Why Topical Retinoids Are Mainstay of Therapy for Acne

Abstract

Acne-focused dermatology expert groups have consistently recommended that most patients with acne be treated with a combination of topical retinoid and antimicrobial therapy. This is based on clinical data as well as evidence that these drug classes have different and complementary mechanisms of action that target multiple aspects of acne's complex pathophysiology. Recent evidence-based guidelines for acne, including those from the American Academy of Dermatology (AAD) and the European Dermatology Forum (EDF), have agreed that retinoids have an essential role in this widespread disease. The AAD states "retinoids are the core of topical therapy for acne because they are comedolytic, resolve the precursor microcomedone lesion, and are anti-inflammatory;" further, they "allow for maintenance of clearance." Despite uniform recommendation for use of topical retinoids, a recent study of prescribing practices from 2012 to 2014 indicated that dermatologists prescribed retinoids just 58.8% of the time while non-dermatologists prescribed them for only 32.4% of cases. In this article, we review the reasons supporting retinoids as the mainstay of acne therapy and discuss some of the perceived barriers that may be limiting use of this important drug class. Further, we discuss how and when titrating retinoid concentrations may be utilized in clinical practice.

Funding: Galderma International.

Keywords: Acne vulgaris; Adapalene; Tazarotene; Topical retinoid; Tretinoin.

Fig. 1

Dose-dependent actions of adapalene at the molecular level. From Tenaud et al. [21]

Fig. 2

Dose-dependent clinical success rate (IGA) of 0.3 A/BPO, A/BPO, and vehicle in patients with severe acne at baseline. From Weiss et al. [68]

Fig. 3

Clinical efficacy of topical retinoid monotherapy on inflammatory lesions after 12 or 15 weeks therapy. From Leyden et al. [37]

Fig. 4

Changes over time in the skin with retinoid therapy, differentiating transient irritation versus inflammation. MoA mechanism of action, IL interleukin, TNF tumor necrosis factor