Caries

From bonepath

Tooth decay, or caries, is caused by oral bacteria (Featherstone 2000, Roberts and Manchester 2005), and is one of the commonest transmissible diseases affecting children (Hong et al. 2011). Carious lesions may present as small white spots on the enamel surface, or as full-blown cavities (as they are colloquially known). Hundreds of species of oral bacteria have been identified, but those most commonly associated with caries belong to the genera Streptococcus, Lactobacillus, Bifidobacterium, and Atopobium (Aas et al. 2005). As these bacteria digest dietary carbohydrates on tooth surfaces, they excrete acid (viz. lactic) that can dissolve the calcium phosphate of tooth crowns and roots. Untreated, caries can decay a tooth so that the pulp cavity is exposed causing pain and abscess, and possibly requiring removal.

The prevalence of caries varies considerably, and differs between sexes, age groups, populations, and social strata (Roberts and Manchester 2005). For example, Wong and colleagues (2011) report that caries prevalence among children under 6 years ranges between 1 – 12% in developed countries, but can be as high as 70% in developing countries and within groups of lower socioeconomic status in developed countries. These authors also found that among a cohort of children in Hong Kong, caries prevalence was higher among children whose parents had less education and lower annual income. Gorbotova and colleagues (2011) report a caries prevalence of nearly 92% among 350 15-year olds in northwest Russia. This study also found that urban adolescents had an lower level of teeth missing due to caries, but more filled-in cavities, than rural counterparts. Similarly, in the United States, caries prevalence ranges between 19 – 25% among children and adolescents, but these values are higher among children of minority and/or low socio-economic status (Borrell and Talih 2011). Indeed, access to preventative and oral health care is probably one of the strongest determinants of caries frequency (Vargas et al. 1998).

Along these lines, it is possible that hypomineralized teeth, such as occurs due to childhood under-nutrition (Roberts and Manchester 2005), may be more susceptible to caries because they are already under-mineralized. Two recent studies (Hong et al. 2009, Carvalho et al. 2011) have suggested that hypo-mineralization is a significant risk factor predisposing children to caries. Intriguingly, however, Carvalho and colleagues (2010) found that within an individual child’s dentition, hypomineralized teeth were more likely to be carious, whereas between children with versus without hypomineralization there was equal likelihood of caries. Other factors that may predispose individuals to caries development include long-term asthma, low salivary rate, and low plaque pH (Stensson et al. 2010), and high dietary sugar (viz. sucrose) intake (Featherstone 2000, Robertson and Manchester 2005, Vartanian et al. 2007).

Caries can be prevented by habitual oral care, as well as fluoridated water (Featherstone 2000). Moreover, saliva contains minerals and proteins which can actually remineralize carious lesions, though only if demineralization is minor. Once a cavity has formed, however, the lesion must be cleaned and filled with a ‘restorative material’ to prevent further tooth decay. Such tooth fillings have traditionally been made of silver amalgam, gold or porcelain, but more recently glass ionomers are the preferred material (Frencken et al. 1996, Forsten 1998).

References

Aas JA, Paster BJ, Stokes LN, Olsen I, Dewhirst FE. 2005. Defining the normal bacterial flora of the oral cavity. Journal of Clinical Microbiology 43:5721-32.

Borrell LN, Talih M. 2011. A symmetrized Theil index measure of health disparities: An example using dental caries in U.S. children and adolescents. Statistics in Medicine 30:277-90.

Carvalho JC, Silva EF, Gomes RR, Fonseca JA, Mestrinho HD. 2011. Impact of enamel defects on early caries development in preschool children. Caries Research 45:353-60.

Featherstone JDB. 2000. The science and practice of caries prevention. The Journal of the American Dental Association 131:887.

Forsten L. 1998. Fluoride release and uptake by glass-ionomers and related materials and its clinical effect. Biomaterials 19:503-8.

Frencken JE, Pilot T, Songpaisan Y, Phantumvanit P. 1996. Atraumatic restorative treatment (ART): rationale, technique, and development. Journal of Public Health Dentistry 56:135-40; discussion 161-3.

Gorbatova MA, Gorbatova LN, Grjibovski AM. 2011. Dental caries experience among 15-year-old adolescents in north-west Russia. International Journal of Circumpolar Health 70:232-5.

Hong L, Levy SM, Warren JJ, Broffitt B. 2009. Association between enamel hypoplasia and dental caries in primary second molars: a cohort study. Caries Research 43:345-53.

Roberts C, Manchester K. 2005. The Archaeology of Disease. Ithaca: Cornell University Press

Stensson M, Wendt LK, Koch G, Oldaeus G, et al. 2010. Caries prevalence, caries-related factors and plaque pH in adolescents with long-term asthma. Caries Research 44:540-6.

Vargas CM, Crall JJ, Schneider DA. 1998. Sociodemographic distribution of pediatric dental caries: NHANES III, 1988--1994. The Journal of the American Dental Association 129:1229.

Vartanian LR, Schwartz MB, Brownell KD. 2007. Effects of soft drink consumption on nutrition and health: a systematic review and meta-analysis. American Journal of Public Health 97:667-75.

Wong HM, McGrath CP, King NM, Lo EC. 2011. Oral health-related quality of life in Hong Kong preschool children. Caries Research 45:370-6.