The oral cavity is host to a complex and diverse microbiota community which plays an important role in health and disease. Major oral infections, i.e., caries and periodontal diseases, are both responsible for and induced by oral microbiota dysbiosis. This dysbiosis is known to have an impact on other chronic systemic diseases, whether triggering or aggravating them, making the oral microbiota a novel target in diagnosing, following, and treating systemic diseases. In this review, we summarize the major roles that oral microbiota can play in systemic disease development and aggravation and also how novel tools can help investigate this complex ecosystem. Finally, we describe new therapeutic approaches based on oral bacterial recolonization or host modulation therapies. Collaboration in diagnosis and treatment between oral specialists and general health specialists is of key importance in bridging oral and systemic health and disease and improving patients’ wellbeing.

The aim of this study was to analyze the link between oral microbiota and obesity in humans. We conducted a pilot study including 19 subjects with periodontitis divided into two groups: normo-weighted subjects (NWS) with a body mass index (BMI) between 20 and 25 (n = 9) and obese subjects (OS) with a BMI > 30 (n = 10). Obesity was associated with a poor oral health status characterized by an increased number of missing teeth and a higher score of periodontal-support loss associated with dysbiotic oral microbiota (39.45 ± 3.74 vs. 26.41 ± 11.21, p = 0.03 for the Chao 1 index). Oral microbiota taxonomic analysis showed that the abundance of the Capnocytophaga genus was higher (2.47% ± 3.02 vs. 0.27% ± 0.29, p = 0.04) in OS compared to NWS. Obese females (OF) were characterized by an increase in the Streptococcus genus (34.12% ± 14.29 vs. 10.55% ± 10.42, p = 0.05) compared to obese males (OM), where the Neisseria genus was increased (5.75% ± 5.03 vs. 58.05% ± 30.64, p = 0.008). These first data suggest that sex/gender is determinant in the link between oral dysbiotic microbiota and obesity in patients with periodontitis. Our results could lead to recommendations concerning therapeutic strategies for obese patients with periodontitis following the sex/gender.

The aim of this study was to analyze the link between periodontal microbiota and obesity in humans. We conducted a cohort study including 45 subjects with periodontitis divided into two groups: normo-weighted subjects with a body mass index (BMI) between 20 and 25 kg/m² (n = 34) and obese subjects with a BMI > 30 kg/m² (n = 11). Our results showed that obesity was associated with significantly more severe gingival inflammation according to Periodontal Inflamed Surface Area (PISA index). Periodontal microbiota taxonomic analysis showed that the obese (OB) subjects with periodontitis were characterized by a specific signature of subgingival microbiota with an increase in Gram-positive bacteria in periodontal pockets, associated with a decrease in microbiota diversity compared to that of normo-weighted subjects with periodontitis. Finally, periodontal treatment response was less effective in OB subjects with persisting periodontal inflammation, reflecting a still unstable periodontal condition and a risk of recurrence. To our knowledge, this study is the first exploring both salivary and subgingival microbiota of OB subjects. Considering that OB subjects are at higher periodontal risk, this could lead to more personalized preventive or therapeutic strategies for obese patients regarding periodontitis through the specific management of oral microbiota of obese patients.

(1) Background: In developed countries, the prevalence of apical periodontitis (AP) varies from 20% to 50% for reasons that could be associated with the apical periodontitis microbiota ecology. (2) Methods: We performed a clinical study in the Odontology department of Toulouse hospital in France, to sequence the 16S rRNA gene of AP microbiota and collect clinical parameters from 94 patients. Forty-four patients were characterized with a PAI (periapical index of AP severity) score lower or equal to 3, while the others had superior scores (n = 50). (3) Results: The low diversity of granuloma microbiota is associated with the highest severity (PAI = 5) of periapical lesions (Odds Ratio 4.592, IC 95% [1.6329; 14.0728]; p = 0.001; notably, a lower relative abundance of Burkholderiaceae and a higher relative abundance of Pseudomonas and Prevotella). We also identified that high blood pressure (HBP) is associated with the increase in PAI scores. (4) Conclusions: Our data show that a low diversity of bacterial ecology of the AP is associated with severe PAI scores, suggesting a causal mechanism. Furthermore, a second risk factor was blood pressure associated with the severity of apical periodontitis.

Over the past decade, there have been significant advancements in the high-flow analysis of “omics,” shedding light on the relationship between the microbiota and the host. However, the full recognition of this relationship and its implications in cardiometabolic diseases are still underway, despite advancements in understanding the pathophysiology of these conditions. Cardiometabolic diseases, which include a range of conditions from insulin resistance to cardiovascular disease and type 2 diabetes, continue to be the leading cause of mortality worldwide, with a persistently high morbidity rate. While the link between the intestinal microbiota and cardiometabolic risks has been extensively explored, the role of the oral microbiota, the second-largest microbiota in the human body, and specifically the dysbiosis of this microbiota in causing these complications, remains incompletely defined. This review aims to examine the association between the oral microbiota and cardiometabolic diseases, focusing on the dysbiosis of the oral microbiota, particularly in periodontal disease. Additionally, we will dive into the mechanistic aspects of this dysbiosis that contribute to the development of these complications. Finally, we will discuss potential prevention and treatment strategies, including the use of prebiotics, probiotics, and other interventions.

The long-standing view of sterile internal tissues has been challenged by accumulating evidence that microbial material, and under specific conditions, viable bacteria may translocate from the gut and oral cavity into metabolic and cardiovascular tissues. This review synthesizes current knowledge on the mechanisms underlying bacterial translocation and its implications for cardiometabolic disease, complemented by original experimental data. Dysbiosis and epithelial barrier disruption facilitate the passage of microbial components and, in some settings, culturable bacteria across mucosal surfaces, triggering local and systemic inflammation. In our murine models, high-fat feeding markedly increased the recovery of culturable bacteria from visceral adipose tissue and spleen, with tissue-specific bacterial signatures enriched in pro-inflammatory taxa. GFP-labelled E. coli translocated more abundantly under metabolic stress, while CD14 deficiency significantly reduced dissemination, highlighting the role of LPS–CD14 signaling. Clinical studies consistently report bacterial DNA and, in some cases, viable bacteria in adipose tissue, liver, atherosclerotic plaques, and heart valves, correlating with immune cell infiltration, cytokine production, and disease severity. However, because internal organs are low-biomass environments, interpretation requires stringent contamination controls and orthogonal evidence of viability and localization. Together, these findings support bacterial translocation as a plausible contributor to chronic low-grade inflammation, insulin resistance, and cardiometabolic pathology. Targeting microbial translocation through barrier reinforcement, microbiota modulation, and metabolite inhibition may offer novel preventive and therapeutic strategies that warrant careful validation.