An irreversible alopecia of the scalp occurs in negro women who straighten their hair with hot combs. The disease is common and distinctive, clinically and histopathologically. . . . Hot petrolatum used with the comb causes a chronic inflammation around the upper segment of the hair follicle leading to degeneration of the external root sheath. LoPresti P, Papa CM, Kligman AM. Hot comb alopecia. Arch Dermatol 1968;98:234-38.
We recommend that the condition [“hot comb alopecia”] be called the follicular degeneration syndrome. . . . Historical information is incompatible with the hypothesis that hot comb usage causes the alopecia. Premature desquamation of the inner root sheath serves as a histologic marker for FDS [follicular degeneration syndrome], and may be an important pathogenic factor. Sperling LC, Sau P. The follicular degeneration syndrome in black patients: “hot comb alopecia” revisited and revised. Arch Dermatol 1992;128:68-74.
The “follicular degeneration syndrome,” described by Sperling and Spau in 1992 and elaborated on by Sperling et al. in 1994, is said by them to represent a “clinically and histologically distinct form of scarring alopecia” that was “formerly called hot comb alopecia” by LoPresti, Papa, and Kligman who, in 1968, had given that latter name to irreversible, partial, scarring alopecia of the crown of the scalp of African-American women. Those three authors claimed that the alopecia was distinctive clinically and histopathologically. As the appellation “hot comb alopecia” implies, the loss of hair was thought by them to be a consequence of the effects of heated combs that African-American women employed commonly in the past, and even nowadays, to straighten their hair. The procedure consists of passing a hot comb through hair that already had been stretched and covered with petrolatum. Sections of tissue of biopsy specimens taken from the alopecia that results from the procedure were said by LoPresti and coworkers to be characterized by a “chronic inflammatory reaction around the upper portion of the follicle” that led to “degeneration of the upper segment of the external root sheath” and eventually to destruction of the entire follicle, which was replaced by a band of fibrous tissue. Furthermore, the epidermis was said to become altered and to display thin, elongated rete ridges, thin suprapapillary plates, hypogranulosis, and a normal cornified layer.
LoPresti and coauthors implied that a burn from the hot petrolatum was responsible for the alopecia, but the histopathologic findings in hot comb alopecia, as described by LoPresti et al. and presented in their photomicrographs are not those of scarring secondary to a burn; the fibrosis is not diffuse across at least the upper part of the dermis, altered bundles of collagen are not oriented parallel to the skin surface, and venules are not disposed perpendicular to the surface. Fibrosis in hot comb alopecia was purported to occur only at discrete sites where follicles were affected individually. An alopecia caused by a burn from hot petrolatum should involve all follicles diffusely, not individual ones randomly.
After the seminal presentation of hot-comb alopecia by Lo Presti and collaborators, the histopathologic findings in that particular condition do not seem to have been the subject of any other article in any journal for more than two decades. During that period, the popularity of hot combs for straightening hair began to decline slowly, but steadily, as chemical products for that purpose became available. The condition, nonetheless, continues to be common in black women. In 1992, Sperling and Sau proposed both a new term for hot comb alopecia, namely, follicular degeneration syndrome, and a new hypothesis for it, to wit, degeneration of follicles as the cause. The designation “degeneration” for a follicle is itself perplexing, considering that a follicle is made up entirely of epithelium and in classic pathology only non-epithelial elements undergo degeneration, for example, “fatty,” “mucinous,” and “hyaline” types.
Synonymy of "Follicular Degeneration Syndrome" and "Hot Comb Alopecia"
Hot comb alopecia and follicular degeneration syndrome were both said to have predilection for African-American women (although in 1994, Sperling and coworkers asserted that follicular degeneration syndrome also was common in black men) and to have several features in common: localization to the crown of the scalp; infiltration of lymphocytes followed by fibroplasia around the upper part of follicles; complete destruction eventually of follicles with replacement of them by “dense collagen”; and sparing of muscles of hair erection. But based on what has been written about these conditions by Lo Presti et al. and by Sperling, some clinical and histopathologic differences would seem to exist between hot comb alopecia and follicular degeneration syndrome. Those differences, culled from articles by those authors, are listed in the table that follows (Table 1).
