INTRODUCTION
Central centrifugal cicatricial alopecia (CCCA) is a scarring alopecia primarily affecting Black women.1 Patients typically present with hair loss that starts at the vertex and progresses centrifugally, resulting in shiny patches of alopecia with loss of follicular ostia. Hair loss in CCCA may be associated with hair breakage or scalp pruritus, pain, tenderness, scaling, follicular papules, or irritation.1,2 The pathogenesis of CCCA is poorly characterized. However, underlying genetic predispositions, such as a peptidyl arginine deiminase type III (PADI3) mutation, and environmental triggers, namely various hair care practices, are hypothesized to result in premature desquamation of the inner root sheath and inflammation that permanently damages hair follicles.3,4 Unsurprisingly, CCCA has a significant negative impact on quality of life and has a high disease burden.5,6
To date, treatment strategies rely on anecdotal evidence as there is a paucity of published trials and an absence of standardized treatment regimens or approved medications for CCCA.2,7,8 Medical therapies are aimed at preventing disease progression through suppression of active inflammation and maximization of growth within viable follicles. To that end, systemic agents, including doxycycline and hydroxychloroquine are often used for finite periods. Duration of treatment and optimal therapies have not been characterized. Similarly, the literature on inflammatory pathways and cytokines involved in CCCA are poorly understood and not well studied. Implicated genes upregulated in CCCA affected tissue are wide ranging and include platelet-derived growth factors, collagen types I and III, several matrix metalloproteinases (MMP), interleukin (IL)-6, IL-36, and tumor necrosis factor (TNF).9
To date, treatment strategies rely on anecdotal evidence as there is a paucity of published trials and an absence of standardized treatment regimens or approved medications for CCCA.2,7,8 Medical therapies are aimed at preventing disease progression through suppression of active inflammation and maximization of growth within viable follicles. To that end, systemic agents, including doxycycline and hydroxychloroquine are often used for finite periods. Duration of treatment and optimal therapies have not been characterized. Similarly, the literature on inflammatory pathways and cytokines involved in CCCA are poorly understood and not well studied. Implicated genes upregulated in CCCA affected tissue are wide ranging and include platelet-derived growth factors, collagen types I and III, several matrix metalloproteinases (MMP), interleukin (IL)-6, IL-36, and tumor necrosis factor (TNF).9
