Hair loss and Regrowth

Hair Loss Treatment at the Proctor Clinic

J Am Acad Dermatol. 1980 Dec;3(6):623-6.

Analysis of hair from alopecia congenita.
Baden HP, Kubilus J.

Edited for hair loss blog use

Two patients with alopecia congenita had short vellus hairs of the scalp but some apparently normal-sized hairs in other areas. Both fibrous and matrix proteins were detected in the scalp hairs by polyacrylamide gel electrophoresis (PAGE), and x-ray diffraction analysis revealed a normal alpha pattern. Amino acid analysis showed a decreased cystine content suggesting a quantitative or qualitative change in the matrix component. Scanning electron microscopic examination revealed pits and bulges in the cuticle cells which may be related to wearing a wig. The data suggest a defect in the development of the follicle rather than an abnormality in a component of the hair.

Skin Pharmacol. 1993;6:170
Potassium channel openers and whole hair follicle cultures.
Harmon CS, Lutz D, Ducote J.

(edited for hair loss blog)

snip.. the extent of stimulation of epidermal keratinocyte DNA synthesis by minoxidil increased as the rate of DNA synthesis in control cultures declined. Minoxidil stimulation of DNA synthesis in cultures required prolonged exposure to the hair growth agent. Pinacidil and diazoxide also stimulated DNA synthesis in mouse epidermal keratinocyte cultures. In addition, minoxidil, pinacidil, diazoxide, and cromakalim stimulated DNA synthesis in whole-organ cultures of mouse hair follicles. That is, K-channel openers retard the loss of proliferative activity of differentiating keratinocytes. This supports the hypothesis that these agents stimulate hair regrowth through a direct effect on hair follicles.

The familial occurrence of universal congenital hair loss conjoined with nonprogressive central nervous system abnormalities in this and other kindreds defines a nosologic group of neurocutaneous disorders in which congenital hair loss is the solitary cutaneous manifestation.

Ann Dermatol Venereol. 1986;113(9):767

Stereology of the dermo-epithelial interface of the matrix-papilla unit of the hair bulb. Computerized processing of tridimensional images

Van Neste D, et al

Images of the spatial relations of the matrix-papilla unit of the human hair bulb are shown. Hair bulbs were reconstructed in 3 dimensions by a computer graphics system from measurements made on horizontal sections parallel to the scalp surface. …snip… As an end result, the hair bulbs appear as wire frame structures in which the boundaries between consecutive segments have been connected to improve rendering of the dermal papilla interacting with the overlying epithelial hair matrix. This computerized method has been used to evaluate dermal-epithelial stereology of the interacting dermal papilla and epithelial hair matrix in hair bulbs. ..snip.. This method could be useful to demonstrate disturbed dermal-epithelial interactions in other types of alopecia and to evaluate potential biological effects of drugs used in the treatment of hair loss.

Am J Dermatopathol.1984;6:553

The recognition of early stages of catagen.

Weedon D, Strutton G.

Several criteria for recognition of follicles in catagen the early stage of the hair-loss phase ) have been advanced, namely, loss of metachromasia in the hair papilla, subsidence of mitotic activity there, retraction of the lower portion of the follicle, and thickening and corrugation of the fibrous root sheath. The presence of scattered apoptotic cells in the outer root sheath is an additional marker of early catagen.

edited

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Rapidly debilitating disease with generalized lymphadenopathy, skin involvement and interstitial pulmonary infiltration

Haferkamp O, et al
Generalized but well-circumscribed lymphadenopathy and rash-like skin changes were observed in three men, aged 58 to 75 years. There was a reticular appearance in the chest X-ray. Dyspnoea, weakness, marked weight loss, changing but marked lymphopenia, markedly increased blood-sedimentation rate, and an always negative Tine test were present in all three. Despite antibiotics, cytostatic drugs and prednisolone the disease quickly ended fatally with high fever, general debilitation and pneumonia. …snip… Spleen, lung tissue and lymphatics, the skin in the area of the small vessels, hair follicles and sweat glands contained lymphocytes, plasma cells and eosinophilic leucocytes. snip..There was RBC phagocytosis in the macrophages of bone marrow and in Kupffer cells of all three cases.

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Am J Dermatopathol. 1991;13(3):248
Cell degeneration in alopecia areata. An ultrastructural study.

