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Scarring Alopecia

  • Author: Basil M Hantash, MD, PhD, MBA; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Feb 26, 2016
 

Background

A systematic approach to the evaluation of alopecia allows for more effective management. Below is a step-by-step approach that can be used in scarring alopecia:

  • Initial classification of alopecia type
  • Applying scarring alopecia terminology based on clinical features
  • Using histology findings to further support/define the diagnosis
  • Providing an overall evaluation/diagnosis with treatment options

Initial classification

The initial determination of alopecia type usually begins with the establishment of alopecia as either a scarring (cicatricial) alopecia or nonscarring alopecia. Nonscarring alopecias tend to have preserved follicular ostia. No clinically visible inflammation is noted in most presentations, although histologic inflammation may be present. The most common nonscarring alopecias include alopecia areata and telogen effluvium.

Scarring alopecias have loss of follicular ostia, or atrophy. Clinical inflammation is frequently, but not always, present. Histologic inflammation may be present. Ultimately, histologic confirmation is the best method to confirm the presence of a fibrosing/scarring process with loss of hair follicles.

Many alopecia types are biphasic. For example, androgenetic alopecia eventually results in loss of ostia and thus may appear like a scarring alopecia. This article focuses on the alopecia types that are believed to be due to an inflammatory response with rapid secondary scarring if not controlled.

Scarring alopecia terminology based on clinical features

Once the patient is determined to have scarring alopecia, establishing and clarifying the diagnostic options and terminology is important to assist in confirming the diagnosis, initiating treatment, and suggesting a prognosis. Several manuscripts have examined and attempted to clarify the literature findings,[1, 2, 3] as summarized below.

Also important to note is that examination alone cannot be the final step; the literature is filled with examples of misdiagnosis and diagnostic mimics in alopecia.[4, 5, 6, 7] This includes patients presenting with nonscarring, noninflammatory alopecia that is later found to be scarring and inflammatory.[8] Even amongst the scarring alopecia presentation, it is sometimes debated as to the role of immune alteration versus pure external factors that cause the scarring alopecia. Much of the confusion is often based in the similarities of clinical presentation, which emphasizes again the importance of not basing diagnosis purely on clinical examination findings alone.[9]

Diagnoses in which lymphocytes predominate are as follows:

Lichen planopilaris

The diagnosis of lichen planopilaris (LPP) is confirmed by a combination of clinical and histologic features. The following subtypes are recognized[10] :

  • Frontal fibrosing alopecia (FFA): This is a potential clinical variant of lichen planopilaris, with similar histologic features. Frontal fibrosing alopecia has been associated with the postmenopausal state (ie, postmenopausal frontal fibrosing alopecia), although not all patients with this diagnosis are postmenopausal. Note the image below.
    End-stage scarring alopecia (ESSA) with prior hist End-stage scarring alopecia (ESSA) with prior history of itching and burning, along with a receding hairline. Started as the lichen planopilaris variant, frontal fibrosing alopecia. Used with permission, rights retained, courtesy of Rashid M. Rashid, MD, PhD, Morzak Research Collaborative.
  • Fibrosing alopecia in pattern distribution (FAPD): This also is a potential clinical variant of lichen planopilaris, with similar histologic features. Additionally, fibrosing alopecia in pattern distribution has some histologic/clinical overlap with androgenetic alopecia. Fibrosing alopecia in pattern distribution may also be an overlap of lichen planopilaris with androgenetic alopecia.
  • Graham-Little syndrome: This entity is also a possible overlapping condition, with features of lichen planopilaris and other alopecia types.

Central centrifugal cicatricial alopecia (CCCA)

CCCA is a diagnostic category adopted by the North American Hair Research Society to encompass terms such as hot comb alopecia, follicular degeneration syndrome, pseudopelade in African Americans, and central elliptical pseudopelade in whites.[10] Despite the many attempts to clarify and unify the terminology of central CCCA patterns of scarring alopecia, CCCA is not clearly a diagnostic entity in and of itself.

