Cases Of Scarring Alopecia Research Articles

Expression of hair follicle stem cell markers CD34 and CK15 in scarring alopecia

Introduction Pathogenesis of scarring alopecia (SA) is poorly understood with recent studies implicating loss of follicle stem cells (FSC). Objectives The aim of the present study was to examine the expression patterns of FSC markers CK15 and CD34 in SA and to compare them with biopsies from normal and non-SA cases. Materials and methods Twenty-one cases of SA were assessed using CK15 and CD34 immunostains. Biopsies from normal scalp and alopecia areata (AA) cases were studied for comparison. Results CD34 was expressed in the outer root sheath of the lower segment of follicles in all normal, 33% of the AA and 33% of the SA cases. CK15 was seen in the outer root sheath of the upper segment of hair follicles in 100% of normal and AA biopsies, compared with 91% of SA. CK15 was expressed in the lower segment of the follicle in 9/10 cases of SA, which is hitherto undescribed. CK15 was also retained in the bulge in 84% of the SA cases. Conclusion CD34 FSCs are lost in most SA cases. CK15 FSC are retained in both the bulge and the rest of the follicle, signifying that stem cell destruction alone does not eventuate in hair loss. The aberrant distribution of CK15 also suggests that there may be compensatory mechanisms yet to be understood.

The Spectrum of Histopathological Lesions in Scarring Alopecia: A Prospective Study

The aim of the article was to study the histopathological features of various lesions of Scarring Alopecia (SA) and to classify Primary SA on the basis of the predominant type of inflammatory cell component. Scarring or cicatricial alopecias are those that are produced as a result of the malformation, damage or destruction of the pilosebaceous follicles, which are replaced by cicatricial tissue, in such a way that they cannot again produce hair. This prospective study included 32 biopsy - proven cases of SA, who had attended our hospital. Primary SA was classified according to the North American Hair Research Society. The informed consents of the subjects and the institutional ethical clearance was obtained for the study. The SPSS, version 14 software was used to analyse the data. Frequencies and percentages were used to describe the data. During the study period, 32 cases of scarring alopecia were diagnosed, of which 24 were primary SA and 8 were secondary SA. Among the primary SA, there were 23 cases of lymphocyte associated primary scarring alopecias, of which, 19 of lupus erythematosus, 3 of lichen planopilaris (LPP) and one case of non specific SA. 1 case of neutrophil associated primary scarring (folliculitis decalvans) was also noted and among the secondary SA, there were 4 cases of morphea and 1 case each of lupus vulgaris, congenital absence of skin, burn and sarcoidosis. To conclude, histopathology is a dependable tool for identifying the underlying cause in scarring alopecia, which is helpful for an early diagnosis and treatment.

Sebaceous gland loss and inflammation in scarring alopecia: A potential role in pathogenesis

Primary scarring alopecia (SA) comprises a group of disorders with poorly defined origins. Improving diagnostic and therapeutic capabilities requires a better understanding of their pathogenesis. We sought to assess the frequency of sebaceous gland loss in SA and to identify the role of sebaceous gland and sebaceous gland duct inflammation in the pathogenesis of SA. Ninety specimens submitted with a clinical history of alopecia, both scarring and nonscarring, were reviewed. Samples were scored based on sebaceous gland, sebaceous duct, and follicle inflammation. Sebaceous gland loss was much more common in cases of SA (>53% of follicles on average) than non-SA (<5% of follicles on average). Many cases of SA showed residual affected follicles with an absence of sebaceous glands. Sebaceous gland duct inflammation was often more frequent and severe than gland inflammation in SA. Sample size was limited in some alopecia entities. Inflammation was graded by means of subjective observation. This study demonstrates that sebaceous gland loss is a common and early finding among SA. In addition, sebaceous gland and/or duct inflammation may play a role in initiating or accelerating follicular damage during the development of SA.

D2-40 Expression in Primary Scarring and Nonscarring Alopecia

The pathogenesis of scarring alopecia is believed to be related to damage to stem cells within, and outside the confines of, the follicular bulge region. Scattered reports indicate that D2-40, a monoclonal antibody that specifically detects a fixation-resistant epitope on podoplanin, highlights the basal cell layer of the outer root sheath. Given this, we sought to ascertain involvement of the same in a total of 52 cases of alopecia (33 scarring and 19 nonscarring). D2-40 expression, noted in the peripheral layer of the outer root sheath (above and below attachment of the pilar muscle), was similar in 24/33 (73%) and increased in 9/33 (27%) in the infundibular region of cases of scarring alopecia in comparison to its expression in 17/19 (90%; no expression noted in the other 2) of cases of nonscarring alopecia. The absence of a unifying diagnosis in entities demonstrating an increase precludes any correlation from being made regarding D2-40 expression and histologic diagnosis. However, more recently, podoplanin has been shown to be a novel Fos target gene in some skin cancers. Thus, from a scientific perspective, involvement of Fos-dependent transcription mechanisms in the etiopathogenesis of select scarring alopecias does not seem entirely unreasonable although studies defining the role of the Fos-podoplanin axis in development of the normal hair follicle are required before a definitive conclusion can be drawn.

A case of scarring alopecia

A case of scarring alopecia

Scarring alopecia in neonates as a consequence of hypoxaemia-hypoperfusion.

Scarring alopecia is relatively uncommon in infants and children and rarely discussed in the paediatric literature. It does not appear to have been previously documented as a consequence of compromised oxygenation and blood supply in the neonatal population or as a complication of extracorporeal membrane oxygenation (ECMO) treatment. During a six month period, we observed five patients who presented to our neonatal intensive care unit with pressure ulcers that eventuated in scarring alopecia. The patients were all > or = 2500 g at birth, had some disruption of the cardiac circulation, were hypoxaemic and acidotic, and required vasopressor treatment. Institution of a positioning schedule and use of a thermostable Spenco gel pad during the subsequent six month period eliminated the presence of pressure ulceration and scarring alopecia in this at-risk population. Although scarring alopecia is a permanent condition, skin changes preceding its development in this setting are recognisable and follow a predictable pattern and time course, and should therefore allow for intervention at an earlier stage. Neonatal ECMO patients, as well as those who suffer hypoxaemia-hypoperfusion, but do not require circulatory bypass, appear to be at increased risk for development of the pressure ulcers that precede scarring alopecia. Paediatricians should consider this possibility and seek the appropriate historical information when confronted with a case of scarring alopecia after the neonatal period.