Skip to main content
Journal of Pharmacy & Bioallied Sciences logoLink to Journal of Pharmacy & Bioallied Sciences
. 2015 Aug;7(Suppl 2):S320–S324. doi: 10.4103/0975-7406.163436

Caries management by risk assessment: A review on current strategies for caries prevention and management

S Uma Maheswari 1, Jacob Raja 1, Arvind Kumar 1, R Gnana Seelan 1,
PMCID: PMC4606612  PMID: 26538870

Abstract

The current trend in treating dental caries is using nondestructive risk-based caries management strategies rather than focusing on the restorative treatment alone. Currently, there have been many changes in understanding of the multifaceted nature of caries process and its management. Caries Management by Risk Assessment (CAMBRA) which is an evidence-based approach focuses on determining many factors causing the expression of disease and take corrective action. The clinicians can ascertain what behaviors are increasing a patient's risk for disease and disease progression by evaluating the current caries risk of a patient. With this modern CAMBRA protocol, a novel treatment plan can be designed to arrest dental caries thereby decreasing the chance of cavitation. After the recognition of the multi factorial nature of caries involving the biofilm, the contemporary approaches focused mainly on the various options to cope with the locally out-of-balance oral biofilm and stop the progression of the disease. The initial caries lesions can be diagnosed with modern diagnostic aids and with the help of CAMBRA, reestablishment of the integrity of the tooth surface early on in the caries process will bring great rewards for patients. This review focuses on the repair of hard tooth tissues using noninvasive strategies.

KEY WORDS: Caries management by risk assessment, lesion activity, resin infiltrant


Dental caries occurs through a complex interaction over time between acidogenic microorganisms and fermentable carbohydrate, and host factors including teeth and saliva.[1] The caries process can be described as a dynamic balance between re- and demineralization, and if more minerals are lost than gained from the hard tissues over time, a lesion occurs as a sign of the disease.[2] Dental caries, if allowed to progress will result in non-cavitated caries lesions initially on tooth surfaces, and eventually can progress to cavitation. There has been a general trend in clinical practice that caries lesion management focus primarily on operative treatment rather than using preventive noninvasive strategies. This will lead to several replacements over time with increasing restoration size and produces iatrogenic damage. It has been reported that, 71% of all restorations are performed on previously restored teeth, with secondary carious lesions as a major cause.[3] This shows that although the carious lesion was repaired, the dental caries was not adequately treated, since the actual cause and risk factors were not adequately resolved. Recently, the concept of caries management has been changed and focused mainly on the multifaceted nature of caries and biofilm involvement. Currently, it has been shown that the success to caries prevention and management lies with altering the complex dental biofilm changing the oral factors to favor health.[4,5,6] Caries management by risk assessment (CAMBRA) is an evidence-based approach for preventing, reversing and, when necessary, repairing early damage to teeth tissue.[4,7] This article gives current management strategies for caries prevention and management by balancing the multifactorial etiological factors of dental caries.

Caries Management by Risk Assessment

An approach to oral health care requires clinical decision-making based on the integration of systemic assessments of clinically relevant scientific evidence relating to the patient's oral and medical condition and history; the clinical expertise; and the patient's treatment needs and preferences.[8] A current caries management strategy based on the individual patient risk assessment since each one have their own unique set of pathologic and protective factors. CAMBRA was developed to promote the clinical management philosophy in which the caries disease process is managed following the medical model. This involves an evaluation of the etiologic and protective factors and the establishment of the risk for future disease, followed by the development of a patient-centered evidence-based caries management plan.[4] The philosophy of CAMBRA was first introduced nearly a decade ago when an unofficial group called the Western CAMBRA Coalition was formed based in the western region of the USA.[9]

