PURPOSE: Coated and noncoated Wallstents were implanted in dogs with experimental benign common bile duct stenoses to monitor the long-term patency of self-expanding stents in the biliary system. MATERIALS AND METHODS: Experimental common bile duct stenoses were induced with a thermal laser in 12 dogs. Three silicone-coated and 14 noncoated stents were implanted. The animals were followed up from 3 to 25 months by means of cholangiography, cholangioscopy, measurements of liver enzyme levels, autopsy, and histology. RESULTS: Silicone coated stents failed in all cases, resulting in two total occlusions and one stent dislodgment to the bowel. Noncoated stents led to marked mucosal hyperplasia and stent narrowing in most cases, but with follow-up of more than 12 months, hyperplasia underwent regression and--except in one case--neither an increase in liver enzyme levels nor stent occlusion occurred. Histologically, the extent of hyperplasia was related to the stent position within the duct wall. With stents in the mucosal layer, hyperplasia was excessive. Once the stent entered the submucosal layer, hyperplasia was decreased. CONCLUSION: In an experimental setting, mucosal hyperplasia did not compromise patency of noncoated stents in benign bile duct stenosis and regressed with late follow-up after 12 months.
PURPOSE: Coated and noncoated Wallstents were implanted in dogs with experimental benign common bile duct stenoses to monitor the long-term patency of self-expanding stents in the biliary system. MATERIALS AND METHODS: Experimental common bile duct stenoses were induced with a thermal laser in 12 dogs. Three silicone-coated and 14 noncoated stents were implanted. The animals were followed up from 3 to 25 months by means of cholangiography, cholangioscopy, measurements of liver enzyme levels, autopsy, and histology. RESULTS:Silicone coated stents failed in all cases, resulting in two total occlusions and one stent dislodgment to the bowel. Noncoated stents led to marked mucosal hyperplasia and stent narrowing in most cases, but with follow-up of more than 12 months, hyperplasia underwent regression and--except in one case--neither an increase in liver enzyme levels nor stent occlusion occurred. Histologically, the extent of hyperplasia was related to the stent position within the duct wall. With stents in the mucosal layer, hyperplasia was excessive. Once the stent entered the submucosal layer, hyperplasia was decreased. CONCLUSION: In an experimental setting, mucosal hyperplasia did not compromise patency of noncoated stents in benign bile duct stenosis and regressed with late follow-up after 12 months.