ABSTRACT
Connective tissue investing the human orbit appears to be particularly susceptible to the factors directly responsible for the pathogenesis of Graves’ disease. The orbital disease, termed thyroid-associated ophthalmopathy (TAO), involves the extensive remodeling of connective tissue (1). While the proximate connection between the glandular disease and TAO remains unknown, trafficking of activated T lymphocytes to the thyroid gland and orbit represents a prominent feature of both. Why the connective/adipose tissue of the orbit should be singled out for disease targeting is uncertain but intrinsic differences in the resident cells might underlie this susceptibility. Another open question relates to the variations in clinical presentations among patients with TAO. Some manifest predominantly eye muscle enlargement while others exhibit disease limited to the fat/connective tissue depot behind the eye. The basis for this differential presentation could be related to distinct populations of fibroblasts inhabiting the extraocular muscles and adipose/connective tissue compartments.