Dental caries is caused by bacterial pathogens that are a part of complex biofilm in which Streptococcus mutans and Lactobacilli were prevalently involved. These acidogenic bacteria alter their environment to favor their own viability. These are modulated by environmental changes with a sucrose-rich diet, which is an important risk factor. If the infectious disease is allowed to progress and demineralization is not countered with remineralization, cavitations will result.[10] Once cavitation through enamel allows bacteria to invade dentin, restoration by minimally invasive methods may be appropriate and necessary.[11] Unlike the traditional method, which provide treatment only after the advanced destruction of tooth tissue, this current method prevent and manage before cavitation occurs. Appropriate CAMBRA management mainly depends on the stage of the disease process and the subsequent severity of the damage to the teeth.[12,13] It includes the consideration of strategies that delay and reduce the early transmission of cariogenic microflora, control the infection, prevent or remineralize the early manifestations of the disease in the teeth and appropriately manage the more advanced stages of tooth demineralization and cavitation. CAMBRA supports the use of remineralization with chemical agents for early precavitated lesions sealing of occlusal non-cavitated lesions[14,15] along with tooth-preserving and minimally invasive restorative techniques when deemed necessary in treating cavitated lesions.

Caries Balance and Imbalance Concept

The Caries balance and imbalance model was created to represent the multifactorial nature of dental caries disease and to emphasize the balance between pathological and protective factors in the caries disease process.[2,7] If pathological factors predominate protective factors, the caries disease process progresses. It is a dynamic and delicate balance, tipping either way several times a day. Progression or reversal of caries disease is determined by the imbalance between disease indicators and risk factors on one side and the competing protective factors on the opposite.

Disease Indicators

Caries disease indicators are explained as physical signs of the presence of current dental caries disease or past dental caries disease history and activity. These indicators act as strong predictors of caries continuing unless implementation of the therapeutic intervention is made.[16]

The four disease indicators:

  • Visible white spots on smooth surfaces

  • Last 3 years restorations placed in the oral cavity as a result of caries

  • Lesions approximating enamel visible on dental radiographs

  • Carious cavitation lesions are showing radiographic penetration into the dentin.

Clinical Examination

The findings are obtained from the patient interview and clinical examination. The CAMBRA philosophy advocates the detection of the carious lesion at the earliest possible stage so the process can be reversed or arrested before cavitation, and subsequent restoration is needed. The most commonly used method for detecting carious lesions is a visual-tactile inspection. The technique of using a sharp dental explorer pushed into the pits and fissures of the tooth surface to check for “stickiness” is controversial, as the potential to cause an opening (cavitation) is high, thus allowing for the penetration of pathologic bacteria. It has been suggested that an appropriate use of the explorer is to use it to remove plaque and to determine surface roughness of non-cavitated lesions by running the explorer across the tooth surface.[16] Bitewing radiographs are used for examination of the approximal surfaces. However, one of the important caveats in using radiographs for lesion detection is the fact that a radiograph will not give information about lesion activity. The radiographic images underestimate the actual lesion depth and cannot identify initial enamel carious lesions.[17] It is important to remember that caries lesion detection is site specific requiring different methodologies.

Caries Lesion Activity Assessment and Diagnosis

Caries lesion activity assessment is different from the detection of caries lesion. The assessment of lesion activity as well as lesion detection, both are essential to arrive at the disease diagnosis and the appropriate clinical treatment decision.[18,19,20,21] The lesion activity assessment must also consider etiologic factor evaluations, such as oral hygiene, count of cariogenic microorganisms in plaque and saliva, use of fluoride, carbohydrate intake and socio-economic aspects, such as family income and level of education.[18,20,22]

In response to these limitations in detection and diagnosis of dental caries disease, new technologies have been developed. Digital radiography has been shown to provide an advantage in lesion detection compared with conventional radiography.[23,24] Few of these technologies include fiber optic transillumination (fiber optic technologies injection and digital imaging fiber optic transillumination), electronic caries monitor, quantitative light-induced fluorescence, diode laser fluorescence, and light-emitting diode light reflectance and refraction. Though many of these technologies show higher precision in carious lesion detection, it is important for clinicians to not rely solely on these modalities and to continue to use their clinical experience and judgment in their diagnosis.[25] Since, there is a lack of a universally accepted carious lesion detection system, the International Caries Detection Assessment System was created in 2002 in Scotland.[26] This visual system was developed as a detection system for occlusal carious lesions, with a two-digit coding system.

Risk Factors

Caries risk factors are described as biological reasons that cause or promote current or future caries disease. Because of their pathologic nature, risk factors can also serve as an explanation of what could be corrected in order to improve the imbalance that exists.[27]

The Caries imbalance model denotes three risk factors that are supported in the literature as causative for dental caries:

  • Bad bacteria, meaning acidogenic, aciduric or cariogenic bacteria

  • Absence of saliva, meaning hyposalivation or salivary hypofunction

  • Habits such as frequent ingestion of fermentable carbohydrates, and poor oral hygiene.

