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Review
. 2018 Dec 3:7:F1000 Faculty Rev-1885.
doi: 10.12688/f1000research.16537.1. eCollection 2018.

Recent advances in understanding and managing rosacea

Joerg Buddenkotte  1   2 , Martin Steinhoff  1   2   3   4   5
Affiliations
Review

Recent advances in understanding and managing rosacea

Joerg Buddenkotte et al. F1000Res. .

Abstract

Rosacea is a common chronic inflammatory skin disease of the central facial skin and is of unknown origin. Currently, two classifications of rosacea exist that are based on either "preformed" clinical subtypes (erythematotelangiectatic, papulopustular, phymatous, and ocular) or patient-tailored analysis of the presented rosacea phenotype. Rosacea etiology and pathophysiology are poorly understood. However, recent findings indicate that genetic and environmental components can trigger rosacea initiation and aggravation by dysregulation of the innate and adaptive immune system. Trigger factors also lead to the release of various mediators such as keratinocytes (for example, cathelicidin, vascular endothelial growth factor, and endothelin-1), endothelial cells (nitric oxide), mast cells (cathelicidin and matrix metalloproteinases), macrophages (interferon-gamma, tumor necrosis factor, matrix metalloproteinases, and interleukin-26), and T helper type 1 (T H1) and T H17 cells. Additionally, trigger factors can directly communicate to the cutaneous nervous system and, by neurovascular and neuro-immune active neuropeptides, lead to the manifestation of rosacea lesions. Here, we aim to summarize the recent advances that preceded the new rosacea classification and address a symptom-based approach in the management of patients with rosacea.

Keywords: Cathelicidin; Classification; Immunity; Inflammation; Pathophysiology; Rosacea; Therapy.

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Conflict of interest statement

No competing interests were disclosed.No competing interests were disclosed.No competing interests were disclosed.Competing interests: This reviewer has received support from Galderma.

Figures

Figure 1.
Figure 1.. Current understanding of the pathomechanisms in rosacea.
Rosacea triggers lead to the activation of downstream effectors (white boxes) in various cell types (gray boxes) probably by the activation of a few specific receptors and channels (white boxes), which in cooperation nurture processes of (neurogenic) inflammation, including edema and vasodilation, fibrosis, pain, and angiogenesis (lilac boxes). For instance, epidermal and probably immune cell-expressed proteinase-activated receptor-2 (PAR 2) and Toll-like receptor-2 (TLR-2) are activated by rosacea-associated bacterial and Demodex-derived proteases, leading to the induction of the inflammasome and subsequent release of pro-inflammatory agents such as tumor necrosis factor-alpha (TNF-α) and interleukin-1 (IL-1) as well as enhanced expression of the innate immune peptide LL-37. ATP, adenosine triphosphate; CGRP, calcitonin gene-related peptide; ET1, endothelin-1; ETAR, endothelin A receptor; KLK-5, kallikrein-5; LL-37, cathelicidin; MMP, matrix metalloproteinase; NALP3, NACHT, LRR, and PYD domain-containing protein 3; PACAP, pituitary adenylate cyclase-activating peptide; SP, substance P; TGF-β, transforming growth factor-beta; TRP, transient receptor potential; TSLP, thymic stromal lymphopoietin; VEGF, vascular endothelial growth factor.
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    2. F1000 Recommendation

Grants and funding

The author(s) declared that no grants were involved in supporting this work.