High‐fat diet aggravates the liver disease caused by periodontitis in rats

Abstract

Background: Periodontitis is an inflammatory disease that causes periodontium and hepatic alterations. Liver disease is related to the intake of foods rich in fat and sugars (high-fat). The objective of this study was to evaluate whether a high-fat diet can aggravate the liver disease caused by ligature-induced periodontitis in rats.Methods: Twenty-one female rats were divided into three groups (n = 7 in each group): control; periodontitis (periodontitis induced with ligature) and high-fat + periodontitis (received hypercaloric diet and induction of periodontitis). The rats were submitted to the analyses of the following periodontal parameters: gingival bleeding index (GBI), probing pocket depth (PPD), tooth mobility (TM), and alveolar bone height. In the hepatic tissue, the levels of malondialdehyde (MDA), glutathione (GSH), total cholesterol, and myeloperoxidase activity (MPO) were measured. Liver samples were also histopathologically evaluated. Finally, blood levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), glucose, total cholesterol, cholesterol high-density lipoprotein (HDL), and uric acid were measured. Results:The high-fat + periodontitis group presented an increase in the steatosis score (P < 0.05) for the histopathologic evaluation, when compared with the periodontitis group. MDA, uric acid and ALT levels also increased, whereas GSH and HDL levels showed lower values. Conclusion:A high-fat diet aggravates the liver disease caused by ligature-induced periodontitis in rats.

A Diet Rich in Saturated Fat and Cholesterol Aggravates the Effect of Bacterial Lipopolysaccharide on Alveolar Bone Loss in a Rabbit Model of Periodontal Disease

“…Furthermore, similarly to other infectious or chronic inflammatory diseases [59], periodontal diseases might alter concentration and composition of plasma lipids and lipoproteins [60], promoting atherosclerosis and NAFLD progression. In fact, studies on different experimental periodontitis rodent models suggest that this condition led to increases in TGs [61,62] and total cholesterol and to a decrease in HDL-cholesterol [62,63]. However, Ebersole et al [64] reported an increase in serum cholesterol, but no change in TGs in a non-human primate model of ligature-induced periodontitis.…”

Periodontal disease–related nonalcoholic fatty liver disease and nonalcoholic steatohepatitis: An emerging concept of oral‐liver axis

“…Other studies also reported that ligature‐induced periodontitis in rats induced mild hepatic damage through increased malondialdehyde and decreased antioxidant glutathione production present in both the blood and liver 50,51,57,150 . Furthermore, a high‐fat or high cholesterol diet cooperatively with periodontitis enhanced intrahepatic oxidative stress, resulting in exacerbation of steatohepatitis 152,154 …”

“…Moreover, in animal models of metabolic diseases showing obesity or diabetes, periodontal inflammation and bacterial infection enhanced metabolic disorders in the liver, resulting in accelerated progression of nonalcoholic fatty liver disease. 23 , 55 , 151 , 152 , 153 , 154 Although not all mechanisms explaining the interaction between periodontal disease and metabolic diseases are known, diffusion of inflammatory mediators and reactive oxygen species from inflamed periodontal tissues into the circulation can mediate low‐grade systemic inflammation, and thereby exacerbate insulin resistance in obesity and diabetes. 155 Ishikawa et al reported that hyperglycemia promotes translocation of P. gingivalis from the oral cavity to the liver and reduces hepatic insulin‐induced glycogen biosynthesis in mice.…”

“… 50 , 51 , 57 , 150 Furthermore, a high‐fat or high cholesterol diet cooperatively with periodontitis enhanced intrahepatic oxidative stress, resulting in exacerbation of steatohepatitis. 152 , 154 …”

Untargeted and targeted gingival metabolome in rodents reveal metabolic links between high‐fat diet‐induced obesity and periodontitis

“…Obesity is characterized by inflammation‐related impairment of lipid and glucose metabolism in many organs (Gonzalez‐Muniesa et al, 2017), while periodontitis is manifested by inflammation‐based dysregulation of collagen and alveolar bone metabolism (Crotti et al, 2015; Franco et al, 2017). In this context, the two conditions have been interacted via impaired metabolic response in lipid (Cury et al, 2018; Zelkha et al, 2010), glucose (Martinez‐Herrera et al, 2017; Solini et al, 2019; Song et al, 2016) and bone metabolism (Dittmann et al, 2015), oxidative stress (Bullon et al, 2009) and other metabolic pathways (Andrade et al, 2019; Kuraji et al, 2018). These metabolic links between obesity and periodontitis are targeted but also limited.…”