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Secondary
scarring alopecias from physical and chemical causes
Cicatricial alopecia is often an outcome of chemical and physical
injuries to the skin. Skin injuries, if they are severe enough,
prompt necrosis (the sum of the morphological changes indicative
of cell death and caused by the progressive degradative action of
enzymes, it may affect groups of cells or part of a structure or
an organ). In its most acute form, necrosis is accompanied by severe
inflammation and crusting of the affected skin. As the problem gets
worse, diffuse fibrosis (excessive growth of fibrous connective
tissue, especially in response to any injury) reaching varying depths
takes place and the scarring alopecia finds an expression as a flesh-colored
or atrophic (a wasted away body part, organ or tissue) patch or
plaque.
Post-labor and post-operative hair loss can sometimes be attributed
to the presence of prolonged and unrelieved pressure on hair bearing
regions of skin. Pressure necrosis of the scalp (in the case of
infants) is the result of excessive pressure the infant’s
head experiences during protracted labor. Similarly, postoperative
alopecia is the direct consequence of continual pressure experienced
by patients during surgery. If the patient’s head rests on
a hard surface, as it often does in surgical operating rooms, for
a prolonged period of time, the blood supply may be restricted.
If the surgery takes many hours and the patient’s head is
not moved during this time, the lack of blood supply can lead to
tissue damage. This kind of alopecia generally affects the occiput
(back part of the head and skull) which is usually carrying the
weight of the head when a patient is on the operating table. The
initial stages of post-operative hair loss are marked by local tenderness,
erythema, swelling, exudation, and crusting. Hair loss starts between
the first and the fourth week after the operation.
Scarring alopecia induced by physical or chemical means is often
an upshot of ischemia (a lack of blood supply in an organ or tissue).
Occasionally certain drugs used during surgery or disease treatment
can promote vasoconstriction (the diminution of the calibre of
vessels, especially constriction of arterioles leading to decreased
blood flow to a part) and further exacerbate the problem. Repeated
pulling and traction, such as that from tight braids, extensions,
foam rollers and generally pulling on the hair, etc., can eventually
lead to cicatricial alopecia.
Secondary
scarring alopecia - radiation alopecia
Exposure to radiation also prompts hair loss. The degree and permanence
of alopecia is dependent on a multiplicity of factors such as the
type of radiation, dose fraction, frequency of treatment, total
dosage, etc. Permanent alopecia conditions resulting from radiation
shows loss of all dermal adnexal structures (including the follicular
unit). Diffuse hyalinization of the dermal collagen, along with
ectatic (a dilatation of a hollow organ or of a canal) vessels,
atypical fibroblasts, and radiation elastosis also accompany the
above abnormality. Radiation induced alopecia severe enough to lead
to permanent scarring alopecia is quite rare today as most X-ray
units in hospitals are well aware of the issues surrounding radiation.
However, individuals receiving repeated radiation treatments, as
some cancer patients do, may find permanent hair loss is a problem.
Secondary
scarring alopecia from drug reactions
Drug induced alopecias or hair loss resulting from drug reactions
can be both permanent and temporary in nature. In fact, most of
the drugs that affect hair growth bring about a telogen effluvium
(increased transient shedding of normal club hairs by premature
development of telogen in anagen follicles resulting from various
kinds of stress) rather than permanent hair loss and normal hair
growth is usually restored on discontinuation of these drugs.
However, drugs that stimulate papulosquamous (scaly, elevated skin),
lichenoid or bullous dermatosis of the scalp can promote a permanent
alopecia. Permanent alopecia has also been reported after bone marrow
transplants. This permanence of the alopecia condition seems to
be a consequence of the graft recipient’s response to the
bone marrow grafting involved, though the mechanism of scarring
alopecia development is not clear. Bone marrow transplants utilizing
busulphan in the drug conditioning regimen are particularly associated
with permanent alopecia.
Cancer patients undergoing chemotherapy receive a cocktail of drugs
that often have the common property of inhibiting cell proliferation.
If the drug treatment is intense enough, it is possible that the
drug regimen may bring about a permanent alopecia. The reason for
this is not clear, but it may be that the drugs, when given in a
strong enough dosage regimen, destroy the hair follicle stem cells
or damage the dermal papilla cells. Loss of either would stop hair
follicles from growing.
Secondary
scarring alopecias from autoimmune disorders
Autoimmune disorders (disorders that result from the production
of antibodies and cause enough damage to normal body components)
often instigate unique reactions, which run riot with the normal
telogen-anagen cycle and ultimately cause cicatricial alopecia.
Secondary scarring alopecias resulting from autoimmune disorders
are – (i) those arising from host disease response to grafting
(as in bone marrow transplants – though technically this is
not a true autoimmune reaction), (ii) Scleroderma (En coup de sabre) & (iii)
Lichen sclerosis et atrophicus.
Scleroderma is a hardening and thickening of the skin due to abnormal
fibrous tissue growth. It has been classified into two distinct
diseases – localized to the skin and systemic affecting the
entire body system. Clinically the skin localized type is represented
as deep, linear plaques or as widespread bullae. (Linear scleroderma
of the fronto-parietal scalp is termed en coup de sabre). Lichen
sclerosis et atrophicus also presents generalized bullae.
Standard histologic analyses of scleroderma reveal expanded collagen
(an essential component of wound healing) bundles, reduced follicular
units and adnexae, hyalinized dermal collagen and fibrous tracts.
Studies also prove the presence of lymphocytes and plasma cells
around the follicles and its adnexal structures. Elastin stains
showing scattered elastin (between hyperplastic, hyalinized collagen)
bear proof of the existence of eosinophilic elastic fibers; condensed
elastin is observed within and on the borders of the hyalinized
fibrous tracts.
Administering intralesional corticosteroids in acute stages of
scleroderma has borne excellent results. Long-term intake of antibiotics
has also proved an effective treatment for localized scleroderma.
The role of antimalarial agents in localized scleroderma is not
yet fully established though some doctors use them. Topical medication
such as calcipotriol has shown satisfactory results. The evolution
of hair transplantation techniques has added a new dimension to
the treatment of scarring alopecias.
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