Trimethylamine N-oxide (TMAO) is a metabolite produced by the gut microbiota and has been mainly associated with an increased incidence of cardiovascular diseases (CVDs) in humans. There are factors that affect one’s TMAO level, such as diet, drugs, age, and hormones, among others. Gut dysbiosis in the host has been studied recently as a new approach to understanding chronic inflammatory and degenerative diseases, including cardiovascular diseases, metabolic diseases, and Alzheimer’s disease. These disease types as well as COVID-19 are known to modulate host immunity. Diabetic and obese patients have been observed to have an increase in their level of TMAO, which has a direct correlation with CVDs. This metabolite is attributed to enhancing the inflammatory pathways through cholesterol and bile acid dysregulation, promoting foam cell formation. Additionally, TMAO activates the transcription factor NF-κB, which, in turn, triggers cytokine production. The result can be an exaggerated inflammatory response capable of inducing endoplasmic reticulum stress, which is responsible for various diseases. Due to the deleterious effects that this metabolite causes in its host, it is important to search for new therapeutic agents that allow a reduction in the TMAO levels of patients and that, thus, allow patients to be able to avoid a severe cardiovascular event. The present review discussed the synthesis of TMAO and its contribution to the pathogenesis of various inflammatory diseases.

Introduction: Marfan syndrome (MFS) is an autosomal dominant genetic disorder, caused by a mutation in the FBN-1 gene, affecting the cardiovascular, musculoskeletal, ocular, and central nervous systems. Cardiovascular abnormalities associated with MFS lead to different pathological conditions, such as cardiac arrhythmias, coronary artery disease, and aortic dilatation. The latter are the primary causes of mortality in MFS patients. To date, the role of altered oral microbiota (OM) in MFS is unknown, and so the aim of our study was to determine whether there are differences in the oral microbiota of MFS patients with aortic dilatation and non-dilatation. Methods: We enrolled 36 MFS patients, who were divided into groups with aortic non-dilatation (n = 12) and with aortic dilatation (n = 24). Dental plaque samples were used for OM analysis, and serum was used for cytokine evaluation. Results: The main genera were compared between patients with aortic dilatation and non-dilatation, revealing three genera with significant differences: Actinomyces (p = 0.007) and Rothia (p = 0.002) were more abundant in those with aortic dilatation, while Fusobacterium (p = 0.044) was more abundant in non-dilatation patients. However, no significant differences in cytokine levels were observed between the presence and absence of aortic dilatation, except that the IL-1β levels were higher in non-dilatation patients (165.09 pg/mL) than in those with dilatation (117.15 pg/mL), with a significance of p = 0.057. Conclusions: This study represents the initial, tentative pilot study to understand the relationship between oral health and systemic conditions in patients with Marfan syndrome.