old frozen mummy that was discovered more than 20 years ago.¹ Tattoos were thought to be a form of therapy used to decrease joint pain. On the other hand, the ancient Egyptians used tattoos as symbols of wealth and high status; surprisingly, only women were tattooed. Fletcher also reported that tattoos were used as a form of therapy during pregnancy in upper-class women.¹

Tattoos have served different purposes in the last few centuries, making their way to the United States at the start of the 20th century.² New York City became the tattoo capital of the country. During this early period, male artists often would tattoo their wives so that they could advertise their work. After the Prohibition era, tattoos became widely used within the US Military, becoming a way to show pride and patriotism.²

Due to the permanent nature of tattoos, we sought to understand the reasons for obtaining this particular genre of body art. The purpose of this study was to provide a greater understanding of the current demographics of individuals who get tattoos, looking at specific trends in age and level of education of those who get tattoos as well as the motivation for tattoo placement. As dermatologists, it is essential to understand this patient population to be able to provide services (ie, tattoo removal) in the safe setting of a physician’s office.

Methods

The study was conducted at a private dermatology clinic in the Chicago (Illinois) metropolitan area with no institutional review board approval. Between January 2011 and December 2012, local patients with at least 1 tattoo were asked, with assumed consent, to fill out an investigator-developed survey containing 18 multiple-choice questions regarding age, educational and family background, and other factors. The race and gender of the respondents as well as the number of patients who declined to complete the survey were not recorded.

Results

A total of 363 patients completed the in-person survey. Responses were tabulated and converted into percentages for comparison (N=363). Data analysis was divided into 3 parameters: education level, health concerns, and motivation for getting a tattoo. Figure 1 shows that 70% of respondents had obtained a college degree or higher.

With regard to health concerns associated with tattoos, the majority of respondents (71%) claimed they were not concerned with the health risks (eg, infection with human immunodeficiency virus or hepatitis C virus) associated with getting a tattoo. Also, only 6% of respondents admitted to being under the influence of drugs or alcohol at the time of getting a tattoo. Of 21 respondents who claimed drugs and/or alcohol were part of their tattoo experience, the highest level of education was high school in 7 respondents and 2 got their first tattoo when they were younger than 14 years.

Survey results revealed that the majority of respondents got a tattoo as an act of rememberance (Figure 2). For example, one respondent reported getting a tattoo for religious purposes, while another got a tattoo to celebrate and mark each level of completed education (ie, high school, college, graduate school). However, a high percentage of respondents (26%) got a tattoo for fun.

Comment

Although ancient tattoos were used for therapeutic purposes, this study revealed that tattoos are now obtained by individuals with higher levels of education to remember a loved one or purely for enjoyment. The potential health risks associated with getting a tattoo did not deter the respondents in this study. Converse to the popular belief that individuals are under the influence of drugs and/or alcohol when getting a tattoo, our study found that only 6% of respondents were under the influence. A comparable trend was found among US military service members in a similar study.³ The majority of respondents did not regret their tattoos and did not report taking a mind-altering substance. Tattoos serve as a symbol of one’s proud individualism.³ However, a 2001 study found a correlation between greater use of alcohol and marijuana among college students with tattoos and piecings.⁴ These circumstances may lead patients to seek consultation from a dermatologist for tattoo removal. Therefore, it is important to have a better understanding of this particular patient population to facilitate care in an efficient manner.

Evaluation of the gender and race of survey respondents would be useful in the future. Financial status of respondents also may be explored, as wealth and status were used by the ancient Egyptians to determine who could get a tattoo. A follow-up analysis on removal of tattoos also will be explored in the future.

Tattoos have been viewed as one of the most exotic forms of art for thousands of years. In ancient times, tattoos were used mainly for therapeutic and status purposes. According to British archeologist Joann Fletcher, the oldest evidence of tattoo use was found on the famous “Iceman,” a 5200-year-old frozen mummy that was discovered more than 20 years ago.¹ Tattoos were thought to be a form of therapy used to decrease joint pain. On the other hand, the ancient Egyptians used tattoos as symbols of wealth and high status; surprisingly, only women were tattooed. Fletcher also reported that tattoos were used as a form of therapy during pregnancy in upper-class women.¹

Tattoos have served different purposes in the last few centuries, making their way to the United States at the start of the 20th century.² New York City became the tattoo capital of the country. During this early period, male artists often would tattoo their wives so that they could advertise their work. After the Prohibition era, tattoos became widely used within the US Military, becoming a way to show pride and patriotism.²

Due to the permanent nature of tattoos, we sought to understand the reasons for obtaining this particular genre of body art. The purpose of this study was to provide a greater understanding of the current demographics of individuals who get tattoos, looking at specific trends in age and level of education of those who get tattoos as well as the motivation for tattoo placement. As dermatologists, it is essential to understand this patient population to be able to provide services (ie, tattoo removal) in the safe setting of a physician’s office.

Methods

The study was conducted at a private dermatology clinic in the Chicago (Illinois) metropolitan area with no institutional review board approval. Between January 2011 and December 2012, local patients with at least 1 tattoo were asked, with assumed consent, to fill out an investigator-developed survey containing 18 multiple-choice questions regarding age, educational and family background, and other factors. The race and gender of the respondents as well as the number of patients who declined to complete the survey were not recorded.

Results

A total of 363 patients completed the in-person survey. Responses were tabulated and converted into percentages for comparison (N=363). Data analysis was divided into 3 parameters: education level, health concerns, and motivation for getting a tattoo. Figure 1 shows that 70% of respondents had obtained a college degree or higher.

With regard to health concerns associated with tattoos, the majority of respondents (71%) claimed they were not concerned with the health risks (eg, infection with human immunodeficiency virus or hepatitis C virus) associated with getting a tattoo. Also, only 6% of respondents admitted to being under the influence of drugs or alcohol at the time of getting a tattoo. Of 21 respondents who claimed drugs and/or alcohol were part of their tattoo experience, the highest level of education was high school in 7 respondents and 2 got their first tattoo when they were younger than 14 years.

Survey results revealed that the majority of respondents got a tattoo as an act of rememberance (Figure 2). For example, one respondent reported getting a tattoo for religious purposes, while another got a tattoo to celebrate and mark each level of completed education (ie, high school, college, graduate school). However, a high percentage of respondents (26%) got a tattoo for fun.

Comment

Although ancient tattoos were used for therapeutic purposes, this study revealed that tattoos are now obtained by individuals with higher levels of education to remember a loved one or purely for enjoyment. The potential health risks associated with getting a tattoo did not deter the respondents in this study. Converse to the popular belief that individuals are under the influence of drugs and/or alcohol when getting a tattoo, our study found that only 6% of respondents were under the influence. A comparable trend was found among US military service members in a similar study.³ The majority of respondents did not regret their tattoos and did not report taking a mind-altering substance. Tattoos serve as a symbol of one’s proud individualism.³ However, a 2001 study found a correlation between greater use of alcohol and marijuana among college students with tattoos and piecings.⁴ These circumstances may lead patients to seek consultation from a dermatologist for tattoo removal. Therefore, it is important to have a better understanding of this particular patient population to facilitate care in an efficient manner.

Evaluation of the gender and race of survey respondents would be useful in the future. Financial status of respondents also may be explored, as wealth and status were used by the ancient Egyptians to determine who could get a tattoo. A follow-up analysis on removal of tattoos also will be explored in the future.

Tattoos have been viewed as one of the most exotic forms of art for thousands of years. In ancient times, tattoos were used mainly for therapeutic and status purposes. According to British archeologist Joann Fletcher, the oldest evidence of tattoo use was found on the famous “Iceman,” a 5200-year-old frozen mummy that was discovered more than 20 years ago.¹ Tattoos were thought to be a form of therapy used to decrease joint pain. On the other hand, the ancient Egyptians used tattoos as symbols of wealth and high status; surprisingly, only women were tattooed. Fletcher also reported that tattoos were used as a form of therapy during pregnancy in upper-class women.¹

Tattoos have served different purposes in the last few centuries, making their way to the United States at the start of the 20th century.² New York City became the tattoo capital of the country. During this early period, male artists often would tattoo their wives so that they could advertise their work. After the Prohibition era, tattoos became widely used within the US Military, becoming a way to show pride and patriotism.²

Due to the permanent nature of tattoos, we sought to understand the reasons for obtaining this particular genre of body art. The purpose of this study was to provide a greater understanding of the current demographics of individuals who get tattoos, looking at specific trends in age and level of education of those who get tattoos as well as the motivation for tattoo placement. As dermatologists, it is essential to understand this patient population to be able to provide services (ie, tattoo removal) in the safe setting of a physician’s office.

