Plaque control alleviated renal damage that was aggravated by experimental periodontitis in obese rats

This study aimed to evaluate the influence of experimental periodontitis on renal damage in obese rats.

Thirty-two male Sprague Dawley rats were randomly allocated into 4 groups with 8 animals each: obese rats (obese group), obese rats with periodontitis (periodontitis obese group), obese rats with periodontitis that underwent plaque control (plaque-control obese group), and healthy rats (healthy group). Rats were fed a high-fat diet to establish an obesity model. Experimental periodontitis was induced by local ligation with silk around the bilateral maxillary second molars. The plaque control was accomplished by removing ligations and local wiping with an antiseptic rinse. Histology was used to observe the gingival inflammation and clinical attachment level (CAL) to further assess bone loss and to also observe renal structure. Serum creatinine, urea nitrogen, and kidney injury molecule-1 (KIM-1) levels were measured to evaluate renal function. Renal Toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-κB), serum C-reactive protein (CRP), lipopolysaccharides (LPS), and interleukin-1β (IL-1β) were measured to evaluate renal and systemic inflammation.

Periodontal histology showed that in the periodontitis obese group, the epithelial barrier was considerably eroded by inflammatory cells, which infiltrated into the subepithelial connective tissue and lamina propria. A periodontal pocket was forming accompanied by the loss of attachment. The extent of infiltration of inflammatory cells and the CAL were significantly higher than those of the obese group (p < .001). In the plaque-control obese group, although the inflammatory condition was significantly improved than in the periodontitis obese group, the clinical attachment level with the presence of fiber hyperplasia could not be restored. Renal histology showed that renal tubular structural damage was aggravated in the periodontitis obese group, including vacuolar degeneration, exfoliation of the proximal tubular epithelial cell lining, multifocal loss of the brush border, and movement of several nuclei from the basement membrane to the lumen. These alterations were improved in the plaque-control obese group. Kidney TLR4 and NF-κB mRNA levels increased significantly in the periodontitis obese group compared to the obese group (p = .015 and p = .015, respectively) and decreased significantly in the plaque-control obese group (p = .028 and p = .021, respectively). Kidney TLR4 and NF-κB protein expression in the plaque-control obese group were significantly lower than those in the periodontitis obese group (p < .001 and p = .043, respectively). Serum creatinine and KIM-1 levels significantly decreased in the plaque-control obese group compared to the periodontitis obese group (p = .001 and p = .002, respectively). At 21 weeks (1 week after periodontal ligation), serum CRP levels in the periodontitis obese group were significantly higher than that in the healthy group (p = .017). Other serum inflammatory markers (LPS and IL-1β) did not change significantly.

Experimental periodontitis induced dysfunction and structural destruction of the kidney in obese rats. Plaque control relieved renal damage.