Dental Caries - A New Look at an Old Disease
May 1, 2009
Volume 5
,
Issue 5
,
May 2009
V. Kim Kutsch, DMD
Dental caries is an infectious transmissible biofilm disease of the teeth driven by protracted periods of low pH that results in net mineral loss of the calcified tissues.1 Ultimately, if left untreated it results in pulpal death and loss of teeth. Dental caries is the number one childhood disease in the United States.2 Although dental caries (tooth decay) is largely preventable, it remains the most common chronic disease of children aged 5 to 17 years—5 times more common than asthma (59% versus 11%).2 In addition, it affects adults as well, 27% of adults aged 35 to 44 years have untreated dental caries.2 Thirty percent of senior adults over the age of 65 also have untreated dental caries.2 This very common disease is perhaps the most difficult to diagnose and the most difficult to treat. There are four recognized disease indicators and multiple risk factors for the disease.3 These risks may also be specific by site or tooth surface, individual tooth location, tooth anatomy, individual, age, population and socioeconomic demographic strata.4 It is a very complex disease with a rapidly emerging understanding from the development of the biofilm scientific evidence.5 It is a disease that is not understood by the public and, for the most part, is not well understood by the profession dedicated to treating it.
Just the term dental caries by itself can be confusing. While the CDC lists the demographic data by untreated “dental caries,” what they most typically refer to is the presence of untreated caries lesions or cavities.6 (A list of terms and abbreviations is included to facilitate the reading and interpretation of the diagnostic criteria and results. Dental examiners were trained to use modified Radike’s criteria5 to diagnose dental caries and its sequelae (missing teeth [due to disease] and filled teeth). The modification consisted of eliminating the “extraction indicated” code. Dental examiners were asked to dry the tooth surfaces with compressed air and use a non-magnifying mirror and a No. 23 dental explorer to assess for the presence of carious and restored (filled) lesions. To be consistent with the NHANES 1988–1994 protocols and diagnostic criteria, pits and fissures were coded as carious if the explorer would catch after insertion with moderate, firm pressure, accompanied with either softness at the base of the lesion or an opacity adjacent to or evidence of undermining enamel. Four surfaces of incisors and canines and five surfaces, including the occlusal surface, of premolars and molars were examined. No radiographs were taken. Detailed diagnostic and coding guidelines were included in the procedures manuals for dental examiners and recorders available at the NHANES web site.1)
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To effectively understand this disease we must separate the signs and symptoms from the etiology and diagnosis of the disease process proper. The CDC data provides a clear picture of the number of untreated cavities in a population group, which creates meaningful data to track over time, but assumes the cavity is the disease, which is not the case.7 Dental caries is the infectious transmissible biofilm disease that causes the cavities. The presence of this disease and/or risk factors among these populations is not well accounted for simply by identifying cavities. The presence of other disease factors, such as enamel white-spot lesions, radiographic interproximal lesions, and a history of caries lesions, provides a much more accurate profile of this disease in any population.3 The dental profession is beginning to recognize the significance between identifying lesions and diagnosing the disease process.8 Simply restoring the caries lesions does not effectively treat the disease process. To effectively treat dental caries requires an understanding of the local, microbial, behavioral, environmental, and socioeconomic factors contributing to the disease.9
Disease Models
Until recently, dental caries was thought to be a fairly simple disease. It was caused primarily by two bacteria, Mutans streptococci and Lactobacillus10,11 and required only refined sugar and tooth structure to occur. The traditional disease model was supported by an abundance of scientific studies linking Mutans streptococci and Lactobacillus levels to caries risk in children.12,13 But as the field of biofilm research developed, a broader, more complex picture became apparent. More bacteria were implicated in the disease process by different researchers worldwide.14 Now oral biofilms can be studied with forensic-type precision by identifying the bacteria with the 16S gene sequence of their rRNA.15 This has added additional species to the growing list of implicated dental caries pathogens.16-28 As early as 1989, Marsh demonstrated that the selection pressure for the acidogenic/aciduric bacteria in a mixed culture biofilm was a function of pH and not sugar availability.29 This early research later led to his description of the Ecological Plaque Hypothesis.30 In this biofilm disease model, the environmental factor of low pH drives the selection of cariogenic bacteria in a patient’s dental biofilm, causing mineral loss and cavitation of the teeth.31 Studying the effects of different risk factors, Featherstone introduced the concept of the caries balance in 2004. He demonstrated that dental caries and health are also a function of a balance—or rather an imbalance—between the pathologic and the protective factors for the disease.32 So the understanding of the disease model became more complex: one of disease indicators and risk factors, protective factors, and numerous pathogens present in a biofilm behaving based on ecological principles.