Methods

The study was conducted at a private dermatology clinic in the Chicago (Illinois) metropolitan area with no institutional review board approval. Between January 2011 and December 2012, local patients with at least 1 tattoo were asked, with assumed consent, to fill out an investigator-developed survey containing 18 multiple-choice questions regarding age, educational and family background, and other factors. The race and gender of the respondents as well as the number of patients who declined to complete the survey were not recorded.

Results

A total of 363 patients completed the in-person survey. Responses were tabulated and converted into percentages for comparison (N=363). Data analysis was divided into 3 parameters: education level, health concerns, and motivation for getting a tattoo. Figure 1 shows that 70% of respondents had obtained a college degree or higher.

With regard to health concerns associated with tattoos, the majority of respondents (71%) claimed they were not concerned with the health risks (eg, infection with human immunodeficiency virus or hepatitis C virus) associated with getting a tattoo. Also, only 6% of respondents admitted to being under the influence of drugs or alcohol at the time of getting a tattoo. Of 21 respondents who claimed drugs and/or alcohol were part of their tattoo experience, the highest level of education was high school in 7 respondents and 2 got their first tattoo when they were younger than 14 years.

Survey results revealed that the majority of respondents got a tattoo as an act of rememberance (Figure 2). For example, one respondent reported getting a tattoo for religious purposes, while another got a tattoo to celebrate and mark each level of completed education (ie, high school, college, graduate school). However, a high percentage of respondents (26%) got a tattoo for fun.

Comment

Although ancient tattoos were used for therapeutic purposes, this study revealed that tattoos are now obtained by individuals with higher levels of education to remember a loved one or purely for enjoyment. The potential health risks associated with getting a tattoo did not deter the respondents in this study. Converse to the popular belief that individuals are under the influence of drugs and/or alcohol when getting a tattoo, our study found that only 6% of respondents were under the influence. A comparable trend was found among US military service members in a similar study.³ The majority of respondents did not regret their tattoos and did not report taking a mind-altering substance. Tattoos serve as a symbol of one’s proud individualism.³ However, a 2001 study found a correlation between greater use of alcohol and marijuana among college students with tattoos and piecings.⁴ These circumstances may lead patients to seek consultation from a dermatologist for tattoo removal. Therefore, it is important to have a better understanding of this particular patient population to facilitate care in an efficient manner.

Evaluation of the gender and race of survey respondents would be useful in the future. Financial status of respondents also may be explored, as wealth and status were used by the ancient Egyptians to determine who could get a tattoo. A follow-up analysis on removal of tattoos also will be explored in the future.

Due to a submission error, the article “A Boxed Warning for Inadequate Psoriasis Treatment” (Cutis. 2016;98:206-207) did not contain the complete author disclosure information. The corrected disclosure statement appears below:

Ms. Kagha and Ms. Anderson report no conflict of interest. Dr. Blauvelt has served as a clinical study investigator and scientific adviser for AbbVie Inc; Amgen, Inc; Boehringer Ingelheim; Celgene Corporation; Dermira Inc; Eli Lilly and Company; Genentech, Inc; GlaxoSmithKline; Janssen Biotech, Inc; Merck & Co; Novartis; Pfizer Inc; Regeneron Pharmaceuticals, Inc; Sandoz, a Novartis Division; Sanofi; Sun Pharmaceutical Industries, Ltd; UCB; and Valeant Pharmaceuticals International, Inc, as well as a paid speaker for Eli Lilly and Company. Dr. Leonardi has served as an advisory board member and consultant for AbbVie Inc; Amgen, Inc; Boehringer Ingelheim; Dermira Inc; Eli Lilly and Company; Janssen Biotech, Inc; LEO Pharma; Pfizer Inc; Sandoz, a Novartis Division; UCB; and Vitae Pharmaceuticals. He also has been an investigator for AbbVie Inc; Actavis Pharma, Inc; Amgen, Inc; Boehringer Ingelheim; Celgene Corporation; Coherus BioSciences; Corrona, LLC; Dermira Inc; Eli Lilly and Company; Galderma Laboratories, LP; Glenmark Pharmaceuticals Inc; Janssen Biotech, Inc; LEO Pharma; Merck & Co; Novartis; Pfizer Inc; Sandoz, a Novartis Division; Stiefel, a GSK company; and Wyeth Pharmaceuticals, Inc. Dr. Leonardi also has been on the speaker’s bureau for AbbVie Inc; Celgene Corporation; Eli Lilly and Company; and Novartis. Dr. Feldman is a consultant, researcher, and/or speaker for AbbVie Inc; Amgen, Inc; Baxter; Boehringer Ingelheim; Celgene Corporation; Janssen Biotech, Inc; Merck & Co; Mylan; Novartis; Pfizer Inc; and Valeant Pharmaceuticals International, Inc.

The staff of Cutis^® makes every possible effort to ensure accuracy in its articles and apologizes for the mistake.

Due to a submission error, the article “A Boxed Warning for Inadequate Psoriasis Treatment” (Cutis. 2016;98:206-207) did not contain the complete author disclosure information. The corrected disclosure statement appears below:

Ms. Kagha and Ms. Anderson report no conflict of interest. Dr. Blauvelt has served as a clinical study investigator and scientific adviser for AbbVie Inc; Amgen, Inc; Boehringer Ingelheim; Celgene Corporation; Dermira Inc; Eli Lilly and Company; Genentech, Inc; GlaxoSmithKline; Janssen Biotech, Inc; Merck & Co; Novartis; Pfizer Inc; Regeneron Pharmaceuticals, Inc; Sandoz, a Novartis Division; Sanofi; Sun Pharmaceutical Industries, Ltd; UCB; and Valeant Pharmaceuticals International, Inc, as well as a paid speaker for Eli Lilly and Company. Dr. Leonardi has served as an advisory board member and consultant for AbbVie Inc; Amgen, Inc; Boehringer Ingelheim; Dermira Inc; Eli Lilly and Company; Janssen Biotech, Inc; LEO Pharma; Pfizer Inc; Sandoz, a Novartis Division; UCB; and Vitae Pharmaceuticals. He also has been an investigator for AbbVie Inc; Actavis Pharma, Inc; Amgen, Inc; Boehringer Ingelheim; Celgene Corporation; Coherus BioSciences; Corrona, LLC; Dermira Inc; Eli Lilly and Company; Galderma Laboratories, LP; Glenmark Pharmaceuticals Inc; Janssen Biotech, Inc; LEO Pharma; Merck & Co; Novartis; Pfizer Inc; Sandoz, a Novartis Division; Stiefel, a GSK company; and Wyeth Pharmaceuticals, Inc. Dr. Leonardi also has been on the speaker’s bureau for AbbVie Inc; Celgene Corporation; Eli Lilly and Company; and Novartis. Dr. Feldman is a consultant, researcher, and/or speaker for AbbVie Inc; Amgen, Inc; Baxter; Boehringer Ingelheim; Celgene Corporation; Janssen Biotech, Inc; Merck & Co; Mylan; Novartis; Pfizer Inc; and Valeant Pharmaceuticals International, Inc.

The staff of Cutis^® makes every possible effort to ensure accuracy in its articles and apologizes for the mistake.

