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Inside Dentistry

May 2009, Volume 5, Issue 5
Published by AEGIS Communications


Dental Caries: A New Look at an Old Disease

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)

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.

Clinical Implications

The new biofilm science and disease model has significant clinical implications for the practitioner treating patients with dental caries, or with caries risk. Currently there has been a lot of information and research performed on laser caries fluorescence as a diagnostic tool.36 In light of the new disease model, it is important to distinguish between lesion detection or identification and caries diagnosis. Instruments like the DIAGNOdent (Kavo Corporation, Lake Zurich, IL) are invaluable clinical instruments that have dramatically improved the precision in lesion detection,37 and bring new objective technology to replace the mirror and explorer.38,39 They also play a role in the diagnosis phase of dental caries. However, the diagnosis of the disease process is not limited to the presence and extent of lesions. Diagnosis of dental caries requires all diagnostic data to be gathered and a clinical decision to be made in the best sound judgment of the practitioner. This should include: an oral examination looking for disease indicators previously discussed, a radiographic exam, an evaluation of risk factors, use of a validated caries risk assessment form (Figure 1 and Figure 2), a microbial metric, and, if one exists, the patient’s previous history with the practitioner.40 Previous microbial metrics involved culturing saliva samples for Mutans streptococci.41 Based on the biofilm disease model, a better metric might be ATP bioluminescence.42 The survival of acidogenic/aciduric bacteria depends on their ability to produce enough ATP to effectively transport the H+ ions out of the cell, thereby maintaining intracellular neutrality.43 The concept of ATP bioluminescence has been tested with excellent correlation values in dental caries risk assessment, and fits the non-specific bacterial biofilm model.42 A diagnosis is then made based on weighing all of the evidence. The caries risk assessment form and risk factors further identifies specific contributing conditions to the disease process for each individual patient, and provides a starting point in the design of the evidence based therapy.44

The caries risk assessment for children age 5 and under includes disease indicators: caries activity status of the mother/primary caregiver, socioeconomic status, visible cavitations, cavity history in the previous 2 years and obvious white-spot lesions (Figure 3).45 Caries risk factors for children include: obvious plaque on teeth, the gingiva bleeds easily, inadequate saliva flow, appliances present, no dental home with episodic regular care, developmental problems/special needs, medications inducing xerostomia, continuous availability of a bottle containing anything but water, opportunity to nurse on demand, and frequent snacking.45 For children over the age of 6, adolescents, and adults, the caries risk assessment form should include disease factors (Figure 4): visible cavitations, radiographic interproximal lesions penetrating to the dentin or D1 lesions, obvious white-spot lesions, and a cavity in the previous 3 years.46 Risk factors for this group should include: visible plaque on the teeth, inadequate saliva flow, hyposalivary medications, frequent acidic beverages, frequent snacking between meals, appliances present, and deep developmental occlusal pits and fissures.3 Taking these disease indicators and risk factors into account with the rest of the diagnostic data, the practitioner can make the best diagnosis and simultaneously develop the most effective treatment plan. The ADA Council on Scientific Affairs established a guideline and definition for these risk categories,47 and now also endorses caries risk assessment and has developed a form for practitioners.48

CAMBRA is a risk assessment based medical management model for dental caries.49 The CAMBRA model protects, preserves, and remineralizes dental hard tissues. CAMBRA is based on risk assessment, followed by diagnosis of the disease process and the appropriate evidence-based treatment strategies based on the patient’s individual risk factors and restorative needs. These treatment strategies include: reparative strategies (remineralization for non-cavitated and/ or white-spot lesions and restorative for cavitated lesions), therapeutic (antimicrobial to reduce total bacterial load, metabolic to inhibit growth of bacteria, and pH-neutralizing strategies to stimulate non-Mutans streptococci and Actinomyces species) and behavioral (modifiable behavior with nutrition counseling and homecare instruction and non-modifiable risk factors such as hyposalivary medications or special needs individuals).5 In the past, the profession has depended on fluoride as an anti-caries strategy, and while it aids in remineralization and may inhibit some cariogenic bacteria, fluoride therapy alone has not been enough to control this disease. Chlorhexidine has been a standard antimicrobial in dentistry, and while it is an effective agent for periodontal pathogens, and against Mutans streptococci, it has little effect against Lactobacilli and its effectiveness against the rest of the implicated cariogenic bacteria remains uncertain.50 Sodium hypochlorite is an effective broad-spectrum antimicrobial agent with little adverse effects, and is an elevated pH.51 Based on Takahashi and Nyvads’ work, pH neutralization strategies appear to be the best fit for the present understanding of the disease model and are a promising although not yet well-tested strategy.52

