INTRODUCTION
Despite being an exceptionally common disease, the exact pathogenesis of acne has not yet been fully elucidated. The hair follicle and sebaceous gland make up the pilosebaceous unit and acne vulgaris is the most common inflammatory disorder of the pilosebaceous unit. There are four key pathogenic factors in acne development: 1) increased sebum production, 2) presence of Cutibacterium acnes (C. acnes, formerly known as Propionibacterium acnes), 3) inflammation, and 4) follicular hyperkeratinization.1
However, the temporal order and the individual impact of each of these steps are debated and uncertain. As one example of this temporal confusion, it was long assumed that the comedo was the initial lesion incited by hyperkeratinization. It has therefore long oft been referred to as a "non-inflammatory" lesion as it was assumed that inflammation had not yet afflicted this early lesion in acne pathogenesis and that inflammation was reserved for papules, pustules, and nodules. However, as will be discussed in further detail later, inflammation has been found even in micro-comedones making the reference to comedones as "non-inflammatory" lesions incorrect and outdated. While each of the four pathogenic steps plays a role in lesion development, we cannot say for certain that one of these steps proceeds the other or is more important than the other. As will be evident from the science presented herein, each step influences the other and the pathogenesis of acne is likely a complicated dance amongst sebum, hyperkeratinization, C. acnes, and inflammation.
While there is no single topical therapeutic agent that affects all four steps in acne pathogenesis, clinicians often use multiple topical therapies in combination to obtain maximal reduction in acne lesions. Knowledge of which pharmaceutical affects which step in acne pathogenesis will allow the clinician to choose products wisely, picking combinations of products that are not redundant but add a different mechanism of action and therefore block additional steps in the formation of acne. Theoretically, a topical agent that combats the most steps in the pathogenesis of acne will have the greatest success in treating this common pilosebaceous disease. The clinician must have a basic understanding of acne pathogenesis as well as an understanding of how various therapeutics target acne pathogenesis to choose the best anti-acne topical medication for their patient. We herein will present an overview of acne pathogenesis as well as a review of the mechanisms of action of topical acne medications.
However, the temporal order and the individual impact of each of these steps are debated and uncertain. As one example of this temporal confusion, it was long assumed that the comedo was the initial lesion incited by hyperkeratinization. It has therefore long oft been referred to as a "non-inflammatory" lesion as it was assumed that inflammation had not yet afflicted this early lesion in acne pathogenesis and that inflammation was reserved for papules, pustules, and nodules. However, as will be discussed in further detail later, inflammation has been found even in micro-comedones making the reference to comedones as "non-inflammatory" lesions incorrect and outdated. While each of the four pathogenic steps plays a role in lesion development, we cannot say for certain that one of these steps proceeds the other or is more important than the other. As will be evident from the science presented herein, each step influences the other and the pathogenesis of acne is likely a complicated dance amongst sebum, hyperkeratinization, C. acnes, and inflammation.
While there is no single topical therapeutic agent that affects all four steps in acne pathogenesis, clinicians often use multiple topical therapies in combination to obtain maximal reduction in acne lesions. Knowledge of which pharmaceutical affects which step in acne pathogenesis will allow the clinician to choose products wisely, picking combinations of products that are not redundant but add a different mechanism of action and therefore block additional steps in the formation of acne. Theoretically, a topical agent that combats the most steps in the pathogenesis of acne will have the greatest success in treating this common pilosebaceous disease. The clinician must have a basic understanding of acne pathogenesis as well as an understanding of how various therapeutics target acne pathogenesis to choose the best anti-acne topical medication for their patient. We herein will present an overview of acne pathogenesis as well as a review of the mechanisms of action of topical acne medications.
