Restenosis after stent implantation is mainly characterized by an inflammatory 
response to the procedural injury and an intense fibrocellular response 
including smooth muscle cell (SMC) proliferation. After angioplasty alone, the 
restenosis process also involves thrombus formation and negative remodeling. Due 
to the pleiotropic mode of action exerted by glucocorticoids which include 
profound anti-inflammatory and immunosuppressive effects, direct inhibition on 
SMC proliferation and apoptosis, their potential in the prevention of restenosis 
has gained widespread interest. Over the last decade, preclinical and clinical 
data have not been able to conclusively document a robust therapeutic effect on 
restenosis after angioplasty or stent implantation. Only recently, preclinical 
data and limited observations in humans using drug eluting stents for local drug 
delivery have suggested beneficial effects of dexamethasone on neointimal 
proliferation. Randomized clinical trials using local drug delivery are expected 
to start in the near future. In the light of these ongoing developments, this 
review summarizes the pathophysiological basis of glucocorticoid action in the 
context of restenosis, provides an overview of the animal data available and 
discusses the clinical results that have been gathered over the last decade with 
particular emphasis on dexamethasone.