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Pathogenesis of Graves' ophthalmopathy: recent controversies and progress

Graves' ophthalmopathy (GO) is a medically incurable, chronic autoimmune process that affects the retroorbital space and appears to have strong etiological links with autoimmune thyroid disease. The close clinical association between immunogenic hyperthyroidism (Graves' disease), ophthalmopathy and pretibial dermopathy suggests that the antigen responsible for these diverse conditions may be common to the thyroid gland, the retroorbital tissue and the pretibial skin. The varied clinical expressions of GO, including proptosis, extraocular muscle dysfunction, periorbital and lid edema, chemosis and conjunctival congestion, can be explained mechanically by an increase in connective tissue and extraocular muscle volume within the confines of the bony orbits, resulting from the accumulation of collagen, glycosaminoglycans (GAGs) and the attendant edema within these tissues. This process is likely to be driven by T cells that access and infiltrate the orbital space via certain adhesion molecules, and release various cytokines capable of stimulating cell proliferation, GAG synthesis and

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