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Some scientists believe that inflammation may be an important factor in the etiology or the origin of pattern baldness, or also known as “male pattern baldness”.

At an early study, there was reference to an inflammatory infiltrate of mononuclear cells and lymphocytes in about 50 percent of the scalp samples observed. Another study conducted on 412 patients (193 men and 219 women) also showed, in at least 37 percent of pattern baldness cases, the presence of a significant degree of inflammation and fibrosis. The term ‘micro inflammation’ was proposed by Mahe and colleagues because the process of inflammation in pattern baldness adopts a slow, subtle, painless and lethargic course, in contrast to the inflammatory and destructive process that has been seen in the classical inflammatory scarring alopecias.

Whiting has documented that the horizontal sections of scalp biopsies indicated that the perifollicular fibrosis is generally mild. The layer being generally mild -- its concentric layers of collagen, the fibrous protein that makes up connective tissues, are loose, a characteristic that distinguishes it from cicatricial alopecia.

Jaworsky et al. in 1992 pointed out in regions of actively progressing alopecia to an inflammatory infiltrate of activated T cells and macrophages in the upper third of the hair follicles. The area pointed out was associated with an enlargement of the follicular dermal-sheath composed of collagen bundles (perifollicular fibrosis). The location clearly differentiates pattern baldness from alopecia areata, As androgenic alopecia has its infiltrate near the infrainfundibulum.

The significance of these findings remains controversial.

Inflammatory phenomena

An important fact to be established is how the inflammatory reaction pattern in pattern baldness is generated around the individual hair follicle. Inflammation is regarded as a multi-step process assigned to a central major mediator or pathway. Mahe et al believe that the presence of a perifollicular infiltrate in the upper follicle near the infundibulum points to the fact that the primary causal event for the triggering of inflammation might occur near the infundibulum.

Some researchers speculate, on the basis of this localization and the microbial colonization of the follicular infundibulum, that microbial toxins or antigens could be involved in the generation of the inflammatory response. The production of porphyrins has also been considered to be a possible cofactor of this initial pro-inflammatory stress.

Alternatively, keratinocytes themselves are considered as they respond to chemical stress from irritants, pollutants, and UV irradiation. They produce radical oxygen species and nitric oxide, release intracellularly stored IL-1a. These are pro-inflammatory. The mentioned cytokine by itself has been shown to inhibit the growth of isolated hair follicles in culture. Skin keratinocytes could, theoretically speaking, induce white blood cell or T-Cell proliferation as a response to bacterial antigens. These antigens, after they have been “tagged”, are then selectively destroyed by infiltrating macrophages – the cells that act as scavengers within the body. Langerhans cells, dendritic cells in the skin, then pick up an antigen and transport it to the lymph nodes or commonly called as natural killer cells. Lymph nodes are called natural killer cells because they are immune system cells that destroy foreign bodies or abnormal cells that are marked with antibodies. Their goal is to dispose the marked antigen.

The above-mentioned casual agents as they dispose of the antigen may also lead to the sustained inflammation of the hair follicle. This is due to tissue remodeling where collagenases play an active role. Collagenases are suspected to contribute to the tissue changes and the so-called “perifollicular fibrosis” because they “prepare” tissue matrix and basal membranes where the various enzymes catalyze the hydrosis of collagen and gelatin for macrophages and T-cell adhesion.

Formation of fibrous tissue or fibroplasia of the dermal sheath, which surrounds the hair follicle, is now suspected to be a common terminal process resulting in the miniaturization. Involution of the pilosebaceous unit in this form of baldness and sustained microscopic follicular inflammation with connective tissue remodeling, eventually resulting in permanent hair loss, is considered a possible cofactor in the complex etiology of pattern baldness.

Relations between inflammation and steroidogenesis

It has been proven that androgens, in the form of testosterone or its metabolites are the prerequisites for development of common male pattern baldness. According to Mahe, the only apparent link that can be established between androgen metabolism and the complex inflammatory process is sebum production. The sebum production is controlled by androgens. As sebum harbors a large amount of microorganisms, which use lipids as nutrients, it is possible that, at least for some individuals, androgen metabolism, by microorganisms, may pave way to a possibility of the colonization of the sebaceous infundibulum and sebaceous ducts. These involve microorganisms to be a possible agent in the first steps of pilosebaceous unit inflammation.


Mahe and his team were able to deduce that the genetic factors and androgen metabolism are responsible for about 30 percent of tested pattern baldness cases. The factors that lead to fatal damages by the microinflammatory process include androgens, microbial flora, endogenous or exogenous stress, and genetic imbalance.

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