Scarring alopecia

All skin lesions that lead to cicatricial changes also cause the death of hair follicles. The causes of cicatricial alopecia are very diverse. These are developmental defects and genodermatoses, skin damage caused by physical obligatory factors (mechanical, chemical, radiation), skin neoplasms (benign and malignant), nevoid formations of the skin and its appendages, acute and chronic infectious skin diseases and a number of other skin diseases. Histologically, cicatricial, sometimes inflammatory or neoplastic changes in the dermis with partially damaged or completely destroyed and replaced by connective tissue hair follicles are detected.

The listed causes of persistent baldness lead to the formation of two types of cicatricial changes on the scalp: cicatricial alopecia with a dense, rough scar and atrophic cicatricial alopecia with smooth, thinned, shiny skin without openings of hair follicles.

Cicatricial alopecia

Scarring alopecia (SA) may occur at the site of injury (mechanical, radiation, thermal, chemical, etc.). The time and type of exposure can be easily determined from the anamnesis (wound, radiation, burn, etc.), since victims usually remember this. The action of obligate irritants on the scalp leads to acute dermatitis (bullous-ulcerative or ulcerative-necrotic), death of the dermis with hair follicles and replacement with coarse connective tissue. In the occipital region, hypertrophic keloid scars are formed after acne (acne-keloid in patients with severe seborrheic conditions or dark skin color) or after abscessing and undermining perifolliculitis and Hoffmann's folliculitis.

Causes of cicatricial alopecia

Skin damage from physical and chemical irritants

• Mechanical damage
• Thermal damage
• Damage caused by ionizing radiation
• Chemical damage

Infectious skin diseases

• Folliculitis, furuncle, carbuncle
• Acne keloid
• Perifolliculitis and folliculitis abscessing and undermining Hoffmann
• Folliculitis decalvans (Kenko), or lupoid sycosis (Broca)
• Infiltrative-suppurative form of mycosis (kerion)
• Chronic forms of mycosis (chronic trichophytosis, favus, chronic granulomatous candidiasis, etc.)
• Shingles
• Chicken pox
• Lupozny tuberculosis of the skin
• Leishmaniasis
• Syphilis secondary (malignant) and tertiary
• Leprosy

Nevoid skin lesions

• Epidermal nevi
• Nevus sebaceous
• Syringocystadenoma papillary

New growths

• Tumors of the skin appendages
• Basalioma
• Squamous cell skin cancer
• Hemangioma cavernous
• Lymphoma of the skin
• Plasmacytoma
• Melanoma
• Dermatofibrosarcoma protuberans
• Metastases to the skin of tumors of internal organs

Other dermatoses

• Red lichen follicularis and decalvans
• Discoid lupus erythematosus
• Scleroderma plaque
• Follicular mucinosis
• Pemphigoid cicatricial
• Amyloidosis of the skin
• Sarcoidosis of the skin
• Cutaneous Langerhans cell histiocytosis
• Sclerosing and atrophic lichen
• Lipoid necrobiosis
• Skin lesions as a manifestation of graft-versus-host disease
• Eosinophilic pustulosis
• Erosive pustular dermatosis of the scalp

Developmental defects and genodermatoses

• Congenital aplasia cutis
• Hemiatrophy of the face
• Hair follicle hamartomas
• Congenital ichthyosis
• Dyskeratosis follicularis (Darier's disease)
• Epidermolysis congenita bullosa dystrophica
• Incontinence of pigment
• Scarring follicular keratoses
• Porokeratosis of Mibelli

In some cases, compression of the scalp during long surgical interventions leads to prolonged ischemia and, as a consequence, to the development of alopecia, including cicatricial. Since patients under general anesthesia do not feel pain, the traumatic effect remains unnoticed, and the cause of the developed cicatricial alopecia is unclear.