Bacteria

Dental caries disease is bacteria-driven and because carious lesions are late-stage symptoms of the disease, the evaluation of microbiological findings would assist clinicians in implementing early interventions to help arrest the disease. Mitis salivarius (MS) produce both intra and extracellular polysaccharides that assist with acid production and adherence to smooth surfaces.[28,29,30] The other bacteria species of interest in dental caries is lactobacilli, and they prefer to live in low-pH niches that are difficult to clean and near plaque biofilm accumulation.[31] They are more involved in the lesion progression.[32,33]

There has been a correlation between MS levels in plaque biofilm and in saliva.[34,35] It has been reported that if saliva contains high bacterial counts, so does the plaque biofilm. High bacterial counts in saliva correlate to >103 colony-forming units of MS in plaque biofilm.[36] Findings higher than 105 CFU of MS and Lactobacilli show a high-risk for future caries disease.[37,38] Several culture-based methods are commercially available. The cathode ray tube® bacteria caries risk test is sensitive and give information about a level of low, medium or high cariogenic bacterial level.[7] This contains an agar carrier, containing blue MS agar with bacitracin, used to detect MS and de Man, Rogosa and Sharpe agar, used to evaluate LB. On completion of the process, the vial used is removed and opened, and the agar carrier is then evaluated using a chart. MS appear as small blue colonies and LB appear as white colonies. It has been found that higher than 105 CFU of MS and/or LB indicates a high-risk for future caries disease.[37,38] Chairside saliva tests have been developed and are now available. There is now a monoclonal antibody test that uses a specific immunochromatography process that selectively detects the S. mutans species. Another chairside test available to clinicians is a simple 1-min test that uses adenosine triphosphate bioluminescence to identify oral bacterial load. While, there is no exact pH at which demineralization begins, the general range of 5.5 to 5.0 is considered as critical for enamel demineralization. Both quantity and quality of saliva are critical to the development and progression of dental caries disease.

Saliva

The salivary components help modulate the bacterial attachment in plaque biofilm, the pH and buffering capacity of saliva, antibacterial properties, and tooth surface remineralization and demineralization. Without adequate saliva, the oral clearance of sugary or acidic foods will be longer, and less urea is available to help raise plaque biofilm pH. There are easy-to-use chairside tests available to evaluate saliva quality. These tests measure resting flow rate and pH of saliva at rest and in stimulated condition, salivary consistency, and buffer capacity.

Diet

Diet affects the pH, quantity and quality of saliva. Sucrose and other fermentable carbohydrates are broken down by salivary enzymes and lower salivary and plaque biofilm pH.[39] The physical properties of food and the frequency of eating influence the cariogenicity of the patient's diet.

Protective Factors

Caries protective factors are biologic or therapeutic measures that can be used to prevent or arrest the pathologic challenges posed by the caries risk factors. Protective factors also include fluoridated water; regularly using fluoridated toothpaste, low-fluoride oral rinses and xylitol; and receiving topical applications of fluoride, chlorhexidine, and calcium phosphate agents.

Lesion Arrest and Repair

Diet modification, plaque removal and anti-bacterial strategies, stimulation of salivary flow, and sealing of lesions, all lead to reduction or elimination of acid attacks on the tooth surface. The ion exchange dynamics are changed between the hard tissues and the ambient plaque fluids. The basic preventive steps for moderate and high-risk patients are patient motivation, diet counseling, tooth brushing twice daily with fluoride toothpaste, flossing daily, few times a week, sugar-free gum chewing gums, and sealants. When brushing with concentrations >1,000 ppm fluoride, a risk-benefit decision needs to be discussed with caregivers regarding the development of mild fluorosis. The use of 5,000 ppm prescription fluoride toothpaste and home-use fluoride rinses has also been recommended. Along with fluorides calcium based strategies with casein phosphopeptide amorphous calcium phosphate containing chewing gums and more recently bioactive glass that react with the oral environment and releases calcium and phosphate ions. CAMBRA clinical guidelines recommend the use of xylitol to control S. mutans for patients over 6 years of age who are at moderate to extreme risk for caries.[13] More recently CO2 laser in addition to fluoride has been used for caries inhibition.

