Periodontal disease, a common outcome of poor oral health, is closely linked to microbial dysbiosis in the oral cavity. The oral microbiota, second in complexity only to the gut, plays a central role in plaque formation and inflammation, contributing to both local and systemic diseases. Conventional treatments often disrupt the microbiota without addressing underlying causes, prompting interest in biologic strategies. This review provides a comprehensive analysis of the oral microbiota's role in periodontal disease and its systemic connections. We focus on recent advances in probiotics, prebiotics, and postbiotics, evaluating their protective effects and mechanisms of action through evidence from preclinical and clinical studies. The review also discusses current limitations and outlines future directions for translating these findings into effective therapies. Our synthesis offers novel insights into microbiota-targeted strategies for the prevention and treatment of periodontal disease.

Conventional filling therapy fails to fundamentally reduce oral cariogenic bacteria. Thus, oral microbiota follow-up intervention after filling would be necessary for improving dental caries prognosis. We recruited 9 caries-free individuals, and 89 dental caries subjects (5 dropouts). Eighty-nine patients were randomized into three groups: caries (n=8; no treatment), control (n=40; filling), and postbiotics (n=41; filling and 14-day Probio-Eco^® intervention). Salivary samples were collected at 0 day (after filling) and 14 days. Our results showed that the diversity of dental caries oral microbiota was significantly increased compared with healthy subjects, and filling could restore a healthier oral microbiota partially and temporarily. Thepostbiotics intervention keeps a low alpha-diversity. Co-occurrence network analysis showed that a more stable oral microbiota structure after postbiotics intervention. Taxonomic and functional annotation of the microbiota revealed that postbiotics co-treatment significantly: increased the relative abundance of Pseudomonas and P. reactans, decreased the relative abundance of Prevotella shahii, and enriched the energy metabolism-related pathways. BugBase-predicted phenotypes inferred to an oral microbiota with decreased potential pathogenic bacteria and increased oxidative stress-tolerant bacteria after postbiotics intervention. Collectively, it suggested that postbiotics co-treatment could be a promising strategy that restores the oral microecological balance for dental caries.

Probiotics exert beneficial effects on the host. This study aimed to investigate whether maternally ingested Lacticaseibacillus rhamnosus Probio-M9 during pregnancy could access and colonize the infant gut. This study recruited one pregnant woman, who ingested Probio-M9 daily from 35 weeks of gestation to delivery. Feces of the mother-infant pair were regularly collected from one month before delivery to 6 months of infant’s age for metagenomic sequencing. Probio-M9 genomes were mappable to all infant fecal samples, suggesting the ingested probiotics could be vertically transmitted from mother to infant. Infant- or mother-specific differential metabolic pathways were found between the maternal and infant’s gut microbiome, implicating apparent differences in the intestinal metagenomic potential/function between the mother and the infant. In conclusion, maternal ingestion of Probio-M9 during the final weeks of gestation could deliver to the infant gut. The findings provided novel insights into shaping infant’s gut microbiota.

Recently, it has been established that the human resident microbiota plays key roles in health maintenance. Therefore, it has become an emerging prevention and treatment target for metabolic syndrome. The resident microbiota associated with chronic inflammation has been shown to contribute to the onset of type 2 diabetes mellitus (T2DM). Moreover, the microbiota is altered in the development of T2DM and its comorbid medical conditions/diseases, including diabetic retinopathy, kidney toxicity, atherosclerosis, hypertension, diabetic foot ulcers, cycstic fibrosis and Alzheimer’s disease. Besides, some anti-T2DM regimens are also based microbiota metabolism-dependent mechanism. This review summarizes the current knowledge concerning the altered microbiota in the pathogenesis of T2DM and its related complications, which provides novel insights into these diseases and the potential intervention strategies from the microbiology point of view.