A Wound Care Specialist's Approach to Pyoderma Gangrenosum

Abstract

Significance: Pyoderma gangrenosum (PG) is a rare neutrophilic ulcerative dermatosis that poses a high burden of morbidity due to underdiagnosis, resistance to therapy, and limited therapeutic options. Optimization of wound care strategies and multimodal anti-inflammatory approaches are necessary to mitigate multiple converging pathways of inflammation leading to delayed healing, which is further complicated by additional factors such as pathergy.

Recent Advances: PG treatment typically involves reducing inflammation, controlling pain, promoting wound healing, and treating the underlying etiology. Recent advances have been made with regard to targeted therapies for PG with topical, intralesional, and systemic medications. Wound management includes gentle cleansing without sharp debridement, limited topical antibacterial use, and maintenance of a moist environment to promote epithelial migration.

Critical Issues: Wound dressings and compression therapy, in particular, introduce a wide variety of therapeutic options. Dressings should aim to target the specific PG wound type, depending on the depth and exudative nature of the wound, as well as local secondary factors. Superficial wounds, eschar, exudative wounds, granulating wounds, and colonized wounds are managed with variable approaches to the same underlying principles of pathergy avoidance, moisture balance, and reduction of immunogenic inflammatory stimuli. The importance of compression therapy to decrease edema and overgranulation fits within this treatment paradigm.

Future Directions: As each of these treatment modalities offers a complex mixture of advantages and limitations, development of a systematic treatment algorithm in the future can help direct a more tailored path toward wound healing.

Afsaneh Alavi, MD

David Croitoru, MD

Scope and Significance

We have reviewed the wound care literature for evidence-based practices in inflammatory ulcerative dermatosis, as well as our own clinical practice at our academic wound care clinic specializing in pyoderma gangrenosum (PG). The compilation of the available literature and our algorithm for managing the wound care component of a challenging, likely systemic, inflammatory disease may prove valuable for other wound care centers and satellite practices.

We hope to outline the importance of adhering to the general principles of wound care, with special attention to physical, chemical, and immunological pathergy avoidance. These may manifest in ways that are not intuitive to some wound care specialists. The risks of mildly astringent antiseptics, for example, need to be balanced with the inflammatory stimulus caused by wound colonization with bacterial or fungal agents.

Translational Relevance and Clinical Relevance

The findings presented in this review highlight both translational and clinical implications for wound care principles. In terms of translational relevance, we review the cellular mechanisms and signaling milieu of the inflammatory wounds of PG. We discuss this in terms of the basis for use of concomitant topical antibiotic use in wound care, as well as principles of compression for wound healing. This reflects the emerging translational data that PG is a disease of dysregulated innate immune signaling in the face of microbial stimuli.

There is mounting clinical evidence in therapies that reduce inflammation, reduce interstitial edema as one of several possible risk factors for impaired healing with additional attention to reduction of microbial antigenic stimuli. In this context, our clinical experience is also summarized from our subspecialized PG wound care clinic and we discuss strategies for wrap and dressing strategies depending on wound type.

Background and Overview

PG is a rare, neutrophilic dermatosis with an incidence reported between 0.3 and 1/100,000, characterized by progressive ulceration and necrosis.¹ There are several described morphological variants. Classic PG presents as a painful papulonodule or pustule, which ulcerates within days, often with characteristics that include an undermined and violaceous border. Akin to other neutrophilic dermatoses, pathergy is a hallmark and the appearance of new lesions or extension of _current ulcer after local trauma, such as minor surgical procedures and debridement.^2,3 The epidemiology of PG is not well described and there is a lack of patient registries, and its rarity qualifies PG as an orphan disease with high morbidity.⁴ The typical range reported for onset of PG is between 20 and 50 years, however, a recent U.S. cross-sectional study of 1971 patients reported the highest prevalence in those aged 70–79 years.⁵ Approximately 4% of PG cases have been reported in children, often with germ line mutations.⁶ There has been a reported female preponderance although this is variable between studies. The cause of PG is unknown and its high association with systemic inflammatory conditions such as inflammatory bowel disease and inflammatory arthritis is an area of active research.^3,7,8

