Hair loss and hair regrowth

Br J Dermatol. 2010 May 25.

Intermediate hair follicles: a new more clinically relevant model for hair regrowth investigations.
Miranda BH, et al

Edited for hair loss treatment blog

Abstract
ABSTRACT Background: Alopecia ( hair loss ) causes widespread psychological distress, but is relatively poorly controlled. The development of new hair loss treatments is hampered by the lack of suitable human hair follicle models. Although intermediate and vellus hair follicles are the main clinical target for pharmacological therapy, terminal hair follicles are more frequently studied as smaller hair follicles are more difficult to obtain. Objectives: This investigation was designed to quantify in vivo morphological and in vitro behavioural differences in organ culture between matched intermediate and terminal hair follicles, in order to develop a new clinically-relevant model system. Methods: Microdissected terminal and intermediate hair follicles, from the same individuals, were analysed morphometrically (250 follicles; 5 individuals), or observed and measured over 9 days of organ culture (210 follicles; 6 individuals). Results: Intermediate hair follicles were less pigmented and smaller, penetrating less below the skin surface, with smaller fibre, connective tissue sheath, bulb and dermal papilla diameters. Intermediate hair follicle bulbs appeared 'tubular' unlike their 'bulbous' terminal follicle counterparts. In organ culture they also grew more slowly, remained in anagen longe and produced less hair fibre than terminal follicles. Conclusions: Smaller intermediate hair follicles showed major morphological differences to terminal follicles and retained significant, biologically-relevant differences in vitro in organ culture. Therefore, intermediate hair follicles offer a novel, exciting, more clinically-relevant, albeit technically difficult, model for future investigations into hair growth. This should be particularly important for developing new treatmens for hair loss.

Calif Med. 1958;89:322.

Noncicatrizing alopecias; with special reference to hair loss due to alopecia areata.
NEW WN, NICKEL WR.

edited for blog use

....there has been general acceptance of the causal relationship of the male sex hormone testosterone, age and inheritance in development of male pattern baldness. snip... Hair loss that accompanies disease states is probably due to generalized toxemia and disturbances in metabolism. Sometimes male pattern baldness occurs in physiologic states, as exemplified by diffuse hair loss occasionally in the postpartum period. snip... The development of alopecia totalis or universalis in 50 per cent of the prepuberal cases of alopecia areata is of real significance, especially since so very few patients regrow normal scalp hair....snip... A few conditions simulate alopecia areata. Probably the ones which are seen most often are trichotillomania and patchy baldness caused by agents used in hair waving and straightening. In 22 cases we found an inflammatory perivascular and perifollicular infiltrate, massive plugging of the ostia, disappearance of robust hair follicles and diminution in total number of hair follicles and sometimes fibrosis are not necessarily diagnostic of alopecia areata but seem to be very definitely characteristic.Treatment for hair regrowth in alopecia areata is of little avail. snip....

FASEB J. 1992;6:911

Interleukin 1 protects hair follicles from ARA-C-induced hair loss in vivo and in vitro.
Jimenez JJ,

ImuVert, a biologic response modifier, and interleukin 1 (IL 1) have been shown to protect the young rat from hair loss induced by ARA-C. In the present study the inhibition by ARA-C of DNA synthesis in hair follicles and the protective effect of ImuVert and IL 1 were investigated in vivo and in vitro. Both ImuVert and IL 1 were equally effective in protecting rats from ARA-C-induced hair loss. DNA synthesis in HFs isolated from ARA-C-treated animals was 10-20% of untreated controls. Follicles isolated from animals given either ImuVert or IL 1 before ARA-C exhibited normal DNA synthesis. In vitro, the incubation of normal rat HF with ARA-C resulted in 80% inhibition of thymidine uptake. .....

edited for hair regrowth and hair loss blog

J Am Acad Dermatol. 2010 Feb;62:177

Alopecia areata update: part I. Clinical picture, histopathology, and pathogenesis.
Alkhalifah A, et al

Alopecia areata (AA) is an autoimmune disease that presents as nonscarring hair loss, although the exact pathogenesis of the disease remains to be clarified. Disease prevalence rates from 0.1% to 0.2% have been estimated for the United States. AA can affect any hair-bearing area. It often presents as well demarcated patches of nonscarring hair loss on skin of overtly normal appearance. Recently, newer clinical variants have been described. The presence of AA is associated with a higher frequency of other autoimmune diseases. Controversially, there may also be increased psychiatric morbidity in patients with AA. Although some AA features are known poor prognostic signs, the course of the disease is unpredictable and the response to treatment can be variable. Part one of this two-part series on AA describes the clinical presentation and the associated histopathologic picture. It also proposes a hypothesis for AA development based on the most recent knowledge of disease pathogenesis. LEARNING OBJECTIVES: After completing this learning activity, participants should be familiar with the most recent advances in AA pathogenesis, recognize the rare and recently described variants of AA, and be able to distinguish between different histopathologic stages of AA..
hair regrowth

J Dermatol Sci. 2010;58:43. Epub 2010.

