A microbiota oral possui aproximadamente 700 microrganismos simbiontes responsáveis pela homeostase da saúde bucal. Contudo, alterações na microbiota oral podem gerar processos disbióticos que favorecem o agravamento de infecções como a cárie e a doença periodontal. Essas infecções orais, além do acometimento sistêmico, podem comprometer a integridade dos dentes e também da saúde bucal. Dessa forma, a alimentação inadequada mostra-se um fator de risco que influência na prevenção e no tratamento dessas infecções orais. Objetivo: Este estudo visa evidenciar a influência nutricional na modulação da microbiota oral afetando a longo prazo a microbiota intestinal, destacando o uso de probióticos e prebióticos no tratamento de infecções orais através de uma revisão de literatura. Síntese de dados: A suplementação de determinados nutrientes e a ingestão de uma dieta adequada em macronutrientes e micronutrientes influenciam diretamente no estado nutricional e consequentemente na manutenção da homeostase oral-sistêmica. Além disso, devido à multirresistência microbiana, terapias com probióticos e prebióticos têm sido adotadas como auxiliares no tratamento de infecções orais. Conclusão: A Odontologia Personalizada deve integrar conhecimentos multidisciplinares de atenção à saúde. Isso além de saber quando encaminhar e trabalhar junto com o Nutricionista.
Background and Objectives: Periodontitis is a highly prevalent disease in psychiatric patients, including those undergoing symptomatic treatment with second-generation antipsychotics. Some of these drugs, such as clozapine (CLO) and olanzapine (OLA), have prominent metabolic effects such as weight gain, hyperglycemia, and dyslipidemia, which are risk factors for periodontitis. In addition to the metabolic effects, there are reports of changes in salivary flow, gingival bleeding, and caries. In this context, we aimed to evaluate if the metabolic effects of OLA and CLO alter periodontal parameters in an animal model of periodontitis without the environmental and psychosocial biases inherent to human diseases. Methods:In the first set of experiments, male and female adult Wistar rats received oral administration of CLO, OLA, or vehicle for 45 days. They were evaluated for body mass composition and weight gain, blood glucose parameters (fasting and glucose tolerance and insulin resistance tests), and lipid profile (HDL, total cholesterol, and triglycerides). In a second set of experiments, the same measurements were performed in female rats exposed to the antipsychotics for 45 days and ligature-induced peri-
Chagas disease (CD) is a neglected tropical disease caused by Trypanosoma cruzi infection that, despite being discovered over a century ago, remains a public health problem, mainly in developing countries. Since T. cruzi can infect a wide range of mammalian host cells, parasite–host interactions may be critical to infection outcome. The intense immune stimulation that helps the control of the parasite’s replication and dissemination may also be linked with the pathogenesis and symptomatology worsening. Here, we discuss the findings that support the notion that excessive immune system stimulation driven by parasite persistence might elicit a progressive loss and collapse of immune functions. In this context, cellular stress and inflammatory responses elicited by T. cruzi induce fibroblast and other immune cell senescence phenotypes that may compromise the host’s capacity to control the magnitude of T. cruzi-induced inflammation, contributing to parasite persistence and CD progression. A better understanding of the steps involved in the induction of this chronic inflammatory status, which disables host defense capacity, providing an extra advantage to the parasite and predisposing infected hosts prematurely to immunosenescence, may provide insights to designing and developing novel therapeutic approaches to prevent and treat Chagas disease.
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