Treating Inflammation in Rosacea: Current Options and Unmet Needs

Rosacea has been described in the medical literature for centuries.¹ Twentieth-century medical publications referred to multiple phases of rosacea, typically asserting its pathophysiology as “unknown.”² In 2002, the National Rosacea Society Expert Committee described the primary and secondary features for rosacea diagnosis and classified four presentation patterns as subtypes: erythematotelangiectatic (ETR), papulopustular (PPR), ocular, and phymatous.³ However, each subtype contained multiple signs and symptoms, most of which overlapped with one or more other subtypes and did not account for variation in individual patient presentation.⁴ This led to confusion in epidemiological studies, clinical trial patient recruitment, and the development of assessment scales conflated to measure divergent features (eg, erythema and papules/pustules) that did not necessarily respond to interventions in parallel.⁴ Consequently, in 2017 a global panel of rosacea experts updated the diagnostic criteria for rosacea based on clinical features, termed the phenotype approach (Table 1).^5,6

Many recent reviews point to advances in understanding the pathogenesis of rosacea as prompting this shift in the description of rosacea—notably, that most cases seem attributable to aberrations in the immune system.^6,7

This review discusses the underlying inflammatory nature of rosacea, treatments that target these inflammatory processes, and shortcomings of current therapies.

Inflammation in Rosacea
The pathophysiology of rosacea involves the innate and adaptive immune systems, as well as neurovascular dysregulation. External and endogenous triggers initiate and aggravate various pathways in rosacea patients (Figure 1).