Get PDF An Atlas of Hair Pathology with Clinical Correlations, Second Edition

Free download. Book file PDF easily for everyone and every device. You can download and read online An Atlas of Hair Pathology with Clinical Correlations, Second Edition file PDF Book only if you are registered here. And also you can download or read online all Book PDF file that related with An Atlas of Hair Pathology with Clinical Correlations, Second Edition book. Happy reading An Atlas of Hair Pathology with Clinical Correlations, Second Edition Bookeveryone. Download file Free Book PDF An Atlas of Hair Pathology with Clinical Correlations, Second Edition at Complete PDF Library. This Book have some digital formats such us :paperbook, ebook, kindle, epub, fb2 and another formats. Here is The CompletePDF Book Library. It's free to register here to get Book file PDF An Atlas of Hair Pathology with Clinical Correlations, Second Edition Pocket Guide.
Top Authors

  1. 2nd Edition
  2. An Atlas of Hair Pathology with Clinical Correlations - CRC Press Book
  3. Shop now and earn 2 points per $1
  4. An Atlas of Hair Pathology with Clinical Correlations

Only terminal follicles can be found at this level, and they are not yet organized into follicular units. The bulbs of telogen hairs and vellus hairs can also be found at this level, organized into follicular units. In the normal scalp, the terminal: vellus hair ratio should be or greater. The architecture of scalp biopsy specimens should be uniform over Table 3.

Figures 3. Normally, only terminal and indeterminate follicles can be found at this level, and they are not yet organized into follicular units.

  • An Atlas of Hair Pathology with Clinical Correlations | Taylor & Francis Group!
  • Bestselling Series.
  • Angels Watching Over Me (Shenandoah Sisters Book #1).

This specimen contained 16 total follicles. These numbers would be regarded as low for a Caucasian but are normal in African Americans. Original magnification 40 Terminal anagen hairs: Terminal catagen hairs: Terminal telogen hairs: Telogen germinal units: Vellus hairs: Total hairs terminal plus vellus, all phases : Anagen : telogen percentages e. In this particular field, there are 12 terminal anagen hairs and seven terminal telogen hairs, for a total of 19 terminal hairs. This unit contains four terminal hairs and one vellus hair. Mild upper dermal perifollicular inflammation may be present even in normal scalp specimens.

This is especially true for African American patients. This can be summarized in a microscopic description e. A reduced number of hairs are present, and most are miniaturized. One unit contains three terminal anagen hairs and the other contains one terminal anagen and one vellus telogen hair. Even within the same specimen, the number of hairs per follicular unit varies somewhat; so several units need to be examined to arrive at a valid average.

Alternatively, detailed data can be presented in tabular form. A template for a complete report, adapted from that used by David A. Whiting, MD, is presented in Table 3. Such a detailed report not only serves as the basis for the final diagnosis, but also allows for efficient data collection for research purposes. Arch Dermatol ; Solomon A. Arch Dermatol ; Sperling LC. Hair anatomy for the clinician. Various classification schemes for alopecia exist, but all are imperfect.

Most forms of alopecia demonstrate at least some overlapping clinical and histological features. This overlap blurs the distinction between diseases, making classification difficult. It would make the most sense to segregate diseases by etiology, but the causes of many forms of hair loss are unknown, making it difficult to group diseases with confidence.

In this textbook, the terms cicatricial and scarring will be considered to be synonymous and will be used interchangeably. Cicatricial or scarring implies that follicular epithelium has been replaced by connective tissue. However, in some cases of alopecia, follicles seem simply to disappear without noticeable alteration in tissue architecture. The broadest definition of scarring alopecia might include all forms of alopecia in which hair follicles are permanently lost. In contrast, nonscarring alopecia is potentially reversible. However, certain hair diseases demonstrate a biphasic pattern, where nonscarring hair loss is seen early in the course of the disease, and permanent hair loss becomes apparent in the later stages of the disease Figure 4.

Examples of diseases demonstrating this biphasic pattern include androgenetic alopecia, alopecia areata and traction alopecia. These forms of alopecia are generally considered to be non-scarring. However, after many years or decades of continuous active disease, permanent dropout of follicles occurs. There are no characteristic biological markers for most forms of scarring alopecia. We do not know whether the clinical and histological features found in a given patient are. Figure 4. With the passage of time, follicles begin to disappear permanently and histological specimens take on the appearance of a cicatricial alopecia.

Any classification of scarring alopecia should be considered provisional and subject to change as new information becomes available. Scarring alopecia can be subdivided into two categories. The first is primary scarring alopecia, where the target of inflammation appears to be the follicle. In secondary scarring alopecia, the follicle is merely an innocent bystander in the disease process, and is destroyed in a non-specific manner. Examples of secondary scarring alopecia include deep burns, radiation dermatitis, cutaneous. The ovals in this diagram overlap for several reasons.

Second, it is possible that two different entities may some day prove to be variations of the same disease this concept is discussed in Chapter Finally, the overlap of these distinct entities serves as an admission that the conditions are poorly understood, and that their separation in this classification is provisional. The various forms of secondary scarring alopecia should have distinctive histological features typical of the underlying disease.

For example, alopecia caused by cutaneous sarcoidosis should reveal sarcoidal granulomata in the dermis. A discussion of the various forms of secondary scarring alopecia is beyond the scope of this text. Primary scarring alopecia can be divided into six diagnostic groups Figure 4. They are: 1 2 3 4 5 6 Central, centrifugal scarring alopecia; Lichen planopilaris; Chronic, cutaneous lupus erythematosus discoid lupus erythematosus ; Acne keloidalis folliculitis keloidalis; acne keloidalis nuchae ; Dissecting cellulitis perifolliculitis abscedens et suffodiens ; Scarring alopecia, not otherwise classified.