There are two major diagnostic algorithms for approaching ulcerative dermatoses compatible with PG from Su et al. and, more recently, Maverakis et al.^2,3 Maverakis describes one major and eight minor criteria (Table 1); this newer criteria carry a fundamental change in that exclusion of infection is not required for diagnosis. In this diagnostic algorithm, the major criterion is demonstration of neutrophilic infiltrate biopsy, while the minor criteria include 4/8 of the following: (1) exclusion of infection, (2) pathergy, (3) history of inflammatory bowel disease or inflammatory arthritis, (4) history of papule, pustule, or vesicle ulcerating within 4 days of appearing, (5) peripheral erythema, undermining border, and tenderness at ulceration site, (6) multiple ulcerations, at least one on anterior lower leg, (7) cribriform scar at healed ulcer site, and (8) decreased ulcer size within 1 month of initiating immunosuppressive treatment.² In contrast, Su et al. describe two major criteria: rapid progression of a painful, necrolytic cutaneous ulcer with an irregular, violaceous, and undermined border, or papules, pustules, or bullae that evolve to typical ulceration, and exclusion of other causes of cutaneous ulceration.³ Two or more of the following four minor criteria must also be met (2/4): (1) history suggestive of pathergy or clinical finding of cribriform scarring, (2) systemic diseases associated with PG, (3) histopathologic findings, and (4) rapid response to systemic steroid treatment³ (Table 2). Neither diagnostic criteria have been extensively validated in comparative studies and differ, primarily, in their attention to histologic and clinical features of PG.

Table 1.

Diagnostic criteria for pyoderma gangrenosum, proposed from Delphi Consensus 2018^a

Major Criterion	Minor Criteria
Neutrophilic infiltrate in biopsy	Exclusion of infection
	Pathergy
	History of inflammatory bowel disease or inflammatory arthritis
	History of papule, pustule, or vesicle ulcerating within 4 days of appearing
	Peripheral erythema, undermining border, and tenderness at ulceration site
	Multiple ulcerations, at least one on anterior lower leg
	Cribriform scar at healed ulcer site
	Decreased ulcer size within 1 month of initiating immunosuppressive treatment

^aReference.²

Table 2.

Diagnostic criteria for pyoderma gangrenosum initially proposed by Su et al.^a

Major Criteria (Both Required)	Minor Criteria (Two or More Required)
Rapid progression of a painful, necrolytic cutaneous ulcer with an irregular, violaceous, and undermined border, or papules, pustules, or bullae that evolve to typical ulceration	History suggestive of pathergy or clinical finding of cribriform scarring
Other causes of cutaneous ulceration have been excluded	Systemic diseases associated with pyoderma gangrenosum
	Histopathologic findings (sterile dermal neutrophilia with or without mixed inflammation, with or without lymphocytic vasculitis)
	Treatment response (rapid response to systemic steroid treatment)

^aReference.³

The diagnosis of PG is challenging and we use both diagnostic algorithms in our clinical practice. With considerable overlap, one benefit from the original algorithm proposed by Su et al. is that it requires the exclusion of infectious mimickers as one of two major criteria.³ Recently, Maverakis et al. have proposed a criteria with greater attention to the morphological and clinical features, which we do find to be sensitive and specific for PG.² However, we tend to also prioritize ruling out infection by staining for acid fast bacilli (Ziehl-Neelsen or Fite) and fungus (Period Acid Schiff), as well as allocating a transection of our biopsies for extended bacterial and fungal culture before formalin fixation.

PG has four main subtypes, each with unique histopathology, morphology, and treatment options (Table 3). The classic or ulcerative PG is the most common type, with lower extremities being the most common location; postsurgical and peristomal PG are usually ulcerative type and likely a consequence of pathergy. It is, however, worthwhile to note that some controversy exists as to whether peristomal PG represents true pathergy or simply a form of irritant contact dermatitis⁹; the treatment for both is similarly local and heavily focused on wound care, discussed below. Bullous PG is commonly associated with hematological malignancy and in particular acute myeloid leukemia; the occurrence of this variant as an entity separate from bullous Sweet's or neutrophilic dermatosis of the dorsal hands also remains a topic of ongoing discussion by dermatologists and dermatopathologists.^10,11 Pustular PG is highly associated with inflammatory bowel disease (IBD) and has classically required treatment of the underlying disease. Vegetative PG, in contrast, requires less aggressive therapy such as topical or intralesional therapy and has a less aggressive course and commonly with no associated disease.

Table 3.

