Sir,

We read with interest the observations of Tinley et al. We would agree with the authors that inflammation is one of the major contributing factors for such lesions in cases of meibomian gland dysfunction (MGD). In MGD, alterations in lipid secretions and abnormal keratinization of the meibomian gland duct orifices have a profound effect on the quality of tear film and on the ocular surface.1 Inflammatory mediators accumulate in the tear film and the induced inflammation damages the ocular surface.1

Jain et al2 have recently reported similar findings in a case of ocular rosacea, which after negative virologic studies, was successfully treated with topical steroids. However, in the current series, we noted resolution of the refractory lesions (3/5) after putting a bandage contact lens.3 None of the cases were treated with the topical steroids. Increased ocular surface inflammation and mechanical rubbing of the inflamed eyelids on the corneal surface may have been the probable contributing causes for pseudodendritic keratitis. If only inflammation and antigen–antibody reactions were the contributing causes, then our cases would not have shown a resolution only with bandage contact lens. Also, at times, the variability in the presentation of the pseudodendrites may lead to a clinical suspicion of herpetic keratitis. In such cases, it is wise to initiate therapy with topical steroids after ruling out a true dendrite in spite of associated MGD. We would also emphasize that in cases of MGD besides other treatment modalities the underlying dysfunction of meibomian glands should be addressed with appropriate therapy.