Untreated caries in permanent teeth is the most prevalent human disease worldwide, according to the 2015 Global Burden of Disease report. Dental caries is now understood to be multifactorial, with no single causation pathway. In an article published in 2018 in the British Dental Journal Philip et al highlights the “evolution of dental caries etiology theories over the years and how this continues to have important implications for caries prevention, risk assessment, and treatment.”1
By the end of the nineteenth century the cause of dental disease was accepted as an overgrowth of nonspecific bacteria found in dental plaque. This was referred to as the nonspecific plaque hypothesis (NSPH). This hypothesis stated it was the amount of plaque that determined pathogenicity and not the levels of bacterial virulence. This hypothesis brought us to the mechanical removal of plaque via toothbrushing and flossing.
By the mid-twentieth century , Keyes and Fitzgerald demonstrated that dental caries was an “infectious and transmittable disease.” In 1976, Loesche announced his hypothesis, the specific plaque hypothesis (SPH), postulating that dental caries was an “infection caused by specific bacteria within dental plaque.” The specific bacteria were Streptococcus mutans and Streptococcus sobrinus. For many years preventive and therapeutic interventions focused on these microorganisms. The SPH proposed the use of antibiotics as a method to treat and prevent dental caries.
However, Kochs postulate indicates dental caries is not an infectious disease as causative agents of disease are not applicable for microbial community-based diseases. Furthermore, most of the evidence that supports mutans streptococci (MS) as the main concern in dental caries is considered associative rather than causative. This is supported by evidence of individuals with high levels of MS that do not develop carious lesions, while other individuals develop carious lesions in the absence of MS. While there is no question that dental caries is microbially induced, the cause is endogenous bacteria not exogenous bacteria.
Instead of being considered an infectious disease caused by a single pathogen, dental caries is now understood to be a biofilm mediated disease. The ecological plaque hypothesis (EPH) describes the critical factors of disease onset and progression as an “upsurge in the acidogenic/aciduric component of the oral microbiome.” This refers to frequent sugar exposure and salivary dysfunction. Current consensus is that any bacterial species can participate in the caries process as long as they are aciduric and dominant. DNA and RNA molecular studies show that S. mutans only account for a fraction of the bacterial community implicated in the caries process (0.1%-1.6%). Additionally, the presence of Candida albicans enhances biofilm virulence.
Two other evolving factors include the oral microbiome and genetic factors. A healthy oral microbiome can mitigate acid produced by cariogenic bacteria. Less diverse oral microbiomes tend to have higher caries incidence when compared to a more diverse oral microbiome. There is emerging evidence that certain population groups are genetically more susceptible to dental caries. The current landscape of dental caries involves a biofilm model with a complex multifactorial disease influenced by systemic effects, hereditary components, diet, behavioral, environmental, socioeconomic and physiological risk factors.
Prevention strategies are discussed, and they include prebiotics, probiotics, antimicrobial peptides, sugar polyols, phytochemicals, quorum-sensing targets, and genetically modified designer bacteria. The treatment section focuses on minimal invasive dentistry (MID). MID principles include recognition of disease contributory factors, re-orientation of the contributory lifestyle factors, remineralization of both cavitated and non-cavitated lesions, repair (only when other solutions are not possible), and review to ensure healthy oral and life environment is maintained.
Philip et al conclude by stating, “About 700-800 bacterial species have been identified from the human oral microbiome making the mouth the most microbiologically diverse environment in the body. Both traditional as well as newly identified bacterial species have an important role in the caries process, and from an ecological point of view it may be more important to describe what the bacteria are doing in the biofilm community rather than which bacteria are present. Given the polymicrobial nature of dental caries, it is predicted that diagnostic, preventive, and treatment strategies directed toward specific bacterial species will not be universally effective. Another important change in perspective is the realization that there are beneficial members of the oral microbiome, and an understanding of health and disease requires knowledge of all microorganisms, not just select few pathogens.”
Do you currently practice using a model to assess all aspects of the caries process that are mentioned here? Does your practice use MID to reduce tooth loss and recurrent decay? Were you surprised to find out S. mutans play a minor role in the caries process?
- Philip N, Suneja B, Walsh L. Beyond Streptococcus mutans: clinical implications of the evolving dental caries aetiological paradigms and its associated microbiome. Br Dent J. 2018 Feb 23;224(4):219-225. doi: 10.1038/sj.bdj.2018.81. Epub 2018 Feb 16. PMID: 29449651.
