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Symposium-Hair Disorders
2013:79:5;576-590
doi: 10.4103/0378-6323.116726
PMID: 23974576

What's new in cicatricial alopecia?

Sunil Dogra, Rishu Sarangal
 Department of Dermatology, Venereology and Leprology, Postgraduate Institute of Medical Education and Research, Chandigarh, India

Correspondence Address:
Sunil Dogra
Department of Dermatology, Venereology and Leprology, Post Graduate Institute of Medical Education and Research, Chandigarh - 160 012
India
How to cite this article:
Dogra S, Sarangal R. What's new in cicatricial alopecia?. Indian J Dermatol Venereol Leprol 2013;79:576-590
Copyright: (C)2013 Indian Journal of Dermatology, Venereology, and Leprology

Abstract

Scalp hairs complete the body self-image and patients with alopecia suffer from overt disfiguration, leading to psychosocial embarrassment and significant lack of self-esteem. Hence an early diagnosis and an aggressive treatment in the case of active hair loss are crucial in the management of scarring alopecia. This review presents a comprehensive study of newer theories in aetiopathogenesis, evolving diagnostic modalities and a step ladder approach in management of primary cicatricial alopecia.
Keywords: Cicatricial alopecia, primary cicatricial alopecia, secondary cicatricial alopecia, stable alopecia, unstable alopecia

Introduction

Cicatricial alopecias (CAs) or scarring alopecias are a group of uncommon inflammatory hair loss disorders, which are characterized by permanent destruction of hair follicles. Clinically there is loss of visible follicular ostia in the scarring area, with or without epidermal atrophy and histologically there is absence of pilosebaceous structures which are replaced by fibrous tracts. [1],[2],[3],[4],[5] CAs are classified as primary cicatricial alopecia (PCA), secondary cicatricial alopecia (SCA), and developmental/hereditary CA.

PCA is caused by destructive inflammation of the hair follicle. This destruction is attributed to various etiologies, which are predominantly autoimmune processes. In this article, we aim to review newer theories in aetiopathogenesis, recently described clinical patterns, and advances in management of the PCA.

Epidemiology

Very few data on the epidemiology of CA is available in the published literature. One large retrospective study over 10 years showed the frequency of CA as 7.3% of all the hair loss cases. The majority of affected adults were females (2.6:1) and PCA was more common than SCA (4:1). Among causes of PCA, pseudopelade of Brocq (PPB) (40.6%) was most frequent followed by lichen planopilaris (LPP) (12.6%), and folliculitis decalvans (FD) (11.2%). [1]

In another retrospective study, 3.2% patients of hair disorders seen over 5 years had PCA, with majority cases characterized histopathologically by lymphocytic infiltrate (4:1). In this study, discoid lupus erythematosus (DLE) (33.9%) was the most common cause followed by PPB (24.1%) and LPP (22.3%). [2]

A recent questionnaire survey in UK, revealed incidence of PCA as 6.96 cases per 1000 new general dermatology referrals per year, equating to about 9.6 new cases per clinician per year. [3]

Classification

The causes of CA are broadly classified as primary, secondary, and hereditary or developmental defects. [4],[5],[6] In PCA, the hair follicles are the main targets of destructive inflammatory process resulting in irreversible hair loss from the affected site on scalp. The inflammatory cells targets and destroys the stem cells in the bulge area of hair follicles. [4] In SCA, the hair follicles are secondarily damaged as a result of more generalized destructive process within the skin, which ultimately destroys the hair follicle stem cell (HFSC)-based capacity for regeneration. [5] The causes of SCA are trauma (burns, radiation, traction), any infiltrative processes (morphoea, scleroderma, sarcoidosis, neoplasias), and infections (bacterial, fungal, viral, mycobacterial). [6]

