BACKGROUND: Epidemiologic and clinical studies have indicated that periodontal disease (PD) may cause disturbances in general health and even affect diabetes. The aim of this study was to gain knowledge on the effect of PD on diabetes metabolic control in a new model for type 2 diabetes-associated PD (i.e., the Goto-Kakizaki [GK] rat). METHODS: GK rats represented the type 2 diabetes group and were allocated into two groups: diabetes or diabetes+PD group; Wistar rats represented the non-diabetes group and were divided into non-diabetes+PD and non-diabetes groups. PD was induced by placing ligatures around second maxillary molars, and the animals were followed for 6 weeks. Serum insulin, glucose, and free fatty acid levels were evaluated; interleukin (IL)-1beta, IL-6, and tumor necrosis factor-alpha were measured in adipose tissue supernatant; glucose tolerance and insulin resistance were calculated. Further, alveolar bone destruction was estimated morphometrically and radiographically. RESULTS: Rats with diabetes+PD became almost 30% more glucose intolerant (P<0.01) and presented a 25% increase in IL-1beta in adipose tissue (P<0.05) compared to rats from the diabetes group. Moreover, PD associated with diabetes resulted in more alveolar bone destruction in comparison to PD in the absence of diabetes (P<0.01). CONCLUSIONS: Our results indicated that PD deteriorates metabolic control in diabetes, which emphasizes that PD may play a significant role for the course of diabetes. The GK rat can represent a suitable model for further studies on the association between PD and diabetes.
BACKGROUND: Epidemiologic and clinical studies have indicated that periodontal disease (PD) may cause disturbances in general health and even affect diabetes. The aim of this study was to gain knowledge on the effect of PD on diabetes metabolic control in a new model for type 2 diabetes-associated PD (i.e., the Goto-Kakizaki [GK] rat). METHODS: GK rats represented the type 2 diabetes group and were allocated into two groups: diabetes or diabetes+PD group; Wistar rats represented the non-diabetes group and were divided into non-diabetes+PD and non-diabetes groups. PD was induced by placing ligatures around second maxillary molars, and the animals were followed for 6 weeks. Serum insulin, glucose, and free fatty acid levels were evaluated; interleukin (IL)-1beta, IL-6, and tumor necrosis factor-alpha were measured in adipose tissue supernatant; glucose tolerance and insulin resistance were calculated. Further, alveolar bone destruction was estimated morphometrically and radiographically. RESULTS:Rats with diabetes+PD became almost 30% more glucose intolerant (P<0.01) and presented a 25% increase in IL-1beta in adipose tissue (P<0.05) compared to rats from the diabetes group. Moreover, PD associated with diabetes resulted in more alveolar bone destruction in comparison to PD in the absence of diabetes (P<0.01). CONCLUSIONS: Our results indicated that PD deteriorates metabolic control in diabetes, which emphasizes that PD may play a significant role for the course of diabetes. The GK rat can represent a suitable model for further studies on the association between PD and diabetes.
Authors: K Watanabe; T Iizuka; A Adeleke; L Pham; A E Shlimon; M Yasin; P Horvath; T G Unterman Journal: J Periodontal Res Date: 2010-09-22 Impact factor: 4.419