This short list is a simplification of a longer list of confusing, vague and poorly defined diagnostic terms that have been coined and used by various authors during the past century. Notably absent from the above list are terms such as pseudopelade, pseudopelade of Brocq, folliculitis decalvans, tufted folliculitis and a variety of other more obscure terms. These entities are poorly defined, and. Almost all of these older terms can be incorporated into one of the six categories shown in Figure 4. Nevertheless, many of the older terms will be discussed in this text for the sake of clarity.

Cicatricial alopecia and other causes of permanent alopecia. In Olsen EA, ed. Disorders of Hair Growth. The cicatricial alopecias. J Invest Dermatol ; 8: Solomon A. A new look at scarring alopecia. Scarring alopecia: a classification based on microscopic criteria. J Cutan Pathol ; Classification schemes are of little value to pathologists trying to extract the diagnosis from a glass slide. The histological features, in conjunction with a brief clinical description, must somehow guide the pathologist to the correct diagnosis. To assist in this process, some especially important histological features listed below will help to segregate the diagnostic entities.

Identifying additional histological features will make it easier to establish the diagnosis. Frequently, different diseases may share two or more histological features. When this occurs, separating such diseases may rest on good clinical correlation or subtle histological clues. Attempts have been made to create alopecia algorithms for arriving at a diagnosis, but in the authors experience, such algorithms provide little assistance.

The starting point for arriving at a histological diagnosis is recognition of an obvious or dominant histological finding, such as miniaturization of hairs, missing hairs, or perifollicular inflammation. Unfortunately, no single histological feature is sufficient to establish a definitive diagnosis in any form of hair loss.

However, a differential diagnosis based on one or two histological features will help to create a short list of possible diagnoses. Additional histological features characteristic of the entities on the short list can then be used to narrow the field of possibilities. Clinical information will often help to decide the issue. Listed below are histological features, and those diseases that often demonstrate the feature. Cicatricial alopecia all forms Congenital hypotrichosis various syndromes End stage traction alopecia an example of the biphasic pattern of hair loss Androgenetic alopecia or hereditary balding very long-standing disease; an example of the biphasic pattern of hair loss.

Figure 5. A transverse section from the normal uninvolved scalp of an African American woman with traction alopecia. The section contains 22 follicles, slightly more than average. A section from the zone of alopecia contains 11 follicles, a marked reduction compared to her normal scalp.

  1. Response to the review from the authors!
  2. Recommended For You.
  3. Cadillac Marketing Analysis.
  4. The Wisdom of Father Brown.
  5. Alopecia areata very long-standing disease; an example of the biphasic pattern of hair loss Aplasia cutis congenita. Telogen effluvium Androgenetic alopecia Temporal triangular alopecia Traction alopecia. This can be explained by an increase in miniaturized hairs producing no hair shaft. All forms of cicatricial alopecia Alopecia areata long-standing disease Note: hair density in dark-skinned, kinky-haired individuals e.

    In this case it was because of a massive conversion to telogen hairs. Average hair shaft diameter is 0. Average shaft diameter is 0. See Figures 5. This half is spared lymphocytic inflammation. Note: as mentioned earlier, the diagnostic significance of catagen and telogen hairs is the same, since all catagen hairs become telogen hairs within a few weeks. Vacuolar, basilar degeneration is present. There is perifollicular fibroplasia but not vacuolar interface alteration.

    Alopecia areata predominantly lymphocytic Patchy hair loss in systemic lupus erythematosus predominantly lymphocytic Patchy hair loss in secondary syphilis predominantly lymphocytic with occasional plasma cells. Inflammation spares the lower half of the follicle but premature desquamation of the inner root sheath is present.

    The sebaceous glands have disappeared with the follicles. Lichen planopilaris Frontal, fibrosing alopecia Chronic, cutaneous discoid lupus erythematosus. Without vacuolar interface alteration See Figures 5. Acne keloidalis Central, centrifugal scarring alopecia also known as follicular degeneration syndrome and pseudopelade.

    Cicatricial alopecia: all forms. Normal follicles with intact inner root sheaths are present for comparison. With associated sebaceous glands intact See Figure 5. Traction alopecia end stage Androgenetic alopecia very advanced and long-standing Alopecia areata very advanced and long-standing. The hair shaft is distorted in shape, irregularly pigmented and incompletely cornified. Trichotillomania Acute traction alopecia Pressure-induced alopecia Alopecia areata. Clinicians who contribute even a brief clinical description and differential diagnosis are of considerable assistance to the pathologist.

    Some clinical features that may be described include: Pattern of hair loss Evidence of inflammation Evidence of hair breakage hairs of uneven length Evidence of permanent hair loss Obliteration of follicular ostia Abnormal hair density. The most important feature is the pattern of hair loss. Hair loss can be diffuse or patterned. Patterned hair loss implies that the area of alopecia is confined to one or several portions of the scalp, leaving at least a portion of the scalp uninvolved.

    Truly diffuse hair loss suggests a uniform reduction in hair density over all portions of the scalp. Telogen effluvium Figure 6. Patchy alopecia areata is one example of patterned alopecia. The various patterns of thier loss are listed below. Figure 6. Hair thinning is uniform over the crown, occiput and sides of the head. Randomly scattered, irregularly shaped patches of partial or complete hair loss e.

