Dental caries etiopathogenesismicrobial composition, functional activity and host recognition

Resumen

For decades, the sugar-fermenting, acidogenic species Streptococcus mutans has been considered the main causative agent of dental caries and most diagnostic and therapeutic strategies have been targeted toward this microorganism. However, the DNA- and RNA-based studies from carious lesions reported in this thesis, have uncovered an extraordinarily diverse ecosystem where S. mutans accounts only for a tiny fraction of the bacterial community. This supports the concept that consortia formed by multiple microorganisms act collectively, probably synergistically, to initiate and expand the carious lesion. The data also show that these microbial consortia are different between individuals, between the affected tissue, and even between different lesions from the same individual. Thus, antimicrobial therapies are not expected to be effective in the treatment of caries and other polymicrobial diseases that do not follow Koch's postulates, and that I propose cannot be considered infectious diseases in classical terms. In addition, the data also indicate a prominent role for the immune system in caries risk, suggesting that therapies directed towards stimulating immunological competence should be explored. Based on the results from this Thesis, I propose that dental caries is a dysbiotic polymicrobial disease caused by pathobionts.