Further, the working classification of PCA is based on the most representative pathological finding on scalp biopsies. PCAs are divided into subgroups depending upon the predominant inflammatory infiltrates, that is, lymphocytic, neutrophilic, and mixed [Table - 1], [Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6], [Figure - 7], [Figure - 8], [Figure - 9] and [Figure - 10]. Chronic cutaneous lupus erythematosus (CCLE), LPP, classic PPB, central centrifugal cicatricial alopecia (CCCA), alopecia mucinosa (AM), and keratosis follicularis spinulosa decalvans (KFSD) are categorized under "lymphocytic" PCA. Frontal fibrosing alopecia (FFA) and Graham-Little-Piccardi (GLP) syndrome are considered as LPP variants. The neutrophilic PCA group comprises FD and dissecting cellulitis/folliculitis of scalp (perifolliculitis abscedens et suffodiens). Acne keloidalis nuchae (AK), acne necrotica (AN), and eruptive pustular dermatosis (EPD) are classified as "mixed" cell infiltrate PCA. In addition, nonspecific CA is defined as "idiopathic scarring with inconclusive clinical and histopathological findings". There have been debates whether this classification is satisfactory or not, however, it provides a practical and reasonable standard for clinical and basic studies thus has been widely used. [5],[6],[7]

Table 1: Clinical and histopathological characteristics of primary cicatricial alopecia
Figure 1: Scalp DLE, showing erythematous atrophic plaque with central depigmentation, dilated follicular orifices, follicular plugging, and loss of follicular ostia
Figure 2: Patch of LPP, showing violaceous, peri-follicular papules in the periphery and loss of follicular ostia, dyspigmentation in the center
Figure 3: Violaceous pigmented spots of LP on face along with scarring alopecia
Figure 4: (a) Microphotograph showing hyperkeratosis with peri-follicular inflammation and atrophy of sebaceous unit in a case of LPP (H and E, ×20), (b) Heavy lymphocytic infiltrate around dermoepidermal junction and peri-follicular area (H and E, ×40)
Figure 5: Wide band of bald frontal scalp with bilateral symmetrical thinning of lateral eyebrows in postmenopausal women suffering from FFA
Figure 6: Closer view of the frontal scalp of the same patient suffering from FFA, showing perifollicular erythematous papules at the hair margin (in the active stage of disease)
Figure 7: Multifocal, skin-colored plaques of pseudopelade of Brocq with complete loss of follicular ostia and no signs of inflammation
Figure 8: (a and b) Microphotograph showing thinned out epidermis with total loss of hair follicles, replaced by collagen in a case of PPB (H and E, ×20)
Figure 9: Multiple scarring alopecia areas seen in beard and eyebrows in a patient of KFSD
Figure 10: Folliculitis Decalvans showing scarred scalp with yellowish, crusted pustules at the periphery with matted and tufted hairs in the centre of plaque

Another classification proposed to facilitate determination of the most suitable surgical corrective therapies for CA, categorize it into "stable" and "unstable" type [Table - 2]. [8] "Stable" CAs are secondary to isolated events that cause permanent scarring in a hair-bearing region. Once corrected surgically, there is no need for constant vigilance. Whereas "unstable" cicatricial alopecias (UCAs) are secondary to disorders that have a tendency to progress and recur intermittently over the course of time. Therefore, prior to considering any surgical treatment, it is vital to identify the type of alopecia and also to confirm quiescence preferably for at least 1 year so that they can be successfully treated medically before scarring actually occurs. [8]

Table 2: Stable and unstable cicatricial alopecia

Pathogenesis

PCA is characterized by permanent destruction of hair follicles, progressive deposition of collagen, and is frequently associated with loss of sebaceous glands. The pathogenesis of PCA revolves mainly around the destruction of slow-cycling, pluripotent HFSCs. [9] These HFSCs are located in the ′bulge′ region of hair follicle in outer root sheath (i.e., at the site of attachment of the arrector pili muscle to the outer root sheath). These stem cells are thought to produce secondary germ cells or transient amplifying cells that migrate in a bidirectional fashion, undergoing coordinated differentiation to restore and renew the upper follicle, including the sebaceous gland, and adjacent epidermis; and regrow the lower hair follicle during normal telogen-anagen cycling. [10]

But, HFSCs destruction alone cannot explain the full phenotypic profile seen in different PCA entities like erythema, epidermal atrophy, follicular plugging. Therefore, other pathogenic processes may account for such changes. [11]

The newer insights into the pathogenesis of PCA mainly involves the HFSCs destruction theories, impairment of self maintenance of HFSCs, alteration of lipid metabolism, neurogenic inflammation theory, environment, and genetic factors. [4],[11],[12],[13],[14],[15],[16],[17],[18],[19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[31],[32],[33],[34],[35],[36],[37],[38],[39],[40],[41],[42],[43],[44],[45],[46],[47],[48],[49],[50],[51],[52],[53],[54]

