There are many myths surrounding the cause of cavities, and maybe you have heard a few. “Maybe you just have soft teeth.” “Sugar causes cavities.” “Just brushing and flossing twice a day will prevent cavities.” “Fillings will stop the decay process.” “You can’t ‘catch a cavity’ from someone else.” “Fluoride is a conspiracy, and it doesn’t actually help prevent cavities.”

While some of these sayings are partially based on facts, and some are simply not true, actual research exists and reveals the truth. Cavities, also known as dental caries, are caused by a bacterial imbalance on the teeth. This imbalance occurs based on each individual’s oral environment, dietary habits, and hygiene habits. By understanding what causes an imbalance in the oral environment, and by making adjustments, the bacterial imbalance can be controlled and a patient’s cavity rate can be either reduced or eliminated. 

According to the CDC (Centers for Disease Control and Prevention), dental caries is an epidemic in the United States; and although it is largely preventable, it remains the most common chronic disease of children aged 5 to 17 years—4 times more common than asthma (42% versus 9.5%). According to the CDC in the US population,

  • 28% of children aged 2–5 have already had decay in their primary (baby) teeth;
  • 50% of children have experienced tooth decay by age 11;
  • 68% of 19-year-olds have experienced tooth decay in their permanent teeth—more than two-thirds;
  • low-income children are twice as likely to experience decay as children of higher-income families.
  • 52,000,000 school hours are lost each year due to dental disease;
  • much of the dental disease in both children and adults go untreated;
  • 16% of children aged 6–19 years have untreated dental caries;
  • 23% of adults aged 20–64 years have untreated dental caries;
  • most adults will experience dental disease, and many will lose teeth;
  • 85% of all adults experience tooth decay;[1] and
  • more than 60% of adults will lose a permanent tooth due to cavities.[2]

According to the American Dental Association and the American Academy of Pediatric Dentistry, the new dental standard of care for managing a patient’s risk and preventing dental disease is to perform an individual “caries risk assessment” analysis during dental appointments. Dental disease (caries) today is best assessed, diagnosed, and managed by identifying disease indicators and risk factors, and examining the balance between pathogenic and protective risk factors.[3, 4, 5, 6, 7] This process provides both patients and practitioners with specific future decay risk probability that is specific to each patient. Patients found to be at risk can then be presented early intervention advice, educational materials, and prescription/professional therapies.

Everyone with teeth is at some form of risk for the infection that causes decay. Based on a major population study of close to 13,000 patients, even low-risk individuals have a 23.6 % chance of developing new cavities in the next 12 months. Conversely, high/extreme-risk patients have an 88% chance of developing new cavities in the next 12 months (See Figure 1). Patients can lower their risk by choosing to change some of their lifestyle habits, change their dental home care program and the products they use, and regularly visit their dental professional to monitor progress. The process of caries risk assessment in the private dental practice was first introduced in 2003, and published and unpublished studies have shown that caries risk assessment, along with early intervention professional products, can lower decay rates anywhere from 24% to 74%.[8] For some patients, this means a reduction in their decay rate from 10 new cavities per year down to fewer than 3. Some patients with nonmodifiable caries risk factors may only experience a limited benefit, but for many, it means a lifetime of being cavity or decay free.

Unfortunately, there is no “silver bullet,” “magic pill,” “guarantee,” or “vaccine” for dental decay; and educated dental professionals do not see one coming in the near future. Dental caries is a multifactorial, multiple-pathogen biofilm disease.[9] While some progress has been made in the immunization against Streptococcus mutans and genetically modified bacteria, typically, complex biofilm diseases do not respond readily to vaccines, antibiotics, or replacement therapies.[10] Not to mention the current dental caries disease model also includes potential systemic effects on the rest of your body from the disease. Streptococcus mutans (a cavity-causing bacterial species) is the most common oral bacteria found on heart valves and coronary arteries when it is found in the mouth of an individual.[11] This species has been demonstrated to invade artery lining tissues and may be responsible for infections in the heart and valves, bacterial endocarditis, and may also have other potential risks for heart diseases.[12] Other oral bacterial species that have been identified with dental caries may also play a role in other systemic infections and complications.[13]Every patient’s oral bacterial profile is as specific to them as their own fingerprint, and the guidance of a trained dental professional is absolutely essential to their oral and overall health.[14]

  1. Oral Health America: A Report of the US Surgeon General 63 (2000):79–94, 245.
  2. National Institute of Health, US Dept. of Health and Human Services, “Diagnosis and Management of Dental Caries throughout Life” 18, no.1 (March 2001).
  3. O. Fejerskov and E. Kidd, Dental Caries: The Disease and Its Clinical Management (Oxford, UK: Blackwell Munksgaard, 2003), 4–5.
  4. D. A. Young, V. K. Kutsch, and J. Whitehouse, “A Clinician’s Guide to CAMBRA: A Simple Approach,” Compend Contin Educ Dent 30, no. 2(2009): 92–98.
  5. D. A. Young, J. D. Featherstone, J. R. Roth, M. Anderson, J. Autio-Gold, G. J. Christensen, M. Fontana, V. K. Kutsch, M. C. Peters, R. J. Simonsen, and M. S. Wolff, “Caries Management by Risk Assessment: Implementation Guidelines,” J Calif Dent Assoc 35, no. 11 ( Nov. 2007):799–805.
  6. J. D. B. Featherstone, “The Science and Practice of Caries Prevention,”J Am Dent Assoc 131, no. 7 (2000): 887–899.
  7. V. Uskokovic´, W. Li, and S. Habelitz, “Amelogenin as a Promoter of Nucleation and Crystal Growth of Apatite,” J of Crystal Growth 316, no. 1 (2011): 106–117.
  8. J. D. B. Featherstone, J. M. White, C. I. Hoover, M. Rapozo-Hilo, J. A.Weintraub, R. S. Wilson, L. Zhan, and S. A. Gansky, “A Randomized Clinical Trial of Anticaries Therapies Targeted according to Risk Assessment (Caries Management by Risk Assessment),” Caries Res 46(2012): 118–129.
  9. O. Fejerskov and E. Kidd, Dental Caries: The Disease and Its Clinical Management (Oxford, UK: Blackwell Munksgaard, 2003).
  10. H. J. Busscher and L. V. Evan, Oral Biofilms and Plaque Control (Amsterdam, the Netherlands: Harwood Academic Publishers, 1998).
  11. K. Nakano, H. Nemoto, R. Nomura, H. Inaba, H. Yoshioka, K. Taniguchi, A. Amano, and T. Ooshima, “Detection of Oral Bacteria in Cardiovascular Specimens,” Oral MicrobiolImmunol 24, no. 1 (2009):64–68.
  12. J. Abranches, J. H. Miller, A. R. Martinez, P. J. Simpson-Haidaris, R.A. Burne, and J. A. Lemos. “The Collagen-Binding Protein Cnm Is Required for Streptococcus mutans Adherence to and Intracellular Invasion of Human Coronary Artery Endothelial Cells,” Infect Immun79, no. 6 (June 2011): 2277–84.
  13. A. Kojima, K. Nakano, et al., “Infection of Specific Strains of Streptococcus mutans, Oral Bacteria, Confers a Risk of Ulcerative Colitis,” Sci Rep 2 (2012): 332.
  14. S. K. Filoche, D. Soma, M. van Bekkum, and C. H. Sissons, “Plaques from Different Individuals Yields Different Microbiota Responses to Oral-Antiseptic Treatment,” FEMS Immunol Med Microbiol 54 (2008):27–36.