Table 1 Supposed Differences Between “Hot Comb Alopecia” and “Follicular Degeneration Syndrome” (Traction Alopecia Both)
|Hot Comb Alopecia||Follicular Degeneration Syndrome|
|Affects black women only||Affects black women and black men|
|Caused by hot petrolatum||Not related to use of a hot comb or any method of grooming|
|Scalp sore||“Pins-and-needles” sensation in the scalp; itching and/or slight tenderness sometimes|
|No treatment specified||Topical corticosteroids and tetracycline effective|
|Polytrichia common||Polytrichia rare|
|External root sheath degenerates secondary to effects of hot petrolatum||External root sheath not affected|
|Inner root sheath not involved by the primary process||Premature desquamation of the inner sheath responsible for the alopecia|
|Epidermal changes are usually present, i.e., thin suprapapillary plates and inconspicuous granular layer||Epidermal changes not prominent|
|Increased number of fibrocytes around the upper part of a follicle, but no concentration of fibrocytes at the isthmus||Lamellar fibroplasia at the level of the isthmus|
Despite this set of contrasting findings, it is likely, based on all the information available, that follicular degeneration syndrome is synonymous with hot comb alopecia. The term follicular degeneration, as it is used in the phrase follicular degeneration syndrome, turns on a single histopathologic finding in tissue sections cut horizontally, a finding that Sperling claimed to be specific for it – namely, premature “disintegration of the inner sheath.” He averred that even a single affected follicle was sufficient to enable coiled hairs to spring through the “soft” outer sheath and to initiate perifolliculitis, which in turn leads in time to permanent alopecia. In brief, the absence of an inner sheath as a result of premature desquamation of it is supposed to be the basis for so-called follicular degeneration syndrome.
Importance of Knowledge of Histology and the Follicular Cycle
Before one can begin to consider the question of the authenticity of the concept of follicular “degeneration” as it relates to a “syndrome,” it is essential to attain thorough familiarity with the rudiments of histologic aspects of a follicle. A follicle may be divided histologically into an upper segment and a lower segment. The upper segment is permanent and consists of an infundibulum and an isthmus. The boundaries of the infundibulum are the ostium of the follicle above and the point of entry of the sebaceous duct below. The boundaries of the isthmus are the point of entry of the sebaceous duct above and the site where corneocytes of the inner sheath desquamate below. The lower segment is transient and consists of a stem and a bulb. The stem stretches from the base of the isthmus to the summit of the bulb (marked by Adamson’s fringe, i.e., the end of the keratogenous zone where nucleated corneocytes of an emerging hair become anucleate), and the bulb extends from Adamson’s fringe to the base of the follicle. Viewed in cross section, the stem, throughout its length, consists of an outer sheath, an inner sheath, and a hair. The inner sheath comes into being as a consequence of maturation of matrical cells in the bulb and is recognizable there by the presence of bright red trichohyalin granules, and in the stem it is identifiable by the presence of blue-gray corneocytes arranged compactly. Never do the corneocytes that make up the inner sheath “degenerate” or “disintegrate;” they eventually desquamate at a site that becomes the lower boundary of the isthmus.
Crtitique of the Notion of "Follicular Degeneration"
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).
*All are patients of Norman W. Walton, III, M.D.
Rollers as a Cause of Traction Alopecia. Rollers are the major inducer of traction alopecia in African-American girls and women. On the right are three examples of permanent alopecia whose staggered pattern reflects the effects of longstanding traction by rollers placed in the same position repeatedly.
Elastic Bands, Plaits, and Extensions as Causes of Traction Alopecia. Permanent alopecia shown here is a consequence of longstanding traction from elastic bands, plaits, and extensions. The pattern of the patches of alopecia, especially the linearity of it, corresponds to sites where traction had been applied for many years.
The Periphery of The Scalp as a Site of Predilection for the Effects of Traction. Permanent alopecia pictured here followed on the effects of traction over the course of many years. The periphery of the hair-bearing scalp is involved predominantly in these women, the predilection for that site being the result of the pull on hair having been greatest there.
