No photomicrograph published by Sperling and his coworkers as illustrative of the follicular degeneration syndrome shows the inner sheath missing at the stem. In the absence of a demonstration of that finding, the assertion that the inner sheath desquamates prematurely is unverified. All of the photomicrographs alleged by Sperling to show "transverse sections of normal hair follicles sectioned at the level of the isthmus" are actually follicles sectioned at the level of the stem; each sports a fully formed inner sheath, in contrast with the situation at the isthmus where, by definition, there is no inner sheath. Furthermore, in figure 4 of an article by Sperling et al. published in 1994 in the Archives of Dermatology, an arrow points to a structure in follicle C that surely is an intact inner sheath, yet the legend states that the "IRS [inner root sheath] of follicle C has desquamated far below the isthmus;" figure 6 is said to show follicles that "demonstrate premature desquamation of their inner sheaths," but the inner sheaths are actually completely cohesive; and figure 7 is alleged to illustrate follicles that "are sectioned at a level just below the isthmus," but the section really is through the upper segment of both follicles and possibly even through infundibula, as may be inferred from the epithelium being epidermoid. Last, in routine sections, some corneocytes of the inner sheath appear to be separated from one another, a finding that is mere artifact produced by the blade of a microtome. It seems to have been this artifact of processing that Sperling misconstrued as the cause of the follicular degeneration syndrome.

In short, premature desquamation of the inner sheath is not a feature of follicular degeneration syndrome—or of any condition for that matter—and that finding alone, even if it were demonstrable, would not constitute a syndrome.

In a recent editorial, Sperling and coworkers proposed the term central centrifugal scarring alopecia for what, according to them, encompasses four patterns of scarring alopecia: 1) follicular degeneration syndrome, 2) pseudopelade, 3) folliculitis decalvans, and 4) tufted folliculitis. These patterns of alopecia are grouped under the same heading because, in the judgment of the authors, they have these features in common: 1) hair loss centered on the crown or vertex of the scalp, 2) chronic and progressive disease with eventual "burnout," 3) roughly symmetrical expansion with the disease being most active at the periphery of lesions, and 4) both clinical and histopathologic evidence of inflammation in the zone of activity at the periphery. The authors exclude traction alopecia (which they consider to be an entity different from follicular degeneration syndrome) from this group of scarring alopecia because they believe that it behaves in a biphasic pattern, with non-scarring hair loss early in the course of the disease and permanent hair loss at a later stage. This statement is not in consonance with their own definition, progressive disease with eventual burnout being considered by them to be one of the essential features of central centrifugal scarring alopecia. Moreover, traction alopecia may show all four features said to be characteristic of central centrifugal scarring alopecia.

Although the "follicular degeneration syndrome" does not exist as a specific condition that results from premature "degeneration" or "disintegration" of the inner sheath, patients who are described in articles devoted to that subject clearly exhibit a distinctive type of alopecia. We have been fortunate to study, clinically and histopathologically, more than 200 patients with what has been called hot comb alopecia or follicular degeneration syndrome.* It became apparent to us that the cause of hot comb alopecia/follicular degeneration syndrome is traction—and traction alone. The patients, virtually all of whom were African-American women, either used rollers under tension in their hair or plaited their hair. Many admitted that hot combs had been applied to their hair by attentive mothers when they were still young girls. These procedures affected numerous foci on the scalp, from the frontotemporal to the nape, in repeatable patterns. The alopecia began in those particular foci, but in time—that is, over many years—extended slowly from those sites to involve the crown in confluence and at other times nearly the entire scalp. The hairs at the periphery of the scalp are spared (Figures 1, 2, 3, 4, 5 and 6).