Due to a submission error, the article “A Boxed Warning for Inadequate Psoriasis Treatment” (Cutis. 2016;98:206-207) did not contain the complete author disclosure information. The corrected disclosure statement appears below:

Ms. Kagha and Ms. Anderson report no conflict of interest. Dr. Blauvelt has served as a clinical study investigator and scientific adviser for AbbVie Inc; Amgen, Inc; Boehringer Ingelheim; Celgene Corporation; Dermira Inc; Eli Lilly and Company; Genentech, Inc; GlaxoSmithKline; Janssen Biotech, Inc; Merck & Co; Novartis; Pfizer Inc; Regeneron Pharmaceuticals, Inc; Sandoz, a Novartis Division; Sanofi; Sun Pharmaceutical Industries, Ltd; UCB; and Valeant Pharmaceuticals International, Inc, as well as a paid speaker for Eli Lilly and Company. Dr. Leonardi has served as an advisory board member and consultant for AbbVie Inc; Amgen, Inc; Boehringer Ingelheim; Dermira Inc; Eli Lilly and Company; Janssen Biotech, Inc; LEO Pharma; Pfizer Inc; Sandoz, a Novartis Division; UCB; and Vitae Pharmaceuticals. He also has been an investigator for AbbVie Inc; Actavis Pharma, Inc; Amgen, Inc; Boehringer Ingelheim; Celgene Corporation; Coherus BioSciences; Corrona, LLC; Dermira Inc; Eli Lilly and Company; Galderma Laboratories, LP; Glenmark Pharmaceuticals Inc; Janssen Biotech, Inc; LEO Pharma; Merck & Co; Novartis; Pfizer Inc; Sandoz, a Novartis Division; Stiefel, a GSK company; and Wyeth Pharmaceuticals, Inc. Dr. Leonardi also has been on the speaker’s bureau for AbbVie Inc; Celgene Corporation; Eli Lilly and Company; and Novartis. Dr. Feldman is a consultant, researcher, and/or speaker for AbbVie Inc; Amgen, Inc; Baxter; Boehringer Ingelheim; Celgene Corporation; Janssen Biotech, Inc; Merck & Co; Mylan; Novartis; Pfizer Inc; and Valeant Pharmaceuticals International, Inc.

The staff of Cutis^® makes every possible effort to ensure accuracy in its articles and apologizes for the mistake.

It is an exciting time for dermatologists. In the 16 years that I have been in practice our knowledge of disease pathogenesis has increased and has shaped treatments that can now offer life-changing improvement for patients with extensive dermatologic disease. The everyday practice of cosmetic dermatology also has advanced. Sixteen years ago the only cosmetic options we had for our patients were bovine or human collagen injections, traditional CO₂ laser resurfacing, and the older generations of pulsed dye lasers. Neuromodulators were just being introduced. We quickly learned the limitations and complications associated with these modalities. Collagen injections were directed at fine perioral lines and lasted 3 to 4 months. The worst complication would be a bruise or an allergic reaction to the bovine collagen. If we really needed to restore volume beyond the perioral regions, our only option was autologous fat transfer. CO₂ laser resurfacing was used to firm skin, erase deep wrinkles, and improve sun damage, but its use was limited to older, fair-skinned individuals due to the inherent risk for hypopigmentation and depigmentation. Pulsed dye lasers similarly had no means of cooling the skin, thus they were limited to lighter-skinned individuals and had notable risk for blisters, burns, and hypopigmentation. Since then, our understanding of skin healing, laser-tissue interaction, and facial aging has driven the field to new heights of technological advances and safety. Just as I tell my patients and residents, there is no better time to be in this field than at this moment. Dermatologists have driven the advances behind many of the technologies that are now in widespread use among physicians in a variety of specialties.

Our understanding of facial aging has evolved to include the complex interplay of skeletal change, fat atrophy, and skin aging, which must all be considered when improving a patient’s appearance. Fillers have evolved in physical characteristics to give us the ability to choose between lift, spread, neocollagenesis, or water absorption. Thus, we can select the proper filler for the specific anatomic area we are rejuvenating.

Our understanding of photoaging and laser-tissue physics has allowed for the development of a newer generation of lasers ranging from fractionated lasers to noninvasive modalities that can safely be used in a variety of ethnic skin types to address acne scars, wrinkles, and inflammatory processes such as acne and rosacea. Similarly, the desire to tighten redundant skin has continued to drive ultrasound and radiofrequency technology and sparked growth in a newer field of cryolipolysis and chemical lipolysis agents.

Our dialogue with patients also has evolved to include the 4 R’s of antiaging: resurfacing the skin (eg, lasers, peels), refilling the lost volume (eg, fillers, fat), redraping the excess skin (eg, radiofrequency, ultrasound, laser, surgery), and relaxing dynamic lines (eg, neuromodulators). I propose an additional R: renewal! We must focus on the need for constant renewal so that patients maintain the results we have achieved. I apply the analogy of exercising to get into shape. One must go to the gym regularly to get to the desired level of fitness, but you do not stop exercising, otherwise you will quickly relapse to your former lack of fitness. Similarly, patients should receive the appropriate treatments to bring them to the desired level of rejuvenation, but then some form of constant renewal process is needed to maintain them at that level. Without the stimulation of the skin, the aging process continues and the cycle begins all over again.

In my practice, renewal is achieved by driving the skin to maintain the glow and smoothness that enhances the results of the fillers, neuromodulators, lasers, and peels that we have used. The skin is the first thing people notice. Without the glow, the patient will look good but not great. I tell patients that this part of the process is their responsibility. They must adhere to the skin care regimen specifically designed to address their needs. By incorporating the patient in the rejuvenation process, he/she is empowered to take control over the aging process and has grown more confident in you as a physician.

These are exciting times and there is still so much in the pipeline. By continually learning, reading, and attending workshops and meetings, you can make sure our specialty continue to be the leader in the antiaging field.

It is an exciting time for dermatologists. In the 16 years that I have been in practice our knowledge of disease pathogenesis has increased and has shaped treatments that can now offer life-changing improvement for patients with extensive dermatologic disease. The everyday practice of cosmetic dermatology also has advanced. Sixteen years ago the only cosmetic options we had for our patients were bovine or human collagen injections, traditional CO₂ laser resurfacing, and the older generations of pulsed dye lasers. Neuromodulators were just being introduced. We quickly learned the limitations and complications associated with these modalities. Collagen injections were directed at fine perioral lines and lasted 3 to 4 months. The worst complication would be a bruise or an allergic reaction to the bovine collagen. If we really needed to restore volume beyond the perioral regions, our only option was autologous fat transfer. CO₂ laser resurfacing was used to firm skin, erase deep wrinkles, and improve sun damage, but its use was limited to older, fair-skinned individuals due to the inherent risk for hypopigmentation and depigmentation. Pulsed dye lasers similarly had no means of cooling the skin, thus they were limited to lighter-skinned individuals and had notable risk for blisters, burns, and hypopigmentation. Since then, our understanding of skin healing, laser-tissue interaction, and facial aging has driven the field to new heights of technological advances and safety. Just as I tell my patients and residents, there is no better time to be in this field than at this moment. Dermatologists have driven the advances behind many of the technologies that are now in widespread use among physicians in a variety of specialties.

Our understanding of facial aging has evolved to include the complex interplay of skeletal change, fat atrophy, and skin aging, which must all be considered when improving a patient’s appearance. Fillers have evolved in physical characteristics to give us the ability to choose between lift, spread, neocollagenesis, or water absorption. Thus, we can select the proper filler for the specific anatomic area we are rejuvenating.

Our understanding of photoaging and laser-tissue physics has allowed for the development of a newer generation of lasers ranging from fractionated lasers to noninvasive modalities that can safely be used in a variety of ethnic skin types to address acne scars, wrinkles, and inflammatory processes such as acne and rosacea. Similarly, the desire to tighten redundant skin has continued to drive ultrasound and radiofrequency technology and sparked growth in a newer field of cryolipolysis and chemical lipolysis agents.

Our dialogue with patients also has evolved to include the 4 R’s of antiaging: resurfacing the skin (eg, lasers, peels), refilling the lost volume (eg, fillers, fat), redraping the excess skin (eg, radiofrequency, ultrasound, laser, surgery), and relaxing dynamic lines (eg, neuromodulators). I propose an additional R: renewal! We must focus on the need for constant renewal so that patients maintain the results we have achieved. I apply the analogy of exercising to get into shape. One must go to the gym regularly to get to the desired level of fitness, but you do not stop exercising, otherwise you will quickly relapse to your former lack of fitness. Similarly, patients should receive the appropriate treatments to bring them to the desired level of rejuvenation, but then some form of constant renewal process is needed to maintain them at that level. Without the stimulation of the skin, the aging process continues and the cycle begins all over again.

In my practice, renewal is achieved by driving the skin to maintain the glow and smoothness that enhances the results of the fillers, neuromodulators, lasers, and peels that we have used. The skin is the first thing people notice. Without the glow, the patient will look good but not great. I tell patients that this part of the process is their responsibility. They must adhere to the skin care regimen specifically designed to address their needs. By incorporating the patient in the rejuvenation process, he/she is empowered to take control over the aging process and has grown more confident in you as a physician.

These are exciting times and there is still so much in the pipeline. By continually learning, reading, and attending workshops and meetings, you can make sure our specialty continue to be the leader in the antiaging field.