Pseudopelade

Pseudopelade is a term used to describe a clinically noninflammatory patchy alopecia. The most common condition to produce this appearance is lichen planopilaris. The term “idiopathic pseudopelade” refers to a distinct fibrosing alopecia characterized by a thin dermis, with dense eosinophilic dermal collagen and thick recoiled elastic fibers. The fibrous tracts are broad and may contain granulomas, but the surrounding elastic sheath is preserved.

Traction alopecia

As the name implies, traction alopecia is alopecia secondary to physical traction. Variant presentations exist with terminology that is optional for differentiating purposes. This includes alopecia linearis frontalis (ALF), more commonly known as marginal alopecia, and chignon alopecia, which is when a tight hair bun causes the traction changes.

Secondary systemic scarring alopecia

Secondary systemic scarring alopecia is a term used when the alopecia is a feature of a systemic disease (eg, scleroderma, discoid lupus erythematosus). Discoid lupus erythematosus is often a cause of alopecia. In the classic lupus classifications scheme, discoid lupus erythematosus is one of the chronic cutaneous lupus types (along with tumid lupus and lupus panniculitis).

Trichotillomania

Trichotillomania is a nonscarring psychiatric alopecia that can have a scarring clinical presentation. Trichotillosis is an alternative term that some physicians believe is more acceptable to patients.[11]

Chemotherapy alopecia

Chemotherapy alopecia is often thought of as nonscarring alopecia; however, reports of permanent alopecia suggest that hair stem cells can be permanently destroyed. Note the image below.

Alopecia due to primary cutaneous follicular cente Alopecia due to primary cutaneous follicular center cell lymphoma. Used with permission, rights retained, courtesy of Rashid M. Rashid, MD, PhD, Morzak Research Collaborative.

Alopecia mucinosa

Follicular mucinosis can exist by itself or can be a manifestation of mycosis fungoides.

Keratosis pilaris atrophicans

Keratosis pilaris atrophicans involves a spectrum of conditions that resemble keratosis pilaris, but result in hair loss.

Diagnoses in which neutrophils predominate are as follows:

  • Folliculitis decalvans: Folliculitis decalvans presents with recurrent crops of follicular pustules that result in permanent epilation. Staphylococci are often cultured from pustules, but this condition does not respond the standard antibiotic regimens. The best results are obtained by long-term use of topical corticosteroids together with an oral tetracycline.
  • Perifolliculitis capitis abscedens et suffodiens: Other terms used for perifolliculitis capitis abscedens et suffodiens include dissecting cellulitis and Hoffman disease. It resembles hidradenitis suppurativa and the 2 often occur together.
  • Tufted hair folliculitis: Tufted hair folliculitis often contains Staphylococcus aureus, but it is unclear if a preexisting abnormality predisposes to staphylococcal infection. Clinically, 5-20 hairs emerge from a common dilated follicular orifice, producing a clinical resemblance to doll hair. This is often seen as a reactive pattern present in multiple types of scarring alopecia and even as a reaction to medications. [12]

Diagnoses in which a mix of cell types predominate are as follows:

  • Acne keloidalis: Others terms used for this condition include acne keloidalis nuchae, dermatitis papillaris capillitii, sycosis nuchae, and folliculitis keloidalis. Patients present with pustules, alopecia, and hypertrophic scarring on the posterior neck. Many plasma cells are typically present in the infiltrate.
  • Acne necrotica: Acne necrotica is sometimes also called folliculitis necrotica. This condition is rare and exists in 2 variants. The first is acne necrotica varioliformis, which is a distinctive necrotizing disorder of the hair follicle that heals with varioliform scars. The second is acne necrotica miliaris, which is a nonscarring folliculitis.
  • Erosive pustular dermatosis of the scalp: This condition often follows surgery or other trauma. It presents with an expanding patch of crusts and pustules. [13] It has been reported to respond to potent topical corticosteroids, tacrolimus, and light therapy.

