RESUMEN
Bacteria in the oral cavity, including commensals and opportunistic pathogens, are organized into highly specialized sessile communities, coexisting in homeostasis with the host under healthy conditions. A dysbiotic environment during biofilm evolution, however, allows opportunistic pathogens to become the dominant species at caries-affected sites at the expense of health-associated taxa. Combining tooth brushing with dentifrices or rinses combat the onset of caries by partially removes plaque, but resulting in the biofilm remaining in an immature state with undesirables' consequences on homeostasis and oral ecosystem. This leads to the need for therapeutic pathways that focus on preserving balance in the oral microbiota and applying strategies to combat caries by maintaining biofilm integrity and homeostasis during the rapid phase of supragingival plaque formation. Adhesion, nutrition, and communication are fundamental in this phase in which the bacteria that have survived these adverse conditions rebuild and reorganize the biofilm, and are considered targets for designing preventive strategies to guide the biofilm towards a composition compatible with health. The present review summarizes the most important advances and future prospects for therapies based on the maintenance of biofilm integrity and homeostasis as a preventive measure of dysbiosis focused on these three key factors during the rapid phase of plaque formation.
RESUMEN
The ecological dysbiosis of a biofilm includes not only bacterial changes but also changes in their metabolism. Related to oral biofilms, changes in metabolic activity are crucial endpoint, linked directly to the pathogenicity of oral diseases. Despite the advances in caries research, detailed microbial and metabolomic etiology is yet to be fully clarified. To advance this knowledge, a meta-taxonomic approach based on 16S rRNA gene sequencing and an untargeted metabolomic approach based on an ultra-high performance liquid chromatography-quadrupole time-of-flight mass spectrometry analysis (UHPLC/Q-TOF-MS) were conducted. To this end, an in vitro biofilm model derived from the saliva of healthy participants were developed, under commensal and cariogenic conditions by adding sucrose as the disease trigger. The cariogenic biofilms showed a significant increase of Firmicutes phyla (p = 0.019), due to the significant increase in the genus Streptococcus (p = 0.010), and Fusobacter (p < 0.001), by increase Fusobacterium (p < 0.001) and Sphingomonas (p = 0.024), while suffered a decrease in Actinobacteria (p < 0.001). As a consequence of the shift in microbiota composition, significant extracellular metabolomics changes were detected, showed 59 metabolites of the 120 identified significantly different in terms of relative abundance between the cariogenic/commensal biofilms (Rate of change > 2 and FDR < 0.05). Forty-two metabolites were significantly higher in abundance in the cariogenic biofilms, whereas 17 metabolites were associated significantly with the commensal biofilms, principally related protein metabolism, with peptides and amino acids as protagonists, latter represented by histidine, arginine, l-methionine, glutamic acid, and phenylalanine derivatives.