It is an exciting time for dermatologists. In the 16 years that I have been in practice our knowledge of disease pathogenesis has increased and has shaped treatments that can now offer life-changing improvement for patients with extensive dermatologic disease. The everyday practice of cosmetic dermatology also has advanced. Sixteen years ago the only cosmetic options we had for our patients were bovine or human collagen injections, traditional CO₂ laser resurfacing, and the older generations of pulsed dye lasers. Neuromodulators were just being introduced. We quickly learned the limitations and complications associated with these modalities. Collagen injections were directed at fine perioral lines and lasted 3 to 4 months. The worst complication would be a bruise or an allergic reaction to the bovine collagen. If we really needed to restore volume beyond the perioral regions, our only option was autologous fat transfer. CO₂ laser resurfacing was used to firm skin, erase deep wrinkles, and improve sun damage, but its use was limited to older, fair-skinned individuals due to the inherent risk for hypopigmentation and depigmentation. Pulsed dye lasers similarly had no means of cooling the skin, thus they were limited to lighter-skinned individuals and had notable risk for blisters, burns, and hypopigmentation. Since then, our understanding of skin healing, laser-tissue interaction, and facial aging has driven the field to new heights of technological advances and safety. Just as I tell my patients and residents, there is no better time to be in this field than at this moment. Dermatologists have driven the advances behind many of the technologies that are now in widespread use among physicians in a variety of specialties.

Our understanding of facial aging has evolved to include the complex interplay of skeletal change, fat atrophy, and skin aging, which must all be considered when improving a patient’s appearance. Fillers have evolved in physical characteristics to give us the ability to choose between lift, spread, neocollagenesis, or water absorption. Thus, we can select the proper filler for the specific anatomic area we are rejuvenating.

Our understanding of photoaging and laser-tissue physics has allowed for the development of a newer generation of lasers ranging from fractionated lasers to noninvasive modalities that can safely be used in a variety of ethnic skin types to address acne scars, wrinkles, and inflammatory processes such as acne and rosacea. Similarly, the desire to tighten redundant skin has continued to drive ultrasound and radiofrequency technology and sparked growth in a newer field of cryolipolysis and chemical lipolysis agents.

Our dialogue with patients also has evolved to include the 4 R’s of antiaging: resurfacing the skin (eg, lasers, peels), refilling the lost volume (eg, fillers, fat), redraping the excess skin (eg, radiofrequency, ultrasound, laser, surgery), and relaxing dynamic lines (eg, neuromodulators). I propose an additional R: renewal! We must focus on the need for constant renewal so that patients maintain the results we have achieved. I apply the analogy of exercising to get into shape. One must go to the gym regularly to get to the desired level of fitness, but you do not stop exercising, otherwise you will quickly relapse to your former lack of fitness. Similarly, patients should receive the appropriate treatments to bring them to the desired level of rejuvenation, but then some form of constant renewal process is needed to maintain them at that level. Without the stimulation of the skin, the aging process continues and the cycle begins all over again.

In my practice, renewal is achieved by driving the skin to maintain the glow and smoothness that enhances the results of the fillers, neuromodulators, lasers, and peels that we have used. The skin is the first thing people notice. Without the glow, the patient will look good but not great. I tell patients that this part of the process is their responsibility. They must adhere to the skin care regimen specifically designed to address their needs. By incorporating the patient in the rejuvenation process, he/she is empowered to take control over the aging process and has grown more confident in you as a physician.

These are exciting times and there is still so much in the pipeline. By continually learning, reading, and attending workshops and meetings, you can make sure our specialty continue to be the leader in the antiaging field.

How do we increase patient adherence to therapy? This question fascinates me. As dermatologists, we will see thousands of patients over the course of our careers, most with treatable conditions that will improve with therapy and others with chronic or genetic conditions that will at least be made more tolerable with therapy. Only 50% of patients with a chronic condition are adherent to therapy.¹ Why some patients adhere to treatment and others do not can be difficult to understand. The emotional makeup, culture, family background, socioeconomic status, and motivation of each person is unique, which leads to complexity. This column is not meant to answer a question that is both complex and broad; rather, it is meant to survey and summarize the literature on this topic.  

Education

Health literacy is defined as cognitive and social skills that determine the motivation and ability of individuals to gain access to, understand, and use information in ways that promote and maintain good health.² Greater health literacy leads to improved compliance and health outcomes.^3,4 When we take the time to educate patients about their condition, it improves health literacy, treatment compliance, and patient safety and satisfaction, factors that ultimately are linked to better health outcomes.^3-8

There are many practical ways of educating patients. Interestingly, one meta-analysis found that no single strategy is more effective than another.⁶ This analysis found that "[c]omprehensive interventions combining cognitive, behavioral, and affective components were more effective than single-focus interventions."⁶ The Centers for Disease Control and Prevention (CDC) website is an excellent source of information on how to educate patients and increase patient treatment compliance.² The CDC website offers a free tool kit on how to design educational information to your target audience, resources for children, a database of health-related educational images, an electronic textbook on teaching patients with low literacy skills, a summary of evidence-based ideas on how to improve patient adherence to medications used long-term, and more.²

Facilitating Adherence

The World Health Organization (WHO) emphasizes 5 dimensions of patient adherence: health system, socioeconomic, condition-related, therapy-related, and patient-related factors.⁹ Becker and Maiman⁵ summarized it eloquently when they wrote that we must take "clinically appropriate steps to reduce the cost, complexity, duration, and amount of behavioral change required by the regimen and increasing the regimen's convenience through 'tailoring' and other approaches." It is a broad ultimatum that will require creativity and persistence on the part of the dermatology community.

Some common patient-related factors associated with nonadherence to treatment are lack of information and skills as they pertain to self-management, difficulty with motivation and self-efficacy, and lack of support for behavioral changes.⁹ It is interesting that low socioeconomic status has not been consistently shown to portend low treatment adherence. It has been shown that children, especially adolescents, and elderly patients tend to be the least adherent.^9-11

Dermatologists Take Action

As dermatologists, the WHO encourages us (physicians) to promote optimism, provide enthusiasm, and encourage maintenance of healthy behaviors.⁹ Comprehensive interventions that have had a positive impact on patient adherence to therapy for diseases such as diabetes mellitus, asthma, and hypertension may serve as motivating examples.⁹ Some specific dermatologic conditions that will benefit from increased patient adherence include acne, vesiculobullous disease, psoriasis, and atopic dermatitis. We can lend support to efforts to reduce the cost of dermatologic medications and be aware of the populations most at risk for low adherence to treatment.^9-12

Final Thoughts

As we work to increase patient adherence to therapy in dermatology, we will help improve health literacy, patient safety, and patient satisfaction. These factors are ultimately linked to better health outcomes. The CDC and WHO websites are excellent sources of information on practical methods for doing so.^2,9

How do we increase patient adherence to therapy? This question fascinates me. As dermatologists, we will see thousands of patients over the course of our careers, most with treatable conditions that will improve with therapy and others with chronic or genetic conditions that will at least be made more tolerable with therapy. Only 50% of patients with a chronic condition are adherent to therapy.¹ Why some patients adhere to treatment and others do not can be difficult to understand. The emotional makeup, culture, family background, socioeconomic status, and motivation of each person is unique, which leads to complexity. This column is not meant to answer a question that is both complex and broad; rather, it is meant to survey and summarize the literature on this topic.  

Education

Health literacy is defined as cognitive and social skills that determine the motivation and ability of individuals to gain access to, understand, and use information in ways that promote and maintain good health.² Greater health literacy leads to improved compliance and health outcomes.^3,4 When we take the time to educate patients about their condition, it improves health literacy, treatment compliance, and patient safety and satisfaction, factors that ultimately are linked to better health outcomes.^3-8

There are many practical ways of educating patients. Interestingly, one meta-analysis found that no single strategy is more effective than another.⁶ This analysis found that "[c]omprehensive interventions combining cognitive, behavioral, and affective components were more effective than single-focus interventions."⁶ The Centers for Disease Control and Prevention (CDC) website is an excellent source of information on how to educate patients and increase patient treatment compliance.² The CDC website offers a free tool kit on how to design educational information to your target audience, resources for children, a database of health-related educational images, an electronic textbook on teaching patients with low literacy skills, a summary of evidence-based ideas on how to improve patient adherence to medications used long-term, and more.²

Facilitating Adherence

The World Health Organization (WHO) emphasizes 5 dimensions of patient adherence: health system, socioeconomic, condition-related, therapy-related, and patient-related factors.⁹ Becker and Maiman⁵ summarized it eloquently when they wrote that we must take "clinically appropriate steps to reduce the cost, complexity, duration, and amount of behavioral change required by the regimen and increasing the regimen's convenience through 'tailoring' and other approaches." It is a broad ultimatum that will require creativity and persistence on the part of the dermatology community.