Diagnoses for which the least evidence-based characterization is available are as follows:

  • Pressure alopecia: Pressure alopecia is due to constant pressure to the region. Often described as a nonscarring reversible alopecia, it has also been reported to result in permanent scarring. This may be more accurately termed externally traumatic alopecia or iatrogenic alopecia. [14] As in chemotherapy alopecia, the rapidly growing hair follicle and hair cell source (bulge and associated regions) may be especially susceptible to antimetabolic insult, such as lack of blood flow.
  • Lipedematous alopecia: Lipedematous alopecia is a rare condition with unknown scarring potential. It is also referred to as lipedematous scalp.
  • Senescent alopecia: Senescent alopecia is also known as senile alopecia, a diffuse thinning due to decreased terminal hairs but without increased miniaturization. [15] It is thought to affect people aged 40-50 years or older with no family history or evidence of pattern balding. Senescent alopecia is not a primary diagnosis in all clinics and often is debated as a diagnosis as actually being late-onset androgenetic alopecia. [16]
  • Keratosis follicularis atrophicans
  • Possible variants include keratosis pilaris decalvans, an X-linked and sporadic condition, and folliculitis spinulosa decalvans, which is autosomal dominant.
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Pathophysiology

The etiology for most forms of scarring alopecia is largely unknown and represents a fertile area for research.

One study suggested an autosomal dominant pattern of inheritance with CCCA, with hairstyling and gender as strong contributing factors.[17]  A population study of environmental and medical risk factors for CCCA development described a possible correlation between the clinical presentation of CCCA and the finding of diabetes. The study also reminds us that traction makes alopecia, including CCCA worse; hot comb use does not necessarily play a role.[18] The major limitations of this study should be acknowledged and include the lack of biopsies and the reliance on self-reporting. Clinical CCCA does not always translate into histological CCCA because clinical mimics are common in alopecia.

For lichen planopilaris, related entities include frontal fibrosing alopecia and fibrosing alopecia in pattern distribution. Research has suggested that dysfunction in the PPAR receptor plays a role in the pathophysiology of lichen planopilaris. The dysfunction results in toxic fatty acid buildup.[19]

Studies have also show a significantly higher ratio of Langerhans cells to T lymphocytes in lichen planopilaris compared with that seen in traction alopecia.[9]

Sebaceous gland damage is also believed to be more common in scarring alopecia and can be a histologic clue to scarring.[20] Although it is not clear if a difference exists between external trauma–induced scarring alopecia and internal dysfunction, such as in lichen planopilaris. Nevertheless, it can be a good clue to differentiate from clinical mimics that can be seen in nonscarring alopecia.

Scarring alopecia can also result from rather unexpected causes. In particular, epidermal growth factor receptor inhibitors and chemotherapy-induced scarring/permanent alopecia have been reported.[21]

Traction alopecia is believed to be related directly to external factors, such as traction or trauma resulting from activities such as break dancing.[22]

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Epidemiology

Frequency

United States

Epidemiology studies are mostly from clinics dedicated to alopecia. Within the alopecia population, the prevalence of scarring alopecia is believed to be approximately 7%.[23] The relative prevalence of each type of scarring alopecia varies by different reports and is highly clinic dependent.[23]

No large evidence-based medicine studies are available to report the epidemiology of lichen planopilaris, central centrifugal cicatricial alopecia, or pseudopelade in the general population.

Traction alopecia is most commonly seen in the African American population because of the practice of styling the hair in tight braids or the use of chemical hair straighteners. Female athletes who pull their hair back tightly have been found to develop from this problem. Traction alopecia is also reported in nurses who secure their nurse's caps to their scalp with bobby pins.[14, 15] The exact frequency of traction alopecia in the United States has yet to be documented.

International

Traction alopecia is seen worldwide. Its frequency usually depends on cultural customs. Japanese women who wear a traditional hairdo, Sikh men in India, and others who wear ponytails are examples of individuals who may be affected.

Population studies show a prevalence of 17.1% in African schoolgirls (6-21 y) and of 31.7% in women (18-86 y).[24] This is by far one of the most frequent types of scarring alopecia presentations.

Scarring alopecia prevalence studies are otherwise still lacking. Partial hindrance of such data production is based on the lack of well-established diagnostic criteria. Prevalence from specialty clinics has been estimated, although extrapolation to the general population is still difficult.[25]

Race

Large race-based studies are not yet available. Central centrifugal cicatricial alopecia is believed to be predominant in African Americans, while lichen planopilaris occurs mostly in lighter-skinned patients.