Sun exposure of the fronto-parietal region in men with early-onset androgenetic alopecia (types VI-VIII) can cause actinic keratosis, especially in blondes and redheads. It manifests itself as dry skin, flat yellowish papules covered with brown keratotic crusts, and numerous, merging areas of smooth, atrophic, and in places slightly hyperemic skin with dyschromia and telangiectasias. Against the background of actinic keratosis, which is a precancerous condition, squamous cell skin cancer can develop.

Atrophy of the scalp is possible in patients who have undergone X-ray therapy for malignant tumors of this localization. The degree of skin damage after exposure to various types of ionizing radiation (X-ray, neutron, etc.) depends on the type of radiation, dose, area of the site and its localization. Radiation dermatitis always occurs within the irradiated area of the skin. According to clinical manifestations, it can be acute and chronic with subsequent formation of pigmentation and skin atrophy with alopecia and telangiectasia at the site of exposure to ionizing radiation. Skin changes after radiation therapy also predispose to the development of cancer in this localization.

Hair follicles can be destroyed by various infectious agents (staphylococci, chickenpox virus, herpes zoster, dermatophytes, mycobacteria of tuberculosis and leprosy, pale treponema, leishmania, etc.). Thus, after a furuncle, deep folliculitis, carbuncle, abscess, infiltrative-suppurative mycosis, etc., scars of different sizes and shapes remain on the scalp, sometimes - skin atrophy with a peripheral zone of temporary hair loss.

In other cases, the destruction of hair follicles is associated with benign and nevoid formations of the scalp and its appendages (sebaceous gland adenoma, seborrheic keratosis, cavernous hemangioma, syringoma, papillary syringocystadenoma, eccrine cylindroma of the skin - "turban tumor", etc.), as well as malignant neoplasms (basalioma, squamous cell carcinoma, lymphoma, melanoma, metastasis to the scalp of internal organ cancer, protruding dermatofibrosarcoma, etc.

Scarring alopecia on the scalp may occur in developmental defects and genodermatoses. Of particular note are rare hereditary dermatoses from the group of follicular scarring keratoses, such as follicular spinous decalvans keratosis (Siemens syndrome), fusiform hair aplasia, or monilethrix, and follicular serpiginous keratosis of Lutz.

Acquired dermatoses, which mainly cause skin atrophy with baldness, are combined into group 5 and will be discussed below.

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Atrophic alopecia

It is recognized clinically by characteristic signs: smooth, shiny, taut, thinned skin, lacking hair and openings of hair follicles. Atrophic alopecia is usually clearly limited, with long-term progression it can sometimes occupy a large part of the scalp (subtotal and total atrophic baldness). Formation of smooth atrophic scars and absence of rough cicatricial changes of the skin are characteristic. Most atrophic alopecias, clinically similar to pseudopelade of Broca, are designated as a condition of pseudopelade. Many authors identify the condition of atrophic alopecia and pseudopelade. Some acquired dermatoses and genodermatoses can lead to such a condition, some - often, others - rarely. In cases where neither anamnestic, nor clinical, nor histological data reveal any data in favor of one of the known dermatoses that could cause atrophic focal alopecia, Broca's pseudopelade is diagnosed as an independent disease of unknown etiology.

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Dermatoses leading to pseudopelade state

Frequent acquired dermatoses

• Lichen planus, atrophic forms
• Discoid lupus erythematosus
• Limited scleroderma
• Folliculitis decalvans Kenko

Rare acquired dermatoses

• Lipoid necrobiosis
• Granuloma annulare
• Sarcoidosis
• Neoplasms (metastases)
• Superciliary cicatricial erythema
• Favus

Genodermatoses

• Ichthyosis vulgaris (X-linked recessive)
• Congenital ichthyosis
• Incontinence of pigment (Bloch-Sulzberger)
• Conradi-Hunnermann syndrome (autosomal recessive)
• Chondrodysplasia punctata (X-dominant)
• Epidermolysis bullosa congenita dystrophica (Hallopeau-Siemens, autosomal recessive)
• Follicular keratosis awl-shaped decalvans (X-chromosome dominant)

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