    Although on rare occasions the balding process seems to affect the entire scalp, including the occiput, in the vast majority of cases the crown of the scalp including frontal and vertex regions is predominandy involved. Therefore, the condition has a distinctive pattern of thinning Figures 6. Hair shaft disorders associated with hair fragility, such as trichorrhexis nodosa, tend to cause localized zones of alopecia containing hairs of uneven length.

    When the hair is particularly fragile, as is true in monilethrix, patches of hair stubble will be found. In disorders caused by hair shaft fragility, the shaft defect is usually readily apparent under the light microscope. In trichotillomania, the patches of alopecia are seldom totally bald. Usually there are several short hairs of varying lengths scattered over the involved area. Clinicians should examine the scalp surface in all cases of hair loss.

    An Atlas of Prostatic Diseases CD ROM

    Abnormalities may or may not be related to the hair loss but need to be documented. Erythema, pustules, follicular papules and perifollicular scaling or hyperpigmentation suggest an inflammatory form of alopecia. Wide spacing between follicles, clusters of shafts exiting single follicular ostia polytrichia or tufting and the obliteration of follicular openings are all signs of scarring alopecia.

    Follicular plugging, with dilated ostia devoid of hair shafts, can be another indication of follicular destruction, as seen in discoid lupus erythematosus. Marked erythema and scaling or numerous papular lesions without a loss of follicular density suggests a primary scalp disorder as opposed to a hair disorder. Psoriasis, seborrheic dermatitis and Langerhans cell.

    The crown is diffusely and symmetrically affected with relative sparing of the occiput as seen in Figure 6. The evaluation of hair loss. Hair diseases. Med Clin North Am ; Pure senescent alopecia is found in patients who boast a full head of hair well into middle age, and who typically deny a family history of balding. Patients with senescent alopecia note a very slow but steady, diffuse thinning of scalp hair starting at age 50 and older.

    Women who complain of a marked degree of thinning in the few years following menopause probably have a component of androgenetic alopecia. Many and perhaps most patients with senescent alopecia also have mild concomitant androgenetic alopecia, and the superimposed clinical and histological features of common balding and senescent alopecia may be impossible to separate. Several authors have assessed the effect of aging on hair density by studying the scalp surface i.

    The results of these studies indicate that the density of hair follicles decreases steadily with aging. There is little information available on the histological evaluation of scalp biopsy specimens taken from normal individuals of various ages. Compared to normal or youthful scalp, more follicles are in the telogen phase, but the telogen count may still be within the range of normal. Inflammation is uncommon, and fibrous streamers such as those found in androgenetic alopecia are absent. The follicles are not as long or as wide as normal, but miniaturization such as that seen in androgenetic alopecia is absent.

    All these subtle findings would be uniform over the scalp surface. The following combination of histological findings based on 4-mm punch biopsy specimens is typical of senescent alopecia Figures 7. Figure 7. The specimen is from an elderly patient with mild, diffuse thinning of hair who complained of gradual hair loss over a period of several years.

    The two specimens here and in Figure 7. This contrasts with androgenetic alopecia, where histological changes in the occiput if present are less dramatic than at the vertex or crown. SUMMARY Clinical correlation: an elderly person who admits to very gradual thinning of the hair; hair density appears normal for age or diffusely thinned over the entire scalp.

    Histological findings:. The comparative histopathology of male-pattern baldness and senescent baldness. Androgenetic alopecia is also known as common balding, hereditary balding, male-pattern balding and female-pattern balding. Some authors speculate that the pathogenesis of balding differs between men and women. However, the histopathological findings are similar in both sexes.

    Many women with a genetic predisposition to baldness first notice the onset or an acceleration of shedding and thinning around the time of menopause. However, some less fortunate women, especially those with strong family histories for balding, begin to thin in early adulthood. In the majority of cases, thinning is localized to the crown of the scalp, with sparing of the occipital and lower parietal fringe of hair Figures 8. Two patterns of hair loss can be seen: Hamiltons male pattern and Ludwigs female pattern. In fact, there is considerable overlap between the sexes, with many women demonstrating a male pattern of hair loss, and some men showing a female pattern, with diffuse crown thinning and retention of the frontal hairline.

    In exceptional cases, the pattern of hair loss in both men and women with androgenetic alopecia can be truly diffuse authors personal observation , with thinning of the occiput as well as the crown. In these cases, histological confirmation may be required to establish the diagnosis with certainty. The diagnostic breakthrough has been the study of transverse sections of scalp biopsies, a technique popularized through the efforts of Headington and others.

    The microscopic diagnosis of androgenetic alopecia depends more on quantitative than qualitative features. Therefore, the ability to identify all follicles within a biopsy specimen is required to establish the diagnosis. All specimens should be sectioned horizontally. Uninvolved skin can serve as the patient s normal control. If the condition is advanced, a single specimen from balding skin may be sufficient. Figure 8. Thinning is most prominent over the crown. Androgenetic alopecia is characterized by progressive miniaturization of hair follicles.

    This results in a mixture of hairs with various bulb depths and shaft diameters. When one examines a specimen from a normal scalp, sectioned transversely through the lower dermis, one gets the global impression that all hairs are terminal hairs of similar size diameter. A biopsy specimen from a patient with androgenetic alopecia, sectioned at the same level, will show hairs that appear vastly different in diameter Figures 8.

    Below each miniaturized follicle is a streamer, the collapsed connective tissue sheath that once surrounded the formerly deep-seated, terminal hair. Streamers can also be found beneath follicles that have become temporarily miniaturized, as in alopecia areata. After a streamer has been present for years as in late androgenetic alopecia , the streamer becomes less vascular and assumes a grayish hue when stained with hematoxylin and eosin Figures 8. In advanced cases, the number of vellus and indeterminate hairs will actually surpass the number of terminal hairs Figures 8.

