The importance of human hair in view of social communication and sexual attraction is enormous. Thus, diseases that lead to hair loss (alopecia), structural hair shaft defects or excessive hair growth on the body are often accompanied by a diminished sense of personal well-being and self-esteem, leading to depressive moods and withdrawal from social interims.
Following are the main types of alopecia:
ANDROGENETIC ALOPECIA: AGA or pattern hair loss is by far the most common type of hair loss in men and women. Male pattern hair loss (MPHL) (also known as male AGA, male balding) is a hormone (androgen) dependent, genetically determined trait. Female pattern hair loss (FPHL) (or female androgenetic alopecia) is believed to be the same entity. However, the requirement of androgens is less clear cut than in men and the distribution of hair loss is generally different. In both, men and women, AGA is characterized by a progressive decline in the duration of anagen (active growth phase), an increase in the duration of telogen (terminal phase) and miniaturization of scalp hair follicles.
Men: Estimates of the prevalence of AGA vary widely. Most men will develop some degree of a recession of the hairline during their lifetime. Some hair loss is seen in around 50% of men and women beyond 40 years of age. The risk of male pattern baldness depends on the family history in the father, the mother, or the maternal grandfather. Men whose father had hair loss were twice as likely to have hair loss as men whose father showed no hair loss. Ethnic variation in the incidence of AGA has been reported. AGA seems to be four times less frequent in men of African ancestry, around three times less frequent in Korean men and approximately 1.5 times less frequent in men originating from China, Japan or Thailand.
Women: Female Pattern Hair Loss (FPHL) is less common than Male Pattern Hair Loss (MPHL) but shows a similar age-related increase in frequency and severity. However, the condition can start as early as the prepubertal period both in men and women. Around 40% of Caucasian women have developed some degree of FPHL at age 70. FPHL seems to be less frequent in Asian women.
Pathophysiology: The underlying causes of patterned hair loss have yet to be determined. In men, MPHL appears to result from a combination of androgen (mainly testosterone) hyperactivity, a genetic predisposition to hair loss-related sensitivity to androgen action as well as an androgen-independent genetic predisposition. For females, the condition known as female pattern hair loss (FPHL) may have a more complex etiology. However, androgen action combined with genetic sensitivity to those actions seems to play a dominant role in most cases, and indeed these factors may be present generally in FPHL. In AGA, large, pigmented hairs, called terminal hairs, are gradually replaced by fine (nearly invisible) colorless vellus hairs. This transformation follows a progressive course with each hair cycle in the following manner. Scalp hair develops in three phases: (1) a growth phase, or anagen, of approximately 2–6 years; (2) a short (2–3 weeks) phase, catagen, which actually represents the termination of anagen; and (3) transition to the telogen phase. A telogen hair does not grow and is shed from the follicle after about 12 weeks. MPHL and FPHL exhibit a progressive decrease in anagen duration with each cycle, producing shorter, thinner hairs. Finally, the interval between late telogen hair shedding (exogen) and new hair growth with initiation of anagen increases, resulting in more follicles without hair and an apparent reduction in scalp hair density.
Epidemiology: The second most common cause of hair loss in women after FPHL is TE. The latter presents as a nonpatterned increase in shedding of terminal hairs, diffusely over the entire scalp, and can produce an apparent thinning of hair in severe cases. While both genders can experience TE, attitudes toward hair loss result in a greater proportion of females who complain. TE can co-present with AGA, particularly in early-onset situations, and this can complicate diagnosis and treatment. TE differs from AGA in that it is not androgen-sensitive and does not appear to be inherited. TE also tends to be related to external causes and is often reversed when the exogenous stimuli are removed.
