Food restriction reduces hepatic alterations associated with experimental periodontitis.

BACKGROUND: Periodontitis is a chronic inflammatory and multifactorial disease that affects the periodontal structures and can cause alterations in the hepatic tissue. The aim of the present study was to evaluate whether a diet with food restriction can decrease oral and liver alterations associated with ligature-induced periodontitis. METHODS: Twenty-four female Wistar rats were used in this study, randomized into three groups (n = 8 for each group): control (regular food); periodontitis (regular food + periodontitis induced with ligatures); and food restriction (diet with food restriction and periodontitis induction). The following periodontium parameters were analyzed tooth mobility (TM), probing pocket depth (PPD), gingival bleeding index (GBI), and alveolar bone height (ABH). In the liver, the levels of oxidative stress markers-malondialdehyde (MDA), glutathione (GSH), total cholesterol, and levels of myeloperoxidase (MPO) activity were measured. Liver samples were analyzed for histopathological score. In the blood tissue, the levels of enzymes alanine aminotransferase (ALT), aspartate aminotransferase (AST), glucose, total cholesterol, and the high-density lipoprotein (HDL) were also evaluated. RESULTS: The animals that received a diet with food restriction + periodontitis showed a decrease in hepatic histopathological score (P < 0.05) when compared with the periodontitis group, the same for glucose, total cholesterol, ALT, AST, and ABH data. The group with food restriction + periodontitis showed a decrease in the histopathological liver score (P < 0.05) compared with the group with periodontitis. CONCLUSION: This study revealed that food restriction reduced oral damages, as well as hepatic, blood and alveolar bone alterations associated with ligature-induced periodontitis in rats.

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

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.

Periodontitis causes abnormalities in the liver of rats.

BACKGROUND: Periodontitis not only causes injury to the periodontium, but also damages other tissues such as: articulate, renal, cardiac, and hepatic. The objective of this study was to investigate periodontitis induced alterations in liver function and structure using an experimental model. METHODS: Twenty female rats (Rattus norvegicus) were allocated into two groups: control and periodontitis. Gingival bleeding index and oxidative stress parameters and specific circulating biomarkers were measured. Immunohistochemistry was carried out using alkaline phosphatase (AlkP) staining of the liver. Hepatic tissues, cytokines, and lipid contents were measured. Histopathologic evaluation of the liver was carried out using light and electron microscopy. RESULTS: Liver histopathologic and immunohistochemistry assessment showed increase in steatosis score, and presence of binucleate hepatocytes and positive cells for AlkP in periodontitis versus control group. Ultrastructural evaluation showed significant increase in size and number of lipid droplets (LD), distance between the cisterns of rough endoplasmic reticulum (RER), mitochondria size, foamy cytoplasm, and glycogen accumulation in the liver of the periodontitis group compared with the control group. In addition, plasma levels of AlkP, high-density lipoprotein (HDL), triglycerides, and total cholesterol were also changed. CONCLUSION: Experimental periodontitis caused immunohistochemistry, histopathologic, ultrastructural, oxidative, and biochemical changes in the liver of rats.

Corrigendum to "Biological Effects of Medicinal Plants on Induced Periodontitis: A Systematic Review".

[This corrects the article DOI: 10.1155/2016/3719879.].