Efeitos Locais E Sistêmicos Da Dehidroepiandrosterona (Dhea) Em Ratos Após Periodontite Induzida

Abstract

Periodontitis is a bacterial inflammatory disease characterized by connective tissue rupture, loss of attachment of ligaments and resorption of alveolar bone, which may lead to tooth loss. Dehydroepiandrosterone (DHEA) is the most abundant steroid hormone in the human body and is associated with the production of the hormones estrogen and testosterone. This study aimed to investigate the local and systemic effects of dehydroepiandrosterone supplementation on periodontitis in ovariectomized rats submitted to a model of induction of periodontitis by ligature. The study methodology consisted of performing ovariectomy on the rats and subsequently inducing periodontitis, after which the pharmaceutical solutions proposed in the work were administered for a period of 20 days. After the experimental days, the analysis of the oral clinical parameters, alveolar bone height and the presence of the myeloperoxidase enzyme in the gingival tissue was carried out. To evaluate the hepatic and uterine tissues, the dosage of the myeloperoxidase enzyme and histopathological evaluation were performed. Ligature-induced periodontitis caused clinical and morphometric changes in periodontal tissue, as evidenced by increased alveolar bone loss, gingival bleeding rates and pocket depth. The treatment of animals with DHEA was not able to reduce the oral inflammatory parameters and alveolar bone loss characteristic of the disease. In addition, the study demonstrates that periodontitis can induce uterine inflammation in ovariectomized animals, considering that the group of ovariectomized animals with induced periodontitis showed significant oxidative stress in the uterine tissue and histology compatible with an inflammatory process. It was possible to observe a positive effect of DHEA supplementation on the liver tissue of ovariectomized animals with periodontitis. There was preservation of the structure of hepatocytes and sinusoid spaces in the supplemented groups, which was not observed in the group without supplementation. The treatment of animals with DHEA was not able to reduce the oral inflammatory parameters and alveolar bone loss characteristic of the disease. Therefore, new experiments with different doses of DHEA are necessary to evaluate the effects of supplementation of the substance in relation to periodontitis. Although it does not have a protective action on the gingival tissue, and may even accentuate the oxidative stress resulting from the ovariectomy, the induction of periodontitis or the combination of both, it may have protected the uterine tissue against the action of inflammation at a dose of 25 mg/kg, considering the myeloperoxidase analysis and the histology of the uterine tissue. In addition, the study demonstrates that periodontitis can induce uterine inflammation in ovariectomized animals, considering that the group of ovariectomized animals with induced periodontitis showed significant oxidative stress in the uterine tissue and histology compatible with an inflammatory process. It was possible to observe a positive effect of DHEA supplementation on the liver tissue of ovariectomized animals with periodontitis.