THE PATHOLOGY OF DRY EYE - THE INTERACTION BETWEEN THE OCULAR SURFACEAND LACRIMAL GLANDS

Background. Most dry-eye symptoms result from an abnormal, nonlubricat ive ocular surface that increases shear forces under the eyelids and d iminishes the ability of the ocular surface to respond to environmenta l challenges. This ocular-surface dysfunction may result from immunoco mpromise due to systemic autoimmune disease or may occur locally from a decrease in systemic androgen support to the lacrimal gland as seen in aging, most frequently in the menopausal female. Hypothesis. Compon ents of the ocular surface (cornea, conjunctiva, accessory lacrimal gl ands, and meibomian glands), the main lacrimal gland, and interconnect ing innervation act as a functional unit. When one portion is compromi sed, normal lacrimal support of the ocular surface is impaired. Result ing immune-based inflammation can lead to lacrimal gland and neural dy sfunction. This progression yields the OS symptoms associated with dry eye. Therapy. Restoration of lacrimal function involves resolution of lymphocytic activation and inflammation. This has been demonstrated i n the MRL/lpr mouse using systemic androgens or cyclosporine and in th e dry-eye dog using topical cyclosporine. The efficacy of cyclosporine may be due to its immunomodulatory and antiinflammatory (phosphatase inhibitory capability) functions on the ocular surface, resulting in a normalization of nerve traffic. Conclusion. Although the etiologies o f dry eye an varied, common to all ocular-surface disease is an underl ying cytokine/receptor-mediated inflammatory process. By treating this process, it may be possible to normalize the ocular surface/lacrimal neural reflex and facilitate ocular surface healing.