The effects of diet on the incidence of periodontitis in rats

Abstract

SummaryFour groups of 60 male Alpk:APfSD rats were fed different nutritionally comparable diets for 107 weeks with interim sacrifices at 26, 53 and 77 weeks in order to compare the effect of diet on the incidence of oral disease. Changes in the oral and nasal cavities were assessed by histopathology. Oro-nasal fistulation and severe periodontitis were associated with diets containing fibres originating from oats and barley. An expanded ground diet induced the most severe lesions. Aspects of the pathogenesis of the lesions observed are discussed.

N‐Acetylcysteine, a Thiol Antioxidant, Decreases Alveolar Bone Loss in Experimental Periodontitis in Rats

“…Several models of experimental periodontitis, such as dietary manipulation, the introduction of pathogenic microorganisms, and placement of a ligature, have been described in the literature 26–28 . Ligature methods have been accepted as useful experimental models of periodontitis with alveolar bone resorption 26,29,30 .…”

The influence of diet consistence, drinking water and bedding on periodontal disease in Sprague‐Dawley rats

“…A similar relationship was also found in roughly half of 956 Mol:Wistar Han rats, 132–137 weeks old, used in an experimental carcinogenesis study, where impaction clusters of oats and barley from the diet were found in the gingival sulcus accompanying various degrees of alveolar bone resorption (22). The effect of various forms of Porton combined diet (PCD) and Central Toxicology Laboratory Diet 1 (CT1) on the incidence of periodontitis and oro‐nasal fistulation in Wistar rats was investigated in another study (18) where rats were sacrificed after 26–107 weeks. The highest incidence and most severe periodontitis of the upper molars were generally found in rats fed PCD expanded diet, which was looser and less ground than the other types of PCD.…”

Ameliorative effect of quercetin on the destruction caused by experimental periodontitis in rats

“…In periodontitis, bacteria and their products induce polymorphonuclear leukocyte infiltration, edema and vascular dilatation in inflamed periodontal tissues (3). Periodontal disease can be induced in rats by dietary manipulation (4), introduction of pathogenic microorganisms (5), placement of a ligature that acts as a site for bacterial colonization (6) or injection of bacterial toxins (7). It has been suggested that LPS can penetrate gingival connective tissue and induce a local inflammatory response that leads to periodontal bone resorption (8,9).…”