Microbiota, intestine, and brain interact one with another through the afferent fibers of the vagus nerve, which is the major linkage of this one. It has been established that long-term dietary habits influence gut bacterial diversity and are capable of inducing changes in hypothalamic energy homeostasis. The biological effects are mediated by microglial activation, systemic inflammation, and vagal afferent nerve signaling, culminating in neuroinflammation. It has been emphasized the need for a further approach regarding the influence of the dietary factors as well as their direct impacts or outcomes on the gut dysbiosis. This review aimed to understand the role of some dietary triggers of neuroinflammation on changes in the gut microbiota. Each of the diets significantly altered the microbial composition in distinct ways, leading to neuroadaptations. Hyperlipidic diets (SFA and MUFA) can stimulate TLR4 inflammatory pathway by increased LPS translocation and LBP activation and modulate brain functions, mainly in the center of feeding. Overconsumption of sucrose seems to be more detrimental for metabolic alterations, whereas fructose has a more pronounced effect on gut barrier dysfunction and subclinical inflammation; nevertheless, sucrose absorption favors fructose bioavailability, contributing to adiposity and sugar addiction.

Sex differences in gut microbiota are acknowledged, and evidence suggests that gut microbiota may have a role in higher incidence and/or severity of autoimmune diseases in females. Additionally, it has been suggested that oral, vaginal and gut microbiota composition can be regulated by estrogen levels. The association of vaginal microbiota with vulvovaginal atrophy at menopause is well described in the literature. However, the relevance of oral and gut microbiota modulation in the immune system during estrogen deficiency and its effect on inflammatory diseases is not well explored. Estrogen deficiency is a condition that occurs in menopausal women, and it can last approximately 30 years of a woman’s life. The purpose of this mini- review is to highlight the importance of alterations in the oral and gut microbiota during estrogen deficiency and their effect on oral and inflammatory diseases that are associated with menopause. Considering that hormone replacement therapy is not always recommended or sufficient to prevent or treat menopause-related disease, we will also discuss the use of probiotics and prebiotics as an option for the prevention or treatment of these diseases.

Mineral trioxide aggregate (MTA) and Portland cement are being used in dentistry as root end-filling materials. However, biocompatibility data concerning genotoxicity and cytotoxicity are needed for complete risk assessment of these compounds. In the present study, genotoxic and cytotoxic effects of MTA and Portland cements were evaluated in vitro using the alkaline single cell gel (comet) assay and trypan blue exclusion test, respectively, on mouse lymphoma cells. The results demonstrated that the single cell gel (comet) assay failed to detect DNA damage after a treatment of cells by MTA and Portland cements for concentrations up to 1000 μg/ml. Similarly, results showed that none of the compounds tested were cytotoxic. Taken together, these results seem to indicate that MTA and Portland cements are not genotoxins and do not induce cellular death.