Resin Sealants and Infiltrants

Sealants protect the surface by blocking continuous attacks by plaque acids. This will prevent plaque accumulation and dissolution of minerals from the tooth tissues. Resin infiltrants act by concurrent sealing of the caries lesion from the oral environment, the progression of the lesion is halted. When the demineralized enamel is filled with resin, it has been claimed that its refractory index changes also. The lesion may become less opaque and thus less visible as it regains translucency.

Antimicrobial Agents

Antimicrobial agents destroy or suppress the growth or multiplication of microorganisms, including bacteria. CAMBRA clinical guidelines recommend the use of antimicrobials for patients over 6 years of age who are classified as being at high or extreme risk for caries.[13,40]

Antimicrobials require repeated applications at various intervals, depending on the agent. Chlorhexidine gluconate rinse has been widely studied that when used as a 30 s rinse every day of the 1st week of every month, reduces MS bacterial level but is not as effective against LB.[41] Chlorhexidine gels are the next most efficacious, followed by oral rinses for patients at moderate to extreme risk.[42] It also reduces the root carious lesions in a geriatric population.[43,44] The application of chlorhexidine varnish, every three to 4 months may be a more viable option than the use of chlorhexidine rinses, especially for caregivers of children.

Habits

While the use of fluoride has decreased the need for strict dietary control of sucrose, dental caries disease does not occur in the absence of dietary fermentable carbohydrates. Reducing the amount and frequency of carbohydrate consumption, continues to be important for patients at high-risk for caries.[45] Arginine rich proteins include a variety of nuts (peanuts, almonds, walnuts, cashews, pistachios), seeds (sunflower, pumpkin, squash), kidney beans, soybeans, watermelon, and tuna. While most research concerning power toothbrushes focuses on the ability of the brush to remove plaque biofilm, power toothbrushes may be helpful in the delivery and retention of fluoride. Recent research has shown that one sonic toothbrush enhances effects of fluoride on the plaque biofilm, causing increased fluoride delivery and retention at the tooth surface.[46] In addition, for patients at extreme risk the sonic power toothbrush has been shown to increase salivary flow and decrease the numbers of incipient caries and root caries.[47,48] Patient adherence to the recommendations made by the dentists is critical to successful implementation of these caries protective factors. It is well understood among dental professionals that adherence and motivation are issues for many patients, and lack of adherence or noncompliance affects outcomes across all dental disciplines. The ability of the clinician to motivate the patient to make positive behavior change is crucial. One technique gaining popularity among patient-centered clinicians is motivational interviewing. The strategies involved in motivational interviewing are more persuasive and supportive and argumentative and are designed for the patient's intrinsic motivation.[49]

Conclusion

The strategies used for treating dental caries should have individualized consideration of the underlying disease process for each patient. Many factors such as bacteria, carbohydrate diet, and host response, cause initiation of dental caries, and its progression. Assessment of the caries risk of the individual patient is a critical component in determining an appropriate management strategy. Along with patient motivation and risk assessment, successful outcome for caries management can be achieved. For low-risk patients the considerations must be given for remineralization, the arrest of incipient caries or pit, and fissure sealant application, which provides ultimate conservation of tooth. For the preservation of the tooth structure and slow caries progression, minimal intervention program can be considered for high-risk patients. There is a great variation in the interplay between all known and unknown factors that are involved in caries development and the strategy have to be balanced with the clinician's professional judgment and the patient's history and preference. Since, CAMBRA approach is based on research, clinical expertise, and the patient's preferences and individual needs, implementation of this new protocol will provide ultraconservative tooth preservation that gives good patient care.

Footnotes

Source of Support: Nil

Conflict of Interest: None declared.

