Tariq Al-Zaid1, Stefan Vanderweil2, Artur Zembowicz3, Stephen Lyle4. 1. Department of Pathology, Tufts Medical Center, Tufts University Medical School, Boston, Massachusetts. 2. Departments of Cancer Biology and Pathology, UMass Memorial Medical Center, University of Massachusetts Medical School, Worcester, Massachusetts. 3. Department of Pathology, Lahey Clinic Medical Center, Tufts University Medical School, Burlington, Massachusetts. 4. Departments of Cancer Biology and Pathology, UMass Memorial Medical Center, University of Massachusetts Medical School, Worcester, Massachusetts. Electronic address: stephen.lyle@umassmed.edu.
Abstract
BACKGROUND: 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. OBJECTIVES: 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. METHODS: 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. RESULTS: 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. LIMITATIONS: Sample size was limited in some alopecia entities. Inflammation was graded by means of subjective observation. CONCLUSIONS: 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.
BACKGROUND: 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. OBJECTIVES: 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. METHODS: 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. RESULTS: 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. LIMITATIONS: Sample size was limited in some alopecia entities. Inflammation was graded by means of subjective observation. CONCLUSIONS: 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.
Authors: Helen B Everts; Kathleen A Silva; Shalise Montgomery; Liye Suo; Monica Menser; Amy S Valet; Lloyd E King; David E Ong; John P Sundberg Journal: J Invest Dermatol Date: 2012-10-25 Impact factor: 8.551