Clinical characteristics of different pyoderma gangrenosum types with their corresponding wound type characteristics and recommended wound dressings

Increasing Moisture/Purulence
	Superficial	Eschar	Granulating	Fibrinous	Exudative	Deep	Infected	Histopathology	Prognosis	Morphology
Wound dressing category	Films PMDs	Hydrogels Hydrocolloids PMDs	Hydrocolloid Hydrogels Foams PMDs	Protease-Ia Hydrogels Hydrocolloid	Alginates Hydrofiber Foams PMDs	PMDs Alginates Hydrofiber PHMB	Silver Iodine
Variant Morph	Ulcerative	Ulcerative	Ulcerative	Ulcerative	Ulcerative	Ulcerative	Ulcerative	Edema, neutrophilia, secondary lymphocytic vasculitis	Variable	Tender ulceration, undermined border
Variant Morph	Bullous		Bullous	Bullous				Epidermal necrosis with neutrophilia, subepidermal bulla	Poor	Rapidly evolving vesicles/bullae, central necrosis and erosions
Variant Morph	Pustular	Pustular	Pustular	Pustular	Pustular			Epidermal and dermal neutrophilia	Good	Multiple pustules, surrounded by a halo
Variant Morph	Vegetative	Vegetative	Vegetative	Vegetative				Neutrophilic and eosinophilic infiltrate, subepidermal granuloma	Good	Verrucous and ulcerative lesions

Inhibitors. Histopathological differences are listed for each morphological variant with prognosis and detailed morphology adjacent (adapted from Bhat⁴ and Dabiri et al.²⁵).

^aProtease.

PHMB, polyhexamethylene biguanide; PMDs, polymeric membrane dressings.

Discussion

Pathogenesis and the role of bacteria

A predominant neutrophilic infiltrate, which features as a criterion on both proposed diagnostic tools for PG, highlights the role of innate immune signaling in disease pathogenesis. This has been speculated to result from baseline immunologic and inflammasome reactivity, with a possible genetic basis for dysregulation (Fig. 1).⁷ Defects in matrix metalloproteinases (MMPs) have been found to be linked to neutrophilic activation in PG, and thus serve as a target gene in the genetic studies.⁸ MMP overactivity is speculated, in part, to be stimulated or contributed by factors that include pathergic exogenous triggers such as trauma and medication, but the role of innate immune stimulus secondary to bacterial antigen is unknown. There have been several case reports of PG treated with antibiotics, with improvement as mono- and polytherapy.¹² While the limited reports on treatment of PG with antibiotics may suggest a role for bacteria in PG pathogenesis, more data are required to sufficiently characterize antimicrobial efficacy and mechanism of action versus an anti-inflammatory role. It is important to note that the role of antimicrobials may be historically confounded by cases of misdiagnosed PG that were bacterial or nontuberculous mycobacterial in nature. At this time, we recommend the treatment of cutaneous secondary infections with systemic antibiotics, but avoid the routine use of both systemic and topical antimicrobials unless there is (1) evidence of critical wound colonization indicated by odor, purulence, and hypergranulation in the absence of edema and (2) signs of active soft-tissue infection, acute or chronic (osteomyelitis).

Figure 1.

Multifactorial disease pathophysiology and suggested treatment algorithm. We have modified this from the suggested approach from Bhat.⁴ We have added the suggestion screen for systemic disease in all patients with PG and added to the systemic treatment options (ustekinumab) based on emerging literature.

Systemic management update

PG treatment is largely aimed at reducing inflammation, controlling pain, promoting wound re-epithelization, and treating the underlying etiology, if applicable. This often depends on the number, size, depth, and growth of skin ulcers. Bhat has suggested an algorithm for PG treatment, which we have modified and included below (Fig. 1).⁴ We have expanded this algorithm by suggesting to screen for associated not only in cases of extensive PG or in the presence of pathergy, but that everyone with PG should be screened given the high systemic associations as well, however, no such guidelines yet exist.¹³ The first line of treatment has traditionally been corticosteroids, but steroid-sparing drugs such as cyclosporine and antitumor necrosis factor therapies have been demonstrated in randomized clinical trials.^14,15 Cyclosporine must be administered cautiously given the high side effect profile, adverse event rate (renal toxicity, hypertension), and risk of sepsis.¹⁵ Recently, IL-12/23 inhibition has also shown to be beneficial as monotherapy in a small subset (6/9) of a 52-patient cohort receiving systemic therapies, with 4/9 (44%) achieving complete remission.¹⁶ The importance of analgesia, aside from the obvious duty to the patient's comfort, resides in facilitating appropriate compression and dressing changes. This is furthermore reflected in patient-reported anxiolytic quality and improved quality of life within the wound healing process.¹⁷ The role of surgical grafting and use of negative pressure wound therapy (NPWT) are increasingly being utilized as adjunct to systemic therapy in large ulcers; a 2017 systematic review of 115 patients demonstrated successful treatment in 84 cases.¹⁸ Notably, one reported case resolved with use of split-thickness skin grafting and NPWT alone.