References

  • 1.Selwitz RH, Ismail AI, Pitts NB. Dental caries. Lancet. 2007;369:51–9. doi: 10.1016/S0140-6736(07)60031-2. [DOI] [PubMed] [Google Scholar]
  • 2.Featherstone JD. The caries balance: The basis for caries management by risk assessment. Oral Health Prev Dent. 2004;2(Suppl 1):259–64. [PubMed] [Google Scholar]
  • 3.Fontana M, González-Cabezas C. Secondary caries and restoration replacement: An unresolved problem. (21-4).Compend Contin Educ Dent. 2000;21:15–8. 26. [PubMed] [Google Scholar]
  • 4.Young DA, Featherstone JD, Roth JR. Curing the silent epidemic: Caries management in the 21st century and beyond. J Calif Dent Assoc. 2007;35:681–5. [PubMed] [Google Scholar]
  • 5.Marsh PD. Microbiology of dental plaque biofilms and their role in oral health and caries. Dent Clin North Am. 2010;54:441–54. doi: 10.1016/j.cden.2010.03.002. [DOI] [PubMed] [Google Scholar]
  • 6.Hara AT, Zero DT. The caries environment: Saliva, pellicle, diet, and hard tissue ultrastructure. Dent Clin North Am. 2010;54:455–67. doi: 10.1016/j.cden.2010.03.008. [DOI] [PubMed] [Google Scholar]
  • 7.Featherstone JD, Domejean-Orliaguet S, Jenson L, Wolff M, Young DA. Caries risk assessment in practice for age 6 through adult. (710-3).J Calif Dent Assoc. 2007;35:703–7. [PubMed] [Google Scholar]
  • 8.American Dental Association Council on Scientific Affairs. Professionally applied topical fluoride: Evidence-based clinical recommendations. J Am Dent Assoc. 2006;137:1151–9. doi: 10.14219/jada.archive.2006.0356. [DOI] [PubMed] [Google Scholar]
  • 9.Young DA, Buchanan PM, Lubman RG, Badway NN. New directions in interorganizational collaboration in dentistry: The CAMBRA Coalition model. J Dent Educ. 2007;71:595–600. [PubMed] [Google Scholar]
  • 10.Featherstone JD. The science and practice of caries prevention. J Am Dent Assoc. 2000;131:887–99. doi: 10.14219/jada.archive.2000.0307. [DOI] [PubMed] [Google Scholar]
  • 11.Featherstone JD, Cutress TW, Rodgers BE, Dennison PJ. Remineralization of artificial caries-like lesions in vivo by a self-administered mouthrinse or paste. Caries Res. 1982;16:235–42. doi: 10.1159/000260603. [DOI] [PubMed] [Google Scholar]
  • 12.Ramos-Gomez FJ, Crall J, Gansky SA, Slayton RL, Featherstone JD. Caries risk assessment appropriate for the age 1 visit (infants and toddlers) J Calif Dent Assoc. 2007;35:687–702. [PubMed] [Google Scholar]
  • 13.Jenson L, Budenz AW, Featherstone JD, Ramos-Gomez FJ, Spolsky VW, Young DA. Clinical protocols for caries management by risk assessment. J Calif Dent Assoc. 2007;35:714–23. [PubMed] [Google Scholar]
  • 14.Beauchamp J, Caufield PW, Crall JJ, Donly K, Feigal R, Gooch B, et al. Evidence-based clinical recommendations for the use of pit-and-fissure sealants: A report of the American Dental Association Council on Scientific Affairs. J Am Dent Assoc. 2008;139:257–68. doi: 10.14219/jada.archive.2008.0155. [DOI] [PubMed] [Google Scholar]
  • 15.Griffin SO, Oong E, Kohn W, Vidakovic B, Gooch BF, Bader J, et al. CDC Dental Sealant Systematic Review Work Group. The effectiveness of sealants in managing caries lesions. J Dent Res. 2008;87:169–74. doi: 10.1177/154405910808700211. [DOI] [PubMed] [Google Scholar]
  • 16.Hamilton JC, Stookey G. Should a dental explorer be used to probe suspected carious lesions? J Am Dent Assoc. 2005;136:1526–32. doi: 10.14219/jada.archive.2005.0082. [DOI] [PubMed] [Google Scholar]
  • 17.Baelum V. What is an appropriate caries diagnosis? Acta Odontol Scand. 2010;68:65–79. doi: 10.3109/00016350903530786. [DOI] [PubMed] [Google Scholar]
