ABSTRACT
Human skin is continually exposed to internal and external forces, dynamic as well as static. The skin is normally flexible and can resist mechanical trauma due to friction, pressure, vibration, suction and laceration to a considerable degree. However, an excess of these forces can abnormally affect the structure and function of the skin, setting the stage for the development of a skin disorder. Repetitive trauma can cause lichenification, hyperpigmentation, erythema, scaling, fissuring, blisters, ulceration and chronic alterations. Frictional dermatoses is an under-recognised entity with no clear-cut definition and encompasses a variety of terms such as frictional dermatitis, frictional melanosis, frictional pigmentary dermatoses and certain other named entities, many of which are confusing. The authors propose to define frictional dermatoses as ‘a group of disorders caused by repetitive trauma to the skin as a result of friction of varied aetiology which can have a wide range of cutaneous manifestations depending on the type of insult.’ The exact prevalence of frictional dermatoses as a separate entity is unknown. Authors who conducted this review include a group of dermatologists and post graduate students from various institutions. Literature was reviewed through PubMed, Medscape, Medline, ResearchGate and Google Scholar using the terms ‘frictional dermatitis,’ ‘friction and skin,’ ‘dermatoses and culture,’ ‘clothing dermatitis,’ ‘friction melanosis,’ ‘PPE induced dermatoses in COVID-19 era,’ etc. A total of 122 articles were reviewed and 100 articles among them were shortlisted and included in the study, after removing duplications. The review was followed up with further deliberation which resulted in the formulation of a new definition and classification of frictional dermatoses taking into account the morphology, histopathological characteristics, anatomical region affected and the major predisposing factors. The rising incidence of mechanical dermatoses in the COVID-19 era was also emphasised.
ABSTRACT
Background: Alopecia areata is an autoimmune disease that occurs as a result of the loss of the inherent immune privilege of the hair follicle. It has been recently demonstrated that the interferon-γ/interleukin-15 feedback loop that signals via the Janus kinase–signal transducer and activator of transcription pathway is critical to the breakdown of this immune privilege. Aims: To evaluate the immunological distribution of CD4+ T-cells, CD8+ T-cells, phosphorylated signal transducer and activator of transcription 1 and study its relation with the clinical and histopathological findings of the disease. Materials and Methods: A total of 30 patients of alopecia areata were included in the study. Following a detailed history and clinical examination, a scalp biopsy was performed. Histopathology was studied and immunohistochemistry was done to demonstrate the positivity and distribution of CD4+ T-cells, CD8+ T-cells and phosphorylated signal transducer and activator of transcription 1. Results: The follicular count, number of anagen and terminal hair were found to be decreased, whereas the catagen, telogen and vellus hair were found to be increased in number. A peribulbar CD4+ T-cell infiltrate was seen in 70% cases, whereas a CD8+ T-cell infiltrate was seen in 83.3% cases. An intrabulbar CD4+ T-cell infiltrate was seen in 26.7% cases, whereas a CD8+ T-cell infiltrate was seen in 70% cases. Among the 25 hair follicles dermal papilla identified, 36.8% cases were found to be positive for phospho-signal transducer and activation of transcription-1. Limitations: The drawbacks of our study included a small sample size and the use of only vertical sectioning for the scalp biopsy samples. Conclusion: Phosphorylated signal transducer and activator of transcription 1 positivity as an indicator of signalling via the Janus kinase-1/2 pathway was seen in 36.8% of our cases highlighting the integral role of this pathway in the pathogenesis of alopecia areata.