Reproducibly, specialized wound care and compression therapies improve the quality of life of patients, while limiting wound pathergy and shortening the time to healing, discussed below.

The role of adequate wound care in PG

Once inflammation is maintained by local or systemic suppressive therapies, the importance of site-specific wound care is of highest consideration. So far, there have been no validated measures to objectively assess wound inflammatory activity, and classically, erythema, tenderness, and undermining have been used as surrogated markers, as reflected by Maverakis et al. Wound care involves adequate and gentle cleansing to remove epithelial debris, fibrinoid, and necrotic tissue, which is necessary to promote keratinocyte migration. Gentle mechanical debridement, considering risk of pathergy, an exaggerated skin injury occurring after minor trauma, and inhibition of critical colonization are essential throughout the phases of wound healing. For inflammatory ulcers such as PG, the disproportionate level of pain may require preanalgesia preferably with nonopiate or non-steroid anti inflammatory drug analgesics. While pathergy is a risk, intralesional lidocaine or topical anesthetics to open areas of ulceration without border disturbance have proven to be highly effective in our clinical experience. In our opinion, this is preferable to opiate analgesia as premedication, which carries with it escalating risks of chronic dependency and eventual baseline hyperesthesia.¹⁹ Topical antibacterial use in cases of critical colonization and maintenance of an appropriately moist environment are necessary to promote epithelial migration with any acute or chronic cutaneous ulceration.^17,20,21

At each clinical encounter, at minimum, all lesions should have a comprehensive assessment of their wound bed and border. Particular attention is paid to the amount and type of exudate, evidence of erythematous/violaceous wound margins or undermining, as well as the level of pain the patient is experiencing as signs of inflammatory activity. Secondary infection should be assessed with such clinical features as spreading erythema, malodor, and lymphangitis. The length, width, and depth of the wound should always be measured to aid in accurate longitudinal assessment; imaging with photographs and applied thermometry are becoming increasingly important and useful for clinical tracking.

Generally, the tissue debridement, control of tissue, debridement, control of infection/inflammation, moisture balance, and edge effect (TIME) principle, a guide for local wound care: the TIME.²² The TIME system was developed more than a decade ago to provide a structured wound care approach and is a useful framework for the management of chronic wounds.²² Overall, dressings should be nonadherent to the wound bed and removed easily to minimize trauma and subsequent pain, as well as pathergy.

Critical colonization is often managed with antimicrobial dressings as well as topical antiseptics.⁶ The use of systemic antimicrobials may yield an additional anti-inflammatory effect, which is yet to be fully elucidated in PG and other autoinflammatory neutrophilic wound disorders such as hidradenitis suppurativa (HS).²³

Management according to wound features

Wound dressings

A variety of dressings are recommended for different wound types, primarily depending on moisture balance and peripheral skin integrity, including hydrogels, films, hydrocolloids, alginates, and foams.

For eschars

Hydrogels and hydrocolloids help to promote autolytic debridement, which is favorable in wounds with little exudate, overdrying may cause pain upon removal.²⁴ The use of hydrogel and other autolytic agents promotes endogenous enzymatic degradation of inhibitory wound products with wound fluid activation, demonstrated to limit pain and benefit re-epithelization.²⁵

For highly exudative wounds

Foams, alginates, and superabsorbents help increase absorption and improve moisture balance. The neutrophilic and inflammatory nature of PG produces excess wound fluid, often requiring dressings that control the exudate to limit periwound maceration and infection, while promoting a moisture balance that still allows for epithelial migration. Having a powerful absorptive capacity minimizes inflammation of surrounding healthy skin. Upon contact with a moist wound, calcium alginate dressings produce the gel calcium/sodium alginate; since alginates can absorb up to 20 times their weight in wound fluid, they are ideal for moderate to heavy exudate.^24,25 Recent attention to the importance of limiting maceration has been evidenced by efficacy of window-colloidal dressings for periostomy PG, which serve to only protect affected skin.²⁶ This can be further modified to a partial window to decrease the burden of wound care materials and has been beneficial in cases of peristomal PG or irritant contact dermatitis. Foam can provide a tempting choice, but the importance of protection is often outweighed by the need for frequent dressing changes given the relative lack of absorptivity.²⁵ We reserve foam only for situations when PG occurs on promontory or sites of repeated trauma and require some form of physical protection or the amount of drainage is not heavy.

