scientists believe that inflammation may be an important factor in the
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
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
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
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
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