Hair follicle stem cells destruction theory

This theory is based upon the observation of the peri-follicular inflammatory infiltrate relative to the two key structures of the hair follicle, the hair bulb (where the hair shaft is generated), and the hair bulge. In the prototypic reversible autoimmune hair loss disorder alopecia areata (AA), the inflammatory infiltrate is centered around the hair bulb; whereas in PCA, the infiltrate is mainly located around the bulge region and distal (noncycling) follicle. This marked difference in the intradermal location of the inflammatory infiltrate has major clinical consequences, that is, reversible versus permanent hair loss. [11],[12],[13]

Further, immuno-staining of keratin 15, (a recognized hair ′bulge′ marker in humans) has shown to be diminished or absent from the bulge region in LPP and CCLE with predominantly dense peri-follicular inflammatory infiltrates, suggesting that the inflammatory process is destroying the HFSCs pool. [14],[15]

Similarly, other studies showed that the bulge region, marked by the biomarkers such as keratin-15 and -19 and CD200, is preferentially affected and replaced by fibrotic tissue in PCA leading to permanent hair loss. [16],[17] Recent studies reported some cell populations marked by MTS24, [18] Lrig1, [19] Nestin, [20] Lgr5, [21] and Lgr6 [22] are also capable of reconstituting hair follicles, suggesting that these cells are endowed with some stem cell characteristics. But the inflammation and subsequent fibrosis in PCA affect most of these cell populations also, except Lgr5 expressing cells. [4]

Collapse of hair follicle immune privilege

Hair follicles provide major portal for entry of microbial agents but in immuno-competent individuals the clinical consequences of such invasions are rare, this is because of anti-infection defense mechanisms like intraepithelial T-cells, Langerhans cells, perifollicular mast cells, macrophages, and antimicrobial peptides (human β2-defensin, psoriasin, cathelicidin, and RNAse7). These substances together with various chemokines and proinflammatory molecules can cause massive inflammation, which can also breach the follicular epithelium. But the hair follicle has established a state of immuno-suppression known as ′immune privilege′ in its bulb and bulge region. This is done by the expression of potent endogenous immuno-suppressants like TGF-β1 and 2 (secretes macrophage inhibitory factor), α-MSH in hair follicular epithelium and low or absent expression of MHC class I and II molecules around the bulb and bulge. [11]

′Hair follicle immune privilege collapse′ is thus an attractive theory to explain the exposure of HFSCs to immune-mediated attack in PCA. The data supporting this show the immune reactivity of MHC class I, β2-microblobulin, and MHC class II, is upregulated in the hair ′bulge′ region of lesional skin, compared with uninvolved skin, in different PCA entities. [23]

Cytotoxic cell mediated hair follicle damage and proinflammatory response leading to PCA

This hypothesis is based upon the inflammatory infiltrate observed in the scalp biopsies of CCLE, LPP, and FD. In scarred areas of CCLE, there is upregulation of γδ-T-lymphocytes with increased expression of chemokine 4, co-localization of skin homing marker cutaneous lymphocyte antigen (CLA) with the cytotoxic marker granzyme B leading to direct cytotoxic tissue damage. [4],[11] Various proinflammatory cytokines like INF-γ, TNF-α, IL-2 are upregulated in the lesional skin of LPP, CCLE, and FD, leading to direct tissue damage and hence scarring. [4],[11]

Increased apoptosis in PCA

Apoptotic keratinocytes are commonly observed during the histological assessment of PCA, suggesting a potential role of apoptosis in these disorders. In CCLE, apoptosis is increased in the hair follicle epidermis with the upregulation of epithelial proliferation marker Ki-67 and the tumor suppressor gene p53. The p53 direct the damaged cells into apoptosis. [24],[25] Also, the expression of the constitutive apoptosis inhibitor Bcl-2 is reduced in CCLE, further predisposing to apoptosis-related tissue injury. [23] Peri-follicular FASL+ infiltrate is thought to play a key role in the follicular destruction commonly seen in CCLE through inappropriate apoptosis induction. [24],[26]

Lipid metabolism dysregulation in PCA pathogenesis

With an insufficient evidence, this hypothesis is based upon the observation of spontaneous mutation, in widely studied mouse model for PCA. [27] It states that defect in stearoyl-CoA desaturase 1 (required for sebaceous gland fatty acid composition) results in sebaceous glands atrophy and abnormal gland secretions, which in turn lead to delayed inner root sheath disintegration, retrograde hair shaft growth and penetration of the bulb, with resulting foreign body reaction and eventual destruction of the hair follicle. [27],[28] This supports the idea that inflammation in scarring alopecia is a secondary event resulting from a primary defect in the pilosebaceous unit. [29]