The Crown of the Scalp as a Site of Predilection for the Effects of Traction. Permanent alopecia secondary to traction applied for many years. The crown of the scalp is involved predominantly in these women, the predilection for that site being the result of traction having been greatest there.
Traction Alopecia and Attempts to Disguise it. Some attempts to disguise the permanent alopecia caused by traction of long-standing are shown here. On the right are examples of efforts to cover zones of alopecia pictured in the same person on the left. All too often, only a wig can conceal the extensive alopecia.
Chronic and Acute Effects of Traction. Some complications of prolonged traction are illustrated here. The top four photographs show only permanent alopecia and the bottom two exhibit pustules that represent suppurative folliculitis in addition to alopecia.
Histopathologic Findings in Chronological Sequence
Examination of tissue sections from biopsy specimens obtained from affected foci on the scalp revealed different findings at different stages of the process (Figures 7, 8, 9 and 10). Unfortunately, we have no instructive examples of very early lesions, that is, lesions that appear before alopecia is obvious clinically. The earliest findings observed by us are a superficial perivascular and lichenoid peri-infundibular infiltrate of lymphocytes followed in time by peri-infundibular fibroplasia. As the process progresses, the lichenoid infiltrate wanes and the fibrosis waxes, the fibroplasia giving the appearance of “strangling” the epithelium of the upper segment of the follicle. The number of follicles in anagen is decreased, and the number in catagen and telogen is increased. Later still, the number of follicles in anagen decreases further and, at sites where follicles resided formerly, fibrous tracks are widened by thickened bundles of collagen. Degenerated glassy membranes (basement membranes that envelop the lower segment of follicles normally), often several of them, are situated within the altered fibrous tracks and represent the residuum of the inferior segment of follicles which have participated in more cycles of progressively lessened length. Follicles still in anagen are shortened and thinned. At the end of the process, hardly a follicle is terminal and in anagen; the few follicles in anagen are vellus. Most of the follicles are in telogen. Altered fibrous tracks dominate. Subtle fibrosis may be present in the upper part of the dermis. Episodically, hair shafts are noted within the reticular dermis, having been wrenched by traction from the viable component of follicles, and there are surrounded by histiocytes, some of them multinucleate, in the manner of a foreign-body reaction.
Traction Alopecia: Relatively Early. Clinico-pathologic correlation. (A) At a relatively early stage, traction alopecia is typified histopathologically by a lichenoid perifolliculitis in which infundibula are enveloped by lymphocytes. (B) At a stage later than that pictured in (A), the lichenoid infiltrate of lymphocytes is now separated from a markedly thinned infundibulum by a prominent zone of fibroplasia.
Traction Alopecia: Fully Developed. Clinico-pathologic correlation. Fully developed traction alopecia is characterized by sparse perivascular infiltrates of lymphocytes, a markedly thinned lower part of the infundibulum and the entire isthmus consequent to the effects of a band of fibroplasia, and a foreign- body granulomatous reaction to infundibular cornified cells that lie outside a follicle in the dermis.
Traction Alopecia: Late. Clinico-pathologic correlation. (A) At this late stage of traction alopecia, the number of follicles is decreased and thickened fibrous tracks made up of thickened bundles of collagen extend throughout much of the reticular dermis and well into the subcutaneous fat. Also abnormal is the finding of numerous collagen bundles in fat lobules. (B) At this late stage of traction alopecia, the number of follicles is decreased, follicles are thinned as a consequence of fibroplasia that envelops them, and many collagen bundles are present in lobules of the subcutaneous fat.
Traction Alopecia: Late. Clinico-pathologic correlation. (A) At the end stage of traction alopecia, the following changes are apparent: a decreased number of follicles, peri-infundibular fibroplasia of a follicle in the upper-left of the photomicrograph “shot” at scanning magnification, a fibrous track thickened markedly by thickened bundles of collagen, thickened collagen bundles aligned parallel to one another and to the skin surface in the lower part of the reticular dermis, many collagen bundles in lobules of the subcutaneous fat, and absence of inflammatory cells. (B) At the end stage of traction alopecia, several degenerated glassy membranes are seen to reside within a thickened fibrous track and numerous collagen bundles are observed to repose in lobules of the subcutaneous fat.
