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T He Alo Pecias t he a lo pecias hair follicles can be noted as early as 4 days following 2. Camacho F, Montagna W. Trichologie-maladies radiation. Similar effects are noted with x-rays and elec- du follicule pilosébacé. Madrid, Spain: Grupo Aula tron beam radiation. The earliest change is thinning of Médica SA; 1997. the hair bulb, especially in the area of the matrix. Two or 3. Olsen EA. Disorders of Hair Growth—Diagnosis and 3 weeks following irradiation, hairs with tapered shafts Treatment. New York, NY: McGraw-Hill; 1997. are apparent. The number of follicles showing radiation 4. Bouhanna P. Alopécies traumatiques. In: Bouhanna P, effects is roughly proportional to the dose of radiation. Reygagne P, ed. Pathologie du cheveu et du cuir chev- The definitive treatment is the scar excision or, better, a elu. Paris, France: Masson; 1999:145–152. hair transplant restoration (Figure 10.18a and b). 5. Tosti A, Miteva M, Torres F, Vincenzi C, Romanelli P. Hair casts are a dermoscopic clue for the diagnosis of traction alopecia. Br J Dermatol. 2010;163:1353–1355. CONCLUSION 6. Tosti A. Dermascopy of Hair and Scalp Disorders. Traction alopecia and trichotillomania are types of physi- London: Informa Healthcare; 2007. cal trauma that can lead to alopecia. 7. Bouhanna P. Les alopécies traumatiques, une triple Traction alopecia is seen most commonly in black orientation diagnostique. In: Bouhanna P, ed. Les alo- females. Trichotillomania is a traction alopecia related to pécies—de la clinique au traitement. Collection Guide a compulsive disorder. In the long term, permanent alo- Pratique de Dermatologie. Paris, France: Med’Com;2004. pecia may occur. 8. Ferrando J. Alopecias: Guia de diagnostico y trata- miento. Barcelona, Spain: Pulso; 2000. REFERENCES 9. Camacho FM, Tosti A. Montagna tercera Edicion— 1. Rook A, Dawber R. Diseases of the Hair and Scalp. Tricologia Enfermedades del foliculo pilosabaceo. Oxford, UK: Blackwell Scientific P blications; 1982. Madrid, Spain: Biblioteca Aula Medica Editions; 2014. 98 11 Management of acquired primary cicatricial alopecia Salvador Villablanca and Juan Ferrando INTRODUCTION The ratio between PCA and SCA is estimated at 1:15, and Human hair involves aspects of self-image, identity, the ratio between neutrophilic and lymphocytic PCA is ethnicity, and health, among other attributes. This is why 1:4.3 it is no surprise that diseases that cause alopecia can cause Between 30% and 40% of patients with PCA in a hair altered self-perception and psychosocial interactions.1 research institution are cataloged as pseudopelade (or Alopecia can be classified as cicatricial (or scarring) and noncicatricial. In turn, cicatricial alopecia (CA) is subdivided into primary cicatricial alopecia (PCA) and Table 11.1 Causes of Secondary Cicatricial Alopecia secondary cicatricial alopecia (SCA). The PCAs represent Physical/ • Chemical burns a rare and heterogeneous group of diseases, clinically chemical agents • Insect bites characterized by the absence of follicular ostium and his- • Mechanical trauma, traction, tologically by the replacement of hair follicle structures compression or laceration by fibrous tissue making the alopecia irreversible. From • Radiation dermatitis a physiopathological point of view, the scar is the end • Thermal burns point of reparative fibrosis with permanent destruction of the preexisting tissue.2–4 In PCA the hair follicle is the Dermal • Fungic infections granulomatous main target of the inflammatory process, as evidenced • Protozoa infiltrations • Tuberculosis microscopically as a preferential destruction of follicu- (infectious • Syphilis lar epithelium and/or adventitial dermis associated with origin) relative preservation of interfollicular reticular dermis.5,6 • Viral infections In secondary CA, the destruction of the hair follicle is Dermal • Necrobiosis lipoidica not the primary pathological event. It results from non- granulomatous • Sarcoidosis follicular damage that eventually destroys the follicle. In infiltrations • Amyloidosis these cases, the permanent follicular scarring develops (noninfectious) • Actinic granuloma when the involved pathological process is close to the fol- licular unit. Exogenous factors such as trauma (burns, Sclerosing • Lichen sclerosus et atrophicus radiation, and traction) and infiltrative and inflamma- disorders • Morphea tory endogenous processes (sarcoidosis, pemphigus vul- • Scleroderma garis, and scleroderma) may result in secondary scarring • Sclerotic porphyria cutanea tarda alopecia2,4,7 (Table 11.1). Neoplastic • Basal cell carcinoma Primary CA may become a true clinical challenge due infiltrations • Squamous cell carcinoma to the limited knowledge of the natural history of the dis- ease. Many do not have a known cause. Clinical