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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. 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. 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. 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.

Liver disease is global health problem. Paracetamol (APAP) is used as an analgesic drug and is considered safe at therapeutic doses, but at higher doses, it causes acute liver injury. N-acetyl-p- Benzoquinone Imine (NAPQI) is a reactive toxic metabolite produced by biotransformation of APAP. NAPQI damages the liver by oxidative stress and the formation of protein adducts. The glutathione precursor N-acetylcysteine (NAC) is the only approved antidote against APAP hepatotoxicity, but it has limited hepatoprotective effects. The search for new drugs and novel therapeutic intervention strategies increasingly includes testing plant extracts and other natural products. Plumeria pudica (Jacq., 1760) is a plant that produces latex containing molecules with therapeutic potential. Proteins obtained from this latex (LPPp), a well-defined mixture of chitinases, proteinases proteinase inhibitors have shown anti-inflammatory, antinociceptive, antidiarrheal effects as well as a protective effect against ulcerative colitis. These studies have demonstrated that LPPp acts on parameters such as Glutathione (GSH) and Malondialdehyde (MDA) concentration, Superoxide Dismutase (SOD) activity, Myeloperoxidase (MPO) activity, and TNF- α IL1-β levels. Since oxidative stress and inflammation have been reported to affect the initiation and progression of liver injury caused by APAP, it is suggested that LPPp can act on aspects related to paracetamol hepatoxicity. This article brings new insights into the potential of the laticifer proteins extracted from the latex of P. pudica and opens new perspectives for the treatment of this type of liver disease with LPPp.

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. 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. 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. A high‐fat diet aggravates the liver disease caused by ligature‐induced periodontitis in rats.

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. 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. 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. Experimental periodontitis caused immunohistochemistry, histopathologic, ultrastructural, oxidative, and biochemical changes in the liver of rats.

Background:Damage caused by periodontitis not only affects periodontal tissues, but also increases the severity of various illnesses such as rheumatoid arthritis, diabetes, and liver diseases. The aim of this study is to investigate the association between induced periodontitis and damage caused through its systemic effects on the liver. Methods:Twenty rats were divided into two groups: control and periodontitis. The following parameters were evaluated: gingival bleeding index (GBI), probing depth (PD), myeloperoxidase (MPO) activity, alveolar bone loss (ABL) for periodontal tissues; histopathologic examination of gingival and liver tissues; immunohistochemistry to cells positive for neural/glial antigen 2 (NG2) expressed in hepatic pericytes, glutathione (GSH), and malondialdehyde (MDA) concentrations in liver; and serum levels of alanine aminotransferase and aspartate aminotransferase. Results:GBI, PD, MPO, ABL, and histopathologic examinations demonstrated the development of periodontitis. There was a significant increase in microvesicular steatosis accompanied by a marked reduction in NG2+ pericytes in the periodontitis group compared with the control group. The periodontitis group had significantly lower GSH and higher MDA concentration in the liver compared with the control group. Conclusions:The present study results link the systemic effects of induced periodontitis with changes in hepatic tissues such as microvesicular steatosis, likely caused by an increase in oxidative stress and lipid peroxidation. The findings from the present study implicate an association between a decrease of pericytes and liver disease caused by ligature‐induced periodontitis in rats.

Background:Intermittent administration of parathyroid hormone (PTH) promotes new bone formation in patients with osteoporosis and bone fractures. It was shown previously that PTH also reduces periodontitis‐related bone loss. The aim of this study is to evaluate the effect of treatment with PTH on periodontal healing in rats. Methods:Fenestration defects were created at the buccal surface of the distal root of the mandibular first molars, and both periodontal ligament (PDL) and cementum were removed. Animals were then assigned to two groups (eight animals per group): group 1: control, placebo administration; and group 2: test, human PTH (hPTH) 1‐34 administration at a concentration of 40 μg/kg. For both groups, the animals were injected every 2 days, and the animals were sacrificed at 14 and 21 days after surgery. Specimens were harvested and processed for routine decalcified histologic sections. The following parameters were assessed: 1) remaining bone defect extension (RBDE); 2) newly formed bone density (NFBD); 3) total callus area (TCA); 4) osteoclast number (ON) in the callus region; and 5) newly formed dental cementum‐like tissue (NFC). Birefringence of root PDL reattachment was also evaluated. Results:Birefringence analysis showed root PDL reattachment for both groups 21 days after treatment. Intermittent hPTH 1‐34 administration decreased RBDE (P<0.01) and increased NFBD (P<0.01), TCA (P<0.01), area of NFC (P<0.01), and ON in the callus region (P<0.01). Conclusion:Within the limits of the present study, intermittent administration of hPTH 1‐34 led to an enhanced periodontal healing process compared with non‐treated animals.