![]() The hyperthyroid condition itself does not impact directly on the accumulation of connective tissue within the orbit ( 1, 2). ![]() ![]() The close association of TED with Graves' disease of the thyroid provides clues to its etiology. Understanding the pathogenetic mechanisms underlying TED should yield the identification of predictive biomarkers of progressive disease and effective and specific treatments. They do nothing to prevent or reverse pathological remodeling of orbital tissues ( 10). These interventions are aimed at the consequences of the disease rather than targeting its cause, which remains poorly understood ( 5, 6, 10, 11). Current therapeutic options include corticosteroids, external beam radiation, and surgery. To date, there are no effective means of preventing the disease or reliably altering its course. The increased volume of orbital connective tissue leads to protrusion of the eye (exophthalmos) ( 2, 9). The most dramatic pathological findings in end-stage TED include glycosaminoglycan (GAG) deposition (accompanied by dramatic swelling resulting from the water-binding capacity of these macromolecules) and fibrosis affecting the extraocular muscles and fat accumulation in the orbit ( 5– 8). TED affects many eye functions, including wetting of the ocular surface, eye motility, optic nerve function, and eyelid anatomy ( 2, 5). TED occurs more frequently in patients older than 50 years of age and in males, smokers, and those with microvascular disease ( 2, 4). Besides hyperthyroidism, up to 60% of patients with Graves' disease develop a manifestation localizing to the orbit called Graves' ophthalmopathy or thyroid eye disease (TED) ( 2, 3). ![]() G raves' disease is an autoimmune condition in which the thyroid-stimulating hormone receptor (TSH-R) displayed on thyrocytes is targeted by autoantibodies, inducing the production of excess thyroid hormone ( 1). Although the mechanisms underlying these processes are not completely understood, several currently available therapeutic strategies might interrupt the signaling between B and T cells and fibroblasts, thereby treating the clinical manifestations of TED. These interactions ultimately result in fibroblasts expressing extracellular matrix molecules, proliferating and differentiating into myofibroblasts or lipofibroblasts. When orbital fibroblasts are activated, possibly by Graves' disease–related autoantibodies, they release T cell chemoattractants, initiating an interaction in which these cells activate each other. Recent findings have uncovered the importance of intercellular communication between autoreactive T cells and orbital fibroblasts. Such treatments may become available as a result of research aimed at understanding the mechanism by which Graves' disease leads to specific remodeling of orbital tissues. Current treatments are sometimes effective in alleviating the symptoms of the disease, but there remains a demand for treatments that prevent or reverse the pathological alterations of orbital tissues. This dramatic remodeling results in protrusion of the eye, also known as exophthalmos. During the course of TED, fibrosis can develop around the extraocular muscles, and excess extracellular matrix and fat accumulates in the periorbital space. Thyroid eye disease (TED) is an inflammatory condition of the orbit closely associated with Graves' disease. ![]()
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