After extensive histological and ultrastructural studies of AKN lesions, Herzberg et al proposed that a series of events must happen in order for acne keloidalis nuchae to occur, namely the following [10] :
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The initial process begins as acute perifollicular inflammation followed by weakening of the follicular wall at the level of the lower infundibulum, the isthmus, or both.
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The naked hair shaft is then released into the surrounding dermis, which acts as a foreign-body and incites further acute and chronic granulomatous inflammation. This process is clinically manifested by small follicular-based papules and pustules. The nape of the neck has almost twice the number of mast cells compared with the anterior scalp and therefore may contribute to the pruritic sensation in this location. [11]
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Subsequently, fibroblasts deposit new collagen and fibrosis ensues.
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Distortion and occlusion of the follicular lumen by the fibrosis results in retention of the hair shaft in the inferior aspect of the follicle, thereby perpetuating the granulomatous inflammation and scarring. This stage is marked by plaques of hypertrophic scar and irreversible alopecia.
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Numerous acne keloidalis papules and plaques in a white man with straight hair.
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A large acne keloidalis plaque in a bandlike distribution at the posterior occiput in an African American man.
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A large acne keloidalis plaque on the occipital region in an African American patient. This man also had perifolliculitis of the scalp and acne conglobata (the follicular occlusion triad).
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Numerous papules that have coalesced into a large plaque, within which are tufts of hairs with several hair shafts exiting the same follicular orifice.
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A dense plasma cell infiltrate surrounding a hair follicle.
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Naked hair shafts embedded within a fibrotic dermis.