Sex

The sex distribution of scarring alopecia is anecdotally believed to be predominantly favoring the female population.

Age

Traction alopecia is initially seen in children and young adults. Traction alopecia is an uncommon overall cause of hair loss in adults. However, in the African American population, this entity is a significant cause of alopecia. The exact frequency has yet to be documented in children, young adults, and adults.

Age distribution on the other scarring alopecia types has not been well studied. The majority of case reports suggest these conditions present in persons older than 20 years.

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Contributor Information and Disclosures
Author

Basil M Hantash, MD, PhD, MBA Medical Director, Advanced Skin Institute

Basil M Hantash, MD, PhD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Society for Dermatologic Surgery, Sigma Xi, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Coauthor(s)

Mayla T Carlos, PA-C, MPH, MSPAS Physician Assistant for Dermatology Practice, Advanced Skin Institute

Mayla T Carlos, PA-C, MPH, MSPAS is a member of the following medical societies: American Academy of Physician Assistants, California Academy of Physician Assistants

Disclosure: Nothing to disclose.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: American Medical Association, Alpha Omega Alpha, Association of Military Dermatologists, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Phi Beta Kappa

Disclosure: Nothing to disclose.

Warren R Heymann, MD Head, Division of Dermatology, Professor, Department of Internal Medicine, Rutgers New Jersey Medical School

Warren R Heymann, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Jaggi Rao, MD, FRCPC Clinical Professor of Medicine, Division of Dermatology and Cutaneous Sciences, Director of Dermatology Residency Program, University of Alberta Faculty of Medicine and Dentistry

Jaggi Rao, MD, FRCPC is a member of the following medical societies: American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for Laser Medicine and Surgery, Canadian Medical Association, Pacific Dermatologic Association, Royal College of Physicians and Surgeons of Canada, Canadian Medical Protective Association, Canadian Dermatology Association

Disclosure: Nothing to disclose.

Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, Rutgers New Jersey Medical School; Visiting Professor, Rutgers University School of Public Affairs and Administration

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, New York Academy of Medicine, American Academy of Dermatology, American College of Physicians, Sigma Xi

Disclosure: Nothing to disclose.

Rashid M Rashid, MD, PhD Director, Mosaic Clinic Hair Transplant Center of Houston

Rashid M Rashid, MD, PhD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Texas Dermatological Society, International Society of Hair Restoration Surgery, Council for Nail Disorders, Houston Dermatological Society

Disclosure: Nothing to disclose.

References
  1. Chiu HY, Lin SJ. Fibrosing alopecia in a pattern distribution. J Eur Acad Dermatol Venereol. 2010 Feb 2. [Medline].

  2. Olsen EA. Female pattern hair loss and its relationship to permanent/cicatricial alopecia: a new perspective. J Investig Dermatol Symp Proc. 2005 Dec. 10(3):217-21. [Medline].

  3. Ross EK, Tan E, Shapiro J. Update on primary cicatricial alopecias. J Am Acad Dermatol. 2005 Jul. 53(1):1-37; quiz 38-40. [Medline].

  4. Nusbaum BP, Nusbaum AG. Frontal fibrosing alopecia in a man: results of follicular unit test grafting. Dermatol Surg. 2010 Jun. 36(6):959-62. [Medline].

  5. Rashid RM, Thomas V. Androgenic pattern presentation of scarring and inflammatory alopecia. J Eur Acad Dermatol Venereol. 2010 Jan 6. [Medline].

  6. Rakowska A, Slowinska M, Kowalska-Oledzka E, Olszewska M, Czuwara J, Rudnicka L. Alopecia areata incognita: true or false?. J Am Acad Dermatol. 2009 Jan. 60(1):162-3. [Medline].

  7. Abraham LS, Torres FN, Azulay-Abulafia L. Dermoscopic clues to distinguish trichotillomania from patchy alopecia areata. An Bras Dermatol. 2010 Oct. 85(5):723-6. [Medline].

  8. Iorizzo M, El Shabrawi Caelen L, Vincenzi C, Misciali C, Tosti A. Folliculotropic mycosis fungoides masquerading as alopecia areata. J Am Acad Dermatol. 2010 Aug. 63(2):e50-2. [Medline].