    Early in the course of balding, the total number of follicles present remains normal. Also, sebaceous glands persist even when the hairs have greatly miniaturized Figure 8. However, in very long-standing balding, there is an actual decrease in follicular density as well as follicular size. Therefore, androgenetic alopecia shows a biphasic pattern of hair loss and may eventually resemble cicatricial alopecia.

    As hairs miniaturize, the anagen phase becomes shorter. Therefore, the balding scalp shows an increase in the telogen count, since miniaturized hairs spend a greater proportion of each hair cycle in the telogen phase. In well-established androgenetic alopecia, the majority of telogen follicles will be miniaturized follicles Figure 8. Successful treatment with minoxidil or finasteride will increase the size of follicles and reduce the telogen count, presumably by lengthening the duration of anagen.

    In this woman with early androgenetic alopecia, the number of follicles in the vertex specimen is similar to the number in the occipital specimen Figure 8. However, follicles in the vertex specimen show considerable variation in diameter, and many are quite small. Inflammation has been described as a histological feature of androgenetic alopecia, but balding should be regarded as a form of non-inflammatory hair loss. Many biopsy specimens of androgenetic alopecia show mild, perifollicular, lymphohistiocytic, upper dermal inflammation, sometimes associated with mild perifollicular fibrosis.

    These changes are subtle and non-specific, and can also be found in many normal scalp specimens. Mild, peri-infundibular chronic inflammation is especially common in African American women and can be regarded as normal. Peribulbar or destructive inflammation is absent in common balding. SUMMARY Clinical correlation: symmetric thinning, predominantly affecting crown, vertex and frontal regions, with relative sparing of the occiput; no evidence of scarring.

    Family history of balding is usually elicited. Histological findings Figures 8. The same specimen as in Figure 8. The marked variation in hair size in the vertex specimen is evident However, the total number of hairs in both vertex and occipital Figure 8. Male pattern alopecia: a histopathologic and histochemical study. Finasteride increases anagen hair in men with androgenetic alopecia. Measuring reversal of hair miniaturization in androgenetic alopecia by follicular counts in horizontal sections of. Original magnification 40 serial scalp biopsies: results of finasteride I mg treatment of men and postmenopausal women.

    Diagnostic and predictive value of horizontal sections of scalp biopsy specimens in male-pattern androgenetic alopecia. J Am Acad Dermatol ; Old streamers, such as those seen here and in Figure 8. Such streamers, found in more recently miniaturized hairs, show more prominent vascularity. When multiple follicular units from the balding scalp are examined, most will show that vellus hairs equal or even outnumber terminal hairs. Here, when multiple follicular units from the normal scalp are examined, terminal hairs outnumber vellus hairs. Even so, the sebaceous glands remain intact.

    The percentage of telogen hairs is increased, but the majority of telogen hairs are vellus or indeterminate hairs. A telogen effluvium occurs when abnormally large numbers of anagen hairs from all areas of the scalp enter the telogen phase. This may be caused by some sort of endogenous stress to the follicles, such as a metabolic disturbance, nutritional deficiency, or serious systemic illness.

    Other cases of telogen effluvium are physiological, and not indicative of disease. The many possible causes are listed in Table 9. In response to the causative factor, many hairs prematurely enter the catagen phase. This is a committed step for follicles; having entered catagen they must proceed through the telogen phase and shedding before a new anagen hair can regrow.

    Telogen effluvium is probably the most common form of hair loss associated with systemic diseases, especially chronic and debilitating conditions. Most drugs that have been associated with hair loss, with the exception of anticancer medicines and other toxins, cause hair loss by way of a telogen effluvium. Physiological forms of telogen effluvium include postpartum and neonatal hair loss. In postpartum telogen effluvium, numerous hair follicles are artificially maintained in the anagen state under the influence of gestational hormones.

    This is reflected in the lower telogen counts that occur towards the end of pregnancy. Telogen effluvium of the newborn represents the nearly universal shedding of scalp hair during the first Table 9. Post-surgical implies major surgical procedure Hypothyroidism, hyperthyroidism and other endocrinopathies Crash or liquid protein diets; starvation Drugs retinoids e. This may occur rapidly, resulting in obvious alopecia, or may proceed slowly and imperceptibly. In either case, large numbers of anagen hairs enter telogen within a period of months.

    Many adult women suffer from a chronic telogen effluvium with no definable precipitating event. This has been termed chronic telogen effluvium, and is a diagnosis of exclusion. Many or most of these women have self-limited disease, although the condition may last for several years before spontaneous resolution. The early stage of androgenetic alopecia has features of a chronic, localized form of telogen effluvium. The vertex and frontal hairs of the balding scalp experience a marked reduction in the length of anagen. A much higher proportion of hairs are thus entering telogen at any given time.

    Hair shedding is only obvious during the early stages of the balding process, when large, terminal hairs are being shed. Once hairs have miniaturized, the shedding of vellus telogen hairs is not apparent. Patients with acute forms of telogen effluvium notice hair loss about 3 or 4 months after the precipitating event. This corresponds to the time it takes for a hair to move through catagen and the early stages of telogen. Scalp hair density may appear normal, despite the patients complaint of profuse hair loss.