Acute Telogen Effluvium: The pathophysiology underlying TE is best characterized as a premature shift of hairs from the anagen (growth) phase into the catagen (resting) and telogen (terminal) phases. However, there are variants: anagen may be prolonged, or telogen may instead be shortened or prolonged. Which type of shift occurs depends on the stimulus producing the shift, with the main clinical difference being the latency of effluvial onset following the stimulus. The hair loss that commonly occurs following pregnancy is generally seen 2 or 3 months after birth, although some individuals can exhibit longer times to onset. While this is classic TE, the mechanism has been shown to involve a delayed transition from anagen to catagen/telogen, which results in a simultaneous shedding of large numbers of terminal hairs. This hair does eventually regrow; however, the returning hair may show changes in texture, color, and curliness, and may not attain its previous length. As such, pregnancy (parturition or abortion) may in some cases produce permanent changes in anagen length. Other perturbations can produce TE, usually involving premature termination of the anagen phase. Some women experience transient TE 2–3 months after discontinuing or changing oral contraceptive medication; the delayed onset of TE in these cases distinguishes it from the anagen effluvium (AE) initiated by certain drugs. In the 1970s, the popularity of fad “crash” diets resulted in many cases TE about 3 months after initiation of these spartan regimens, depending on the severity of weight loss. Sudden deprivation of amino acids and other dietary factors most likely produced the condition, and the hair tended to regrow following cessation of the diets. Surgical procedures, psychological traumas, and febrile illness have all been reported to produce TE events. Drugs are widely reported to produce temporary hair loss. This is usually, but not necessarily, of the AE variety, since, depending on the causal agent, the time course and severity may suggest a diagnosis of TE to be appropriate. Agents producing TE include cimetidine, enalapril and captopril, propranolol, and lithium among others. Finally, hair loss occurring following environmental contamination or poisoning, for example with selenium, arsenic, thallium, mercury, and lead, displays an AE-like rapid onset.
Chronic Telogen Effluvium: Chronic Telogen Effluvium (CTE) is used in distinguishing the abrupt-onset, short-acting type TE, usually caused by exogenous triggers or parturition, from a more durable condition (CTE) that may not be so clearly related to any external event. While “crash” diets have been pinpointed as potential triggers for acute TE, chronic malnutrition can analogously lead to CTE. Protein deficiency is the likely mechanism in this type of balding. It is less clear whether zinc or biotin deficiencies are also correlated with chronic diffuse hair loss. Although controversial, iron deficiency, as evidenced by decreased serum ferritin and anemia, may be a trigger for CTE. Hypothyroidism has also been associated with CTE.
Epidemiology: At any given time, approximately 0.2% of the world population is suffering from alopecia areata with an estimated lifetime risk of 1.7%. It is a common cause of abrupt-onset hair loss but occurs less frequently than androgenic alopecia or TE. Both sexes are affected equally. Although it may occur at any age, incidence at a younger age is higher. Alopecia areata is the most common form of alopecia seen in children. The familial occurrence is around 15% but the expression of the disorder is variable among different family members. 5% of patients suffering from alopecia areata develop hair loss of their entire scalp hair (alopecia totalis), and 1% of patients develop loss of total body hair (alopecia universalis) at some point.
Pathophysiology: Alopecia areata is a chronic, organ-specific autoimmune disease, which affects hair follicles and sometimes nails. Alopecia areata is thought to be an autoimmune disease with inappropriate immune- response to hair follicle associated proteins. A collapse of the normal immune privilege of the anagen hair bulb may play a key role in the pathogenesis of this disease. There is a high frequency of a positive family history of alopecia areata in affected individuals, ranging from 10% up to 42% of cases, and a much higher incidence of positive family history in early-onset alopecia areata. Many patients report the experience of major emotional stress prior to the onset of alopecia.
Pathophysiology: AE is a result of a disturbance of hair follicle matrix cells. The anagen phase is interrupted and the hair falls out 7–14 days after the initiating event without entering catagen or telogen. Drugs used in chemotherapy quickly produce severe hair loss and even total baldness. A rapid onset undoubtedly indicates an immediate release from anagen hair. Immediate anagen hair release is characterized by an easy release of anagen hairs after gentle pulling.
TEMPORAL TRIANGULAR ALOPECIA
Epidemiology: Lesions can be present at birth or first appear before school age. Temporal triangular alopecia (TTA) has been reported in Asian and Caucasian patients with no sexual predilection. TTA is often misdiagnosed as alopecia areata.