Hair loss and hair regrowth

Br J Dermatol. 2009;160:75
Frontal fibrosing alopecia (hairloss): clinical presentations and prognosis.

edited for hair regrowth blog

Tan KT, Messenger AG.

BACKGROUND: Frontal fibrosing alopecia is an uncommon condition characterized by progressive frontotemporal recession due to inflammatory destruction of hair follicles. Little is known about the natural history of this disease. OBJECTIVES: To determine the clinical features and natural history of frontal fibrosing alopecia. METHODS: We studied the cases notes of patients diagnosed with frontal fibrosing alopecia from 1993 to 2008 at the Royal Hallamshire Hospital, Sheffield. RESULTS: There were 18 patients aged between 34 and 71 years. Three were premenopausal. All had frontotemporal recession with scarring. This was associated with partial or complete loss of eyebrows in 15 patients while four had hair loss at other sites...snip,,, Progression of frontotemporal recession was seen in some patients, but not all. In one patient the hair line receded by 30 mm over 72 months, whereas in another patient there was no positional change in the hair line after 15 years. CONCLUSIONS: Hairloss secondary to frontal fibrosing alopecia is more common in postmenopausal women, but it can occur in younger women. It may be associated with mucocutaneous lichen planus. Recession of the hair line may progress inexorably over many years but this is not inevitable. It is not clear whether or not treatment alters the natural history of the disease...

J Invest Dermatol. 1976;67:98

Hair and hairloss

Ebling FJ.

The psychologic importance of hair to man is in inverse ratio to its physical function. Except for scalp hair and desultory areas of sexual hair, most of man's hair follicles are vestigial. Three problems of hair regrowth remain to be solved: (1) how the intermittent activity of hair follicles in both animals and man is controlled; how the male hormone alters the hair cycle in human skin; and (3) why larger hairs are produced by testosterone in some areas of the body when in some individuals the hair follicles in the scalp regress. Studies in which skin grafts from rats of different ages were exchanged showed that hair follicles are innately programmed but can be slowly influenced by systemic factors. Steroid hormones, especially estrogens, slow down the moult cycle whereas thyroid hormones accelerate it. What establishes the innate rhythm remains problematical. The fact that plucking out the club hair initiates activity in resting follicles has been explained by the hypothesis that the mitotic inhibitor which accumulates during anagen is normally used up or dispersed during telogen or by wounding. However, contrary to this theory, follicular activity is not prolonged by epilation during anagen. Moreover, if rats are epilated within one or two days of eruption, only club hairs are removed since forceps cannot grasp the tips of the new hairs. Such epilation does not affect the anagen in progress, but remarkedly enough the subsequent resting phase is shortened. Both sexual hair and male-pattern baldness depend on androgenic hormones. snip... The major metabolite of testosterone incubated with hair roots in androstenedione, and hirsute women without other obvious endocrine abnormality sometimes excrete high levels of androstanediol. Both steroids stimulated the sebaceous glands of hypophysectomized-castrated rats, which, however, showed only a limited response to testosterone. The androgenic steroids, the enzymes that convert them to their active metabolites, and the proteins that bind them are undoubtedly very important to the problems of the growth of sexual hair and male-pattern baldness.

Clin Interv Aging. 2006;1(:121

Pharmacologic interventions in aging hair
Ralph M Trüeb

Edited exerpt...

Hair loss

Androgenetic alopecia aka male-pattern hair loss or common baldness in men, and female-pattern hair loss in women, affects at least 50% of men by the age of 50 years, and eventually up to 70% of all males . Recent studies assert that 16% of women aged under 50 years are affected, increasing to a proportion of 30%–40% of women aged 70 years and over. The hair loss is heritable, androgen-dependent, and occurs in a defined pattern. This involves replacement of large, pigmented hairs (terminal hairs) by barely visible vellous hair. It is assumed that the genetically predisposed hair follicles are the target for androgen-stimulated hair follicle miniaturization. T^his leads to gradual e, depigmented hairs (vellus hairs) in affected areas. This results in a decline in scalp hair density. snip... major advances have been achieved in understanding principal elements of the androgen metabolism involved in the pathogenesis of pattern hair loss : Androgen-dependent processes are predominantly due to the binding of dihydrotestosterone to the androgen receptor. Dihydrotestosterone-dependent cell functions depend on weak androgens, their conversion to more potent androgens, low enzymatic activity of androgen inactivating enzymes, and functionally active AR present in high numbers. The predisposed scalp exhibits high levels of DHT, and increased expression of the AR. Conversion of testosterone to DHT plays a central role, while androgen-regulated factors deriving from dermal papilla cells are believed to influence growth of other components of the hair follicle. Many hair regrowth-modulating factors, such as androgens, work in the dermal papilla. Thus, research is currently also focused on androgen-regulated factors. Of factors suggested to figure in hair regrowth, so far only insulin-like growth factor is reported to be altered by androgens, and stem cell factor (SCF) has been found to be produced in higher amounts by androgen-dependent beard cells than in control non-balding scalp cells, presumably also in response to androgens. snip..