Some common patient-related factors associated with nonadherence to treatment are lack of information and skills as they pertain to self-management, difficulty with motivation and self-efficacy, and lack of support for behavioral changes.⁹ It is interesting that low socioeconomic status has not been consistently shown to portend low treatment adherence. It has been shown that children, especially adolescents, and elderly patients tend to be the least adherent.^9-11

Dermatologists Take Action

As dermatologists, the WHO encourages us (physicians) to promote optimism, provide enthusiasm, and encourage maintenance of healthy behaviors.⁹ Comprehensive interventions that have had a positive impact on patient adherence to therapy for diseases such as diabetes mellitus, asthma, and hypertension may serve as motivating examples.⁹ Some specific dermatologic conditions that will benefit from increased patient adherence include acne, vesiculobullous disease, psoriasis, and atopic dermatitis. We can lend support to efforts to reduce the cost of dermatologic medications and be aware of the populations most at risk for low adherence to treatment.^9-12

Final Thoughts

As we work to increase patient adherence to therapy in dermatology, we will help improve health literacy, patient safety, and patient satisfaction. These factors are ultimately linked to better health outcomes. The CDC and WHO websites are excellent sources of information on practical methods for doing so.^2,9

How do we increase patient adherence to therapy? This question fascinates me. As dermatologists, we will see thousands of patients over the course of our careers, most with treatable conditions that will improve with therapy and others with chronic or genetic conditions that will at least be made more tolerable with therapy. Only 50% of patients with a chronic condition are adherent to therapy.¹ Why some patients adhere to treatment and others do not can be difficult to understand. The emotional makeup, culture, family background, socioeconomic status, and motivation of each person is unique, which leads to complexity. This column is not meant to answer a question that is both complex and broad; rather, it is meant to survey and summarize the literature on this topic.  

Education

Health literacy is defined as cognitive and social skills that determine the motivation and ability of individuals to gain access to, understand, and use information in ways that promote and maintain good health.² Greater health literacy leads to improved compliance and health outcomes.^3,4 When we take the time to educate patients about their condition, it improves health literacy, treatment compliance, and patient safety and satisfaction, factors that ultimately are linked to better health outcomes.^3-8

There are many practical ways of educating patients. Interestingly, one meta-analysis found that no single strategy is more effective than another.⁶ This analysis found that "[c]omprehensive interventions combining cognitive, behavioral, and affective components were more effective than single-focus interventions."⁶ The Centers for Disease Control and Prevention (CDC) website is an excellent source of information on how to educate patients and increase patient treatment compliance.² The CDC website offers a free tool kit on how to design educational information to your target audience, resources for children, a database of health-related educational images, an electronic textbook on teaching patients with low literacy skills, a summary of evidence-based ideas on how to improve patient adherence to medications used long-term, and more.²

Facilitating Adherence

The World Health Organization (WHO) emphasizes 5 dimensions of patient adherence: health system, socioeconomic, condition-related, therapy-related, and patient-related factors.⁹ Becker and Maiman⁵ summarized it eloquently when they wrote that we must take "clinically appropriate steps to reduce the cost, complexity, duration, and amount of behavioral change required by the regimen and increasing the regimen's convenience through 'tailoring' and other approaches." It is a broad ultimatum that will require creativity and persistence on the part of the dermatology community.

Some common patient-related factors associated with nonadherence to treatment are lack of information and skills as they pertain to self-management, difficulty with motivation and self-efficacy, and lack of support for behavioral changes.⁹ It is interesting that low socioeconomic status has not been consistently shown to portend low treatment adherence. It has been shown that children, especially adolescents, and elderly patients tend to be the least adherent.^9-11

Dermatologists Take Action

As dermatologists, the WHO encourages us (physicians) to promote optimism, provide enthusiasm, and encourage maintenance of healthy behaviors.⁹ Comprehensive interventions that have had a positive impact on patient adherence to therapy for diseases such as diabetes mellitus, asthma, and hypertension may serve as motivating examples.⁹ Some specific dermatologic conditions that will benefit from increased patient adherence include acne, vesiculobullous disease, psoriasis, and atopic dermatitis. We can lend support to efforts to reduce the cost of dermatologic medications and be aware of the populations most at risk for low adherence to treatment.^9-12

Final Thoughts

As we work to increase patient adherence to therapy in dermatology, we will help improve health literacy, patient safety, and patient satisfaction. These factors are ultimately linked to better health outcomes. The CDC and WHO websites are excellent sources of information on practical methods for doing so.^2,9

Review the PDF of the fact sheet on Chemical Peels with board-relevant, easy-to-review material. This fact sheet will review the use of chemical peels for dermatologic indications.

Practice Questions

1. Which peel requires neutralization?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

2. Which peel contains resorcinol?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

3. Which peel would be the best treatment of severe actinic photodamage?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

4. Which peel would not be indicated for treatment of melasma in a patient with Fitzpatrick skin type IV?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

5. Which peel is a β-hydroxy acid?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

Answers to practice questions provided on next page

Practice Question Answers

1. Which peel requires neutralization?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

2. Which peel contains resorcinol?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

3. Which peel would be the best treatment of severe actinic photodamage?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

4. Which peel would not be indicated for treatment of melasma in a patient with Fitzpatrick skin type IV?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

5. Which peel is a β-hydroxy acid?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

Review the PDF of the fact sheet on Chemical Peels with board-relevant, easy-to-review material. This fact sheet will review the use of chemical peels for dermatologic indications.

Practice Questions

1. Which peel requires neutralization?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

2. Which peel contains resorcinol?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

3. Which peel would be the best treatment of severe actinic photodamage?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

4. Which peel would not be indicated for treatment of melasma in a patient with Fitzpatrick skin type IV?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

5. Which peel is a β-hydroxy acid?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

Answers to practice questions provided on next page

Practice Question Answers

1. Which peel requires neutralization?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

2. Which peel contains resorcinol?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

3. Which peel would be the best treatment of severe actinic photodamage?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

4. Which peel would not be indicated for treatment of melasma in a patient with Fitzpatrick skin type IV?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

5. Which peel is a β-hydroxy acid?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

Review the PDF of the fact sheet on Chemical Peels with board-relevant, easy-to-review material. This fact sheet will review the use of chemical peels for dermatologic indications.

Practice Questions

1. Which peel requires neutralization?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

2. Which peel contains resorcinol?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

3. Which peel would be the best treatment of severe actinic photodamage?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

4. Which peel would not be indicated for treatment of melasma in a patient with Fitzpatrick skin type IV?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

5. Which peel is a β-hydroxy acid?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

Answers to practice questions provided on next page

Practice Question Answers

1. Which peel requires neutralization?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

2. Which peel contains resorcinol?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

3. Which peel would be the best treatment of severe actinic photodamage?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

4. Which peel would not be indicated for treatment of melasma in a patient with Fitzpatrick skin type IV?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

5. Which peel is a β-hydroxy acid?

a. Baker-Gordon

b. glycolic acid

c. Jessner

d. salicylic acid

e. trichloroacetic acid

The process of wound healing has been well characterized. Immediately following injury, neutrophils arrive at the site in response to chemotactic factors produced by the coagulation cascade. Monocytes follow 24 to 36 hours later; transform into macrophages; and begin to phagocytose tissue debris, organisms, and any remaining neutrophils. In turn, macrophages release chemotactic factors such as basic fibroblast growth factor to attract fibroblasts to the wound, which then begin the process of synthesizing collagen and ground substance. Fibroblasts then take over as the dominant cell type, with collagen synthesis continuing for approximately 6 weeks. Keratinocytes and endothelial cells also proliferate during this time. After approximately 6 weeks, collagen remodeling begins. Tensile strength of the wound may continue to increase up to one year after the injury.^1,2

Corticosteroids inhibit wound healing in several ways. Notably, they decrease the number of circulating monocytes, leading to fewer macrophages in the tissue at the site of injury, which then leads to impaired phagocytosis and reduced release of chemotactic factors that attract fibroblasts. Additionally, corticosteroids can inhibit collagen synthesis and remodeling, leading to delayed wound healing and decreased tensile strength of the wound as well as impacting capillary proliferation.³