  9. Hutchens KA, Balfour EM, Smoller BR. Comparison between Langerhans cell concentration in lichen planopilaris and traction alopecia with possible immunologic implications. Am J Dermatopathol. 2011 May. 33(3):277-80. [Medline].

  10. Zinkernagel MS, Trüeb RM. Fibrosing alopecia in a pattern distribution: patterned lichen planopilaris or androgenetic alopecia with a lichenoid tissue reaction pattern?. Arch Dermatol. 2000 Feb. 136(2):205-11. [Medline].

  11. Aljabre SH. Trichotillomania: a trichotillosis, a trichotillotic, or a tic trichotillosis. Int J Dermatol. 1993 Nov. 32(11):823-4. [Medline].

  12. Lacarrubba F, Dall'oglio F, Micali G. Massive tufted hair folliculitis associated with chronic use of systemic corticosteroids. G Ital Dermatol Venereol. 2011 Apr. 146(2):164-5. [Medline].

  13. Kim KR, Lee JY, Kim MK, Yoon TY. Erosive pustular dermatosis of the scalp following herpes zoster: successful treatment with topical tacrolimus. Ann Dermatol. 2010 May. 22(2):232-4. [Medline].

  14. Hwang SM, Lee WS, Choi EH, Lee SH, Ahn SK. Nurse's cap alopecia. Int J Dermatol. 1999 Mar. 38(3):187-91. [Medline].

  15. Renna FS, Freedberg IM. Traction alopecia in nurses. Arch Dermatol. 1973 Nov. 108(5):694-5. [Medline].

  16. Whiting DA. How real is senescent alopecia? A histopathologic approach. Clin Dermatol. 2011 Jan-Feb. 29(1):49-53. [Medline].

  17. Dlova NC, Jordaan FH, Sarig O, Sprecher E. Autosomal dominant inheritance of central centrifugal cicatricial alopecia in black South Africans. J Am Acad Dermatol. 2014 Apr. 70 (4):679-682.e1. [Medline]. [Full Text].

  18. Kyei A, Bergfeld WF, Piliang M, Summers P. Medical and environmental risk factors for the development of central centrifugal cicatricial alopecia: a population study. Arch Dermatol. 2011 Aug. 147(8):909-14. [Medline].

  19. Mirmirani P, Karnik P. Lichen planopilaris treated with a peroxisome proliferator-activated receptor gamma agonist. Arch Dermatol. 2009 Dec. 145(12):1363-6. [Medline].

  20. Al-Zaid T, Vanderweil S, Zembowicz A, Lyle S. Sebaceous gland loss and inflammation in scarring alopecia: a potential role in pathogenesis. J Am Acad Dermatol. 2011 Sep. 65(3):597-603. [Medline].

  21. Hepper DM, Wu P, Anadkat MJ. Scarring alopecia associated with the epidermal growth factor receptor inhibitor erlotinib. J Am Acad Dermatol. 2011 May. 64(5):996-8. [Medline].

  22. Monselise A, Chan LJ, Shapiro J. Break dancing: a new risk factor for scarring hair loss. J Cutan Med Surg. 2011 May-Jun. 15(3):177-9. [Medline].

  23. Whiting DA. Cicatricial alopecia: clinico-pathological findings and treatment. Clin Dermatol. 2001 Mar-Apr. 19(2):211-25. [Medline].

  24. Khumalo NP, Jessop S, Gumedze F, Ehrlich R. Determinants of marginal traction alopecia in African girls and women. J Am Acad Dermatol. 2008 Sep. 59(3):432-8. [Medline].

  25. Ochoa BE, King LE Jr, Price VH. Lichen planopilaris: Annual incidence in four hair referral centers in the United States. J Am Acad Dermatol. 2008 Feb. 58(2):352-3. [Medline].

  26. Dorr VJ. A practitioner's guide to cancer-related alopecia. Semin Oncol. 1998 Oct. 25(5):562-70. [Medline].

  27. Matta M, Kibbi AG, Khattar J, Salman SM, Zaynoun ST. Lichen planopilaris: a clinicopathologic study. J Am Acad Dermatol. 1990 Apr. 22(4):594-8. [Medline].