    If alopecia is clinically obvious, the loss appears diffuse, affecting all parts of the scalp Figure 9. A gentle hair pull will yield several hairs with the depigmented, cornified, clubbed morphology of telogen hair roots. A forcible hair pluck will produce a mixture of normal anagen and telogen hairs, as well as an occasional catagen hair Figure 9. The only abnormality in a pure case of telogen effluvium is an increase in the percentage of terminal.

    Figure 9. Therefore, the total number of hairs in the specimen will be normal, but there will appear to be a reduced number of terminal hairs when counted at the dermal-fat junction. Fibrous streamers stelae replace the missing terminal hairs at this level Figures 9.

    These streamers lie beneath the bulbs of the terminal telogen hairs, which are found in the middermis. However, a lower number does not exclude the diagnosis of telogen effluvium. Even lower numbers can be consistent with this diagnosis. There is a mixture of normal-appearing anagen and telogen bulbs, but the telogen bulbs are overrepresented. This specimen, sectioned at the level of the dermal-fat junction, demonstrates a reduced number of terminal anagen hairs.

    However, the terminal anagen hairs present are roughly similar in diameter. The size of hairs is not affected in a telogen effluvium. Abnormally large numbers of terminal large anagen hairs are converted into terminal telogen hairs, but miniaturization does not occur Figure 9. Therefore, the terminal : vellus hair ratio is normal greater than In fact, all body hair will be affected by the disease, which may clinically be evident by thinned eyebrows, pubic hair and axillary hair.

    If paired biopsy specimens crown and occiput are obtained, the histological findings will be similar at both sites. The two terminal telogen hairs in this field have been sectioned through their secondary hair germs SHG. Telogen effluvium is a non-inflammatory form of hair loss, and no significant inflammation is found. In particular, peribulbar inflammation and inflammation affecting the lower two-thirds of the follicles is absent.

    SUMMARY Clinical correlation: history of a precipitating event 2 or 3 months prior to hair loss is often obtainable childbirth, major surgery or severe illness, certain medications, etc. Anagen hairs may fail to replace telogen hairs in early androgenic female alopecia. Dermotology ; Headington JT.

    Telogen effluvium. New concepts and review. Arch Dermatol ; Kligman AM. Pathologic dynamics of reversible hair loss in humans. Arch Dermatol ; Rebora A. Telogen effluvium: an etiopathogenetic theory. Int J Dermatol ; Rebora A. Diffuse alopecia in women. Arch Dermatol ; Whiting DA.

    2nd Edition

    Chronic telogen effluvium: increased scalp hair shedding in middle-aged women. Trichotillomania is caused by the habitual, compulsive or intentional pulling and plucking of hair. Although it can be found in persons who are mentally or emotionally ill, many patients are healthy. However, with careful questioning, a history of significant stress or turmoil at school, home or work can often be obtained.

    Frequently, patients are school-aged children, and often both child and parents deny the possibility of pulling or plucking as a cause of hair loss. Therefore, a biopsy specimen can be crucial for establishing the diagnosis with certainty. Lesions of trichotillomania are often irregularly shaped, with bizarre or geographic outlines. The bald patches are usually sharply demarcated from the surrounding normal scalp, and typically there are several retained short hairs of various lengths within the zone of alopecia Figure The scalp surface is usually not inflamed, but occasionally excoriations from scratching or picking may be present.

    In the process of plucking, some or all of the follicular epithelium may be removed from the follicle, and the residual tissue collapses to fill the void. Normally, the inner root sheath surrounds either a hair shaft or the oval space occupied by the shaft before processing. A collapsed inner root sheath indicates prior extraction of the hair shaft and is the most common histological defect encountered in trichotillomania Figures When both the shaft and the inner root sheath are extracted, the outer root sheath collapses upon itself.

    Infrequently, all or most of the epithelium is removed, and the fibrous root sheath along with any retained epithelial fragments and extravasated red blood cells form a vertical column. Mechanical trauma to the hair frequently propels anagen follicles into the catagen phase. Therefore, increased numbers of catagen and telogen hairs are found in trichotillomania Figure Catagen hairs will be found in areas that have recently been plucked, and telogen hairs are present a few weeks after the traumatic event Figures Figure A terminal anagen hair has lost its shaft from plucking.

    The inner root sheath has collapsed upon itself. Frequently, chunks of pigmented hair matrix or cortex cells are torn from their moorings during the plucking process, and come to rest in superficial portions of the follicles Figure These cells then shrink to form a dark black homogeneous clump called a pigment cast Figure Pigment casts are simply the byproduct of fragmented, ectopic matrix or cortical epithelium.

    If the hair matrix and suprabulbar epithelium is injured, but not severely disrupted, the follicle may remain in the anagen phase, producing a hair shaft. However, the shaft that is formed may be distorted in shape, smaller than normal and incompletely cornified. This is termed trichomalacia Figures Although trichomalacia is very characteristic of trichotillomania, it is not found exclusively in this condition refer to the section on alopecia areata, Chapter Pulling or plucking does not incite inflammation but may cause some hemorrhage within the lower portion of the follicle Figure Even very dramatic cases of trichotillomania are remarkably free of an inflammatory.

    On the right is a normal follicle for comparison. Two catagen hairs are present in this field. The follicle on the right is sectioned through the newly forming club. Very rarely, a few eosinophils are found surrounding the lower portion of a badly traumatized follicle. SUMMARY Clinical correlation: the patient is often a child or teenager, and a history of emotional stress at home, school or work may be elicited.