Recent biofilm research based on 16S gene sequence DNA evidence is also broadening the picture of dental caries.5 It is clear now that some of the previous paradigms on the microbiology of dental caries were wrong.5,28 The mouth represents a unique environment in the body for biofilms. The teeth are the only non-shedding surfaces in the body, so the biofilms on the teeth tend to be more complex and microbiologically diverse than previously thought.33 While more than 700 bacterial phylotypes could potentially be found in the human mouth, a healthy individual will only have around 113 different bacterial species, while a high caries risk individual will have an average of 94, presumably because fewer bacteria are capable of surviving the low pH conditions consistent with the disease.34 There is also an inverse relationship between the bacteria present and absent in healthy versus high caries risk individuals.35 The bacteria are also site-specific on the teeth, with individual sites containing only 20 to 30 different phylotypes for an individual.34 Some bacteria are common to all sites, like Gemella, Granulicatella, Streptococcus, and Veillonella, while others are more site-specific. The occlusal fissures are predominated by Mutans streptococci, but the smooth surfaces contain mostly Actinomyses and other streptococcal species. The interproximal areas are predominated by anaerobic and periodontal species and the cervical regions demonstrate a strong presence of gingival related bacterial.34 The concept of dental caries being a disease of Mutans streptococci and Lactobacilli needs to permanently be put to rest, as the biofilm scientific evidence strongly suggests otherwise.
Most recently, Takahashi and Nyvad provided an even clearer picture of this disease.5 They compiled evidence from a broad range of scientific sources and combined the current DNA biofilm evidence with other known concepts in the caries process. Research indicates that additional streptococcal species are potentially cariogenic, and they described these as low-pH non-Mutan streptococci.5 This group includes Streptococcus mitis, oralis, gordonii, and anginosus. Under prolonged periods of low environmental biofilm pH, these bacteria actually adapt and become acidogenic/aciduric, creating a pH similar to Mutans streptococci and producing acid equally as fast. These bacteria are able to adapt to this environment with four strategies: their cell wall becomes more impervious to the H+ ions, they up regulate ATP-ase activity to increase their metabolism and ability to transport the H+ ions out of their cell, they induce the arginine deaminase system to increase the pH, and they produce stress proteins to protect their intracellular enzymes and DNA.5 The significance of this research is that S gordonii is an early colonizer and, along with S oralis, has previously been widely considered as a healthy member of the biofilm.5,34 Takahashi and Nyvad point out that it is no longer just a consideration of which specific bacteria are present, but rather what those bacteria are doing. Are they behaving as healthy bacteria in a neutral and balanced biofilm, or are they behaving as acidogenic/aciduric bacteria contributing to the dental caries disease process? The question becomes: are they good bacteria or bad bacteria? And the complex answer is yes, both. Takahashi and Nyvad present a broadened view of this disease, the Extended Caries Etiological Hypothesis. In this theory they conclude that because of the complexities of this disease model, traditional treatment methods will fall short. The best approach will not be targeting a specific group of organisms like Mutans streptococcus through gene therapy, vaccine or antimicrobial treatment, but rather environmental measures to be implemented to stimulate the bacteria such as non-Mutans streptococcus and Actinomyces by avoiding acidification of the biofilm. Logical treatment strategies would include pH-neutralizing techniques. While perhaps more challenging, this disease model represents the best current understanding of dental caries.