  • 18.Ekstrand KR, Ricketts DN, Kidd EA. Occlusal caries: Pathology, diagnosis and logical management. Dent Update. 2001;28:380–7. doi: 10.12968/denu.2001.28.8.380. [DOI] [PubMed] [Google Scholar]
  • 19.Nyvad B, Fejerskov O. Assessing the stage of caries lesion activity on the basis of clinical and microbiological examination. Community Dent Oral Epidemiol. 1997;25:69–75. doi: 10.1111/j.1600-0528.1997.tb00901.x. [DOI] [PubMed] [Google Scholar]
  • 20.Basting RT, Serra MC. Occlusal caries: Diagnosis and noninvasive treatments. Quintessence Int. 1999;30:174–8. [PubMed] [Google Scholar]
  • 21.Nyvad B. Diagnosis versus detection of caries. Caries Res. 2004;38:192–8. doi: 10.1159/000077754. [DOI] [PubMed] [Google Scholar]
  • 22.Baelum V, Heidmann J, Nyvad B. Dental caries paradigms in diagnosis and diagnostic research. Eur J Oral Sci. 2006;114:263–77. doi: 10.1111/j.1600-0722.2006.00383.x. [DOI] [PubMed] [Google Scholar]
  • 23.Chong MJ, Seow WK, Purdie DM, Cheng E, Wan V. Visual-tactile examination compared with conventional radiography, digital radiography, and diagnodent in the diagnosis of occlusal occult caries in extracted premolars. J Clin Dent. 2004;15:76–82. [PubMed] [Google Scholar]
  • 24.Senel B, Kamburoglu K, Uçok O, Yüksel SP, Ozen T, Avsever H. Diagnostic accuracy of different imaging modalities in detection of proximal caries. Dentomaxillofac Radiol. 2010;39:501–11. doi: 10.1259/dmfr/28628723. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 25.Strassler HE, Sensi LG. Technology-enhanced caries detection and diagnosis. Compend Contin Educ Dent. 2008;29:464–5. 468, 470. [PubMed] [Google Scholar]
  • 26.Pitts N. “ICDAS” – An international system for caries detection and assessment being developed to facilitate caries epidemiology, research and appropriate clinical management. Community Dent Health. 2004;21:193–8. [PubMed] [Google Scholar]
  • 27.Young DA, Featherstone JD. Implementing caries risk assessment and clinical interventions. Dent Clin North Am. 2010;54:495–505. doi: 10.1016/j.cden.2010.04.002. [DOI] [PubMed] [Google Scholar]
  • 28.Koga T, Asakawa H, Okahashi N, Hamada S. Sucrose-dependent cell adherence and cariogenicity of serotype c Streptococcus mutans. J Gen Microbiol. 1986;132:2873–83. doi: 10.1099/00221287-132-10-2873. [DOI] [PubMed] [Google Scholar]
  • 29.Loesche WJ. Role of Streptococcus mutans in human dental decay. Microbiol Rev. 1986;50:353–80. doi: 10.1128/mr.50.4.353-380.1986. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 30.Hamada S, Slade HD. Biology, immunology, and cariogenicity of Streptococcus mutans. Microbiol Rev. 1980;44:331–84. doi: 10.1128/mr.44.2.331-384.1980. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 31.Beighton DS, Brailsford S. Lactobacilli and actinomyces: Their role in the caries process. In: Stösser L, editor. Caries dynamic and caries risk. Berlin: Quintessenz Verlags-GmbH; 1998. [Google Scholar]
  • 32.van Houte J. Bacterial specificity in the etiology of dental caries. Int Dent J. 1980;30:305–26. [PubMed] [Google Scholar]
  • 33.Kingman A, Little W, Gomez I, Heifetz SB, Driscoll WS, Sheats R, et al. Salivary levels of Streptococcus mutans and lactobacilli and dental caries experiences in a US adolescent population. Community Dent Oral Epidemiol. 1988;16:98–103. doi: 10.1111/j.1600-0528.1988.tb01852.x. [DOI] [PubMed] [Google Scholar]
  • 34.Hardie JM, Thomson PL, South RJ, Marsh PD, Bowden GH, McKee AS, et al. A longitudinal epidemiological study on dental plaque and the development of dental caries – Interim results after two years. J Dent Res. 1977;56(Spec No):C90–8. doi: 10.1177/00220345770560032401. [DOI] [PubMed] [Google Scholar]