    An Atlas of Hair Pathology with Clinical Correlations - CRC Press Book

    The involved areas are irregularly shaped, sharply marginated patches with some retained short hairs of various lengths. The histological differential diagnosis at this level would include telogen effluvium. Eventually, such cells shrink and cornify to form pigment casts. The combined utilization of clinical and histological findings in the diagnosis of trichotillomania. Trichotillomania: a histopathologic study in sixty-six patients. Presentation, etiology, diagnosis and therapy. Dermatopathology of common hair problems. Two black pigment casts and two trichomalacic shafts can be seen.

    Another example with a single trichomalacic shaft. Like trichotillomania, traction alopecia is a form of mechanical, traumatic alopecia. However, trauma to the hair is usually mild and chronic. Although vigorous scratching or combing may cause traction alopecia, most cases are caused by hairstyles involving tight braiding or banding of the hair. The condition is most common among African American girls whose hair-styles involve nearly continual braiding. However, the identical pattern of hair loss can be seen in persons of all races.

    Some girls get the condition after wearing tight ponytail type hairstyles. The hair loss tends to be a peripheral or marginal form of alopecia, i. In girls who wear tight braids, perifollicular erythema and pustule formation may be seen. Whether this inflammation is caused by traction or by cosmetics used in conjunction with hair styling is unknown. Traction alopecia is a biphasic form of hair loss. Initially the hair loss is temporary, hair regrowth occurs and the condition behaves like a non-scarring form of alopecia.

    However, if excessive traction is maintained for years, the hair loss may eventually become permanent end-stage or burnt out; Figure There may be a lag period of a decade or more between the period of traction and the onset of permanent hair loss. Therefore, many African American women present in their thirties and forties with a several-year history of persistent, bitemporal or frontal hair loss.

    These women may deny having worn tight braids since child-hood, although often other forms of traumatic styling e. The acute form, most commonly seen in African American girls or after a short-lived, traumatic hairstyle such as a hair weave or corn row , resembles a mild form of trichotillomania. Occasionally, distorted or incomplete follicular anatomy is seen. Follicular numbers are normal.

    Shop now and earn 2 points per $1

    In end-stage disease, most commonly found in young African American women, the total number of hairs is markedly reduced Figures This is accounted for by the loss of terminal hairs, because vellus hairs are still present in normal numbers Figures Sometimes the missing follicles appear to have disappeared without a trace, because the dermal collagen appears normal, but often some old stelae can be found when deeper levels are examined Figures In many cases, distinct columns of connective tissue replace some follicles, leaving obvious blank spaces Figure The sebaceous glands associated with the remaining hairs are still intact, and often persist in follicular units that seem to have lost all their follicles.

    The presence of sebaceous glands and relative normality of the dermal architecture, despite marked hair loss, is highly characteristic of end-stage traction alopecia. No significant perifollicular inflammation is present in either early or late disease. The number of terminal anagen hairs is reduced in the alopecic zone seen here as compared with normal-appearing perilesional skin see Figure Early or acute diseasepatient is often an African American child whose hair is tightly braided; there is alopecia of the scalp margin or around braids. The reduction in the number of terminal hairs is striking, but sebaceous glands are preserved.

    Figure I 1. No significant inflammation peribulbar inflammation absent End-stage or burnt out disease Figure Terminal hairs are markedly reduced from normal, but normal numbers of vellus hairs persist. Etiologic factors in traction alopecia. Surgical correction of traumatic alopecia marginalis or traction alopecia in black women. Nurses cap alopecia. Traction alopecia in nurses. Corn-row alopecia. Arch Dermatol ; Scott DA.

    Disorders of the hair and scalp in blacks. Dermotol Clin ; When sectioned transversely, these stelae appear as roughly oval condensations of connective tissue containing a few small vascular spaces. Telogen effluvium: a clinically useful concept, with traction alopecia as an example. Cutis ; Trueb RM. Chignon alopecia: a distinctive type of nonmarginal traction alopecia. Cutis ; In some cases, each column may represent the former site of an entire follicular unit.

    This form of hair loss is seen most commonly in patients who have undergone lengthy surgical procedures, and had one portion of their scalp usually the occiput in prolonged contact with the operating table. Postoperative alopecia can occur at any age and is often associated with gynecological and open-heart procedures requiring tracheal intubation. Less commonly, the condition is found in patients who sustain blunt trauma to the scalp.

    Postoperative alopecia typically presents as a solitary, roughly oval patch on the upper occiput Figure Early in the course of the condition, erythema and induration are found in the central portion of the lesion. Nearly total hair loss with fairly sharp demarcation from the surrounding scalp is found just a few weeks after the initial trauma. Usually complete hair regrowth occurs, although several cases of permanent i.

    Early in the course of the disease, before hair loss is complete, vascular thrombosis, inflammation and destruction may be seen in the dermis. Alopecia develops up to 28 days following the surgical procedure. In the typical case of postoperative alopecia, nearly all terminal follicles will be in the catagen or telogen phases Figures Trichomalacia may be present, but not the distorted or incomplete follicular anatomy sometimes found in trichotillomania Figure Pigment casts are also commonly found Figure Variable degrees of dermal fibrosis and chronic inflammation are present in the papillary and upper reticular dermis.

    Focal vascular and tissue necrosis may be present along with an associated chronic inflammatory infiltrate. Fat necrosis is often found, associated with an infiltrate of foamy macrophages and mononuclear cells Figure Inflammation is mild relative to the degree of. A large, nearly hairless, occipital patch was noted 3 weeks after a prolonged surgical procedure. The inflammation does not seem to be centered around hair follicles, but is usually associated with foci of vascular and tissue necrosis.

