ABSTRACT
Thyroid-associated ophthalmopathy (TAO) involves a peculiar remodeling of the orbital connective tissues (1). Many components of this remodeling can be attributed to the activities of resident fibroblasts. Orbital contents, including muscle and connective tissue, occupy a greater volume than normal in many cases of TAO, a consequence at least in part of disordered glycosaminoglycan accumulation. The fatty tissue depot also enlarges and this may result from increased numbers and=or size of adipocytes as well as glycosaminoglycan infiltration. Tissues are often inflamed and become infiltrated with
activated lymphocytes and mast cells (2). The factors driving connective tissue expansion and inflammation in TAO remain unidentified. It is currently believed that cytokines expressed by T-cells and mast cells directly or indirectly activate fibroblasts in the orbit. Recent evidence supports the concept that orbital fibroblasts differ from those inhabiting extraorbital tissue. A number of responses in these cells appear exaggerated when compared to those occurring in cells from other tissues and anatomic regions. I will briefly review the recent advances made in understanding the phenotype of orbital fibroblasts. We hypothesize that the unique attributes of these cells underlie both the targeting of the orbit for disease involvement and the unusual characteristics of the tissue remodeling associated with TAO.
