INTRODUCTION
Acne vulgaris (AV) is the eighth most prevalent disease globally, and a condition reported to affect at least 50 million people in the United States.1 Because AV affects 80% of teenagers, it is generally categorized as a condition of adolescence, yet recent literature indicates that AV can affect both pre-teens and adults, with 40%-50% of women experiencing AV that occurs past the teenage years.2-4 Physical and psychosocial sequelae associated with AV include dyschromia, scarring, poor self-image, depression, anxiety, and avoidance of social interaction.5,6
The pathophysiology of AV is conventionally viewed as resulting from 4 factors occurring at the pilosebaceous unit (PSU): increased sebum, follicular hyperkeratinization, proliferation of Cutibacterium acnes, and inflammation induced by localized immune responses.5 Collectively, this sequence of pathophysiologic events causes marked inflammation in and around the PSU, which results in visible AV lesions and can ultimately lead to both persistent and post-inflammatory hyperpigmentation (PIH) and/or post-inflammatory erythema (PIE) and various forms of scarring.7
However, there is emerging evidence that many dermatologic conditions are associated with generalized underlying immune-inflammatory systemic responses. Psoriasis, once viewed and treated only as a skin disease, is now accepted as a systemic, inflammatory disease managed primarily by immunomodulatory therapies.8 Atopic dermatitis is now approached, based on scientific evidence, as a disorder driven by a variety of pathways of inflammation, both systemic and cutaneous.9 Hair loss and thinning, once thought of as primarily having local pathogenesis, is now accepted as a multi-factorial systemic condition with more similarities than differences across the hair loss disorder spectrum.10
Likewise, evidence now suggests that the localized pathophysiology of AV is not an isolated event but may be induced or exacerbated by an interconnected web of external and internal stressors propagated by various inflammatory signaling pathways.5 Therefore, an important question to address is what systemic drivers are likely to directly contribute to the pathophysiologic development of AV occurring within and around the PSU. If we can address this question, we might then develop and provide a wider range of therapeutic options.