Another evidence supporting this hypothesis, is a recent study on decreased expression of genes for peroxisome proliferator-activated receptor γ (PPARγ) (required for lipid metabolism) and peroxisome biogenesis which triggers the pathogenesis of LPP. [30] The study states that decrease in expression of these genes led to progressive loss of peroxisomes, accumulation of proinflammatory lipids, and infiltration of inflammatory cells around the pilosebaceous structures followed by destruction of the complete pilosebaceous unit. [30] Based upon this theory, the beneficial role of PPARγ agonist in LPP has been described. [31] (Detailed more under "Management" section.)

Impaired self-maintenance of hair follicle stem cells cause hair loss

An experimental study, reported the loss of interaction between Col17a1 and HFSCs (which impairs the self-renewal capacity of stem cells) resulting in permanent hair loss in mice. It also demonstrates the change in microenvironment, including decreased extracellular matrix expression, causing scarring alopecia. Thus, it is possible that impaired self-maintenance or loss of self-regenerative potential due to environmental changes may also be responsible for PCA development. [32]

Neurogenic theory

It explains the possible role of psycho-emotional stress in PCA. The substance P (SP) a neuropeptide molecule, which is increased in the state of psycho-emotional stress, is an inducer of mast-cell dependent neurogenic inflammation. This results in dense peri-follicular inflammatory cell infiltrates (especially around the bulge), accumulation and degranulation of peri-follicular mast cells, increased hair follicular keratinocyte apoptosis and reduced hair matrix keratinocyte proliferation, which is followed by premature entry of hair follicle into catagen. [33],[34],[35]

SP when added to the cultures of human hair follicles in anagen phase, upregulates the expression of MHC class I molecule and β2 microglobulin in peri-follicular region, leading to collapse of immune privilege and thus giving way to HFSCs destruction. [36]

SP is also a known fibroblast growth factor (FGF), thus promoting fibrosis and scar formation after inflammatory damage. [37]

Environmental factors contributing PCA

Various environmental triggering factors for PCA are proposed like infections, trauma, drugs, etc. The role of Staphylococcus aureus in FD is well known, the abnormal host immune responses to the bacterial antigen are responsible for the intense inflammation and scarring alopecia in the disease. [5],[6]

CCCA, [38] FD, [39] AK, [40] and erosive pustular dermatosis of scalp [5],[6] are associated with traumatic hair care practices.

Drug therapies are also implicated in PCAs. Graham-Little syndrome has been reported following hepatitis B vaccination, [41] AK has been associated with anticonvulsant and ciclosporin therapy, [42],[43] and drug-induced cases of AM, [44] CCLE [45] have been described. Similarly, occurrence of LPP is reported after ingestion of gold, [46] hepatitis B vaccination [41] and hepatitis C infection. [47]

Genetic factors related to PCA

Several reports of the familial PCA cases in PPB, FD, GLP syndrome, and KFSD suggested the existence of genetic factors. [48],[49],[50],[51] X-linked KFSD represent genetic scarring alopecia, which is caused by a missense mutation in the MBTSP2 gene. [51] Thus, genetic factors are likely to underline the pathogenesis of several PCA entities in some form, either by predisposing an individual to a certain disorder or through a direct genetic effect, causing the condition. Further genetic studies of the families affected are required to identify the genes associated.

Clinical Features

The characteristic clinical features of each type of PCA are enumerated in [Table - 1]. A new entity described is ′cicatricial marginal alopecia′ (CMA). [67] In this condition, the patient presents with an unusual clinical pattern of alopecia with severe loss of hairs from a wide band-like area on the margins of scalp. The site of involvement most commonly is occipital scalp (40% cases), other being temporal area. On close examination of scalp, there is no clinical appreciable scarring, atrophy, or erythema. Clinical differential diagnosis of CMA includes AA and tractional alopecia (late stages). But there is no history of hair care practices leading to tractional hair loss. Histologically, CMA reveals replacement of hair follicle by columns of fibrous tissue at or below the level of isthmus, with retention of sebaceous glands. This pattern of fibrosis was consistent with scarring alopecia. [67]