  28. Aten E, Brasz L, Bornholdt D, Hooijkaas IB, Porteous ME, Sybert VP. Keratosis follicularis spinulosa decalvans is caused by mutations in MBTPS2. Hum Mutat. 2010 Jul 29. [Medline].

  29. Prevezas C, Matard B, Pinquier L, Reygagne P. Irreversible and severe alopecia following docetaxel or paclitaxel cytotoxic therapy for breast cancer. Br J Dermatol. 2009 Apr. 160(4):883-5. [Medline].

  30. Sullivan JR, Kossard S. Acquired scalp alopecia. Part II: A review. Australas J Dermatol. 1999 May. 40(2):61-70; quiz 71-2. [Medline].

  31. Callen JP. Chronic cutaneous lupus erythematosus. Clinical, laboratory, therapeutic, and prognostic examination of 62 patients. Arch Dermatol. 1982 Jun. 118(6):412-6. [Medline].

  32. George PM, Tunnessen WW Jr. Childhood discoid lupus erythematosus. Arch Dermatol. 1993 May. 129(5):613-7. [Medline].

  33. Assouly P, Happle R. A Hairy Paradox: Congenital Triangular Alopecia with a Central Hair Tuft. Dermatology. 2010 Jun 26. [Medline].

  34. Armenores P, Shirato K, Reid C, Sidhu S. Frontal fibrosing alopecia associated with generalized hair loss. Australas J Dermatol. 2010 Aug. 51(3):183-5. [Medline].

  35. Rashid RM. Alopecia: the case for systemic care and evaluation. Accepted for publication. Skinmed. 2010. to be determined:

  36. Park H, Kim CW, Kim SS, Park CW. The therapeutic effect and the changed serum zinc level after zinc supplementation in alopecia areata patients who had a low serum zinc level. Ann Dermatol. 2009 May. 21(2):142-6. [Medline].

  37. Amor KT, Rashid RM, Mirmirani P. Does D matter? The role of vitamin D in hair disorders and hair follicle cycling. Dermatol Online J. 2010. 16(2):3. [Medline].

  38. Estrada BD, Tamler C, Sodre CT, Barcaui CB, Pereira FB. Dermoscopy patterns of cicatricial alopecia resulting from discoid lupus erythematosus and lichen planopilaris. An Bras Dermatol. 2010 Apr. 85(2):179-83. [Medline].

  39. Ozcan D, Ozen O, Seçkin D. Vertical vs. transverse sections of scalp biopsy specimens: a pilot study on the comparison of the diagnostic value of two techniques in alopecia. Clin Exp Dermatol. 2011 Sep 15. [Medline].

  40. Nguyen JV, Hudacek K, Whitten JA, Rubin AI, Seykora JT. The HoVert technique: a novel method for the sectioning of alopecia biopsies. J Cutan Pathol. 2011 May. 38(5):401-6. [Medline].

  41. Alkhalifah A, Alsantali A, Wang E, McElwee KJ, Shapiro J. Alopecia areata update: part I. Clinical picture, histopathology, and pathogenesis. J Am Acad Dermatol. 2010 Feb. 62(2):177-88, quiz 189-90. [Medline].

  42. Elston DM, McCollough ML, Warschaw KE, Bergfeld WF. Elastic tissue in scars and alopecia. J Cutan Pathol. 2000 Mar. 27(3):147-52. [Medline].

  43. Zinkernagel MS, Trüeb RM. Fibrosing alopecia in a pattern distribution: patterned lichen planopilaris or androgenetic alopecia with a lichenoid tissue reaction pattern?. Arch Dermatol. 2000 Feb. 136(2):205-11. [Medline].

  44. Sullivan JR, Kossard S. Acquired scalp alopecia. Part II: A review. Australas J Dermatol. 1999 May. 40(2):61-70; quiz 71-2. [Medline].

  45. Rhee CH, Kim SM, Kim MH, Cinn YW, Ihm CW. Two cases of linear alopecia on the occipital scalp. Ann Dermatol. 2009 May. 21(2):159-63. [Medline].

