Etiopathogenesis of Punctal Stenosis

Abstract

Inflammation and fibrosis have long been implicated as a common pathogenic mechanism in punctal stenosis [1–3]. Direct histopathological studies of the punctal tissues in stenosis have shown marked subepithelial fibrosis with predominant lymphocytic infiltration by CD45 and CD3 cells [1]. Electron microscopy has shown blunted microvilli, inter- and intracellular edema, irregular deposition of collagen, and activated fibroblasts with typical lymphocytes in their vicinity [1]. The ultrastructural effects to noxious stimuli are likely to be variable and would corroborate with the degree of inflammation. The close proximities of lymphocytes and fibroblasts could possibly signal some intercellular communications and influences. These studies open up more avenues for better understanding of the etiopathogenesis of punctal stenosis and possible preventive strategies.