The subtypes of EDS were reclassified in 1998 by Beighton et al,⁴ and the benign hypermobility type (EDS-BHT)(formerly type III) is considered the least severe. There is some controversy as to whether this subtype constitutes a separate diagnosis from the benign familial joint hypermobility syndrome. It is characterized by hypermobility of the joints (objectively measured with the Beighton scale) and mild hyperextensibility of the skin, and patients often have a history of joint subluxations and dislocations with resultant degenerative joint disease and chronic pain. Manifestations of fragile skin and soft tissue (eg, abnormal wound healing or scarring; spontaneous tearing of the skin, ligaments, tendons, or organs) are notably absent from the findings in this syndrome.⁵ The genetic basis for EDS is unknown in the majority of patients, although a deficiency in tenascin X (secondary to defects in the tenascin XB gene [TNXB]) has been identified in a small subset (<5%) of patients, leading to elastic fiber abnormalities, reduced collagen deposition, and impaired cross-linking of collagen.^6,7 Inheritance usually is autosomal dominant but also can be autosomal recessive. In contrast, the classic type of EDS (formerly types I and II) is associated with atrophic scarring and tissue fragility, in addition to joint hypermobility and skin hyperextensibility. Type V collagen mutations are found in more than half of patients with this disorder.⁸

We present the case of a patient with EDS-BHT who developed large nonhealing cutaneous ulcerations with initiation of high-dose systemic corticosteroids for treatment of dermatomyositis. This case provides a dramatic illustration of the effects of the use of chronic systemic corticosteroids on skin fragility and wound healing in patients with an underlying inherited defect in collagen or connective tissue.

Case Report

A 23-year-old man with an unremarkable medical history was admitted to our inpatient cardiology service with palpitations attributable to new-onset atrial fibrillation. Dermatology was consulted to evaluate a rash of approximately 4 months’ duration that started on the dorsal aspect of the hands, then progressed to involve the extensor elbows and knees. The rash also was associated with fatigue, arthralgia, and proximal muscle weakness. A taper of prednisone that was prescribed approximately 2 months prior to admission by a rheumatologist for presumed dermatomyositis improved his symptoms, but they recurred with discontinuation of the medication.

Physical examination revealed reddish, violaceous and hyperpigmented patches on the dorsal aspect of the hands and digits and the extensor aspect of the knees and elbows. A skin biopsy from the right elbow showed a mild interface reaction and nonspecific direct immunofluorescence, consistent with a diagnosis of dermatomyositis. Autoimmune serologies were negative, including antinuclear, anti–Jo-1, anti–Mi-2, anti–Sjögren syndrome antigen A, anti–Sjögren syndrome antigen B, anti-Smith, and antiribonucleoprotein antibodies. Creatine kinase and rheumatoid factor levels were within reference range. Electromyogram was supportive of the diagnosis of dermatomyositis, showing an irritable myopathy. Cardiac magnetic resonance imaging showed an acute inflammatory process of the myocardium, and a transthoracic echocardiogram revealed a depressed left ventricular ejection fraction of 35% to 40% (reference range, 55%–70%). His cardiac disease also was attributed to dermatomyositis, and he was managed by cardiology with anangiotensin-converting enzyme inhibitor and antiarrhythmic therapy. Rheumatology was consulted and prednisone 60 mg once daily was started, with the patient reporting improvement in his muscle weakness and the rash.

Interestingly, the patient also noted a history of joint hypermobility, and a genetics consultation was obtained during the current hospitalization. He denied a history of abnormal scarring or skin problems, but he did note dislocation of the patella on 2 occasions and an umbilical hernia repair at 3 years of age. A paternal uncle had a history of similar joint hypermobility. His Beighton score was noted to be 8/8 (bending at the waist was unable to be tested due to recent lumbar puncture obtained during this hospitalization). The patient was diagnosed with EDS-BHT, and no further workup was recommended.

Subsequent to his hospitalization for several days, the patient’s prednisone was slowly tapered down from 60 mg once daily to 12.5 mg once daily, and azathioprine was started and titrated up to 150 mg once daily. Approximately 6 months after his initial hospitalization, he was readmitted due to increased pain of the right knee with concern for osteomyelitis. Dermatology was again consulted, and at this time, the patient reported a 4-month history of nonhealing ulcers to the knees and elbows (Figure 1). He stated that the ulcers were initially about the size of a pencil eraser and had started approximately 2 months after the prednisone was started, with subsequent slow enlargement. He noted a stinging sensation with enlargement of the ulcers, but otherwise they were not painful. He denied major trauma to the areas. He noted that his prior rash from the dermatomyositis seemed to have resolved, along with his muscle weakness, and he reported weight gain and improvement in his energy levels. Physical examination at this time revealed several stigmata of chronic systemic corticosteroids, including fatty deposits in the face (moon facies) and between the shoulders (buffalo hump), facial acne, and numerous erythematous striae on the trunk and proximal extremities (Figure 2). Multiple noninflammatory ulcers with punched-out borders ranging in size from 0.5 to 6 cm were seen at sites overlying bony prominences, including the bilateral extensor elbows and knees and the right plantar foot. Similar ulcers were noted on the trunk within the striae. Some of the ulcers were covered with a thick hyperkeratotic crust. A biopsy from the edge of an ulcer on the right side of the flank showed only dermal fibrosis. Workup by orthopedic surgery was felt to be inconsistent with osteomyelitis, and plastic surgery was consulted to consider surgical options for repair. Consequently, the patient was taken to the operating room for primary closure of the ulcers to the bilateral knees and right elbow. He has been followed closely by plastic surgery, with the use of joint immobilization to promote wound healing.

Comment

This case represents a dramatic illustration of the effects of chronic systemic corticosteroids on skin fragility and wound healing in a patient with an underlying genetic defect in the connective tissue. The ulcers were all located within striae or overlying bony prominences where the skin was subjected to increased tension; however, the patient reported no problems with wound healing or scarring at these sites prior to the initiation of corticosteroids, suggesting that the addition of this medication was disruptive to the cutaneous wound healing mechanisms. This case is unique because abnormal wound healing in an EDS patient was so clearly linked to the initiation of systemic steroids.

The exact pathogenesis of the patient’s ulcers is unclear. The diagnosis of EDS was primarily clinical, and without genetic testing, we cannot state with certainty the underlying molecular problem in this patient. Although tenascin X deficiency has been found in a few patients, a genetic defect remains uncharacterized in most patients with EDS-BHT, and in most situations, EDS-BHT remains a clinical diagnosis. In 2001, Schalkwijk et al⁹ first described the association of tenascin X deficiency and EDS in 5 patients, and they noted delayed wound healing in 1 patient who had received systemic corticosteroids for congenital adrenal hyperplasia. The authors remarked that it was not clear whether the abnormality was linked to the patient’s EDS or to his treatment with systemic corticosteroids.⁹ Furthermore, it is possible that our patient in fact has a milder variant of classic type EDS and that the manifestations of tissue fragility remained subclinical until the addition of systemic corticosteroids. It also is interesting to note that muscle weakness can be a symptom of EDS, both classic and BHT of EDS, but our patient’s muscle weakness improved with immunosuppression, supporting an underlying autoimmune disease as the cause for it.¹⁰ Skin ulcerations have been reported as a rare manifestation of dermatomyositis, but it is remarkable that his ulcers progressed as his other dermatomyositis symptoms improved with therapy, suggesting that his autoimmune disease was not the underlying cause for the ulcers.^11-13 This case points to the need to thoughtfully consider the adverse effects of corticosteroids on wound healing in patients with an inherited disorder of collagen or connective tissue such as EDS.

