Scarring Baldness

All skin lesions that lead to her scarring cause the death of hair follicles. Causes of cicatrical alopecia are very diverse. These are developmental defects and genodermatosis, skin damage caused by physical obligate factors (mechanical, chemical, radiation), skin lesions (benign and malignant), non -oidal skin and its appendages, acute and chronic skin infections 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 connective tissue hair follicles.

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

Scarring Baldness

Cicatricial baldness (RO) can occur at the site of trauma (mechanical, radiation, thermal, chemical, etc.). The time and type of exposure can be easily ascertained from an anamnesis (injury, irradiation, burn, etc.), as victims are usually remembered. The effect of obligate stimuli on the skin of the scalp leads to acute dermatitis (bullous-ulcerative or ulcerative-necrotic), death of the dermis with hair follicles and replacement with a coarse connective tissue. In the occipital region, hypertrophic keloid scars form after acne (acne-keloid in patients with severe seborrheic status or dark skin) or after abscessing and undermining perifolliculitis and Goffmann folliculitis.

Causes of cicatrical alopecia

Damage to the skin from physical and chemical irritants

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

Infectious diseases of the skin

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

Nonvoid skin formations

• Epidermal nevi
• Nevus of the sebaceous gland
• Syringocystadenoma papillary

Neoplasms

• Tumors of the appendages of the skin
• Basalioma
• Squamous cell carcinoma of the skin
• Hemangioma cavernous
• Lymphoma of the skin
• Plasmacytoma
• Melanoma
• Dermatofibrosarcoma swelling
• Metastases in the skin of tumors of internal organs

Other dermatoses

• Red lichen follicular and decalcifying
• Lupus erythematosus discoid
• Scleroderma plaque
• Follicular Mucinosis
• Pemphigoid scarring
• Amyloidosis of the skin
• Sarcoidosis of the skin
• Hystiocytosis of the skin from Langerhans cells
• Sclerosing and atrophic lichen
• Lipoid necrobiosis
• Skin lesions as a manifestation of the "graft versus host" reaction
• Eosinophilic pustules
• Erosive pustular scalp dermatosis

Defects of development and genodermatosis

• Congenital skin aplasia
• Face Gematrophy
• Hamartomy hair follicles
• Ichthyosis is congenital
• Folkeric dyskeratosis (Darya disease)
• Epidermolysis congenital bullous dystrophic
• Incontinence of pigment
• Rubbing follicular keratoses
• Porokeratosis Mibelli

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

Irradiation of the frontal parietal region in men with an early formed pronounced androgenetic alopecia (VI-VIII types) can cause, in particular blondes and redheads, actinic keratosis. It is manifested by dry skin, flat yellowish papules, covered with brown keratotic crusts, as well as numerous, merging areas of smooth, atrophic, sometimes slightly hyperemic skin with dyschromia and telangiectasias. Against the backdrop of actinic keratosis, which is a precancer, squamous cell carcinoma can develop.

Atrophy of the scalp is possible in patients who underwent 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 in the place of exposure to ionizing radiation of pigmentation and atrophy of the skin with alopecia and telangiectasias. Skin changes after radiation therapy also predispose to the development of cancer in this localization.

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

In other cases, the destruction of the hair follicles is associated with benign and non-inoid formations of the skin of the scalp and its appendages (adenoma of the sebaceous gland, seborrhoeic keratosis, cavernous hemangioma, syringoma, papillary syringocystadenoma, ekrinnoy skin cylinder - "turbaned tumor", etc.), and malignant neoplasms (basal cell carcinoma, squamous cell carcinoma, lymphoma, melanoma, metastasis of the head skin cancer, dermatofibrosarcoma swollen, etc.

Cicatricial baldness on the scalp can occur with developmental defects and genodermatosis. Particular mention should be made of the rare inherited dermatoses from the group of follicular scarring keratoses, such as follicular subulate decalcifying keratosis (Siemens syndrome), spindle-shaped hair aplasia, or moniteotriks, and follicular seriginous keratosis of Lutz.

Acquired dermatoses that cause predominantly atrophy of the skin with alopecia are grouped into group 5 and will be discussed below.

[1], [2], [3], [4], [5], [6], [7], [8], [9]

Atrophy hair loss

It is recognized clinically by characteristic signs: smooth, shiny, stretched, thinned skin, which does not have hair and holes in the hair follicles. Atrophic alopecia is usually strictly limited, with prolonged progression, it can sometimes occupy a large part of the scalp (subtotal and total atrophic alopecia). Characterized by the formation of smooth atrophic scars and the absence of gross cicatricial changes in the skin. Most atrophic alopecia, clinically similar to Brock's pseudocolus, is referred to as a pseudo-pellet condition. Many authors identify the state of atrophy alopecia and pseudohelps. Some acquired dermatoses and genodermatoses can lead to this condition, some - often, others - rarely. In those cases when neither anamnesis, nor clinically or histologically reveal any evidence in favor of one of the known dermatoses that could cause atrophic focal alopecia, ascertain the Brock pseudocolus as an independent disease of unknown etiology.

[10], [11], [12]

Dermatoses that lead to the condition of pseudo-pancreas

Frequent acquired dermatosis

• Red flat lichen, atrophic forms
• Discoid lupus erythematosus
• Scleroderma limited
• Folliculitis decalving Kenko

Rare acquired dermatoses

• Lipoid necrobiosis
• Ring-shaped granuloma
• Sarcoidosis
• Neoplasms (metastases)
• Nadbrovnaya cicatrizing erythema
• Favus

Genodermatosis

• Vulgar ichthyosis (X-chromosomal recessive)
• Congenital ichthyosis
• Incontinence of the pigment (Bloch-Sulzberger)
• Conradi-Hyunerman syndrome (autosomal recessive)
• Chondrodysplasia point (X-chromosome-dominant)
• Bullous epidermolysis is congenital dystrophic (Allopo-Siemensa, autosomal recessive)
• Follicular keratosis is subulate decolvable (X-chromosome-dominant)

[13], [14], [15], [16], [17]