The Biology of Streptococcus mutans

In 1924, J. Clarke isolated an organism from carious lesions and called it Streptococcus mutans, because he thought the oval‐shaped cells observed were mutant forms of streptococci (1). However, it was in the late 1950s when S. mutans gained widespread attention within the scientific community, and by the mid‐1960s, clinical and animal‐based laboratory studies depicted S. mutans as an important etiologic agent in dental caries (2). The natural habitat of S. mutans is the human oral cavity, more specifically, the dental plaque, a multispecies biofilm formed on hard surfaces of the tooth. It has been largely accepted that the cariogenic potential of S. mutans resides in three core attributes: (i) the ability to synthesize large quantities of extracellular polymers of glucan from sucrose that aid in the permanent colonization of hard surfaces and in the development of the extracellular polymeric matrix in situ, (ii) the ability to transport and metabolize a wide range of carbohydrates into organic acids (acidogenicity), and (iii) the ability to thrive under environmental stress conditions, particularly low pH (aciduricity) (3). While S. mutans does not act alone in the development of dental caries, studies from several laboratories have convincingly demonstrated that S. mutans can alter the local environment by forming an extracellular polysaccharide (EPS)‐rich and low‐pH milieu, thereby creating a favorable niche for other acidogenic and aciduric species to thrive. As a human pathogen, S. mutans is also implicated in subacute bacterial endocarditis, a life‐threatening inflammation of heart valves, while a subset of strains has been linked to other extraoral pathologies such as cerebral microbleeds, IgA nephropathy, and atherosclerosis.