Laminin-511, inducer of hair regrowth, is down-regulated and its suppressor in hair growth, laminin-332 up-regulated in chemotherapy-induced hair loss.
Imanishi H, et al

Chemotherapy-induced alopecia (CIA) or hair loss has a devastating cosmetic effect, especially in the young. Recent data indicate that two major basement membrane components (laminin-332 and -511) of the skin have opposing effects on hair growth. OBJECTIVE: In this study, we examined the role and localization of laminin-332 and -511 in CIA. METHODS: We examined the expression of laminin-332 and -511 during the dystrophic catagen form of CIA induced in C57BL/6 mice by cyclophosphamide (CYP) treatment. RESULTS: Our data indicate that both laminin-332 and its receptor alpha 6 beta 4 integrin are up-regulated (both quantitatively and spatially) after mid to late dystrophic catagen around the outer root sheath (ORS) in the lower third of hair follicles in CIA. This up-regulation also occurs at the transcriptional level. In contrast, laminin-511 is down-regulated after mid dystrophic catagen at the protein level, with transcriptional inactivation of laminin-511 occurring transiently at the early dystrophic catagen stage in both epidermal and ORS keratinocytes. Laminin-511 expression correlates with expression of alpha 3 integrin in CIA and we also demonstrate that laminin-511 can up-regulate the activity of the alpha 3 integrin promoter in cultured keratinocytes. Injection of a laminin-511 rich protein extract, but not recombinant laminin-332, in the back skin of mice delays hair loss in CYP-induced CIA. CONCLUSIONS: We propose that abrupt hair loss in CIA is, at least in part, caused by down-regulation of laminin-511 and up-regulation of laminin-332 at the transcriptional and translational levels.

Cell Stress Chaperones. 2008;13:8

Chemotherapy-induced hair loss.
Jimenez JJ,.et al

edited

Hair loss is experienced by thousands of cancer patients every year. Substantial-to-severe hairloss is induced by anthracyclines, taxanes, alkylating compounds (e.g., cyclophosphamide), and the topisomerase inhibitor etoposide, agents that are widely used in the treatment of leukemias and breast, lung, ovarian, and bladder cancers. Currently, no treatment appears to be generally effective in reliably preventing this secondary effect of chemotherapy. We observed in experiments using different rodent models that localized administration of heat or injection of geldanamycin or 17-(allylamino)-17-demethoxygeldanamycin induced a stress protein response in hair follicles and effectively prevented hair loss from adriamycin, cyclophosphamide, taxol, and etoposide. Model tumor therapy experiments support the presumption that such localized hair-loss preventing treatment does not negatively affect chemotherapy efficacy.

Cell Stress Chaperones. 2008;13:8

Prevention of chemotherapy-induced hair loss in rodent models.
Jimenez JJ,.et al

edited for hair loss blog

Alopecia (hair loss) is experienced by thousands of cancer patients every year. Substantial-to-severe hair loss is induced by anthracyclines (e.g., adriamycin), taxanes (e.g., taxol), alkylating compounds (e.g., cyclophosphamide), and the topisomerase inhibitor etoposide, agents that are widely used in the treatment of leukemias and breast, lung, ovarian, and bladder cancers. Currently, no treatment appears to be generally effective in reliably preventing this secondary effect of chemotherapy. We observed in experiments using different rodent models that localized administration of heat or subcutaneous/intradermal injection of geldanamycin or 17-(allylamino)-17-demethoxygeldanamycin induced a stress protein response in hair follicles and effectively prevented alopecia from adriamycin, cyclophosphamide, taxol, and etoposide. Model tumor therapy experiments support the presumption that such localized hair-saving treatment does not negatively affect chemotherapy efficacy.

Hair regrowth at the Proctor Clinic

edited for hair loss treatment blog

Cancer Epidemiol. 2009;33:293.

The effect of active hexose correlated compound in modulating cytosine arabinoside-induced hair loss, and 6-mercaptopurine- and methotrexate-induced liver injury in rodents.
Sun B,et al
BACKGROUND: Active hexose correlated compound (AHCC)... was used to assess amelioration of alopecia (hair loss) caused by cytosine arabinoside (Ara-C).. Follicular integrity and hair growth was assessed in male and female SD neonatal rats (8 days old) treated with a single dose of Ara-C (30 mg/kg/day, i.p.) and AHCC (500 mg/kg/day, p.o.) for 7 consecutive days. The side effects of a single oral dose of 6-MP plus MTX and their amelioration by treatment with AHCC (1000 mg/kg body weight) for 28 days were assessed in male ddY mice. RESULTS: Of the Ara-C treated rats 71.4% showed severe alopecia and 28.6% showed moderate hair loss. However, the AHCC -treated Ara-C group was significantly protected from alopecia. Ara-treated rats had profound loss of hair follicles but the Ara-C plus AHCC-treated group had mild losses of follicles.snip..

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...