For granulating/epithelializing wounds

In the absence of ongoing inflammation, protease-lowering dressings, such as collagen, help decreasing MMPs and shorten healing time.²⁷ Epithelial migration can also be limited by the quantity of local epidermal loss or ongoing factors such as edema. In addition to long-standing options for skin grafting with both donated tissue and acellular matrices, emerging options for this final wound closure include the bioengineering of stem cell-associated protein polymers. Several studies have demonstrated that use of human-derived adipose and fibroblast stem cells for grafting improves healing time without adverse consequences.^28,29

For colonized wounds

Antimicrobials such as silver or polyhexamethylene biguanide-impregnated dressings are useful to address critical colonization (Table 3).²⁵ The routine use of antiseptics should be avoided and be limited for cases with a high burden of bacteria and used for a limited time. The use of topical antibiotics as prophylactic therapy, due to risk of bacterial resistance and contact dermatitis, is not recommended.³⁰ Antimicrobial dressings can be found in many forms, including semiocclusive dressings, gauze wrap, packing strips, and foam; iodine-based polymer bead absorbs fluid and debris while releasing iodine at nontoxic levels. A recent meta-analysis reported that iodine dressings may be associated with improved healing compared with standard of care.³¹ Silver-releasing agents disrupt bacterial cell walls, damaging membranes and denaturing bacterial DNA and RNA and has an anti-inflammatory effect.³² It is recommended to use sterile water for cleansing before a silver-based dressings as the chloride in normal saline inhibits the cation-mediated action of silver.

Infiltrating ulcers

Dressings are designed to fill the wound cavity in these wounds to absorb exudate. These wounds may extend to the subcutis or beyond and may exhibit undermining of wound edges. Deep wounds are not common in PG, except in cases of severe and active disease. When seen, gentle packing allows for absorbing drainage, cleansing, filling, and moistening wound cavities to promote healing from the inside of the cavity. In these cases, the exclusion of infection, including nontuberculous mycobacterium and deep fungal infections, is of the highest importance. In addition, in these cases, mimickers such as subcutaneous panniculitis-like T cell lymphoma and primary cutaneous gamma delta T cell lymphoma also must be excluded; wound edge biopsies, avoiding lymphocyte crush artifact at collection, with the addition of flow cytometry, when indicated by T cell clonality and atypia on biopsy, are often sufficient to rule out these entities.

Compression therapy

There is a lack of robust evidence to suggest that compression therapy is effective for healing of inflammatory ulcers and preventing recurrent ulcers even though it is a routine practice, which most experts recommend.³³ Compression therapy first reduces inflammation and fluid accumulation, which would otherwise impede wound healing. Low-level local continuous third-spacing and edema occur due to the chronic state of inflammation in PG. A number of options exist for treating local edema, which results in improved tissue oxygenation and promotes an environment conducive to keratinocyte turnover and migration. Of compression options, tubular and compression stockings are the most common followed by wraps and pumping systems or devices.³⁴ A retrospective study of 29 patients with chronic leg ulcers and rheumatologic diseases demonstrated that 17 patients were treated with compression therapy alone, with improvement.³⁵ Furthermore, compression has been shown to relieve pain and improve the odor of the wound.³⁶ This was also demonstrated in a prospective study on 31 patients where compression bandaging was used to reduce the dose of corticosteroids in acute treatment.³⁷ In addition, compression therapy has been found to be an effective treatment for PG without major adverse effects. The efficacy of this therapy has been demonstrated in a study, in which 17 out of 100 patients, who had PG, were treated with compression therapy alone. The leg ulcers of all 17 patients showed significant healing. However, there are challenges to using compression therapy such as adherence to treatment, which can be addressed through proper counseling. Compression therapy has been regarded as a treatment plan that is beneficial for most lower leg ulcers in patients with PG.²¹

Other modalities

Other treatment modalities for PG are dichotomized into topical and systemic therapy.

