Sjögren syndrome: what and where are we looking for?

Sjögren's syndrome affects exocrine glands leading to a dry mouth and dry eyes. Dry eye manifestations can precede the diagnosis of Sjögren's syndrome by many years. Innumerous spontaneous and inducible Sjögren's syndrome models have been used to study the pathogenesis of Sjögren's syndrome. This review focuses on recent human data, ocular and extraglandular manifestations of animal models, what is known, what is still unknown and how we need to look, and their correlation correspondence to human disease.

Hallmarks of dry eye in Sjögren's syndrome include increased corneal staining, goblet cell loss and low tear volume. Confocal microscopy and impression cytology are able to clarify new markers of the ocular disease. Extraglandular manifestations should be an alert more severe complications in the eye. Some models have strong sex and exocrine gland predilection, whereas aging generally worsens the disease phenotype. Although most models do not display a significant increase in corneal staining or tear secretion impairment, conjunctival infiltration and decrease in goblet cells are frequently seen.

We have seen great advances in the role of inflammation in ocular, oral and extra-glandular manifestations of Sjögren's syndrome. Several mechanisms and mediators of Sjögren's syndrome have been elucidated in animal model studies.