Hair loss patterns , known as male-pattern hair loss (MPHL ) when affecting men and female hair loss patterns b> ( FPHL ) when affecting women, is hair loss that mainly affects the top and front of the scalp. In men hair loss often appears as a receding hairline while in women it usually appears as hair thinning.
Male hair loss patterns are believed to be due to a combination of male genetics and dihydrotestosterone hormones. The cause of female hair loss patterns remains unclear.
Management may include accepting only those conditions. Otherwise, treatment may include minoxidil surgery, finasteride, or hair transplant. The evidence for finasteride in women, however, is poor and can result in birth defects if taken during pregnancy.
The pattern of hair loss at age 50 affects about half of men and a quarter of women. This is the most common cause of hair loss.
Video Pattern hair loss
Signs and symptoms
The loss of male hair-the classic pattern begins above the temple and vertex (calvaria) of the scalp. As time passes, the rim of hair on the side and back of the head remains. It has been referred to as 'Hippocratic wreath', and rarely develops to complement baldness. The Hamilton-Norwood scale has been developed to assess androgenic alopecia in males.
Female pattern hair loss more often causes thinning to spread without hair recession; similar to the male partner, female androgenic alopecia rarely causes total hair loss. Ludwig scale severity of female pattern hair loss.
Maps Pattern hair loss
Cause
Hormones
Research shows that early programming of pilosebaceous hair follicle units begins in utero . Physiology is mainly androgenic, with dihydrotestosterone (DHT) being a major contributor to dermal papillae. Men with premature androgenic alopecia tend to have lower than normal globulin sex hormone binding hormone (SHBG), follicle stimulating hormone (FSH), testosterone, and epitestosterone when compared with men without hair loss patterns. Although hair follicles were previously thought to be permanently lost in areas of complete hair loss, they are more likely to be inactive, because recent research shows the scalp contains the stem cell progenitor cells from which the follicles appear.
Transgenic studies have shown that growth and dormancy of hair follicles are associated with growth factor activity such as insulin (IGF) in dermal papillae, which is affected by DHT. Androgens are important in male sexual development around birth and at puberty. They regulate sebaceous glands, apocrine hair growth, and libido. With age, androgens stimulate hair growth on the face, but can suppress it in the temples and scalp vertex, a condition that has been termed the 'androgen paradox'.
Men with androgenic alopecia usually have a higher 5-alpha-reductase, lower total testosterone, higher free/free testosterone, and higher free androgens, including DHT. 5-alpha-reductase converts free testosterone to DHT, and is highest in the scalp and prostate gland. DHT most often formed at the network level by 5? -testosterone reduction. A genetic conclusion encoding this enzyme has been found. Prolactin has also been suggested to have different effects on hair follicles throughout the sexes.
Also, crosstalk occurs between androgens and the Wnt-beta-catenin signaling pathway which causes hair loss. At the level of somatic stem cells, androgens increase papillae differentiation of facial skin, but inhibit it in the scalp. Other studies have demonstrated the enzyme prostaglandin D2 synthase and D2 prostaglandin products (PGD2) in the hair follicles as their contribution.
These observations have led to studies at the level of mesenchymal dermal papillae. Type 1 and 2 5? the enzyme reductase is present in the pilosebaceous unit in the papillae of each hair follicle. They catalyze the formation of testosterone androgens and DHT, which in turn regulates hair growth. Androgens have different effects on different follicles: they stimulate IGF-1 in facial hair, which leads to growth, but also can stimulate TGF? 1, TGF? 2, dickkopf1, and IL-6 on the scalp, leading to the miniaturization of the catagenic. Hair follicles in anaphase express four different caspases.
The fact that hair loss is cumulative with age while decreased androgen levels as well as the fact that finasteride does not reverse the advanced stages of androgenetic alopecia remains a mystery but some explanations may have been posed: 1. Testosterone conversion to a higher DHT locally with higher age of 5-alpha reductase is recorded in bald scalp, and 2. Higher rates of DNA damage in Dermal Papilla as well as aging of Dermal Papilla due to activation of Androgen Receptors and environmental stress. The mechanism by which androgen receptors trigger permanent aging of Dermal Papilla is unknown but may involve IL6, TGFB-1 and oxidative stress. Aging papilla dermis is measured by a lack of mobility, different size and shape, lower replication and different molecular output changes and expression markers. The Dermal Papilla is the prime location of androgen action and migration toward the hair bulge and further signaling and increasing the size necessary to maintain the hair follicle so that aging through the androgen receptor explains a lot of physiology.
Diagnosis
The diagnosis of androgenic alopecia can usually be determined by clinical presentation in men. In women, diagnosis usually requires a more complex diagnostic evaluation. Further evaluation of the differential requires the exclusion of other causes of hair loss, and assesses the progressive hair loss pattern typical of androgenic alopecia. Trichoscopy can be used for further evaluation. Biopsy may be needed to rule out other causes of hair loss, and histology will show peripheracular fibrosis.
Treatment
Medication
Hair loss can be slowed or restored at an early stage with medication. Drugs approved by the US Food and Drug Administration (FDA) to treat hair loss in men include minoxidil and finasteride. The ketoconazole shampoo also exhibits consistent efficacy in enhancing both androgenetic alopecia by either antiandrogenic effects or by increasing seborrhoeic dermatitis which exacerbates androgenetic hair loss.
Androgen-dependent
Finasteride is a drug of the 5th grade? -reductase inhibitors (5-ARIS). By inhibiting type II-5 ARI, finasteride prevents the conversion of testosterone into dihydrotestosterone in various tissues including the scalp. Increased hair on the scalp can be seen within three months since starting treatment of finasteride and long-term studies have shown scalp hair increase at 24 and 48 months with continued use. Treatment with finasteride is more effective at treating male pattern hair loss in the vertex than in male-pattern hair loss patterns on the front of the head and temples.
Dutasteride is a drug in the same class as finasteride but it inhibits both type I and type II 5-alpha reductase. Dutasteride is approved for male pattern hair loss treatments in Korea and Japan, but not in the United States. However, it is usually used off-label to treat hair loss in men. Androgen-independent