Acne and Rosacea

Abstract

Acne, one of the most common skin diseases, affects approximately 85% of the adolescent population, and occurs most prominently at skin sites with a high density of sebaceous glands such as the face, back, and chest. Although often considered a disease of teenagers, acne is occurring at an increasingly early age. Rosacea is a chronic facial inflammatory dermatosis characterized by flushing (or transient facial erythema), persistent central facial erythema, inflammatory papules/pustules, and telangiectasia. Both acne and rosacea have a multifactorial pathology that is incompletely understood. Increased sebum production, keratinocyte hyper-proliferation, inflammation, and altered bacterial colonization with Propionibacterium acnes are considered to be the underlying disease mechanisms in acne, while the multifactorial pathology of rosacea is thought to involve both vasoactive and neurocutaneous mechanisms. Several advances have taken place in the past decade in the research field of acne and rosacea, encompassing pathogenesis and epidemiology, as well as the development of new therapeutic interventions. In this article, we provide an overview of current perspectives on the pathogenesis and treatment of acne and rosacea, including a summary of findings from recent landmark pathophysiology studies considered to have important implications for future clinical practice. The advancement of our knowledge of the different pathways and regulatory mechanisms underlying acne and rosacea is thought to lead to further advances in the therapeutic pipeline for both conditions, ultimately providing a greater array of treatments to address gaps in current management practices.

Keywords: Acne; Acne vulgaris; Adolescent; Pathogenesis; Pediatric; Pre-adolescent; Rosacea; Therapy.

Fig. 1

Primary and secondary factors contributing to acne pathogenesis

Fig. 2

American Acne and Rosacea Society treatment recommendations for mild, moderate, and severe pediatric acne [21] (please refer to your local prescribing information for country-specific guidance). Reproduced with permission from Pediatrics, 131 Suppl 3, S163–6, Copyright © 2013 by the AAP. *Topical fixed-combination prescriptions available. **Assess adherence. ^†Consider dermatology referral

Fig. 3

Factors contributing to rosacea pathogenesis

Fig. 4

Innate and adaptive immune dysfunction in rosacea and potential therapeutic targets. The sequence of innate immune activation in rosacea starts with factors increasing keratinocyte transcription of pro-cathelicidin (including vitamin D activated by UV, UV itself, infection, injury, and other triggers to barrier disruption) [43] and the serine proteases of the KLK family, KLK5 and KLK7 (activation mediated by TLR-2, which is upregulated by environmental and microbial stimuli) [42]. This leads to the formation of LL-37 and other peptides that are inflammatory and angiogenic [44]. Mast cells are pivotal mediators of cathelicidin-initiated skin inflammation—amplifying inflammation, vasodilation, and generation of LL-37 [45]. Chemokine and cytokine signals interact to generate a Th1/Th17-polarized adaptive immune response in rosacea [46]. Increased amounts of serine proteases can activate TRP via upregulation and/or activation of protease-activated receptors. There is co-localization of mast cells with unmyelinated sensory nerves, blood vessels, and myofibroblasts in rosacea (not shown) [41]. Sites of potential therapeutic intervention in these pathways are shown. KLK kallikrein, LL-37 cathelicidin, Th1 type 1 T-helper, Th17 type 17 T-helper, TL Toll-like receptor, UV ultraviolet