The limited success using treatment with hair regrowth promoters or modulators of androgen metabolism means that further pathogenic pathways figure. The implication of microscopic follicular inflammation in the pathogenesis of AGA has recently emerged from several independent studies. There is an inflammatory infiltrate of activated T cells and macrophages in hair follicles, associated with an enlargement of the follicular dermal sheath composed of collagen bundles (perifollicular fibrosis or scaring), in regions of actively progressing hair loss. Horizontal section studies of scalp biopsies indicated that the perifollicular scarring is generally mild. The term “microinflammation” has been proposed because the process involves a slow, subtle, and indolent course, in contrast to the inflammatory and destructive process in the classical inflammatory scarring alopecias. snip.... .. Arguably, microbial toxins or antigens could be involved. Alternatively, keratinocytes themselves may respond to chemical stress from irritants, pollutants, and ultraviolet irradiation, by producing radical oxygen species and nitric oxide, and by releasing intracellularly stored interleukin. snip.. themselves mediators for the recruitment of neutrophils and macrophages, have been shown to be upregulated in the epithelial compartment of the human hair follicle. snip... After processing of localized antigen, Langerhans cells, or alternatively keratinocytes, which may also have antigen presenting capabilities, could then present antigen to newly infiltrating T lymphocytes and induce T-cell proliferation. The antigens are selectively destroyed by infiltrating macrophages, or natural killer cells. On the occasion that the causal agents persist, sustained inflammation is the result, together with connective tissue remodeling, where collagenases, such as matrix metalloproteinase (also transcriptionally driven by pro-inflammatory cytokines) play an active role. Collagenases may contribute to perifollicular fibrosis. The significance is controversial. However, in patients with male pattern hair loss treated with minoxidil, 55% of those with microinflammation had regrowth in response to treatment, in comparison with 77% in those patients without inflammation and fibrosis.

keywards-- hair loss treatment hair regrowth

Am Fam Physician. 200915;80:356

Diagnosing and treating hair loss.
Mounsey AL, Reed SW.

Do not underestimate the emotional impact of hair loss for some patients. Patients may present with focal patches of hair loss or more diffuse hair loss, which may include predominant hair thinning or increased hair shedding. Focal hair loss can be further broken down into scarring and nonscarring. Scarring alopecia is best evaluated by a dermatologist. The cause of focal hair loss may be diagnosed by the appearance of the patch and examination for fungal agents. A scalp biopsy may be necessary if the cause of hair loss is unclear. Alopecia areata presents with smooth hairless patches, which have a high spontaneous rate of resolution. Tinea capitis causes patches of alopecia that may be erythematous and scaly. Male and female pattern hair losses have recognizable patterns and can be treated with topical minoxidil, and also with finasteride in men. Sudden loss of hair is usually telogen effluvium, but can also be diffuse alopecia areata. In telogen effluvium, once the precipitating cause is removed, the hair will regrow.

Loss of hair and alopecia are the most common problems of modern societies, which create many economical and psychological effects. Recently, a great effort has been made to treat hair loss and alopecia, in which some of them were successful. One of the most common types of alopecia is baldness or androgenetic alopecia. This kind of alopecia is recognized by progressive narrowing of hair in the vertex and fronto- temporal area of scalp, in persons with genetic potency. The alopecia is hereditary in nature and is formed due to the high testosterone receptors in scalps of involved persons. Dihydroxy testosterone is an active form of testosterone that is produced by enzyme type II, 5-a reductase from testosterone. [1] Testosterone affects hair follicle, resulting in hair shaft thinning, shortening of anagen phase and prolongation of telogen phase.[2] The most recommended treatment for androgenic alopecia is composed of local minoxidil, hormonal therapy such as local and oral anti- androgen or local progesterone containing products. [3],[4],[5],[6],[7],[8] Finasteride is an effective drug for treatment of male alopecia that can be used orally or locally. The drug decreases loss of hair by inhibiting 5-α reductase enzyme activity, which converts testosterone to its active form, namely di-hydrotestosterone which is the main cause of male pattern hair loss. Topical finasteride is used to treat male pattern hair loss. [10] Since, long-term finasteride is needed for treatment of male pattern hair loss;in treatment of pattern in men. If topical form is effective, it will prevent the undesirable side effects of systemic form of drug. In addition, it will be a suitable treatment for this social problem, especially in adolescence and young age groups in which hair protection, as a cosmetic, is important for them.

Saudi J Kidney Dis Transpl.2008;19:796

Vitamin D dependent rickets type II:
Soni SS, et al

Vitamin D dependent rickets type II is alter­natively known as rickets-alopecia syndrome. The disorder is characterized by end organ resistance to phy­siological doses of 1,25 dihydroxy cholecalci­ferol. The basic defect involves the unrespon­siveness of vitamin D receptor (VDR) to 1,25­dihydroxyvitamin D. Brooks et al [1] in 1978 first reported a 22–year-old African American woman with hypocalcemia, secondary hyper­parathyroidism, osteomalacia, and osteitis fib­rosa cystica in association with normal serum 25–hydroxyvitamin D and markedly increased serum 1,25–dihydroxyvitamin D. They labeled this syndrome as VDDR type II. Many pub­lications followed reporting similar clinical observations of early onset vitamin D unres­ponsive rickets and severe hypocalcemia with or without alopecia ( hair loss ).

Eil et al demonstrated defective nuclear up­take of vitamin D in cultured fibroblasts from these patients. Laboratory clue to diagnosis of VDDR II is high level of 1,25–dihydroxyvitamin D in a patient with hypocalcemia and non-azotemic rickets, as observed in our case. Rapid molecular diag­nosis is also possible by testing the effects of 1,25–(OH)2D3 on thymidine incorporation into PHA-stimulated lymphocytes. The prenatal diagnosis of VDDR-II by analysis of amniotic fluid cells and fetal tissue is indicated in high risk families. These patients are prone for infections because of immune dysfunction and impaired neutrophilic chemotaxis.

VDDR II is an autosomal recessive disorder caused by a defect in the vitamin D receptor gene located on chromosome 12q12–q14. Thus far, 13 mutations have been identified. Treatment with high dose vitamin D analogues is found to be effective as in our case. Takeda E [10] reported a sibling cured by treatment with 50,000 IU of vitamin D2 daily for 2 years without any recurrence for 14 years after cessation of therapy. High dose oral calcium alone or in combination with intravenous cal­cium [12] are also reported to be effective treat­ment options.