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secondary scarring alopecias from infections or dermatoses

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Secondary scarring alopecias from infections

The first, as well as the most dominant, cause of secondary scarring alopecia is infection and it may be of different types including infections resulting from bacterial, fungal and viral attacks.

Bacterial Infection

As in some primary scarring alopecia conditions, tissue homogenate cultures (composed of similar or identical tissues) of bacterial folliculitis (inflammation of a hair follicle or follicles) often bear testimony to the role played by Staphylococcus aureus in this kind of cicatricial alopecia. Folliculitis cultures, at times, also reveal the presence of Corynebacterium acnes. Folliculitis can be part of the larger issue of bacterial infection.

Bacterial folliculitis manifests itself as superficial follicular papules, pustules (a vesicle or an elevation of the cuticle with an inflamed base, containing pus), or as some kind of inflammatory eruption from deep in the skin. As far as histological features of the bacteria infested condition is concerned, the initial stage shows a kind of suppurative (pus forming) infundibular (the upper part of the hair follicle) folliculitis. Later on, the suppurative infundibular folliculitis festers or aggravates into a severe pus containing folliculitis (furuncle or boil) with perifollicular (surrounding a hair follicle, usually used to describe the histopathologic appearance of the infiltrate surrounding a hair follicle) fibrosis (the formation of fibrous tissue). With the condition worsening – due to follicular destruction and extensive fibrosis of the fibrous tract as also of the interstitial (situated between parts or in the interspaces of a tissue) dermis – cicatricial alopecia sets in.

Fungal Infection: A secondary scarring alopecia condition like Tinea capitis shows evidence of the presence of fungal hyphae (the fine, branching tubes which make up the body of a multicellular fungus) in and around the hair shafts but not in overlying epidermis when a scalp-skin sample is viewed under microscope. Tissue cultures also help in the proper diagnosis.

This type of alopecia is characterized by hair loss in all its stages of development. The early stage is characterized by a non-inflammatory alopecia and it develops fine scaling, pustular (pus bearing) folliculitis, seborrhea (a morbidly increased discharge of sebaceous matter upon the skin)-like dermatitis or kerion (a granulomatous secondarily infected lesion complicating fungal infection of the hair; typically, a raised boggy lesion) as the condition deteriorates.

Not all of these presentations, however, show scarring; only the ones with deep inflammation lead to permanent scarring and follicle loss. Initially the inflammation is neutrophilic (pertaining to or characterized by neutrophils, such as an exudate in which the predominant cells are neutrophilic granulocytes) but gradually changes to mixed and granulomatous traits (chronic inflammatory lesion characterized by large numbers of cells of various types – macrophages, lymphocytes, fibroblasts, giant cells – some degrading and some repairing the tissues).

Viral Infection:

Herpes zoster, a form of herpes (an acute inflammatory disease) that infects sensory nerves, causing pain and eruptions, also affects the scalp and can lead to a cicatricial alopecia condition. This condition is marked by the presence of painful grouped vesicles (a closed membrane shell around fluid), ulcers, crusts, or erythematous (unusually reddened) plaques in a dermatomal (dermatome means the area of skin innervated by a single posterior spinal or sensory nerve) distribution.

The histologic changes are inclusive of chronic lymphocytic destructive folliculitis with intra-nuclear viral presence. Viral culture and Tzanck tests help in the proper detection of the condition. As far as remedial measures are concerned, treatment with antiviral agents is known to terminate the process of follicular destruction and avert herpes zoster induced cicatricial alopecia.


Secondary scarring alopecias from dermatoses

Dermatoses, i.e., skin inflammation, especially from two conditions – psoriasis (a common chronic, squamous dermatosis, marked by exacerbations and remissions and having a polygenic inheritance pattern) and pityriasis amiantacea (an inflammatory condition of the scalp in which heavy scales extend onto the hairs and bind the hair fibers together) – can lead to cicatricial alopecia.

What happens in the case of psoriasis of the scalp is that the outbreak of severe inflammation, pustules and persistent scalp plaques in the skin of affected people initiates scarring alopecia in hair follicles of affected skin. In the case of pityriasis amiantacea, the scalp (rather the base of the hair shafts) is covered with mica-like adherent scales. Any attempt at physically removing the scales uproots the hair strands as well. This is effectively a type of traction alopecia. If hair is repeatedly plucked then the hair follicles accumulate damage and disruption. This can promote inflammation around the follicles and the combined result may be scarring alopecia.

The histological presentations of both the disorders exhibit spongiotic infundibular lymphocytic folliculitis and perifolliculitis (the presence of an inflammatory infiltrate surrounding hair follicles; frequently occurs in conjunction with folliculitis). These changes in tissue structures bring about changes in the follicle growth cycle and lead to severe consequences like telogen effluvium and eventual miniaturization of the follicles. With further aggravation, the follicular epithelium is destroyed and becomes bereft of sebaceous, oil secreting glands. Eventually, the condition can provoke a granulomatous reaction and permanent hair loss occurs.

The outbreak of such papulosquamous (denoting an eruption composed of both papules and scales) scalp disorders can be contained by the use of anti-bacterial, anti-fungal, keratolytic (promoting shedding of the epidermis), anti-inflammatory and anti-proliferative agents. As in many cases of scarring alopecia, topical corticosteroid preparations remain a mainstay of treatment.

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