Fox Fordyce Disease

Fox-Fordyce disease has the same anatomical distribution, as well as age and sex incidence as HS. This condition is more convincingly associated with an inflammatory process of the apocrine duct. Of interest there have been descriptions of some cases of Fox-Fordyce disease progressing to HS.

The pathogenesis of acne embraces increased sebum production, follicular hyperkeratosis, colonization with propionibacteria and inflammatory changes. The sebaceous duct hyperkera-tinization is mediated by the production of in-terleukin-1 alpha (IL1-a) and tumour necrosis factor alpha (TNF-a) by keratinocytes and T-lymphocytes. The result is hyperproliferation of keratinocytes, reduced apoptosis and consequent hypergranulosis. As a result the sebaceous follicle becomes blocked with densely packed keratin and so evolves the comedo. Early comedones show a dilated hair follicle associated with infundibular hyperkeratosis. Later due to rupture an acute dermal inflammatory response ensues. This can be complicated by a foreign body granulomatous reaction. In severe cases abscesses frequently present and cysts and sinuses form. Dermal scarring frequently results in these cases.

4.6.3 Follicular Occlusion Triad

In 1956, Pillsbury, Shelley and Kligman coined the term follicular occlusion triad for the common association of acne conglobata, HS and dissecting folliculitis of the scalp. They proposed that the pathological event unique to each disease was follicular hyperkeratinization [19].

All three diseases, HS, acne conglobata and dissecting folliculitis, represent chronic, recurrent deep-seated folliculitis resulting in abscesses followed by sinus tract formation and scarring. In an actively inflamed lesion the sinus contains hairs surrounded by neutrophils, granulation and scar tissue (Fig. 4.7). In an end-stage lesion there is scarring with patchy inflammation, which may track down a healed sinus at the site of a destroyed hair follicle.

The key histological features of all these conditions are:

1. Poral occlusion of the pilosebaceous units within intertriginous skin sites, especially the axillary area and anogenital regions

2. Secondary inflammation of apocrine glands

3. Inflamed nodules and sterile abscesses, which are followed by sinus tracts, fistulae and hypertrophic scars.

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