Tobin DJ, et al

The morphology and prevalence of different forms of cell degeneration in hair follicles in acute alopecia areata were investigated. In addition to apoptosis and necrosis, a third morphological pattern of cell degeneration, dark-cell transformation, was evident. Fifteen patients with hair loss due to untreated acute alopecia areata and three normal adults without hair loss were studied. Electron microscopy revealed that although apoptosis of outer root sheath keratinocytes produces normal hair follicle involution (catagen), increased levels of apoptosis, necrosis, and dark-cell formation appear to be related to the pathology of alopecia areata. Although cell degeneration was generally restricted to keratinocytes of the lower follicle, melanocytes, Langerhans’ and dermal papilla cells were also affected. Keratinocytic degeneration may affect layers of matrix cells in alopecia areata, unlike the apoptosis of scattered outer root sheath cells in normal catagen. The extent of cell death suggests a pathological rather than a physiological event in alopecia areata.

Acta Derm Venereol. 1994 Jan;74(1):28-32.

Cytokeratin expression in alopecia areata hair follicles.

Van Baar HM, et al

Alopecia areata is a human hair-loss disease of unknown etiology. Immunological mechanisms, alterations in the extracellular matrix and follicular growth abnormalities have been suggested as a possible cause. Here we compare the expression of cytokeratins in normal hair follicles to that of alopecia areata using immunohistology with monoclonal antibodies. A number of cytokeratins were specifically expressed in defined anatomical parts of the follicle; however, no gross qualitative or quantitative differences were found between normal and diseased scalp. Interestingly, the expression of cytokeratin 16, which is modulated by conditions that affect the rate of keratinocyte proliferation, was found to be unchanged in the outer root sheet of alopecia areata follicles. This is in contrast with earlier observations of a decrease in the expression of the proliferation-associated, Ki-67 nuclear antigen.

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Z Hautkr. 1985 Apr 1;60(7):576-8.Links

Female pattern androgenic alopecia in the male

Kuhlwein A.

The schematic description of male pattern hair loss neglects the fact that special forms of baldness in males have a rather female pattern aspect. Here we report on a man with female pattern alopecia.

PMID: 3923725

Am J Dermatopathol. 1991 Jun;13(3):248-56.

Cell degeneration in alopecia areata. An ultrastructural study.
Tobin DJ, et al.

The morphology and prevalence of different forms of cell degeneration in hair follicles in acute alopecia areata were investigated. In addition to apoptosis and necrosis, a third morphological pattern of cell degeneration, dark-cell transformation, was evident. Fifteen patients with untreated hair loss due to alopecia areata and three normal adults without hair loss were studied. Electron microscopy revealed that although apoptosis of outer root sheath keratinocytes produces normal hair follicle involution (catagen), increased levels of apoptosis, necrosis, and dark-cell formation appear to be related to the pathology of alopecia areata. Although cell degeneration was generally restricted to keratinocytes of the lower follicle, melanocytes, Langerhans’ and dermal papilla cells were also affected. Keratinocytic degeneration may affect layers of matrix cells in alopecia areata, unlike the apoptosis of scattered outer root sheath cells in normal catagen. The extent of cell death suggests a pathological rather than a physiological event in alopecia areata.

Australas J Dermatol. 1995 May;36(2):51-5; quiz 56-7.

Female pattern hair loss
Callan AW, Montalto J.

Pattern hair loss is an androgen dependent disorder occurring in genetically susceptible individuals. The pattern of hair loss in women differs from that of classical male pattern hair loss, being more diffuse and with retention of the frontal hair line in most cases. snip.. Although research has shown subtle alterations in the androgen status of women with androgenetic alopecia, most patients presenting with this disorder are normal endocrinologically. Anti-androgen therapy will result in some improvement in up to 50% of patients after 6 to 12 months of therapy, but in practice will usually only decrease the rate of hair loss and not result in new hair growth.

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Plast Reconstr Surg. 1978 Sep;62(3):447-51.

Successful replantation of totally avulsed scalp, with profuse regrowth of hair: case report.

Spira M, Daniel RK, Agris J.

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Arch Dermatol. 1982 Aug;118(8):542-5.

Dinitrochlorobenzene treatment of alopecia areata.

de Prost Y, Paquez F, Touraine R.

Forty-two patients with alopecia areata were treated with local applications of dinitrochlorobenzene (DNCB); We used DNCB in two forms, an acetone solution applied weekly or a cream used every day, employing a wide range of DNCB concentrations. The concentration used was varied at the time of each application to produce a contact dermatitis. Seven patients experienced complete and lasting hair regrowth, 17 had poor results, and in 18 patients the treatment was a failure. Acquired tolerance to DNCB was observed in six patients; in five it was abolished by the administration of cimetidine. Certain factors such as the delay in appearance and the intensity of the sensitization reaction influence the hair regrowth. Poor prognostic criteria for treatment effect included a history of previous systemic corticosteroid therapy, atopy, and the presence of alopecia areata in close relatives.

Ann Dermatol Venereol. 1997;124(1):7-11.

Androgenetic alopecia

Esteve E, Aubin F.
Service de Dermatologie, Centre Hospitalier Régional, Orléans.

PMID: 9686040
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