The process of wound healing has been well characterized. Immediately following injury, neutrophils arrive at the site in response to chemotactic factors produced by the coagulation cascade. Monocytes follow 24 to 36 hours later; transform into macrophages; and begin to phagocytose tissue debris, organisms, and any remaining neutrophils. In turn, macrophages release chemotactic factors such as basic fibroblast growth factor to attract fibroblasts to the wound, which then begin the process of synthesizing collagen and ground substance. Fibroblasts then take over as the dominant cell type, with collagen synthesis continuing for approximately 6 weeks. Keratinocytes and endothelial cells also proliferate during this time. After approximately 6 weeks, collagen remodeling begins. Tensile strength of the wound may continue to increase up to one year after the injury.^1,2

Corticosteroids inhibit wound healing in several ways. Notably, they decrease the number of circulating monocytes, leading to fewer macrophages in the tissue at the site of injury, which then leads to impaired phagocytosis and reduced release of chemotactic factors that attract fibroblasts. Additionally, corticosteroids can inhibit collagen synthesis and remodeling, leading to delayed wound healing and decreased tensile strength of the wound as well as impacting capillary proliferation.³

The subtypes of EDS were reclassified in 1998 by Beighton et al,⁴ and the benign hypermobility type (EDS-BHT)(formerly type III) is considered the least severe. There is some controversy as to whether this subtype constitutes a separate diagnosis from the benign familial joint hypermobility syndrome. It is characterized by hypermobility of the joints (objectively measured with the Beighton scale) and mild hyperextensibility of the skin, and patients often have a history of joint subluxations and dislocations with resultant degenerative joint disease and chronic pain. Manifestations of fragile skin and soft tissue (eg, abnormal wound healing or scarring; spontaneous tearing of the skin, ligaments, tendons, or organs) are notably absent from the findings in this syndrome.⁵ The genetic basis for EDS is unknown in the majority of patients, although a deficiency in tenascin X (secondary to defects in the tenascin XB gene [TNXB]) has been identified in a small subset (<5%) of patients, leading to elastic fiber abnormalities, reduced collagen deposition, and impaired cross-linking of collagen.^6,7 Inheritance usually is autosomal dominant but also can be autosomal recessive. In contrast, the classic type of EDS (formerly types I and II) is associated with atrophic scarring and tissue fragility, in addition to joint hypermobility and skin hyperextensibility. Type V collagen mutations are found in more than half of patients with this disorder.⁸

We present the case of a patient with EDS-BHT who developed large nonhealing cutaneous ulcerations with initiation of high-dose systemic corticosteroids for treatment of dermatomyositis. This case provides a dramatic illustration of the effects of the use of chronic systemic corticosteroids on skin fragility and wound healing in patients with an underlying inherited defect in collagen or connective tissue.

Case Report

A 23-year-old man with an unremarkable medical history was admitted to our inpatient cardiology service with palpitations attributable to new-onset atrial fibrillation. Dermatology was consulted to evaluate a rash of approximately 4 months’ duration that started on the dorsal aspect of the hands, then progressed to involve the extensor elbows and knees. The rash also was associated with fatigue, arthralgia, and proximal muscle weakness. A taper of prednisone that was prescribed approximately 2 months prior to admission by a rheumatologist for presumed dermatomyositis improved his symptoms, but they recurred with discontinuation of the medication.

Physical examination revealed reddish, violaceous and hyperpigmented patches on the dorsal aspect of the hands and digits and the extensor aspect of the knees and elbows. A skin biopsy from the right elbow showed a mild interface reaction and nonspecific direct immunofluorescence, consistent with a diagnosis of dermatomyositis. Autoimmune serologies were negative, including antinuclear, anti–Jo-1, anti–Mi-2, anti–Sjögren syndrome antigen A, anti–Sjögren syndrome antigen B, anti-Smith, and antiribonucleoprotein antibodies. Creatine kinase and rheumatoid factor levels were within reference range. Electromyogram was supportive of the diagnosis of dermatomyositis, showing an irritable myopathy. Cardiac magnetic resonance imaging showed an acute inflammatory process of the myocardium, and a transthoracic echocardiogram revealed a depressed left ventricular ejection fraction of 35% to 40% (reference range, 55%–70%). His cardiac disease also was attributed to dermatomyositis, and he was managed by cardiology with anangiotensin-converting enzyme inhibitor and antiarrhythmic therapy. Rheumatology was consulted and prednisone 60 mg once daily was started, with the patient reporting improvement in his muscle weakness and the rash.

Interestingly, the patient also noted a history of joint hypermobility, and a genetics consultation was obtained during the current hospitalization. He denied a history of abnormal scarring or skin problems, but he did note dislocation of the patella on 2 occasions and an umbilical hernia repair at 3 years of age. A paternal uncle had a history of similar joint hypermobility. His Beighton score was noted to be 8/8 (bending at the waist was unable to be tested due to recent lumbar puncture obtained during this hospitalization). The patient was diagnosed with EDS-BHT, and no further workup was recommended.

Subsequent to his hospitalization for several days, the patient’s prednisone was slowly tapered down from 60 mg once daily to 12.5 mg once daily, and azathioprine was started and titrated up to 150 mg once daily. Approximately 6 months after his initial hospitalization, he was readmitted due to increased pain of the right knee with concern for osteomyelitis. Dermatology was again consulted, and at this time, the patient reported a 4-month history of nonhealing ulcers to the knees and elbows (Figure 1). He stated that the ulcers were initially about the size of a pencil eraser and had started approximately 2 months after the prednisone was started, with subsequent slow enlargement. He noted a stinging sensation with enlargement of the ulcers, but otherwise they were not painful. He denied major trauma to the areas. He noted that his prior rash from the dermatomyositis seemed to have resolved, along with his muscle weakness, and he reported weight gain and improvement in his energy levels. Physical examination at this time revealed several stigmata of chronic systemic corticosteroids, including fatty deposits in the face (moon facies) and between the shoulders (buffalo hump), facial acne, and numerous erythematous striae on the trunk and proximal extremities (Figure 2). Multiple noninflammatory ulcers with punched-out borders ranging in size from 0.5 to 6 cm were seen at sites overlying bony prominences, including the bilateral extensor elbows and knees and the right plantar foot. Similar ulcers were noted on the trunk within the striae. Some of the ulcers were covered with a thick hyperkeratotic crust. A biopsy from the edge of an ulcer on the right side of the flank showed only dermal fibrosis. Workup by orthopedic surgery was felt to be inconsistent with osteomyelitis, and plastic surgery was consulted to consider surgical options for repair. Consequently, the patient was taken to the operating room for primary closure of the ulcers to the bilateral knees and right elbow. He has been followed closely by plastic surgery, with the use of joint immobilization to promote wound healing.

Comment

This case represents a dramatic illustration of the effects of chronic systemic corticosteroids on skin fragility and wound healing in a patient with an underlying genetic defect in the connective tissue. The ulcers were all located within striae or overlying bony prominences where the skin was subjected to increased tension; however, the patient reported no problems with wound healing or scarring at these sites prior to the initiation of corticosteroids, suggesting that the addition of this medication was disruptive to the cutaneous wound healing mechanisms. This case is unique because abnormal wound healing in an EDS patient was so clearly linked to the initiation of systemic steroids.

The exact pathogenesis of the patient’s ulcers is unclear. The diagnosis of EDS was primarily clinical, and without genetic testing, we cannot state with certainty the underlying molecular problem in this patient. Although tenascin X deficiency has been found in a few patients, a genetic defect remains uncharacterized in most patients with EDS-BHT, and in most situations, EDS-BHT remains a clinical diagnosis. In 2001, Schalkwijk et al⁹ first described the association of tenascin X deficiency and EDS in 5 patients, and they noted delayed wound healing in 1 patient who had received systemic corticosteroids for congenital adrenal hyperplasia. The authors remarked that it was not clear whether the abnormality was linked to the patient’s EDS or to his treatment with systemic corticosteroids.⁹ Furthermore, it is possible that our patient in fact has a milder variant of classic type EDS and that the manifestations of tissue fragility remained subclinical until the addition of systemic corticosteroids. It also is interesting to note that muscle weakness can be a symptom of EDS, both classic and BHT of EDS, but our patient’s muscle weakness improved with immunosuppression, supporting an underlying autoimmune disease as the cause for it.¹⁰ Skin ulcerations have been reported as a rare manifestation of dermatomyositis, but it is remarkable that his ulcers progressed as his other dermatomyositis symptoms improved with therapy, suggesting that his autoimmune disease was not the underlying cause for the ulcers.^11-13 This case points to the need to thoughtfully consider the adverse effects of corticosteroids on wound healing in patients with an inherited disorder of collagen or connective tissue such as EDS.