    SUMMARY Clinical correlation: a patch of occipital hair loss occurring within a few weeks of a prolonged surgical procedure requiring general anesthesia. Almost all hairs in the catagen or telogen phase Trichomalacia Melanin pigment in collapsed fibrous root sheaths Vascular thrombosis or necrosis with a relatively mild perivascular and perifollicular inflammatory infiltrate Fat necrosis with secondary infiltration by foamy macrophages and a few lymphoid cells.

    Two catagen hairs can be seen. Postoperative alopecia: a case report and literature review. Postoperative alopecia. Postoperative pressure alopecia. Also known as congenital triangular alopecia, temporal triangular alopecia may be present at birth or acquired during the first decade of life. Lesions outside the temporal area, and those acquired in adulthood, can rarely occur. The lancetshaped lesions Figure Lesions appear hairless, but very fine vellus hairs can be seen with magnification. Once present, the patches of alopecia persist for life.

    Microscopically, there are normal numbers of follicles, but almost all are vellus hairs. The small size of the hairs necessitates transverse sectioning for adequate assessment Figures All other features of the epidermis, dermis and other adnexae are entirely normal, and inflammation is absent. The condition appears to be a process of follicular miniaturization confined to a small, lancet-shaped area of the temporal region, resulting in the characteristic bald spot.

    However, fibrous streamers stelae as found in androgenetic alopecia are not found in temporal triangular alopecia Figure Congenital cases presumably undergo the process of follicular miniaturization in utero or terminal hair formation never occurs. SUMMARY Clinical correlation: lancet-shaped bald spot may be bilateral discovered on the temporal region of a newborn or young child; the remainder of the scalp is normal.

    Normal total number of hairs Few, if any, terminal hairs Almost all hairs are vellus hairs No fibrous streamers stelae No significant inflammation or other epidermal or dermal abnormality. This unilateral lesion was first noted when the patient was 3 years old. A section through the deep dermis reveals very few follicles. Congenital triangular alopecia. Pediatr Dermatol ; Bargman H. Congenital temporal triangular alopecia. It is impossible to quantify the total number and average size of follicles using vertical sections.

    Original magnification Feuerman EJ. Congenital triangular alopecia Brauer nevus. Pathological case of the month. Temporal triangular alopecia and aplasia cutis congenita. Congenital triangular alopecia in phakomatosis pigmentovascularis: report of 3 cases. Temporal triangular alopecia in association with mental retardation and epilepsy in a mother and daughter. J Cutan Pothol ; Tosti A. Report of fourteen cases. Temporal triangular alopecia acquired in adulthood.

    The dermis below the miniaturized follicles appears normal, and stelae are not seen. The disease can affect any part of the body Figure Severity ranges from a small, circumscribed bald spot to total scalp hair loss alopecia totalis , and even total body hair loss alopecia universalis. Both the clinical course and histopathological features of relatively mild disease may differ significantly from severe disease alopecia totalis or universalis. Several patterns of partial hair loss can be found, including circumscribed isolated oval patches; Figures In the very unusual diffuse form, hair loss occurs over much of or the entire scalp, but circumscribed bald spots do not form.

    However, hair loss is seldom so uniform or symmetrical that it cannot be distinguished from a telogen effluvium. If the hair steadily and rapidly thins, the diagnosis of alopecia totalis in evolution is more appropriate than that of diffuse alopecia areata Figure Even in alopecia totalis or universalis, isolated hairs or tufts of hairs may continue to grow. The involved scalp is usually normal in color but may show slight erythema or edema.

    Short hairs that taper as they approach the scalp are called exclamation mark hairs, and if present are very characteristic of alopecia areata. Because of shaft narrowing and hypopigmentation near the scalp surface, exclamation mark hairs appear to float on the scalp surface Figures Alopecia areata seems to affect pigmented hairs preferentially, and hair regrowth may occur with depigmented hairs Figure For the purpose of this text, the pathology of alopecia areata will be divided into three stages, a concept that is accepted by other authorities such as David A.

    These stages, which will be called acute, subacute and chronic, reflect the evolution of the. Different stages of disease may be present at the same time at different sites on the same scalp. In any given patient, separate lesions of alopecia areata may begin, evolve, remit and recur independently of one another. The acute stage is seen in rapidly progressive disease or disease of recent onset, as is found in evolving alopecia totalis or at the advancing margin of an enlarging bald spot. The total number of follicles appears normal. Several affected hairs are still terminal anagen follicles, with bulbs in the fat or deep.

    This patient had rapid, diffuse hair loss progressing over a period of just a few months. Some but seldom all anagen phase and early catagen phase hairs demonstrate a peribulbar mononuclear cell inflammatory infiltrate. This hair was easily pulled from the scalp. The wider, distal end right side shows a fracture, and the proximal end is narrow and hypopigmented. Most exclamation mark hairs are in the telogen phase. In some cases, peribulbar inflammation may be subtle or even absent, and other histological features are required to establish the diagnosis.

    The presence of peribulbar inflammation is helpful but not essential to making the diagnosis of alopecia areata. Small numbers of eosinophils may be present, but plasma cells are unusual Figures The infiltrate may invade the dermal papilla and hair matrix, resulting in damage to matrix cells. Especially when exocytosis of inflammatory cells into the hair matrix occurs, but sometimes in its absence as well, the matrix appears blurred and somewhat disorganized Figures There may be both intercellular spongiosis and intracellular edema.

    This change may be subtle or quite prominent, and can affect the suprabulbar as well as the bulbar zone Figures Some anagen follicles show vacuole formation or necrosis of matrix cells located just above the upper pole of the dermal papilla, corresponding to the site of early hair cortex formation Figure This can result in small cystic spaces filled with acantholytic, necrotic cells.

