Patients aftlicted with thyroid eye disease or Graves' ophthamopathy (GO) may experience not only pain and visual loss, but also disfigurement. Full understanding of pathogenesis has been elusive, and treatment modalities are imperfect. As with other conditions, more effective intervention will follow only after a better understanding of pathogenesis is reached. The goal of this volume is to give an overview by leaders in the field of the present state of the art both in pathogenesis and clinical aspects of GO. Much attention has been directed towards determining which cells within the orbit are targets of the autoimmune process, and how these and other cells might participate in the local inflammatory process. It is now generally agreed that orbital fibroblasts, preadipocyte fibroblasts, and adipocytes are the targeted and activated cells in GO and that full-length TSH receptor (TSHr) is expressed in these cells. Further, there is growing consensus that this receptor is up-regulated in the orbit in GO, residing primarily in newly differentiated adipocytes. However, it is also evident, given a sufficiently sensitive assay, that TSHr is detectable in fibroblasts and adipocytes from the normal orbit and other anatomic sites, as well. It will be important to determine whether the observed increase in orbital TSHr expression itself initiates the orbital autoimmune process. Also to be decided is whether orbital lymphocytes from GO patients specifically recognize this receptor, and what factor or factors unique to Graves' dIsease might stimulate TSHr expression in orbital cells. Thyroid Eye Disease is a fitting addition to the Endocrine Updates series. The aim of these publications is to provide the clinician with cutting edge, yet succinct, access to the latest advances in endocrinology. Dr. Bahn and her colleagues have joined her in presenting the most recent and exciting developments. These investigators are increasing the quality of life for thyroid eye disease patients. Thyroid Eye Disease continues the standard of excellence as the fourteenth volume in this series of topical updates. Patients afflicted with thyroid eye disease or Graves' ophthalmopathy (GO) may experience not only pain and visual loss, but also disfigurement. Full understanding of pathogenesis has been elusive, and treatment modalities are imperfect. As with other conditions, more effective intervention will follow only after a better understanding of pathogenesis is reached. The goal of this volume is to give an overview by leaders in the field of the present state of the art both in pathogenesis and clinical aspects of GO Front Matter....Pages i-xii Orbital Autoantigens....Pages 1-20 Orbital Autoimmunity in Graves’ Disease....Pages 21-36 Adipogenesis and TSH Receptor Expression....Pages 37-44 Role of Cytokines in the Pathogenesis of Graves’ Ophthalmopathy....Pages 45-65 Animal Models of Graves’ Ophthalmopathy....Pages 67-81 Participation of Orbital Fibroblasts in the Inflammation of Graves’ Ophthalmopathy....Pages 83-98 Genetic and Environmental Contributions to Pathogenesis....Pages 99-118 Clinical Presentation and Natural History of Graves’ Ophthalmopathy....Pages 119-136 Imaging in Graves’ Ophthalmopathy....Pages 137-162 Quality of Life Measurement in Patients with Graves’ Ophthalmopathy....Pages 163-183 Assessment of Disease Activity....Pages 185-200 Immunosuppressive Therapy....Pages 201-218 Surgical Management of Graves’ Ophthalmopathy....Pages 219-233 Orbital Radiotherapy: An Update....Pages 235-248 Back Matter....Pages 249-253