Alopecia areata vs. Trichotillomania

Differential Diagnosis

Alopecia areata Trichotillomania 1. Sparse infiltrate sometimes of lymphocytes around venules of the superficial and deep plexuses 1. Practically no infiltrate of inflammatory cells 2. In early lesions, infiltrate of lymphocytes in the vicinity immediate of follicular papillae, in fibrous sheaths that surround follicular bulbs, and in fibrous tracks that form normally in catagen 2. Little or no infiltrate of inflammatory cells around the base of hair follicles 3. Increased number of mast cells and melanophages in association with dilated capillaries in arrangement linear in fibrous tracks and at sites where follicular papillae once resided 3. No increase in number of mast cells, melanophages, or blood vessels in follicular papillae or in fibrous tracks 4. More follicles in catagen and telogen than in anagen 4. More follicles usually in anagen than in catagen or telogen 5. Few follicles in anagen 5. At least several follicles in anagen 6. No everted outer sheath of follicles 6. Everted outer sheath of follicles occasionally 7. No trichomalacia 7. Trichomalacia (pleated hair shafts that contain clumps of melanin) in infundibula invariable, but not necessarily in every section of a biopsy specimen 8. In longstanding lesions, at sites of follicular papillae in the deep reticular dermis, whorls of wiry collagen bundles that house degenerated glassy membranes and melanophages 8. No whorls of wiry bundles of collagen 9. No imposition of lichen complex chronicus or association of erosion and crusts 9. Lichen simplex chronicus, in the form of compact orthokeratosis, imposed at times; erosions and crusts, are findings uncommonly

Discussion

Alopecia areata and trichotillomania have several attributes histopathologic in common, namely, some follicles in catagen and often in telogen, long fibrous tracks behind shortened follicles and, in sections from some specimens, and hardly any perivascular infiltrates of inflammatory cells in the dermis. Granulomatous inflammation is a rare denominator in common of alopecia areata and trichotillomania, occurring as it does at the base of every involved follicle in exceptional examples of the former and in a locus of foreign-body reaction to a hair extruded from a follicle in the latter.

Alopecia areata is an inflammatory disease in which the connective tissue at the base of follicles is affected mostly, whereas trichotillomania is a factitious condition that results from persistent twisting, back and forth, of hairs. Plucking and pulling of hairs also are common practices in patients with trichotillomania, but those tugs only send follicles in anagen into catagen; they do not produce signs morphologic of trichomalacia.

Clinically, alopecia areata consists of sharply-circumscribed, smooth, round to oval patches of skin devoid of hairs. It is present especially on the scalp and face but can occur anywhere on the integument. When the process involves the entire scalp, rather than discrete patches of it, the condition is termed alopecia totalis, and when the malady affects the entire hair-bearing skin, it is called alopecia universalis. The more widespread the condition and the longer the duration of it, the worse the prognosis for return of hair. Vitiligo and pitting of nails may be concurrent with alopecia areata and especially the more extensive variants of it.

Histopathologically, fibrous, rather than fibrotic, tracks form in the wake of follicles in catagen in alopecia areata. Those tracks resemble the ones that come into being normally in catagen, but they often house a sprinkling of lymphocytes. In some cases of longstanding alopecia areata and variants of it, whorls of wiry bundles of collagen that contain remnants of thickened, degenerated "glassy" membranes, as well as melanophages, appear in the deep reticular dermis. Those whorls are a sign that units composed of follicular matrix cells and follicular papillae no longer are extant and, as a consequence of the inhospitable collagenous environment, hairs cannot grow at those sites again ever. In the absence of such changes, regrowth of hair is possible in alopecia areata, but, on grounds morphologic alone, no judgment can be made with assurance about that.

Trichotillomania consists clinically of bizarre shaped, partially alopecic, "rat-eaten" patches of hairs that have been broken off at different distances from the surface of the scalp. The patches have a ragged appearance as a result of persistent manipulation, i.e., twisting of the hairs to and fro until they become fractured. If a patient can forego twisting of hairs, the pelage is likely to return to normal.

Trichomalacia, a cardinal histopathologic sign of trichotillomania, results from persistent twisting, back and forth, of hair with consequent fraying and breakage of it, that resulting in dispersal of melanin in variously sized clumps in bits of broken hair shafts. The number of follicles in catagen or telogen in trichotillomania does not depend on how soon after hairs are broken off the biopsy specimen is obtained, but rather on how soon after hairs were pulled out (i.e., the nearer to the time that hairs are plucked, the greater the number of follicles in catagen); in some specimens there are no follicles in catagen or telogen because no hairs were plucked, only twisted. Catagen follicles are identified histologically by the presence of necrotic keratocytes in the outer sheath and by a markedly thickened corrugated glassy membrane that envelops the lower portion of that withered sheath.

The foregoing statements about the interpretation of characteristics histopathologic of alopecia areata and trichotillomania depend on various factors, among them duration of the disease, the site of biopsy, and the breadth and depth of the biopsy specimen. All too often, the biopsy fails to extract the entire dermis, let alone subcutaneous fat, and, in that circumstance, unless trichomalacia is spotted, a histopathologist may not be able to distinguish alopecia areata from trichomalacia.

A not uncommon accompaniment of trichotillomania is one or more signs of lichen simplex chronicus, particularly of the hyperkeratotic variant of that factitious condition. Unlike conventional lichen simplex chronicus, which consequent to prolonged and persistent rubbing of the skin on the neck, trunk, and extremities, and typified not only by uneven psoriasiform acanthosis but by coarse bundles of collagen arranged in vertical streaks in the thickened papillary dermis, the hyperkeratotic variant of lichen simplex chronicus on a scalp (and elsewhere, such as the vulva, scrotum, and perianal region) is characterized by marked compact orthokeratosis and hypergranulosis that resembles the normal stratum corneum on palms and soles. Changes of hyperkeratotic lichen simplex chronicus appear sometimes on the scalp of patients with trichotillomania, in addition to the stereotypical features of trichotillomania already described, a result of the same anxiety that prompts twisting and plucking hairs. Just as the hairs are twisted and the scalp is rubbed forcefully for long as a consequence of unresolved emotional conflicts, so, too, may the scalp be exposed to "neurotic excoriations" which result in production of erosions, ulcerations, and crusts.

Ref:

Differential Diagnosis In Dermatopathology I, Ii, Iii, Iv.chm