"Hot Comb Alopecia" / "Follicular Degeneration Syndrome" is Traction Alopecia
How sustained traction causes permanent alopecia is not known for sure, but the zones of alopecia at first conform precisely to where rollers have been placed and between plaits. We think that the continuous pull on hairs sends follicles into catagen in a fashion somewhat analogous to the change that follows plucking of hairs. Because matrical cells of the follicular bulb are programmed genetically for capability to cycle a limited number of times, the continued use of rollers and the practice of plaiting for years exhaust the possibility for division of these cells, and at one juncture they cease producing hair altogether. A second mechanism that seems to be operative in causing alopecia with finality also results from traction – to wit, perifollicular fibrosis that “chokes” follicular epithelium and eventually replaces it. A third factor that may contribute to the alopecia, again by way of the effects of traction, is extrusion of hairs into the dermis, thereby eliciting a granulomatous reaction of the foreign-body type followed by fibrosis which seems to contribute to the obliteration of follicles.
In our interviews of African-American women who suffer from traction alopecia, it became apparent that they were completely unaware of the cause of the loss of their hair. Most attributed it to a familial tendency to alopecia, offering as explanation the fact that their mothers and grandmothers had the same condition. When queried about whether those relatives also had used “hot combs” and other straighteners, the response invariably was “yes.”
The matter of traction alopecia in African-American women has implications that extend far beyond the usual spheres of interest of dermatologists and dermatopathologists; it has a profound effect on the psyche of these women and, by virtue of that, on the well-being of the society in which they lead their lives. Straighteners often are applied to the hair of young African-American girls and, as a consequence of that, signs of permanent alopecia may be evident even before they reach puberty. The condition under consideration here is first seen in children when rubber bands are used to hold the stretched (traction-subjected) hairs in place all day (8 to 14 hours or so) in the plaits seen commonly in African-American girls. Hairs are placed under traction, too, when “corn row” styling and braids are employed. Rolling hair nightly during hours of sleep was a common practice in the past and accounted for sustained traction applied to a specific site. Because the alopecia may be extensive and therefore embarrassing even before adulthood has been reached, women affected develop imaginative strategies (Figure 5) to cover alopecic patches with hairs still present that are sufficiently long to achieve the aim. Unfortunately, for all too many African-American women the extent of the alopecia is so great that they are forced to resort to the use of extensions of hair and wigs. We estimate that somewhere between 35% and 50% of all African-American females bear evidence, to some degree, of traction alopecia induced by straighteners of various kinds.
Traction alopecia is entirely preventable, but when permanent is resistant to any treatment.** For that reason, it is imperative that physicians of all kinds, especially dermatologists, and of all color skin, understand that “hot comb alopecia” and “follicular degeneration syndrome” are really traction alopecia, and caution women about the inevitable result of using straighteners consistently over the course of years. New hair styles that do not require traction should be adopted. African-American women must be taught the truth about this type of artificially-induced alopecia that afflicts nearly half of them, and about the findings that characterize the condition clinically at a very early stage of the process, thereby enabling them to prevent the devastating effects of it.
**Dr. Walton contends that treatment can prevent spread of the disease.
Drs. Ackerman and Jones are at AmeriPath laboratories (The Ackerman Academy of Dermatopathology in New York City and SkinPath in Birmingham, Alabama, respectively). Dr. Charissi is a Visiting Fellow in Dermatopathology at the Ackerman Academy, and Dr. Walton practices dermatology in Birmingham. Clinical photographs were taken by Dr. Walton and photomicrographs by Dr. Ying Guo.
A lock of hair is extended away from the scalp and liberally greased with petrolatum. The iron comb is then heated by placing it in the flame of the kitchen gas range. While not heated to redness, a guideline to excessive heating is supposedly afforded by touching the iron to a piece of paper. If it bursts into flame, the iron is too hot! The iron is then run up and down the extended lock of hair. By watching this operation, one understands why the disease afflicts the crown and not the peripheral areas. Over the crown, the hot petrolatum runs down the vertical hair shafts and spreads on the skin surface. The lateral hairs are stretched out horizontally and the hot petrolatum is not conducted to the surface. LoPresti R, Papa CM, Kligman AM. Hot comb alopecia. Arch Dermatol 1968;98:234-38.
