Table 1.

Variants of pyoderma gangrenosum with their histological and clinical differences

Variants	Clinical findings	Histological features	Location/Associations	Treatment
Classical	Necrotic deep ulcers with undermined violaceous borders. Cribiform scarring.	Superficial dermal necrosis with intra-dermal neutrophilic abscess formation. Mixed inflammation with occasional giant cells. Leukocytoclastic vasculitis and lymphocytic vasculitis may be present.	Frequently located in the lower extremities (pretibial).	Requires aggressive systemic immunosuppressive therapy.
Pustular	Painful vesiculopustular lesions with a surrounding erythematous halo. Do not evolve to frank ulceration.	Dense dermal neutrophilic infiltrate with sub-corneal neutrophil accumulation and peri-follicular neutrophilic infiltration. Sub-epidermal edema is common.	Associated with inflammatory bowel disease.	Improvement with control of inflammatory bowel disease.
Vegetative “superficial granulomatous pyoderma “	Slowly progressive erythematous plaques with sinus formation. Sometimes superficial ulceration. Not undermined borders or surrounding erythema.	Neutrophilic and histiocytic dermal infiltrate with or without granuloma formation.	Frequently located in the trunk. Usually no association with systemic diseases.	Less commonly requires immunosuppression.
Bullous	Painful vesicles and haemorrhagic bullae with intense red halo rapidly coalescing and evolving to superficial ulcerations. No deep ulceration. Cribiform scarring is not associated.	Neutrophilic dermal infiltrate with sub-epidermal bullae. Epidermal necrosis.	Usually located in the face and upper extremities (dorsal hands). Commonly associated to haematologic malignancy.	Rapid response to steroids.

There are no true variants because the clinical appearance resembles those of the classic lesions: Peri-stomal pyoderma gangrenosum (skin lesions in the peri-stomal area occurring 2 months to 25 years after surgery), genital pyoderma gangrenosum, and infantile pyoderma gangrenosum