INTRODUCTION
Acne vulgaris is a chronic inflammatory skin disease affecting the pilosebaceous follicles.1 It is estimated that 40 to 50 million individuals in the US have acne with an 85% prevalence rate among those aged 12 to 24 years old.1 Most patients affected by acne present with a combination of inflammatory and non-inflammatory lesions. Non-inflammatory acne lesions include open and/or closed comedones, while inflammatory lesions manifest as papules, pustules, nodules, and/or cysts.2,3 The disease is associated with a prolonged, remitting, and relapsing course, generally beginning in adolescence and sometimes continuing into adulthood.4 Physical scars and dyschromias in the skin are also common in the disease.5 Understandably, acne imparts a serious psychological burden on affected individuals, including anxiety, depression, and social withdrawal.6,7
Sebaceous gland differentiation and sebum production are regulated by a complex interplay of hormones, especially androgens.8,9 At the cellular level, peroxisome proliferator-activated receptors located on sebocytes increase sebaceous gland lipogenesis and sebum production.10 Together with the stratum corneum, sebum is important to the integrity and normal function of the skin, acting as a lubricant and barrier to the external environment; however, excess sebum production facilitates Cutibacterium acnes proliferation by providing nutrients and creating an anaerobic environment for bacterial growth. As a result, excess sebum is an important contributor to the inflammatory processes underlying the development of acne vulgaris.11
Sebaceous gland differentiation and sebum production are regulated by a complex interplay of hormones, especially androgens.8,9 At the cellular level, peroxisome proliferator-activated receptors located on sebocytes increase sebaceous gland lipogenesis and sebum production.10 Together with the stratum corneum, sebum is important to the integrity and normal function of the skin, acting as a lubricant and barrier to the external environment; however, excess sebum production facilitates Cutibacterium acnes proliferation by providing nutrients and creating an anaerobic environment for bacterial growth. As a result, excess sebum is an important contributor to the inflammatory processes underlying the development of acne vulgaris.11