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Dental Plaque and Caries Prevention

Dental plaque is a naturally developed biofilm that builds up on the surfaces of teeth. It is a general term for the diverse microbial community embedded in a matrix of polymers of bacterial and salivary origin. The process of attachment, growth, removal, and reattachment of dental plaque to the tooth surface is a continuous and dynamic one. If left uninterrupted and allowed to develop on teeth, the potential for demineralization and caries can increase (Figure 1). In individuals with a high-frequency carbohydrate diet or with a severely compromised salivary flow, the levels of potentially cariogenic bacteria can increase, compromising enamel health. For years, dental professionals have primarily focused on the removal of dental plaque for caries prevention.

The caries process has been well-described in the dental literature. Plaque accumulates on the surfaces of teeth. Certain bacteria within the plaque are acidogenic, meaning they produce acids when they metabolize fermentable carbohydrates.1 The acids proceed to dissolve the calcium phosphate mineral of the tooth enamel, resulting in demineralization which, if not addressed, can result in caries.

Research has shown there are two factors that determine caries progression: 1) pathological factors and 2) protective factors.1 Pathological factors include acidogenic bacteria (mutans streptococci and lactobacilli), salivary dysfunction, and frequency of dietary carbohydrates. Protective factors include salivary calcium, phosphate and proteins, salivary flow, fluoride in saliva, and antibacterial components. Caries progression (demineralization) or reversal (remineralization) is determined by the balance between these two types of factors. The balance is determined by the relative weights of the sums of pathological factors and protective factors.2  


Treatment Paradigms

There has been a shift in the paradigm for treating dental caries. We now know that caries is a reversible multifactorial process. In 2001, the National Institutes of Health sponsored a conference where a “shift toward improved diagnosis of noncavitated, incipient lesions, a treatment for prevention, and arrest of such lesions” were identified.3 There are numerous ways in which a dental practice can achieve successful intervention in the caries process. Steinberg identified a “medical model” consisting of four steps: bacterial control, reduction of risk levels for at-risk patients, reversal of active sites by remineralization, and follow-up and maintenance (Figure 2).4 All the aforementioned steps use a variety of evidence-based methods to prevent dental caries. Considering the pathological factors, acidogenic bacteria; salivary dysfunction; and dietary carbohydrates, regular dental visits; use of antimicrobial agents (eg, chlorhexidine); oral hygiene; and dietary practices can affect caries incidence. Since these are individual behaviors, patient counseling by dental professionals is critically important to the protective and pathological balance.

Assessing the Risk of Caries Development

Caries Risk Assessment is another critical aspect involving the paradigm shift in treating dental caries. Caries risk assessment determines the probability of caries incidence in a certain time period.5 The assessment should evaluate all factors involved with the disease (eg, current caries, diet, fluoride exposure, presence of cariogenic bacteria, salivary status, general medical history, sociodemographic influences).6 Caries risk assessment is receiving considerable attention, and new technologies are being developed to aid practitioners in assessing risk. Chairside molecular probes to assess a patient’s cariogenic bacteria, a caries vaccine, and improved early detection methods are on the horizon. A preventive and restorative management plan and frequency of recall visits should all depend on the patient’s caries risk.

The recent scientific advances in the caries process and prevention focus on the protective factors: salivary calcium, phosphate and proteins, salivary flow, fluoride in saliva and antibacterial components that can assist in the remineralization process. Saliva is essential for the protection of the tooth against dental caries and provides many natural protective factors including calcium, phosphate, and antibacterial components. Salivary flow rate, buffering capacity, antimicrobial activity, microorganism aggregation and clearance from the oral cavity, immune surveillance, and calcium phosphate binding proteins all interact to inhibit or reverse demineralization.7 Topical fluoride therapy has been well established for inhibition of demineralization and enhancing remineralization. It has been found that prolonged and slightly elevated low concentrations of fluoride in the saliva and plaque fluid are beneficial.1 This intake of fluoride is typically derived from beverages, drinking water, foods, and fluoride-containing dental products such as toothpastes and rinses.

Chewing gum containing xylitol has too shown to be very effective for cariogenic bacteria reduction and in caries prevention.8 In fact, studies evaluating the effect of maternal use of chewing gums containing combinations of xylitol, sorbitol, chlorhexidine, and fluoride on caries prevalence in the mother’s children is showing promising results.9  

One of the latest research efforts involves the use of casein phosphopeptide-amophous calcium phosphate (CPP-ACP). Products containing CPP-ACP have been shown to increase resistance to acid thus increasing remineralization (Figure 2). Casein phosphopeptide-amophous calcium phosphate is derived from the milk protein, casein. A tooth-protective effect occurs due to a casein protein called casein phosphopeptide (CPP), which carries calcium and phosphate ions in the form of amorphous calcium phosphate (ACP). Calcium phosphate is normally insoluble at neutral pH; however the CPP keeps the calcium and phosphate in an amorphous non-crystalline state. When CPP-ACP is added to the oral cavity, parts of the CPP component bind directly to the enamel, biofilm, and soft tissue, delivering calcium where and when it is needed. Its incorporation into the salivary pellicle also seems to significantly reduce the adherence of certain plaque bacteria. The free calcium and phosphate ions then move out of the CPP, enter the enamel rods, and reform the apatite crystals, resulting in remineralization. With the addition of CPP-ACP, chewing gum, pastes, mousses, glass ionomers, temporary cements, and rinses have all been examined, showing an increase in enamel remineralization.


The way in which caries is being addressed is changing, being transformed by those investigating the topic from a “surgical” to a “preventive” approach. As a result, the dental hygienist, as a prevention specialist, can now determine dental caries risk factors and introduce remineralization strategies into the dental hygiene diagnosis in an effort to enhance caries prevention.


*Associate Professor and Director, Dental Hygiene, The Ohio State University, Columbus, Ohio.



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  3. National Institutes of Health. Diagnosis and Management of Dental Caries Throughout Life. Bethesda, Maryland: National Institutes of Health; 2001.
  4. Steinberg S. A paradigm shift in the treatment of caries. Gen Dent2002;50:333-338.
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  6. Fontana M, Zero DT. Assessing patient’s caries risk. JADA2006;137:1231-1238.
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  8. Juric H, Dukic W, Jankovic B, et al. Supression of salivary Streptococcus mutans and lactobacilli by topical caries preventive agents. Cent Eur J Public Health2003;11:219-222.
  9. Thorild I, Lindau B, Twetman S. Salivary mutans streptococci and dental caries in three-year-old children after maternal exposure to chewing gums containing combinations of xylitol, sorbitol, chlorhexidine, and fluoride. Acta Odontol Scand2004;62:245-250.
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