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

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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.

Section snippets

Methods

Ninety specimens submitted with a clinical history of alopecia were retrieved from the archives of Lahey Clinic Medical Center and the University of Massachusetts Medical Center with institutional review board approval. Additional consultation cases from dermatopathologyconsultations.com were also obtained. All cases included in the study were re-evaluated, after initial diagnosis, by one of the study dermatopathologists (A. Z. or S. L.). In cases where one of the study pathologists made the

Sebaceous gland loss

Sebaceous gland loss in SA cases was observed as follows: 11 (84.6%) LPP, 13 (76.5%) FDS (Fig 1), 3 (100%) FD, two (100%) AKN, one (100%) lupus, one (100%) SA with hypertrophic scar, and zero (0%) SA with folliculitis, not definitive for FDS, and nonspecific SA cases (Table II). Cases with non-SA showed variable results. Gland loss was identified in one (7.7%) AA case, one (5.9%) AG, and zero (0%) TE. Subtypes TA and TT showed more frequent loss of sebaceous gland: two (66.7%) for each (Table II

Discussion

The origin and pathogenesis of SA remain largely unclear although they are currently treated as inflammatory disorders.1 Several theories that have been proposed to explain the etiopathogenesis of SA are reviewed by McElwee.6 These theories include autoimmune-mediated (through inappropriate presentation of self-antigen to the adaptive immune system) and immune privilege breakdown mechanisms, the danger versus nondanger hypothesis, bulge stem cell destruction, the hair follicle

References (16)

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    Citation Excerpt :

    Sebaceous glands contribute to HF function, and have been suggested to participate in initiating or accelerating HF damage [86]. The loss of sebaceous glands, and an increase in the sebaceous gland area associated with their multilobulation, has been described in different types of alopecia [86,87]. In fact, cultured outer root sheath cells, derma papilla cells and organ culture hair growth were negatively affected by nevus sebaceous sebocyte conditioned medium, and sebaceous gland hamartomas presented as hairless patches [88].

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Funding sources: None.

Conflicts of interest: None declared.

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