    Focal matrix cell vacuolization and necrosis is a characteristic feature of alopecia areata, but it affects relatively few follicles and is found in. This patient had black, but graying hair until his hair loss began. The gray hairs were initially spared, but eventually they too were shed. Nuclear pyknosis and cell death apoptosis occurs not only in matrix keratinocytes, but also in outer root sheath cells and bulbar melanocytes. Amorphous clumps of pigment pigment casts are occasionally found within the follicular epithelium as a byproduct of hair matrix degeneration Figure At this level,the number and size of hairs appears roughly normal, but the presence of several slightly inflamed stelae arrows gives a clue to the diagnosis.

    As a result of damaged bulbar melanocytes and keratinocytes, pigment incontinence is often seen in the dermal papilla and follicular sheath of affected hairs. The second or subacute stage of alopecia areata does not correlate well with the extent or duration of clinical disease. This stage is the one most commonly encountered by pathologists. When all follicles are counted, requiring examination of transverse sections at both deep and superficial levels, the total number of follicles appears normal. Peribulbar inflammation tends to subside after the hair has entered the catagen phase, so that late catagen and telogen hairs are usually free of inflammation Figure Despite the peribulbar inflammation and matrix injury, some anagen hairs continue to produce hair shafts.

    Some of these shafts show trichomalacia, and are. Many follicles produce shafts that become progressively smaller in volume and cross-sectional dimension. These hairs gradually taper down to a point Figure They represent the pencil point hairs which fall from the scalp in great numbers. A transverse section through the site of constriction may show a minute or absent Figure The term. Anagen arrest is characteristic of chemotherapy-induced alopecia, but the initial stages of alopecia areata when terminal hairs are still present also have features of an anagen arrest.

    The outer root sheath of this inflamed follicle see also Figure Some lymphocytes have invaded the outer root sheath. After remaining in the telogen phase for a period of time about days in a normal follicle; an unknown length of time in alopecia areata , hair follicles reenter the anagen phase.

    Unless the disease has spontaneously subsided, an. The third histological stage, which here is referred to as chronic, is found in stable, long-standing bald patches and in well-established alopecia totalis or universalis. Terminal anagen hairs, with or without surrounding mononuclear infiltrate, are rare.

    An Atlas of Hair Pathology with Clinical Correlations

    Thus, the most familiar histological finding of alopecia areata may be absent. In addition, all the follicles may become miniaturized, but the total number of follicles remains normal Figures This remains true for years or even decades, but eventually follicular dropout may occur an example of the biphasic pattern of permanent alopecia; see Figure 4. When follicles are miniaturized, they are often missed on routine vertical sectioning.

    Transverse sections are required to examine and count all follicles. The miniaturized anagen follicles found in chronic disease are situated in the mid- to lower dermis, usually slightly deeper than normal vellus hairs. Normally, anagen hairs develop through a series of developmental stages named anagen I-VI.

    The majority of the miniaturized, diseased follicles in alopecia areata develop to a stage resembling anagen III or IV, but no further. These small, abnormal follicles have been called nanogen hairs nanos, Greek for dwarf , and are a distinctive feature of long-standing alopecia areata. Nanogen hairs are not merely small. Their rapid and distorted life cycle makes them difficult to categorize as anagen, catagen or telogen hairs.

    Shop by category

    The reasons for this are given below. Nanogen hairs have an epithelial matrix that is small relative to the size of the dermal papilla, which is also reduced in volume. Nanogen hairs can be identified in transverse section because they have thin inner and outer root sheaths two or three cell layers , but no central hair shaft, or at most an extremely fine, incompletely cornified shaft Figures The bulb may resemble that of an anagen hair basophilic cells with mitotic activity while the suprabulbar portion. Conversely, the bulb may show features typical of a catagen hair while the suprabulbar zone possesses an anagen-like inner root sheath with trichohyaline granules Figures Nanogen hairs with anagenlike bulbs may have some matrix cells in mitosis while others are undergoing apoptosis Figures Thus, features of active growth mitotic cells and involution apoptotic cells are seen simultaneously.

    Once the inner root sheath has desquamated, the shaft easily fractures at this constriction to form a pencil point hair. Nanogen hair bulbs may be surrounded and sometimes invaded by inflammatory cells, but generally the degree of inflammation is mild and often subtle. The most inflamed nanogen bulbs are those with anagen-like and early catagen-like bulbs Figures Even in the chronic stage of alopecia areata there can be a surprising amount of perifollicular inflammation and infiltration of hair follicles by mononuclear cells.

    However, as in the acute stage, the telogen follicles are relatively spared from an inflammatory infiltrate. This results in a picture of non-inflammatory alopecia areata, a surprising finding in patients who may have very severe and dramatic clinical disease. Below each miniaturized follicle is a collapsed fibrous root sheath stela Figure The student resources previously accessed via GarlandScience. Resources to the following titles can be found at www.

    What are VitalSource eBooks? Disorders in this edition include senescent balding, loose anagen hair syndrome, psoriatic alopecia, and psoriatic alopecia, and chemotherapy-induced alopecia. The book also contains a glossary of terms related to hair pathology. The excellent collection of images and detailed explanation of the clinical conditions will prove invaluable to any budding practitioner of the art and science of "trichopathology.

    Stay on CRCPress. Preview this Book. Cowper, Eleanor A. Add to Wish List. Close Preview. Toggle navigation Additional Book Information. Summary Diagnosing and treating hair disorders is still a subject that is rarely or only superficially covered in residency training.