  46. Kossard S, Collins A, McCrossin I. Necrotizing lymphocytic folliculitis: the early lesion of acne necrotica (varioliformis). J Am Acad Dermatol. 1987 May. 16(5 Pt 1):1007-14. [Medline].

  47. Emer JJ, Stevenson ML, Markowitz O. Novel treatment of female-pattern androgenetic alopecia with injected bimatoprost 0.03% solution. J Drugs Dermatol. 2011 Jul. 10(7):795-8. [Medline].

  48. Rushton DH, Gilkes JJ. Delaying treatment in male-pattern hair loss affects the therapeutic response. Clin Exp Dermatol. 2011 Mar. 36(2):204-5. [Medline].

  49. Chiang C, Sah D, Cho BK, Ochoa BE, Price VH. Hydroxychloroquine and lichen planopilaris: efficacy and introduction of Lichen Planopilaris Activity Index scoring system. J Am Acad Dermatol. 2010 Mar. 62(3):387-92. [Medline].

  50. Grant JE, Odlaug BL, Kim SW. N-acetylcysteine, a glutamate modulator, in the treatment of trichotillomania: a double-blind, placebo-controlled study. Arch Gen Psychiatry. 2009 Jul. 66(7):756-63. [Medline].

  51. Earles RM. Surgical correction of traumatic alopecia marginalis or traction alopecia in black women. J Dermatol Surg Oncol. 1986 Jan. 12(1):78-82. [Medline].

  52. Miranda BH, Farjo N, Farjo B. Eyebrow reconstruction in dormant keratosis pilaris atrophicans. J Plast Reconstr Aesthet Surg. 2011 Jul 1. [Medline].

  53. Jimenez F, Izeta A, Poblet E. Morphometric analysis of the human scalp hair follicle: practical implications for the hair transplant surgeon and hair regeneration studies. Dermatol Surg. 2011 Jan. 37(1):58-64. [Medline].

  54. Meyer-Gonzalez T, Bisanga C. Body-Hair Transplant for Cicatricial Alopecia. Actas Dermosifiliogr. 2011 Aug 25. [Medline].

  55. Amor KT, Rashid RM, Mirmirani P. Does D matter? The role of vitamin D in hair disorders and hair follicle cycling. Dermatol Online J. 2010 Feb 15. 16(2):3. [Medline].

  56. Hantash BM, Schwartz RA. Traction alopecia in children. Cutis. 2003 Jan. 71(1):18-20. [Medline].

 
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Traction alopecia.
Alopecia due to primary cutaneous follicular center cell lymphoma. Used with permission, rights retained, courtesy of Rashid M. Rashid, MD, PhD, Morzak Research Collaborative.
Recalcitrant scarring pressure alopecia several years after an ICU stay. Used with permission, rights retained, courtesy of Rashid M. Rashid, MD, PhD, Morzak Research Collaborative.
End-stage scarring alopecia (ESSA) with prior history of itching and burning, along with a receding hairline. Started as the lichen planopilaris variant, frontal fibrosing alopecia. Used with permission, rights retained, courtesy of Rashid M. Rashid, MD, PhD, Morzak Research Collaborative.
Dissecting scalp cellulitis. Used with permission, rights retained, courtesy of Rashid M. Rashid, MD, PhD, Morzak Research Collaborative.
Armpit scarring alopecia in lichen planopilaris variant. Patient presented with frontal fibrosing alopecia. Used with permission, rights retained, courtesy of Rashid M. Rashid, MD, PhD, Morzak Research Collaborative.
Acne keloidalis. A misnomer term based on clinical examination findings. Used with permission, rights retained, courtesy of Rashid M. Rashid, MD, PhD, Morzak Research Collaborative.
Lichen planopilaris in its active stage presenting in a lighter-skinned patient. Courtesy of Rashid M Rashid, MD, PhD, and Ronald Rapini, MD.
Alopecic and aseptic nodules of the scalp (AANS) is a new entity reported first in Japan as "pseudocyst of the scalp." The main location of the nodules was the occiput. The associated alopecia was nonscarring. Histology is nonspecific but often shows deep granulomas. AANS reponds to tetracyclines. Photo courtesy of Sami Abdennader, MD (rights retained).
 
 
 
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