The pH strategy serves two functions; it elevates the pH to induce remineralization, and it also stimulates or trains the biofilm to behave correctly. Xylitol is an effective metabolic anti-caries agent that provides many benefits and also potentiates the effect of even small amounts of fluoride.53 There are many different strategies available to help practitioners and patients effectively deal with this disease. But the first step is to recognize the need to diagnose the disease and not just identify cavities.54

Conclusion

Biofilm research is rapidly changing the dental profession’s understanding of this very old disease, dental caries. The biofilm science is creating a new model of this complex disease, from which new diagnosis and treatment strategies are developing. CAMBRA represents an effective medical model for caries management in dental practice. While other dental therapies may be controversial, there is no debate that the standard of care requires CAMBRA evaluation and then treatment for susceptible patients. CAMBRA is not controversial because there is no controversy between scientific right and customary ignorance.55

References

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2. Centers for Disease Control, National Center for Chronic Disease Prevention and Health Promotion, November 2005. Chronic Disease Prevention and Health Promotion. Available at: http://www.cdc.gov/NCCdphp/publications/factsheets/Prevention/oh.htm.

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6. Eugenio D, Beltrán-Aguilar, Barker LK, et al. Surveillance for Dental Caries, Dental Sealants, Tooth Retention, Edentulism, and Enamel Fluorosis. United States, 1988-1994 and 1999-2002. MMWR. August 26, 2005:54(03);1-44.

7. Jenson L, Budenz AW, Featherstone JD, et al. Clinical protocols for caries management by risk assessment. J Calif Dent Assoc. 2007;35(10):714-723.

8. Young DA. New caries detection technologies and modern caries management: Merging the strategies. Gen Dent. 2002; 50(4):320-331.

9. Featherstone JD. Dental caries: a dynamic disease process. Aust Dent J. 2008;53(3): 286-291.

10. Theilade E, Fejerskov O, Karring T, Theilade J. Predominante cultivale microflora of human dental fissure plaque. Infect Immun. 1982;36(3):977-982.

11. Arneberg P, Ogaard B, Scheie AA, Rolla G. Selection of Streptococcus mutans and lactobacilli in an intra-oral human caries model. J Dent Res. 1984;63(10):1197-1200.

12. Boue D, Armau E, Tiraby G. A bacteriological study of rampant caries in children. J Dent Res. 1987;66(1):23-28.

13. Kohler B, Bjarnason S. Mutans streptococci, lactobacilli and caries prevalence in 11 and 12-year-old Icelandic children. Community Dent Oral Epidemiol. 1987;15(6): 52-55.

14. Kutsch VK, Kutsch CL, Nelson BC. A clinical look at CAMBRA. Dental Products Report. 2007;41(8):62-67.

15. Munson MA, Banerjee A, Watson TF, Wade WG. Molecular analysis of the microflora associated with dental caries. J Clin Microbiol. 2004;42(7):3023-3029.

16. Becker MR, Paster BJ, Leys EJ, et al. Molecular analysis of bacterial species associated with childhood caries. J Clin Microbiol. 2002;40(3): 1001-1009.

17. Beighton D. The complex oral microflora of high-risk individuals and groups and its role in the caries process. Community Dent Oral Epidemiol. 2005;5(4):248-255.

18. van Houte J, Lopman J, Kent R. The predominant cultivable flora of sound and carious human root surfaces. J Dent Res. 1994;73(11): 1727-1734.

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20. Loesche WJ. Role of streptococcus mutans in human dental decay. Microbiol Review. 1986; 50(4):353-380.

21. Hamada T, Nikawa H, Yamashiro H, et al. In vitro cariogenic potential of Candida Albicans. Mycoses. 2003;46(11-12): 471-478.

22. Kleinberg I. A mixed-bacteria ecological approach to understanding the role of bacteria in dental caries causation: an alternative to Streptococcus mutans and the specific plaque hypothesis. Critical Reviews in Oral Biology and Medicine. 2002;13:108-125.

23. Yip Hk, Guo JH, Wong WH. Incipient caries lesions on cementum by mono and co-culture oral bacteria. J Dent. 2007;35(5):377-382.

24. Tanner AC, Milgrom PM, Kent R Jr, et al. The microbiota of young children from tooth and tongue samples. J Dent Res. 2002; 81(1):53-57.

25. Hoshino E. Predominant obligate anaerobes in human carious dentin. J Dent Res. 1985;64(10):1195-8.

26. Sissons CH, Anderson SA, Wong L, et al. Microbiota of plaque biofilms: effect of three times daily sucrose pulses in different simulated oral environments. Caries Res. 2007;41(5): 413-422.

27. Aas JA, Griffen AL, Dardis SR, et al. Bacteria of dental caries in primary and permanent teeth in children and young adults. J Clin Microbiol. 2008;46(4):1407-1417.

28. Preza D, Olsen I, Aas JA, et al. Bacterial profiles of root caries in elderly patients. J Clin Microbiol. 2008;46(6): 2015-2021.

