PURPOSE: We assessed the effects of hyperglycaemia induced by streptozotocin (STZ) on peri-implantitis developing after implant osseointegration. METHODS: Thirty-six male Wistar rats (4 weeks old) were used. We placed titanium implants 4 weeks after extraction of the maxillary first molars. Healing abutments were attached 4 weeks later. After osseointegration was confirmed, the rats were divided into control, hyperglycaemia (STZ), and STZ with insulin (STZ+INS) groups. Hyperglycaemia was induced by a single injection of 50mg/kg STZ. Silk ligatures were placed on only the right sides (i.e. ligature sides), not on the left sides. Peri-implant tissues extracted at 4 weeks post-ligation were analysed both radiologically (via micro-computed tomography) and histologically (via toluidine blue staining). Total RNA was also extracted and analysed by quantitative PCR to detect TNF-α, IL-1β and the receptor of advanced glycation end products (RAGE). Additionally, advanced glycation end products (AGEs) were measured by ELISA. RESULTS: Radiological and histological analyses showed that bone loss on the non-ligature sides was significantly greater in the STZ than the control group. However, on the ligature sides, bone loss was greater than on the non-ligature sides, and no significant difference was evident among the three groups. The levels of mRNAs encoding TNF-α, IL-1β, RAGE, and AGEs on the ligature sides were significantly upregulated (all P<0.05) in the STZ compared to the control group. CONCLUSIONS: Although hyperglycaemia could be associated with bone loss around implants with increased AGE production and RAGE expression, hyperglycaemia does not become a triggering factor of ligature induced peri-implantitis.
PURPOSE: We assessed the effects of hyperglycaemia induced by streptozotocin (STZ) on peri-implantitis developing after implant osseointegration. METHODS: Thirty-six male Wistar rats (4 weeks old) were used. We placed titanium implants 4 weeks after extraction of the maxillary first molars. Healing abutments were attached 4 weeks later. After osseointegration was confirmed, the rats were divided into control, hyperglycaemia (STZ), and STZ with insulin (STZ+INS) groups. Hyperglycaemia was induced by a single injection of 50mg/kg STZ. Silk ligatures were placed on only the right sides (i.e. ligature sides), not on the left sides. Peri-implant tissues extracted at 4 weeks post-ligation were analysed both radiologically (via micro-computed tomography) and histologically (via toluidine blue staining). Total RNA was also extracted and analysed by quantitative PCR to detect TNF-α, IL-1β and the receptor of advanced glycation end products (RAGE). Additionally, advanced glycation end products (AGEs) were measured by ELISA. RESULTS: Radiological and histological analyses showed that bone loss on the non-ligature sides was significantly greater in the STZ than the control group. However, on the ligature sides, bone loss was greater than on the non-ligature sides, and no significant difference was evident among the three groups. The levels of mRNAs encoding TNF-α, IL-1β, RAGE, and AGEs on the ligature sides were significantly upregulated (all P<0.05) in the STZ compared to the control group. CONCLUSIONS: Although hyperglycaemia could be associated with bone loss around implants with increased AGE production and RAGE expression, hyperglycaemia does not become a triggering factor of ligature induced peri-implantitis.