Rosacea: An Introduction

Rosacea Causes and Pathogenesis

The pathogenesis of rosacea is unknown, but it is presumed to be a genetically determined anomalous vascular response that develops in the third to sixth decades of life.

The hypothesis, that the basic pathogenesis of the disease is a flushing disorder, is based on several findings.

The disease appears to be more frequent and prevalent in northern climates where cold exposure is frequent, and in light-skinned persons in whom flushing is common.

In addition, in the carcinoid syndrome, recurrent flushing over the face and upper chest has resulted in full blown rosacea.

An increase in solar elastosis is present in rosacea biopsy specimens.

Pathologists hypothesize that this altered connective tissue gives inadequate support to small vessels, resulting in prolonged vasodilatation and secondary immune complex deposition.

The presence of pronounced sebaceous gland hypertrophy, as seen in rhinophyma, has resulted in the hypothesis that rosacea is a sebaceous gland disease.

However, sebaceous gland hypertrophy is not a typical feature of early rosacea lesions.

On the other hand, meibomitis is a frequent accompaniment of rosacea, and a diffuse sebaceous gland abnormality has been suggested as the cause of meibomitis.

A variety of hypotheses relating acne rosacea to an underlying gastrointestinal or psychosomatic disorder have not been supported by scientific evidence.

No single hypothesis appears to adequately explain both the vascular changes and the inflammatory reaction seen in acne rosacea, leaving the pathogenesis unclear.

The exact pathogenesis of the corneal (ocular rosacea) findings is not known, although it appears to be closely related to the lid disease.

Meibomian gland dysfunction and S. aureus toxins can produce tear film instability.

An increase in free fatty acids in the tear film may cause conjunctival hyperemia and punctate corneal epithelial breakdown.

This breakdown may allow antigens--probably staphylococcal in origin-access to the corneal stroma where it combines with anti-staphylococcal antibodies.

Antigen-antibody complexes may then activate complement through the classical pathway and generate C5a.

C5a is a potent chemotactic agent for neutrophils resulting in peripheral corneal infiltration and ulceration.

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