Local therapy options, in addition to wound care, include intralesional corticosteroids and topical medications such as calcineurin inhibitors.⁶

Summary of principles and attention to patient factors

Appropriate and individualized wound care is essential in PG—addressing major issues of exudative balance, granulation, pathogen colonization, as well as local inflammation.

While gentle mechanical and autolytic debridement is important, any surgical management of PG is discouraged due to its potentiation of pathergy leading to worsening of the wound. Self-care recommendations and education are vital for any chronic disease where patient self-management is a critical step in the therapeutic plan. Simple behavioral suggestions include minimizing the time for standing to reduce venous stasis, if present, encouragement of routine gentle activity. Due to the limitations of each behavioral modification, dressings and compression bandaging provide a time-efficient, minimally invasive option for protecting the wound against infection, promoting calf-muscle pump function and limiting further insult to lower extremity PG.

A multimodal approach to effective PG treatment has been demonstrated in the literature. The need for local wound care in conjunction with local or systemic immune modulating therapies is highlighted by the modified algorithm from Bhat et al. and apparent to practitioners treating inflammatory wounds. PG likely represents a systemic cause of inflammatory wounds where attention to each factor that contributes to inflammation is addressed and mitigated; this includes drivers of inflammation specific to PG and of chronic wounds, in general. The wound care process in PG always involves gentle cleansing, topical antibacterial use in cases of suspected colonization or infection, as well as maintenance of appropriate fluid balance. Numerous dressings can be used to target the specific wound type in PG, including superficial wounds, eschar, exudative wounds, granulating wounds, and colonized wounds. Compression therapy, while limited in standardized evidence as a modality in PG, is critical to reducing local inflammation and tissue edema, leading to enhanced blood flow directly and indirectly through improved ambulation. A patient-centered approach discussing pain in the wound care encounter is necessary to addressing and treating it, to improve the tolerability and adherence to compressing the wound.

Conclusion

We have highlighted advances in wound materials that limit colonization of microbes, balance moisture, perform gentle debridement for debris, protect the surrounding skin as well as the ulcer edges, and promote re-epithelization.

Take-Home Messages

• In addition to topical and systemic therapeutics, optimized wound care is paramount to the process of healing in PG.

• Inflammatory wound dressings to manage moisture balance, limit irritation and compression therapy are of highest considerations.

• Topical antimicrobials and antiseptics should only be used if evidence of critical colonization or infection.

• Dressing choices must be individualized for the patient depending on the nature of the wound, disease state, and level of pain.

• Consider screening for associated systemic diseases in all patients with PG, despite the severity or localization of disease.

Abbreviations and Acronyms

HS

hidradenitis suppurativa

MMPs

matrix metalloproteinases

NPWT

negative pressure wound therapy

PG

pyoderma gangrenosum

PMDs

polymeric membrane dressings

TIME

tissue, debridement, control of infection/inflammation, moisture balance, and edge effect

Acknowledgments and Funding Sources

There were no sources of funding for this article.

Author Disclosure and Ghostwriting

Afsaneh Alavi received an honoraria as a consultant, speaker, or advisory board participant from AbbVie, Bausch Health, Galderma, Janssen, LEO, Novartis, Sanofi, a Grant from AbbVie, and Research Investigator from AbbVie, Aristea, Asana, Boehringer-Ingelheim, Bristol-Myers Squibb, Dermavant, Eli Lilly, Genetech, Glenmark, Incyte, InflaRx, Janssen, Kyowa, LEO, Novartis, Pfizer, Regeneron, and UCB. No ghostwriters were used to write this article.

About the Authors

David Croitoru, MD, is a PGY3 resident in Dermatology at the University of Toronto and has interest in inflammatory wounds and neutrophilic dermatoses. He has a resident research grant from the Canadian Dermatology Foundation to investigate disease associations in PG. Sheida Naderi-Azad and Muskaan Sachdeva are medical students from the University of Toronto with interest in dermatology and inflammatory wound disorders. Vincent Piguet, MD, PhD, is the Division Head for Dermatology at the University of Toronto and Clinician Scientist with appointment to the Department of Immunology. He has long-standing expertise in the function of dendritic cells in HIV as well as interest in inflammatory wounds, including PG and HS. Afsaneh Alavi, MD, is a wound care specialist at the University of Toronto with the first PG specialty clinic in Canada, perhaps North America. She has special interest in the treatment and research of inflammatory wounds of HS and PG. She is Primary Investigator on numerous projects related to HS and PG, including clinical trials.