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Beyond goosebumps: does the arrector pili muscle have a role in hair loss?

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Beyond goosebumps: does the arrector pili muscle have a role in hair loss? Empty Beyond goosebumps: does the arrector pili muscle have a role in hair loss?

Post  CausticSymmetry Mon Sep 15, 2014 3:24 am

Int J Trichology. 2014 Jul;6(3):88-94. doi: 10.4103/0974-7753.139077.
Beyond goosebumps: does the arrector pili muscle have a role in hair loss?
Torkamani N, Rufaut NW, Jones L, Sinclair RD.

The arrector pili muscle (APM) consists of a small band of smooth muscle that connects the hair follicle to the connective tissue of the basement membrane. The APM mediates thermoregulation by contracting to increase air-trapping, but was thought to be vestigial in humans. The APM attaches proximally to the hair follicle at the bulge, a known stem cell niche. Recent studies have been directed toward this muscle's possible role in maintaining the follicular integrity and stability. This review summarizes APM anatomy and physiology and then discusses the relationship between the follicular unit and the APM. The potential role of the APM in hair loss disorders is also described, and a model explaining APM changes in hair loss is proposed.

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Beyond goosebumps: does the arrector pili muscle have a role in hair loss? Empty Re: Beyond goosebumps: does the arrector pili muscle have a role in hair loss?

Post  CausticSymmetry Mon Sep 15, 2014 3:26 am

An earlier study:

Br J Dermatol. 2014 Jun;170(6):1291-8. doi: 10.1111/bjd.12921.
Destruction of the arrector pili muscle and fat infiltration in androgenic alopecia.
Torkamani N1, Rufaut NW, Jones L, Sinclair R.
BACKGROUND:
Androgenic alopecia (AGA) is the most common hair loss condition in men and women. Hair loss is caused by follicle miniaturization, which is largely irreversible beyond a certain degree of follicular regression. In contrast, hair loss in telogen effluvium (TE) is readily reversible. The arrector pili muscle (APM) connects the follicle to the surrounding skin.
OBJECTIVES:
To compare histopathological features of the APM in AGA and TE.
METHODS:
Archival blocks of 4-mm scalp punch biopsies from eight patients with AGA and five with TE were obtained. New 4-mm biopsies from five normal cases were used as controls. Serial 7-μm sections were stained with a modified Masson's trichrome stain. 'Reconstruct' software was used to construct and evaluate three-dimensional images of the follicle and APM.
RESULTS:
The APM degenerated and was replaced by adipose tissue in all AGA specimens. Remnants of the APM remained attached to the hair follicle. There was no fat in the normal skin specimens. Fat was seen in two of five TE specimens but could be attributed to these patients also showing evidence of AGA. Quantitative analysis showed that muscle volume decreased and fat volume increased significantly (P < 0ยท05) in AGA compared with controls.
CONCLUSIONS:
APM degeneration and replacement with fat in AGA has not previously been described. The underlying mechanism remains to be determined. However, we speculate that this phenomenon might be related to depletion of stem or progenitor cells from the follicle mesenchyme, explaining why AGA is treatment resistant.

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