13.7 Hair Diseases

Question 1

What is Hair?

Answer 1

• Hair is a complex structure composed of keratinized cells that grow from follicles embedded within the skin

Question 2

Scarring and non-scarring alopecia

Answer 2

• Hair loss (called alopecia) can be an isolated problem, or associated with another disease or condition
• It can be non-scarring (temporary or reversible) or scarring (permanent), depending on the cause

Question 3

Non-scarring alopecia
Def
Common causes

Answer 3

• Hair loss with non-scarring damage to the hair follicles (i.e., the hair loss is usually reversible or treatable).

Common causes:
- Alopecia Areata
- Telogen Effluvium
- Male and female pattern hair loss

Question 4

Scarring alopecia
Def
Common causes

Answer 4

• Hair loss characterized by permanent damage to the hair follicles.

Common causes:
- Discoid Lupus Erythematosus
- Lichen Planopilaris
- Chronic bacterial infections
- Chronic fungal infections

Question 5

Alopecia areata

Answer 5

• autoimmune condition resulting in hair loss
• presents with discrete bald patches on the scalp (can cause hair loss from all hair-bearing areas on body)
• immune system mistakenly targets the hair follicles as foreign and launches immune response against them
• exact cause: not yet fully understood
• It is hypothesised that loss of immune privilege in anagen hair follicles plays a key role in the pathogenesis
• Genetic susceptibility is also thought to contribute

Question 6

Pathophysiology of hair loss in alopecia areata – autoimmune response

Answer 6

• The immune system, specifically CD8+ T-lymphocytes, is thought to play a crucial role in the development of alopecia areata
• These T-lymphocytes infiltrate the hair follicles and recognize specific self-antigens expressed in the hair follicle as foreign or abnormal
• Thus an immune response is triggered, which leads to inflammation and subsequent damage to the hair follicles

Question 7

Pathophysiology of hair loss in alopecia areata – genetic and other factors

Answer 7

• Alopecia areata has a strong hereditary component.
• At least 16 genetic risk loci have been detected.
• This includes numerous human leukocyte antigen (HLA) class I and II alleles, and several alleles of genes involved in immune pathways, hair pigmentation, and response to oxidative stress.
• The mode of inheritance seems to be complex, and environmental influences are also at play

Question 8

Telogen effluvium

Answer 8

• In a healthy scalp, about 85% of the hair follicles are actively growing hair (anagen hair) and about 15% are resting hair (telogen hair)
• A few hairs may also be in catagen
• A new anagen hair begins to grow under the resting telogen hair and pushes it out
• A normal or healthy scalp can lose up to about 100 hairs a day on one’s comb, brush, in the basin or on the pillow, as a result of the normal scalp hair cycle
• Telogen effluvium happens when a significant number of hair follicles prematurely enter the telogen phase (resting phase) of the hair growth cycle, leading to increased hair shedding
• If there is some insult to the system, as many as 70% of the anagen hairs can be precipitated into telogen, thus reversing the usual ratio
• This can be triggered by a variety of factors, including physiological, psychological, or environmental stressors

Question 9

Pathophysiology of hair loss in telogen effluvium
Triggering Factors

Answer 9

• Physical or emotional stress (e.g., childbirth, surgery, severe illness, emotional trauma)
• Hormonal changes (e.g., postpartum hormonal fluctuations, thyroid disorders , discontinuing the contraceptive pill)
• Nutritional deficiencies (e.g., iron, zinc, biotin)
• Certain medications (e.g., anticoagulants, retinoids)
• Rapid weight loss
• These triggering factors disrupt the normal balance of the hair growth cycle
• By causing a large number of hairs in the anagen phase (growing phase of the hair cycle) to abruptly enter the telogen (resting) phase
• As a result, there is an increased number of hairs in the telogen phase at any given time
• This then leads to an excess shedding of hair (even with gentle manipulation of the scalp)
• This increased shedding is noticed by the patient as diffuse hair loss or thinning
• Importantly, telogen effluvium is usually a self-limiting condition in the vast majority of people
• Once the underlying triggering factor is resolved or managed, the affected hair follicles gradually return to their normal growth cycle
• New hair begins to grow, and the shedding diminishes over time

Question 10

Male & female pattern hair loss: Androgenetic alopecia

Answer 10

• Male pattern hair loss is the most common type of diffuse thinning of the hair and balding that occurs in adult males
• It is due to a combination of hormones (androgens) and a genetic predisposition
• It is characterised by a receding hairline and hair loss on the top and front of the head.
• A similar type of hair loss in women, female pattern hair loss, results in thinning hair on the mid- frontal area of the scalp and is generally less severe than occurs in males

Question 11

Pathophysiology of male and female pattern hair loss
Genetic Predisposition

Answer 11

• Androgenetic alopecia is considered a genetically determined condition
• It is influenced by both maternal and paternal inherited susceptibility genes
• Several genes have been found to be involved, accounting for differing age of onset, progression, pattern and severity of hair loss in family members