The top of the scalp is sore for a day or two after the use of the hot iron. In some instances, first and even second degree burns occur. LoPresti R, Papa CM, Kligman AM. Hot comb alopecia. Arch Dermatol 1968;98:234-38
Use of the hot comb does not correlate with disease onset or progression in a common, distinctive form of scarring alopecia occurring in black women (formerly called hot comb alopecia). Premature desquamation of the inner root sheath is the first link in a histologic chain of events leading to cicatricial hair loss. Sperling LC, Sau P. The follicular degeneration syndrome in black patients: “Hot comb alopecia” revisited and revised. Arch Dermatol 1992;128:68-74.
Follicular degeneration syndrome is a common form of scarring alopecia in black men, just as it is in black women. In men, there is no association between chemical or mechanical hair styling techniques (e.g., the “hot comb”) and onset, progression, or severity of disease. The histologic features of FDS [follicular degeneration syndrome] in men are identical to those in women. Sperling LC, Skelton HG III, Smith KJ, Sau P, Friedman K. Follicular degeneration syndrome in men. Arch Dermatol 1994 Jun:130(6):763-69.
Some of the clinical and histologic features of FDS are shared by other scalp diseases. The last four histologic stages of FDS [mononuclear cell infiltrate and lamellar fibroplasia at the level of the isthmus, disintegration of the follicular epithelium, disintegration of the “naked” hair shaft with surrounding foreign body giant cell reaction, replacement of the entire follicle by thick fibrous tracts] can be found in other forms of scarring alopecia. . . . The final histologic stages leading to follicular destruction and scarring are remarkably similar in FDS and acne keloidalis nuchae. Sperling LC, Sau P. The follicular degeneration syndrome in black patients: “Hot comb alopecia” revisited and revised. Arch Dermatol 1992;128:68-74.
Premature desquamation of the inner root-sheath and migration of the hair shaft through the outer root sheath serve as histologic markers of FDS and separate it histologically from other forms of scarring alopecia. Sperling LC, Skelton H, Smith K, Sau P, Friedman K. Follicular degeneration syndrome in men. Arch Dermatol 1994;130:763-69.
Our purpose was to assess the impact of combining vertical and transverse sections of scalp biopsy specimens. . . . Transverse sections were superior in cases of lupus erythematosus and lichen planopilaris with focal follicular involvement. Features of the follicular degeneration syndrome were also best demonstrated in transverse sections. Elston DM, McCollough ML, Angeloni VL. Vertical and transverse sections of alopecia biopsy specimens: combining the two to maximize diagnostic yield. J Am Acad Dermatol 1995 Mar;32(3):454-57.
These patterns are grouped under the heading central centrifugal scarring alopecia because they have the following 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 most active disease at the periphery, and 4) both clinical and histologic evidence of inflammation in the active peripheral zone. Sperling LC, Solomon AR, Whiting DA. A new look at scarring alopecia. Editorial. Arch Dermatol 2000;136:235-42.
Prolonged tension created by certain hairstyles, such as braids or pony tails, hair rollers, and hot hair-straightening combs, may result in temporary or, rarely, permanent hair loss in an area corresponding exactly to the stressed hair. The scalp may appear normal or may show evidence of inflammation or scarring. Habif TP. Clinical dermatology. St. Louis: Mosby, 1996:756.
The scarring alopecia resulting from destructive inflammatory folliculitis (including folliculitis decalvans), as well as that following chronic tractional alopecia, hot comb alopecia, and the follicular degeneration syndrome, may create very similar patterns of predominantly focal follicular scarring alopecia, and clinical correlation is always necessary for accurate assessment of biopsy specimens. Abell E. Inflammatory diseases of epidermal appendages and of cartilage. In: Elder D et al, eds. Lever’s histopathology of the skin. 8th ed. Philadelphia: Lippincott-Raven, 1997:414.