Diagnosis

Dermoscopy/Trichoscopy

Dermatoscope is a convenient instrument that aids in diagnosis of skin and scalp lesion. It works on the principal of light reflected by the specimens. This is done by both hand-held dermatoscope using polarized light as well as with video dermatoscopy, which ensures 1000 times magnification. [68],[69]

Dermoscopy of PCA reveals absence of follicular ostia in 100% cases even if it is not evident clinically, other findings suggestive of PCAs are tufted hairs, follicular hyperkeratosis, pili torti, and pink-white appearance. [68],[70],[71] Trichoscopy also helps clinicians assessing PCA disease activity, for example, "follicular red dots", erythematous polycyclic, concentric structures regularly distributed in and around the follicular ostia, are suggestive of active lupus erythematosus of the scalp. [70],[71] A recent review, gives an algorithmic description of trichoscopic features of CA and non-CA [Table - 3]. [71] This further emphasizes that trichoscopy provides the excellent first-line, noninvasive method for assessing scalp and hair characteristics in clinics giving important clues to diagnosis.

Table 3: Algorithm for trichoscopic diagnosis of hair loss diseases

Reflectance confocal microscopy

Reflectance Confocal Microscopy (RCM) is an in vivo, noninvasive, repeatable technique of real-time, en-face microscopic imaging of the superficial layers of the skin down to the superficial reticular dermis, with resolution at cellular level close to conventional histopathology. [72],[73],[74],[75],[76],[77],[78]

RCM has been used for the evaluation of several inflammatory skin conditions, such as acute contact dermatitis, [73] psoriasis, [74] nonscarring alopecia, [75],[76] and in assessment of CCLE. [77]

A study evaluating RCM features of PCA (mainly LPP and CCLE) reveals epidermal disarray, spongiosis, exocytosis of inflammatory cells in the epidermis, interface dermatitis, peri- and intraadnexal infiltration of inflammatory cells, dilated vessels in the dermis, dermal infiltration of inflammatory cells, melanophages, and dermal sclerosis as features of PCA. It also differentiated LPP and CCLE based upon RCM features and has shown strong reduction to disappearance of inflammatory cells with treatment. [78]

Thus, RCM is a high-resolution imaging technique that may be helpful in the diagnosis and follow-up of scarring alopecia. It may also help in choosing the most appropriate biopsy site for more informative histology.

Histopathology

Histopathology of scalp is an essential tool in distinguishing CA from non-CA and in diagnosing the different PCA depending upon the inflammatory infiltrate. For an accurate histopathological diagnosis of PCA, multiple biopsy samples are obtained from active sites and carefully sectioned both vertically and transversely. [2] Unlike in other skin diseases, the information obtained by vertical sections is limited in hair disorders. Transverse sections enable both qualitative (e.g., inflammatory change, fibrosis) and quantitative (e.g., hair follicle numbers, size, phase of hair cycle) examination of scalp biopsy samples. [79]

Recently, the "HoVert" technique, a novel processing technique that produces transverse (horizontal) and vertical sections from a single biopsy has been described. This overcomes the limitation of multiple scalp biopsies [Figure - 11]. [80]

Figure 11: 'Hovert' technique

Based upon the histopathological picture, the CAs are divided mainly into lymphocyte-mediated primary cicatricial alopecia (LMPCA), neutophil-mediated primary cicatricial alopecia (NMPCA), and mixed CA [Table - 1]. [7],[81],[82] The diseases clubbed under LMPCA (LPP, FFA, DLE, CCCA, PPB) are typified by a lymphocyte rich infiltrate in early stages and with variable but limited fibrosis concentrated in the perifollicular adventitial unit in later stages. In contrast, in NMPCA group (FD, TF), there is a neutrophil-rich infiltrate in early disease, a mixed infiltrate in later disease, and marked scarring that extends beyond the peri-follicular dermis and extensively involves the reticular (inter-follicular) dermis. [103],[104] In mixed CA group entities like AKN, AN, EPD inflammatory infiltrate is mixed lympho-plasmacytic or neutrophilic. [7]

