INTRODUCTION
The pathogenesis of acne vulgaris is multifactorial. Four major processes occur in tandem that leads to the development and propagation of acne: (1) excess sebum production, (2) follicular plugging due to epidermal hyperproliferation, (3) proliferation of Cutibacterium acnes (formerly Propionibacterium acnes), and (4) inflammation.1 Dysregulation of the epidermis and pilosebaceous unit due to inflammatory changes and dysbiosis leads to the formation of comedones, papules, pustules, and cystic nodules.2 As such, acne treatment is aimed at mediating these four pillars of pathogenesis.
The need for multiple therapeutic agents to combat acne pathogenesis has traditionally required multiple individual topical therapeutics to be applied at different times of day and with specific layering instructions. Furthermore, simultaneous application of specific active molecules is not advised as they may cause concomitant instability. For example, the oxidative property of BPO causes the degradation of tretinoin rendering it ineffective.9 As a result, acne treatment regimens have required multi-step routines to optimize efficacy. In addition, each individually formulated topical agent has a unique tolerability profile. Thus, the need for a multi-step approach combined with an unpredictable range of tolerability adverse events (AEs) have contributed to poor patient adherence to treatment resulting in treatment failures.10,11
Retinoids are the mainstay of treatment given their pleiotropic effects on sebaceous gland function and epidermal turnover and differentiation.3 Antibiotics such as lincosamides (eg, clindamycin) and tetracyclines are also utilized given their antimicrobial effect on C. acnes as well as their anti-inflammatory effects.4 Benzoyl peroxide (BPO) is a unique antimicrobial exhibiting bactericidal activity through oxidation of bacterial proteins thus damaging the cell wall in a non-targeted manner.5 This mechanism affords BPO as an agent that could not only circumvent but also prevent antibiotic resistance.6 BPO also exhibits comedolytic and keratolytic activity thus aiding with unplugging of the pilosebaceous unit.6
International consensus guidelines for acne treatment recommend topical treatments for any acne disease severity (mild, moderate, or severe).4,7,8 Topical retinoids are considered the first line as they affect almost all pillars of acne pathogenesis. Topical antibiotics are also recommended in combination with retinoids to target the dysbiosis due to C. acnes. However, given the significant concern for antibiotic resistance, BPO is the preferred antimicrobial agent due to its non-targeted mechanism of action as an oxidizing agent.4 Oral antibiotics and oral retinoids are also recommended with increasing disease severity or in the case of failure of topical therapies.
The need for multiple therapeutic agents to combat acne pathogenesis has traditionally required multiple individual topical therapeutics to be applied at different times of day and with specific layering instructions. Furthermore, simultaneous application of specific active molecules is not advised as they may cause concomitant instability. For example, the oxidative property of BPO causes the degradation of tretinoin rendering it ineffective.9 As a result, acne treatment regimens have required multi-step routines to optimize efficacy. In addition, each individually formulated topical agent has a unique tolerability profile. Thus, the need for a multi-step approach combined with an unpredictable range of tolerability adverse events (AEs) have contributed to poor patient adherence to treatment resulting in treatment failures.10,11