findings • Dermatofibrosarcoma protuberans often have limited useful data for the diagnosis, because • Lymphoma of overlapping findings and lack of specific signs. This • Malignant melanoma sometimes makes it difficult to distinguish between the • Metastasic carcinoma different conditions. Also, the clinical and histological • Adnexal Tumor characteristics can change over time, finally resulting in • etc. most cases in hair replacement with scarring tissue. Inherited and • Aplasia cutis, eccrine hamartoma, congenital incontinencia pigmenti, keratosis pilaris EPIDEMIOLOGY disorders spinulosa decalvans, neurofibromatosis, The epidemiology of PCA in the general population is chondrodysplasia punctata, polyostotic unknown. Two retrospective studies in hair research fibrous dysplasia, cutis verticis gyrata, institutions estimated prevalence between 3.2% and Darier disease, epidermal nevi, 7.3%. 2,3 In a recent survey performed in the United epidermolisis bullosa, hair follicle Kingdom, the estimated incidence of PCA was 6.96 per hamartoma, hypotrichosis congenita, 1000 new general dermatology referrals per year, which is ichthyosis (sex-linked recessive), porokeratosis of Mibelli equivalent to about 9.6 new cases per clinician per year.8 99 t he a lo pecias nonspecific cicatricial alopecia).2 This means that one- Table 11.2 Proposed NAHRS Working Classification of third of cases have no specific diagnosis, becoming a Primary Cicatricial Alopecia true diagnostic and therapeutic “desert” for both der- Lymphocytic Chronic cutaneous lupus erythematosus matologists and patients. The diagnosis of PCA is not a Lichen planopilaris purely academic exercise, because early treatment of the Classic lichen planus inflammatory component may prevent the progression Frontal fibrosing alopecia of primary scarring alopecia, and the secondary fibrosis Graham-Little syndrome that gives the alopecia its irreversibility. Within the PCA Classic pseudopelade (Brocq) with predominantly lymphocytic infiltrate, the most fre- Central centrifugal cicatricial alopecia quent condition varies depending on the different series. Alopecia mucinosa, First and second places in frequency are always disputed Keratosis follicularis spinulosa decalvans between lichen planopilaris (and its variants) and cutane- Neutrophilic Folliculitis decalvans ous discoid lupus erythematosus, followed by pseudope- Dissecting cellulitis/folliculitis lade of Brocq (PB).2,3,9 This difference may be influenced (perifolliculitis capitis abscedens et by a discrepancy in the clinicopathological diagnostic cri- suffodiens) teria between authors, especially in regard to the classical Mixed Folliculitis (acne) keloidalis PB (an entity in constant discussion). Among the causes Folliculitis (acne) necrotica of PCA with an initially neutrophilic infiltrate, we should Erosive pustular dermatosis consider folliculitis decalvans (FD) as the most common Nonspecifi form (10% of al PCA), unlike perifolliculitis abscedens et 10 Source: Adapted from Tan E, Martinka M, Ball N et al., J Am suffodiens capitis (less than 5% of PCA). Acad Dermatol. 2004;50:25–32. ETHIOLOGY There is a paucity of data in the literature regarding the origin of PCA. In most of the literature, histopathol- type of predominant inflammatory cell infiltrate (lym- ogy revealed the presence of inflammation affecting the phocytic and neutrophilic), a concept that had been pre- upper portion of the hair, which would explain the irre- viously suggested by other authors, but was improved by versibility of the process, because at this location, stem this working group, adding two more subgroups: mixed cells are housed. This place called the protuberance or and nonspecific (Table 11.2). Although there have been bulge is located in the infundibulum, where the hair debates about whether this classification is satisfactory, erector muscle inserts. In some situations, the trigger it gives us a practical and reasonable view for basic and of this inflammatory response is the result of an anti- clinical research. genic stimulation of Langerhans cells that are located in the pilosebaceous unit. Examples of a possible antigenic CLINICAL PATTERNS OF PRESENTATION stimuli would be ultraviolet radiation in the case of lupus There is a big clinical and histopathological overlap erythematosus, certain medications in the case of lichen between different entities of PCA. There are some forms planopilaris, and Staphylococcus aureus in the case of fol- of PCA whose existence per se is discussed, and among liculitis decalvans. With the new knowledge in respect to them is the pseudopelade of Brocq. its origin, it is known that there is a loss of immune pro- In daily practice we observe two major clinical pat- tection of bulge stem cells,5,11 a dysfunction in the
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