The process of wound healing has been well characterized. Immediately following injury, neutrophils arrive at the site in response to chemotactic factors produced by the coagulation cascade. Monocytes follow 24 to 36 hours later; transform into macrophages; and begin to phagocytose tissue debris, organisms, and any remaining neutrophils. In turn, macrophages release chemotactic factors such as basic fibroblast growth factor to attract fibroblasts to the wound, which then begin the process of synthesizing collagen and ground substance. Fibroblasts then take over as the dominant cell type, with collagen synthesis continuing for approximately 6 weeks. Keratinocytes and endothelial cells also proliferate during this time. After approximately 6 weeks, collagen remodeling begins. Tensile strength of the wound may continue to increase up to one year after the injury.^1,2

Corticosteroids inhibit wound healing in several ways. Notably, they decrease the number of circulating monocytes, leading to fewer macrophages in the tissue at the site of injury, which then leads to impaired phagocytosis and reduced release of chemotactic factors that attract fibroblasts. Additionally, corticosteroids can inhibit collagen synthesis and remodeling, leading to delayed wound healing and decreased tensile strength of the wound as well as impacting capillary proliferation.³

The subtypes of EDS were reclassified in 1998 by Beighton et al,⁴ and the benign hypermobility type (EDS-BHT)(formerly type III) is considered the least severe. There is some controversy as to whether this subtype constitutes a separate diagnosis from the benign familial joint hypermobility syndrome. It is characterized by hypermobility of the joints (objectively measured with the Beighton scale) and mild hyperextensibility of the skin, and patients often have a history of joint subluxations and dislocations with resultant degenerative joint disease and chronic pain. Manifestations of fragile skin and soft tissue (eg, abnormal wound healing or scarring; spontaneous tearing of the skin, ligaments, tendons, or organs) are notably absent from the findings in this syndrome.⁵ The genetic basis for EDS is unknown in the majority of patients, although a deficiency in tenascin X (secondary to defects in the tenascin XB gene [TNXB]) has been identified in a small subset (<5%) of patients, leading to elastic fiber abnormalities, reduced collagen deposition, and impaired cross-linking of collagen.^6,7 Inheritance usually is autosomal dominant but also can be autosomal recessive. In contrast, the classic type of EDS (formerly types I and II) is associated with atrophic scarring and tissue fragility, in addition to joint hypermobility and skin hyperextensibility. Type V collagen mutations are found in more than half of patients with this disorder.⁸

We present the case of a patient with EDS-BHT who developed large nonhealing cutaneous ulcerations with initiation of high-dose systemic corticosteroids for treatment of dermatomyositis. This case provides a dramatic illustration of the effects of the use of chronic systemic corticosteroids on skin fragility and wound healing in patients with an underlying inherited defect in collagen or connective tissue.

Case Report

A 23-year-old man with an unremarkable medical history was admitted to our inpatient cardiology service with palpitations attributable to new-onset atrial fibrillation. Dermatology was consulted to evaluate a rash of approximately 4 months’ duration that started on the dorsal aspect of the hands, then progressed to involve the extensor elbows and knees. The rash also was associated with fatigue, arthralgia, and proximal muscle weakness. A taper of prednisone that was prescribed approximately 2 months prior to admission by a rheumatologist for presumed dermatomyositis improved his symptoms, but they recurred with discontinuation of the medication.

Physical examination revealed reddish, violaceous and hyperpigmented patches on the dorsal aspect of the hands and digits and the extensor aspect of the knees and elbows. A skin biopsy from the right elbow showed a mild interface reaction and nonspecific direct immunofluorescence, consistent with a diagnosis of dermatomyositis. Autoimmune serologies were negative, including antinuclear, anti–Jo-1, anti–Mi-2, anti–Sjögren syndrome antigen A, anti–Sjögren syndrome antigen B, anti-Smith, and antiribonucleoprotein antibodies. Creatine kinase and rheumatoid factor levels were within reference range. Electromyogram was supportive of the diagnosis of dermatomyositis, showing an irritable myopathy. Cardiac magnetic resonance imaging showed an acute inflammatory process of the myocardium, and a transthoracic echocardiogram revealed a depressed left ventricular ejection fraction of 35% to 40% (reference range, 55%–70%). His cardiac disease also was attributed to dermatomyositis, and he was managed by cardiology with anangiotensin-converting enzyme inhibitor and antiarrhythmic therapy. Rheumatology was consulted and prednisone 60 mg once daily was started, with the patient reporting improvement in his muscle weakness and the rash.

Interestingly, the patient also noted a history of joint hypermobility, and a genetics consultation was obtained during the current hospitalization. He denied a history of abnormal scarring or skin problems, but he did note dislocation of the patella on 2 occasions and an umbilical hernia repair at 3 years of age. A paternal uncle had a history of similar joint hypermobility. His Beighton score was noted to be 8/8 (bending at the waist was unable to be tested due to recent lumbar puncture obtained during this hospitalization). The patient was diagnosed with EDS-BHT, and no further workup was recommended.

Subsequent to his hospitalization for several days, the patient’s prednisone was slowly tapered down from 60 mg once daily to 12.5 mg once daily, and azathioprine was started and titrated up to 150 mg once daily. Approximately 6 months after his initial hospitalization, he was readmitted due to increased pain of the right knee with concern for osteomyelitis. Dermatology was again consulted, and at this time, the patient reported a 4-month history of nonhealing ulcers to the knees and elbows (Figure 1). He stated that the ulcers were initially about the size of a pencil eraser and had started approximately 2 months after the prednisone was started, with subsequent slow enlargement. He noted a stinging sensation with enlargement of the ulcers, but otherwise they were not painful. He denied major trauma to the areas. He noted that his prior rash from the dermatomyositis seemed to have resolved, along with his muscle weakness, and he reported weight gain and improvement in his energy levels. Physical examination at this time revealed several stigmata of chronic systemic corticosteroids, including fatty deposits in the face (moon facies) and between the shoulders (buffalo hump), facial acne, and numerous erythematous striae on the trunk and proximal extremities (Figure 2). Multiple noninflammatory ulcers with punched-out borders ranging in size from 0.5 to 6 cm were seen at sites overlying bony prominences, including the bilateral extensor elbows and knees and the right plantar foot. Similar ulcers were noted on the trunk within the striae. Some of the ulcers were covered with a thick hyperkeratotic crust. A biopsy from the edge of an ulcer on the right side of the flank showed only dermal fibrosis. Workup by orthopedic surgery was felt to be inconsistent with osteomyelitis, and plastic surgery was consulted to consider surgical options for repair. Consequently, the patient was taken to the operating room for primary closure of the ulcers to the bilateral knees and right elbow. He has been followed closely by plastic surgery, with the use of joint immobilization to promote wound healing.

Comment

This case represents a dramatic illustration of the effects of chronic systemic corticosteroids on skin fragility and wound healing in a patient with an underlying genetic defect in the connective tissue. The ulcers were all located within striae or overlying bony prominences where the skin was subjected to increased tension; however, the patient reported no problems with wound healing or scarring at these sites prior to the initiation of corticosteroids, suggesting that the addition of this medication was disruptive to the cutaneous wound healing mechanisms. This case is unique because abnormal wound healing in an EDS patient was so clearly linked to the initiation of systemic steroids.

The exact pathogenesis of the patient’s ulcers is unclear. The diagnosis of EDS was primarily clinical, and without genetic testing, we cannot state with certainty the underlying molecular problem in this patient. Although tenascin X deficiency has been found in a few patients, a genetic defect remains uncharacterized in most patients with EDS-BHT, and in most situations, EDS-BHT remains a clinical diagnosis. In 2001, Schalkwijk et al⁹ first described the association of tenascin X deficiency and EDS in 5 patients, and they noted delayed wound healing in 1 patient who had received systemic corticosteroids for congenital adrenal hyperplasia. The authors remarked that it was not clear whether the abnormality was linked to the patient’s EDS or to his treatment with systemic corticosteroids.⁹ Furthermore, it is possible that our patient in fact has a milder variant of classic type EDS and that the manifestations of tissue fragility remained subclinical until the addition of systemic corticosteroids. It also is interesting to note that muscle weakness can be a symptom of EDS, both classic and BHT of EDS, but our patient’s muscle weakness improved with immunosuppression, supporting an underlying autoimmune disease as the cause for it.¹⁰ Skin ulcerations have been reported as a rare manifestation of dermatomyositis, but it is remarkable that his ulcers progressed as his other dermatomyositis symptoms improved with therapy, suggesting that his autoimmune disease was not the underlying cause for the ulcers.^11-13 This case points to the need to thoughtfully consider the adverse effects of corticosteroids on wound healing in patients with an inherited disorder of collagen or connective tissue such as EDS.