The differentiation between the LMPCA and NMPCA group is easier in early stages of inflammation, whereas in later stages the differences in all PCAs as well as late stage of non-CA are subtle. To solve this query one study suggested, that the presence of plasma cells within the infiltrate in a given biopsy serve as a clue to a diagnosis of NMPCA, [83] whereas another points that the presence of ′compound follicle′ (complex follicular unit fused at the level of the infundibulum) are a clue to diagnosis CA. [84] In yet another study, the number of ′compound follicles′ was suggested to distinguish between LMPCA and NMPCA with fewer (two or three) in the former and more melded follicles (four, five or more) in the latter. [85] In a recent study, ′eyes′ or ′goggles′ patterns of fibrosis observed at lower power at the level of infundibulum has been considered to be suggestive of LMPCA. [86]

Direct immunofluorescence study

It is an important diagnostic tool differentiating between PCA due to LPP or CCLE. In CCLE, it shows granular deposits of immunoglobulin (IgG) and complement (C3) at the dermoepidermal junction, while in LPP there are globular deposits of IgM adjacent to the hair follicles or at the dermoepidermal junction [Table - 1]. [52],[53],[54],[55],[56],[87]

Microarray analysis

Microarray analysis represents the global gene expression profile, as a diagnostic tool for clinically or pathologically indistinguishable PCA. Recently, a report of microarray analysis generated from total RNA isolates from active lesions of LPP and PPB, distinguished the two conditions, which were thought to be related. [88] However, further studies in this field may elucidates the genetic and molecular markers of various PCAs.

Management

PCA provides both the diagnostic and therapeutic dilemma to the treating dermatologist. The aim of treatment currently focuses the reduction of symptoms and to reduce or stop the progression of the disease. A general rule followed is to treat LMPCA with immunosuppression and NMPCA with antimicrobials or dapsone. [60] The step ladder treatment of PCA is given in [Table - 4].

Table 4: Therapeutics in primary cicatricial alopecia

Newer in treatment of LPP is the use of PPARγ agonists based upon the recent theory in pathogenesis suggesting the role of abnormal functioning PPARγ receptor as an initial trigger of inflammation in LPP. [30],[31] In a case report, pioglitazone Hcl (PPARγ agonist) 15 mg once daily was given to a patient of unstable LPP, in whom various treatment modalities including oral corticosteriods, antimalarials, MMF, failed to control the disease activity. With 8 months of pioglitazone, there were reportedly decrease in signs and symptoms along with reduction in inflammatory infiltrate in scalp biopsy. [31]

Thiazolidinediones or glitazones act by increasing activity of the nuclear receptor PPARγ and have antiinflammatory, antiproliferative, immunomodulatory effects, which includes downregulation of proinflammatory nuclear transcription factors, proteolytic enzymes, and interleukins. Thus, it helps in lipid biogenesis in pilosebaceous units and is antiinflammatory, immunomodulatory in active stage of LPP. [176],[177]

Surgical treatment of scarring alopecia includes hair transplantation, scalp reduction or alopecia reduction surgeries, tissue expansion, and flap surgeries. [8],[178],[179] Decision for surgical treatment is based upon the stability of the CA, because best results can only be obtained in stable cicatricial alopecia cases. [8] Depending upon the duration of stable disease, some authors recommend the surgical therapies after at least 1 year of quiescence, [8] whereas others state that this should be after 2 years of disease-free interval. [60] The other factors that require consideration before planning the surgical treatment for CA includes vigilance regarding possible evolution of future androgenetic alopecia in the patient under treatment, availability of donor hairs and donor-recipient area ratio, vascular supply to the recipient area, scalp laxity, patient′s healing characteristics, and location of the subsequent scars. [8]

The surgical treatment is individualized depending upon the above mentioned factors but in general surgical excision or alopecia reduction surgeries are preferred for both unstable and stable CA. The success of hair transplantation in CA is limited by various reasons like disproportionate donor-recipient area ratio, decreased survival of hair grafts in scarred area due to compromised vascular supply and relapses of the disease process leading to new areas of scarring alopecia. However, in view of recent platelet rich plasma therapies to provide growth factors for grafted hairs and to increase graft survival at recipient site, hair transplantation will provide better results in stable CA.

Conclusion

PCA is ′trichology emergency′ situation, in which lack of prompt and early treatment will lead to the inevitable loss of hair follicles along with permanent scarring. Newer pathogenesis has given the platform for development of emerging treatment modalities. But still a great deal of research is required in this field, may be developing viable stem cell therapies or bioengineered human hair follicles are the answers to it in future.

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