**5. Pathogenesis**

HS is initially characterized by perifollicular lymphocytic infiltrate, which causes glands' duct occlusion, dilation, and rupture of the follicle. The result is an increased inflammation that leads to the formation of tunnels connected to the surface of the skin and filled with debris (**Figure 1**) [14, 15].

Histologically, the skin is formed by three main layers: epidermis, dermis, and subcutaneous tissue. The invagination of the epidermis develops the skin appendages: hair follicles, apocrine glands, and eccrine glands. The sebaceous glands are located in the mid-dermis and are connected to the hair follicle. They can be unilobular or multilobular holocrine glands that secrete sebum to the skin surface. This oily substance is important to protect the skin from water loss and traumas and to provide antibacterial activity. Eccrine and apocrine glands are the two main types of human sweat glands. The eccrine glands have a straight eccrine duct and secretory coiled portion and are responsible for thermoregulation. The apocrine glands are larger and mainly located at the axillary and anogenital area, areolae, and eyelids [14, 15, 16].

These skin appendages are considered a peripheral endocrine organ, expressing receptors and synthesizing various hormones, especially the androgenic ones. During adolescence, the gonadal cells in the ovary and testis secrete estrogen and testosterone, leading to the development of secondary sexual characteristics, including pubic hairs and axillary hairs. In addition, the apocrine glands grow, and the sebum secretion increases. The body odor is mainly from the axillary apocrine sweat glands, related to the bacterial catabolism of apocrine sweat [14–16].

The HS affects these glands. Histopathological patterns of HS include hyperkeratosis of the terminal follicle openings, hyperplasia of follicular epithelium,

**Figure 1.** *Steps of hidradenitis suppurativa pathology.*

and perifolliculitis. The disease is believed to begin with occlusion and dilation or elongation of the infundibular follicles. The infundibulum of the hair follicles then ruptures, followed by dermal suppurative inflammation with subsequent sinus tract formation and dermal fibrosis. This occlusion cause is not well understood.

*Hidradenitis Suppurativa Perineal and Perianal DOI: http://dx.doi.org/10.5772/intechopen.105632*

The local microbiota may play a role in the innate immune system dysregulation [14, 17, 18].

The damaged skin in HS expresses more keratin 16 at the interfollicular epidermis and infundibulum. Therefore, it is believed that a genetic propensity must be related to the epidermal cell differentiation and innate immunity in HS, leading to ill skin. Infiltrating CD4 + T cells secreting interleukin 17 (IL-17) and interferon-gamma (IFN-γ) are increased in perilesional and lesional skin of patients with HS. In these cases, the keratinocytes also produce significantly more IL-6, IL-8, tumor necrosis factor-alpha (TNF-α), interferon-gamma-induced protein 10, and C-C motif chemokine ligand 5 [16–18].

There are also morphological changes of the apocrine glands in HS, but it is still controversial whether the apocrine glands initiate or participate in the development of HS. The apocrine glands are full of secretory cell-like materials [18, 19]. The basal membrane zone gets thick and inflamed, and secondary bacterial Zcolonization contributes to the diffuse dense inflammatory aggregated in the dermis with dilated vessels, fibrotic changes, and diminished or absent appendageal structures, including apocrine glands. Besides, the number of eccrine sweat glands is reduced, and the sebaceous glands have a smaller volume and less number of sebaceous glands in the axilla and/or groin. The effect of decreased sebaceous glands is a drop in antimicrobial peptides and impaired innate immunity. Expression of integrin α6β4 in sick sebaceous glands may be associated with a bacterial infection [17–19].