Question 12

Pathophysiology of male and female pattern hair loss
Androgen Sensitivity

Answer 12

• The hallmark is the increased sensitivity of hair follicles to androgens, particularly dihydrotestosterone (DHT)
• DHT is a by-product of testosterone conversion facilitated by the enzyme 5-alpha reductase
• DHT is believed to shorten the growth, or anagen, phase of the hair cycle, from a usual duration of 3–6 years to just weeks or months
• This occurs together with miniaturization of the follicles
• Hair follicles located in certain areas of the scalp, particularly the frontal and vertex regions in men and the central scalp in women, are more susceptible to DHT’s effects

Question 13

Pathophysiology of male and female pattern hair loss
Miniaturization of Hair Follicles

Answer 13

• The presence of DHT leads to the gradual miniaturization of hair follicles
• Miniaturization refers to the progressive shrinking of the hair follicles over time
• The affected hair follicles produce thinner, shorter, and less pigmented hairs during each hair growth cycle, eventually leading to the appearance of thinning or balding areas
• A few women present with male pattern hair loss because they have excessive levels of androgens as well as genetic predisposition
• These women also tend to suffer from acne, irregular menses and excessive facial and body hair
• These symptoms are characteristic of polycystic ovarian syndrome (PCOS) although the majority of women with PCOS do not experience hair loss
• Less often, congenital adrenal hyperplasia may be responsible
• Females that are losing their hair with age are more likely to present with female pattern hair loss, in which hormone tests are normal

Question 14

Discoid Lupus Erythmatosus (DLE)

Answer 14

• Discoid lupus erythematosus (DLE) is a chronic scarring skin condition
• It is the most common form of cutaneous lupus erythematosus
• Specifically, it is a sub-type of chronic cutaneous lupus erythematosus
• It is characterised by persistent scaly plaques on the scalp, face, and ears
• which subsequently can progress to scarring, atrophy, dyspigmentation, and permanent hair loss in affected hair-bearing areas

Question 15

Pathophysiology of DLE

Answer 15

• Lupus erythematosus (LE) is a polygenic autoimmune disease linked to various HLA subtypes, immune signalling, and environmental factors, which ultimately leads to autoantibody production and T-cell dysfunction.
• However, the exact aetiology of discoid lupus erythematosus (DLE) is not well understood.
• DLE likely occurs in genetically predisposed individuals, but the exact genetic connection has not been determined.
• Exogenous factors such as smoking and ultraviolet radiation also play a role:
  • A history of smoking has been found to be more common in those with DLE
  • Ultraviolet radiation can provoke DLE as it is a photosensitive disorder. However, it can be found in non-sun exposed areas as well

Question 16

Lichen planopilaris (LPP)

Answer 16

• An uncommon inflammatory condition that can lead to permanent hair loss
• The disease is considered to be a form of lichen planus which affects the hair follicles, and thus
  having a similar pathogenesis.
• It results in patchy, progressive, permanent hair loss mainly on the scalp, although other hair- bearing skin (brows, pubic, and body) may be affected.

Question 17

Pathophysiology of LPP

Answer 17

• The exact cause of lichen planopilaris is unknown
• It is thought to be a cytotoxic autoimmune response to an unknown antigen located in hair follicles
• The exact trigger for this immune response is not fully understood,
• The disease may rarely be gene-related, and is also rarely drug-induced.

Question 18

Pathophysiology of hair loss in chronic bacterial infections

Answer 18

• The specific pathophysiology of hair loss in chronic bacterial infections can vary depending on:
  ➡️the type of bacteria involved (e.g., staphylococcus aureus)
  ➡️the location and severity of the infection (e.g., scalp)
  ➡️individual patient factors (e.g., underlying HIV)
• Bacterial scalp infections presenting as scalp folliculitis do not usually result in scarring hair loss.
• Severe bacterial superinfection of chronic scalp conditions (e.g., seborrhoeic eczema) may result in severe inflammation and damage, and eventually permanent destruction of hair follicles
• Dissecting cellulitis of the scalp is a rare cause of scarring alopecia. This condition is primarily related to follicular hyperkeratosis, rather than infection. However, bacterial superinfection may occur.
• The term folliculitis decalvans is usually applied to forms of highly inflammatory scarring alopecia, where inflammatory, follicular papules and pustules dominate the clinical picture.
  ➡️Often (but not always) Staphylococcus aureus can be grown from pustular or crusted lesions.
  ➡️Some authors believe that a primary staphylococcal infection of the scalp is the cause of folliculitis decalvans.

Question 19

Pathophysiology of hair loss in fungal infections

Answer 19

• Tinea capitis is a common fungal infection of the scalp that most often presents with pruritic, scaling areas of non-scarring hair loss
• Trichophyton and Microsporum species of dermatophyte fungi are the major causes of tinea capitis
• The infection is often contracted from another human or an animal through direct contact
• Tinea capitis does not usually cause a scarring alopecia, unless the infection is long-standing and untreated or severe, or when a clinical variant called a kerion develops

Question 20

Pathophysiology of hair loss in fungal infections - Kerion

Answer 20

• Kerion is a severe manifestation of tinea capitis resulting from a dramatic immune response to the infection
• It is characterized by the development of an inflammatory plaque with pustules, thick crusting, and/or drainage
• Kerions appear most commonly in children ages 5 to 10 and are rare in infancy
• Kerion is most often caused by a zoophilic dermatophyte; however, anthropophilic fungi can also cause a kerion
• Persistent kerion can lead to scarring alopecia