# Revisiting pathologic myopia: imaging evidence of an inflammatory component in the pathogenesis of myopic degeneration

## TL;DR

This paper explores how chronic inflammation may contribute to the development and progression of pathologic myopia, suggesting new treatment possibilities.

## Contribution

The paper introduces evidence that inflammation is a key factor in myopic retinal degeneration, beyond mechanical and ischemic causes.

## Key findings

- Inflammatory patterns like MFC/PIC-like lesions are found in myopic degeneration.
- Cytokine dysregulation and complement cascade activation are observed in myopic eyes.
- Immune activation is linked to choroidal thinning and retinal atrophy.

## Abstract

Pathologic myopia has traditionally been viewed as a degenerative disorder caused by mechanical stretching and choroidal ischemia. However, converging clinical, molecular, and imaging data increasingly suggest that chronic low-grade inflammation contributes to both the onset and progression of myopic retinal degeneration. Recent studies have identified inflammatory patterns—including multifocal choroiditis/punctate inner choroidopathy (MFC/PIC)–like lesions, periatrophic inflammatory “plumes,” and secondary Multiple Evanescent White Dots Syndrome (MEWDS)—often localized at sites of retinal pigment epithelium–Bruch’s membrane disruption. Parallel laboratory evidence indicates dysregulation of cytokines, activation of the complement cascade, and engagement of intracellular signaling pathways such as JAK–STAT within the myopic eye. Together, these findings support a model in which mechanical stress and hypoxia act as triggers for sustained immune activation, promoting extracellular-matrix remodeling, choroidal thinning, and progressive atrophy. Recognizing inflammation as an integral component of the pathophysiology of pathologic myopia may open new therapeutic perspectives, including immunomodulatory or complement-targeting approaches.