29. Marsh PD, Bradshaw DJ, McKee AS. Effects of carbohydrate pulses and pH on population shifts within oral microbial communities in vitro. J Dent Res. 1989;68: 1298-1302.

30. Marsh PD. Are dental diseases examples of ecological catastrophes? Microbiology. 2003;149(Pt2):279-294.

31. Marsh PD. Dental plaque as a biofilm and a microbial community—implications for health and disease. BMC Oral Health. 2006; 6(Suppl 1):S14.

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33. Wilson M. Microbial Inhabitants of Humans. Cambridge Press Publishers; 2005:59-352.

34. Li Y, Ge Y, Saxena D, Caufield PW. Genetic profiling of the oral microbia associated with severe early-childhood caries. J Clin Micro. 2007;45(1):81-87.

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36. Heinrich-Weltzien R, Kuhnisch J, van der Veen M, et al. Quantitative light-induced fluorescence (QLF)—a potential method for the dental practitioner. Quintessence Int. 2003;34(3):181-188.

37. Huth KC, Neuhasu KW, Gugax M, et al. Clinical perfomance of a new laser fluorescence device for detection of occlusal caries in permanent molars. J Dent. 2008 ;36(12)1035-1040.

38. Penning C, van Amerongen JP, Seef RE, ten Cate JM. Validity of probing for fissure caries diagnosis. Caries Res. 1992;26(6): 445-449.

39. Lussi A. Validity of diagnostic and treatment decisions of fissure caries. Caries Res. 1991;25(4):296-303.

40. Fontana M, Zero DT. Assessing patients’ caries risk. J Am Dent Assoc. 2006;137(9): 1231-1239.

41. Nishikawara F, Nomura Y, Imai S, et al. Evaluation of cariogenic bacteria. Eur J Dent. 2007 Jan;1(1):31-9.

42. Sauerwein R, Pellegrini P, Finlayson J, et al. Oregon Health & Science University, Portland, OR. ATP Bioluminescence: Quantitative Assessment of Plaque Bacteria Surrounding Orthodontic Appliances. IADR Abstract #1288;2008.

43. Alice CL Len, Harty DWS, Jaques AJ. Stress-responsive proteins are upregulated in Streptococcus mutans during acid tolerance. Microbiol. 2004;150:159-1351.

44. Selwitz RH, Ismail AI, Pitts NB. Dental caries. Lancet. 2007;369(9562):639.

45. Ramos-Gomez FJ, Crall J, Gansky SA, et al. Caries risk assessment appropriate for the age 1 visit (infants and toddlers). J Calif Dent Assoc. 2007;35(10):687-702.

46. Featherstone JD, Domejean-Orliaguet S, Jenson L, et al. Caries risk assessment in practice for age 6 through adult. J Calif Dent Assoc. 2007;35(10):703-713.

47. American Dental Association Council on Scientific Affairs. J Am Dent Assoc. 2006; 137(8):1151-1159.

48. American Dental Association. Available at: http://www.ada.org/prof/resources/topics/topics_caries_instructions.pdf. Accessed February 27, 2009.

49. Fontana M, Young DA, Wolff MS. Evidence-based caries, risk assessment, and treatment. Dent Clin North Am. 2009;53(1): 149-161.

50. Anderson MH. A review of the efficacy of chlorhexidine on dental caries and the caries infection. J Calif Dent Assoc. 2003; 31(3):211-214.

51. Jorgensen MG, Aalam A, Slots J. Periodontal antimicrobials—finding the right solutions. Int Dent J. 2005;55(1): 3-12.

52. Spolsky VW, Black BP, Jenson L. Products—old, new, and emerging. J Calif Dent Assoc. 2007;35(10):724-737.

53. Maehara H, Iwami Y, Mayanagi H, Takahashi N. Synergistic inhibition by combination of fluoride and xylitol on glycolysis by mutans streptococci and its biochemical mechanism. Caries Res. 2005;39(6): 521-528.

54. Young DA, Featherstone JD, Roth JR, et al. Caries management by risk assessment: implementation guidelines. J Calif Dent Assoc. 2007;35(11):799-805.

55. Kutsch VK, Milicich G, Domb W, et al. How to integrate CAMBRA into private practice. J Calif Dent Assoc. 2007;35(11): 778-785.

About the Author

V. Kim Kutsch, DMD
Private Practice
Albany, Oregon


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Image Gallery

Figure 1  Children’s Caries Risk Assessment Form.

Figure 1

Figure 2  Adult Caries Risk Assessment Form.

Figure 2

Figure 3  Visible plaque on child’s teeth.

Figure 3

Figure 4  Visible cavitations, white-spot lesions, and plaque on an adult’s teeth.

Figure 4