The lacrimal gland, a major contributor to the aqueous component of the tear film, delivers its secretions via ducts opening onto the superotemporal forniceal conjunctiva. Diseases that affect the structure or function of the lacrimal gland result in aqueous tear deficiency. One of the causes of severe aqueous deficiency is Stevens-Johnson syndrome (SJS), an acute self-limiting mucocutaneous blistering disease that often results in chronic ocular sequelae. However, the pathobiological features of aqueous tear deficiency in SJS are not understood fully. A previous report by Singh et al suggests that the aqueous deficiency in SJS could be secondary to fibrosis in the periductal conjunctiva and not the result of primary inflammatory damage to the lacrimal gland itself. Further exploration and confirmation of these initial observations may have significant translational implications because therapeutic approaches can be developed to address the periductal fibrosis, instead of attempting to rejuvenate the entire lacrimal gland.

https://www.aaojournal.org/article/S0161-6420(20)30834-4/fulltext#%20