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Periodontitis causes abnormalities in the liver of rats
Author(s) -
Vasconcelos Any Carolina Cardoso Guimarães,
Vasconcelos Daniel Fernando Pereira,
Pereira da Silva Felipe Rodolfo,
Carvalho França Luiz Felipe,
Alves Even Herlany Pereira,
Lenardo David Di,
dos Santos Pessoa Larissa,
Novaes Pedro Duarte,
Luiz dos Reis Barbosa André,
Mani Arya,
Mariano Flávia Sammartino,
Medeiros JandVenes Rolim,
Oliveira Aldeídia Pereira
Publication year - 2019
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1002/jper.18-0226
Subject(s) - periodontitis , immunohistochemistry , alkaline phosphatase , pathology , steatosis , lipid droplet , cirrhosis , medicine , glycogen , oil red o , liver injury , biology , endocrinology , biochemistry , enzyme , mesenchymal stem cell , adipogenesis
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.