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Granulomatous rosacea: exploratory histological markers

Presented by
Dr EunHye Hong, Hallym University Sacred Heart Hospital, Korea
10:14:56pm> hello nurse from conference
In an initial histological profiling comparing granulomatous rosacea (GR) biopsies to erythematotelangiectatic rosacea (ETR) biopsies and to healthy controls, Dr EunHye Hong (Hallym University Sacred Heart Hospital, Korea) presented her data identifying that elevated numbers of mast cells and higher expression of toll-like receptor 2 (TLR2) are distinct to GR [1].

GR is a unique disease variant of rosacea, characterised by chronic relapsing inflammatory disease with various clinical features such as facial erythema, papules, flushing, pustules, and telangiectasias. Histopathologic findings feature characteristic non-caseated epithelioid granulomas. Little is known about the cell types involved in propagating GR or the underlying signalling that drives this disease. Neurovascular/neuroimmune dysregulation, which includes both anatomic and physiochemical differences present in rosacea-prone skin as compared with healthy facial skin, appears to be a major contributor that exacerbates the vasodilation of facial skin vasculature with increased facial blood flow that occurs during a rosacea flare [2].

Dr Hong and colleagues measured the differences in the expression rate of toll-like receptor 2 (TLR2), neurofilament, and mast cells in ETR (n=12), GR (n=12), and normal skin (n=11). All patients were diagnosed by clinical features and pathology-confirmed biopsies. The researchers performed quantitative analysis of immunohistochemical staining (i.e. number of pixels per image) and found no significant differences in neurofilament staining in any of the groups. GR had significant higher levels of mast cells than either ETR (P<0.05) or the control group (P<0.001); ETR was not significantly higher than the controls. For TLR2 expression, both ETR and GR had significantly higher levels than the control group (P<0.05 for both), although they did not significantly differ from each other.

Mast cells are key effectors in neurogenic inflammation and in rosacea evolution to a chronic stage. Since GR is a later-stage disease than other subtypes, Dr Hong speculated that mast cells may invade when the neurogenic inflammation begins to aggravate. In addition, research supports the observation that TLR2 triggers inflammation by kallikrein 5 (KLK5)-cathelicidin cascade. Increased TLR2 expression may be responsible for abnormal expression of KLK5 and cathelicidin, both of which are important in rosacea. Neurofilament is associated with neurogenic inflammation induced by neuromediators in sensory nerves, but no differences were noted between groups in this study, perhaps due to the sensitivity of the technique used.

The results of this study suggest that the increased expression of mast cell tryptase may be a sign of chronic later-stage GR. Increased expression of TLR2 suggests that cathelicidin-induced neuroimmune pathogenesis also contributes to the pathophysiology of GR. This was a small descriptive study, but it is suggestive that a larger scale immunohistochemical study is needed to confirm results on the pathophysiology of GR.

    1. Hong E. P007, SPIN 2019, 25-27 April, Paris, France.

    2. Two AM, Del Rosso JQ. J Clin Aesthet Dermatol. 2014 Jan;7(1):20-5.

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