  • 35.Mundorff SA, Eisenberg AD, Leverett DH, Espeland MA, Proskin HM. Correlations between numbers of microflora in plaque and saliva. Caries Res. 1990;24:312–7. doi: 10.1159/000261289. [DOI] [PubMed] [Google Scholar]
  • 36.Sullivan A, Borgström MK, Granath L, Nilsson G. Number of mutans streptococci or lactobacilli in a total dental plaque sample does not explain the variation in caries better than the numbers in stimulated whole saliva. Community Dent Oral Epidemiol. 1996;24:159–63. doi: 10.1111/j.1600-0528.1996.tb00834.x. [DOI] [PubMed] [Google Scholar]
  • 37.Kneist S, Laurisch L, Heinrich-Weltzien R, Stösser L. A modified mitis salivarius medium for a caries diagnostic test. J Dent Res. 1998;77:970. Abstr 2712. [Google Scholar]
  • 38.Krasse B. Biological factors as indicators of future caries. Int Dent J. 1988;38:219–25. [PubMed] [Google Scholar]
  • 39.Touger-Decker R, van Loveren C. Sugars and dental caries. Am J Clin Nutr. 2003;78:881S–92. doi: 10.1093/ajcn/78.4.881S. [DOI] [PubMed] [Google Scholar]
  • 40.Ramos-Gomez FJ, Crystal YO, Ng MW, Crall JJ, Featherstone JD. Pediatric dental care: Prevention and management protocols based on caries risk assessment. J Calif Dent Assoc. 2010;38:746–61. [PMC free article] [PubMed] [Google Scholar]
  • 41.Anderson MH. A review of the efficacy of chlorhexidine on dental caries and the caries infection. J Calif Dent Assoc. 2003;31:211–4. [PubMed] [Google Scholar]
  • 42.Zhang Q, van Palenstein Helderman WH, van’t Hof MA, Truin GJ. Chlorhexidine varnish for preventing dental caries in children, adolescents and young adults: A systematic review. Eur J Oral Sci. 2006;114:449–55. doi: 10.1111/j.1600-0722.2006.00392.x. [DOI] [PubMed] [Google Scholar]
  • 43.Baca P, Clavero J, Baca AP, González-Rodríguez MP, Bravo M, Valderrama MJ. Effect of chlorhexidine-thymol varnish on root caries in a geriatric population: A randomized double-blind clinical trial. J Dent. 2009;37:679–85. doi: 10.1016/j.jdent.2009.05.001. [DOI] [PubMed] [Google Scholar]
  • 44.Tan HP, Lo EC, Dyson JE, Luo Y, Corbet EF. A randomized trial on root caries prevention in elders. J Dent Res. 2010;89:1086–90. doi: 10.1177/0022034510375825. [DOI] [PubMed] [Google Scholar]
  • 45.Burt BA, Pai S. Sugar consumption and caries risk: A systematic review. J Dent Educ. 2001;65:1017–23. [PubMed] [Google Scholar]
  • 46.Aspiras M, Stoodley P, Nistico L, Longwell M, de Jager M. Clinical implications of power toothbrushing on fluoride delivery: Effects on biofilm plaque metabolism and physiology. Int J Dent 2010. 2010 doi: 10.1155/2010/651869. 651869. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 47.Papas A, Singh M, Harrington D, Rodríguez S, Ortblad K, de Jager M, et al. Stimulation of salivary flow with a powered toothbrush in a xerostomic population. Spec Care Dentist. 2006;26:241–6. doi: 10.1111/j.1754-4505.2006.tb01661.x. [DOI] [PubMed] [Google Scholar]
  • 48.Papas AS, Singh M, Harrington D, Ortblad K, de Jager M, Nunn M. Reduction in caries rate among patients with xerostomia using a power toothbrush. Spec Care Dentist. 2007;27:46–51. doi: 10.1111/j.1754-4505.2007.tb00327.x. [DOI] [PubMed] [Google Scholar]
  • 49.Rollnick S, Miller WR, Butler CC. Helping Patients Change Behavior. New York, NY: Guilford Press; 2008. Motivational Interviewing in Health Care. [Google Scholar]

Articles from Journal of Pharmacy & Bioallied Sciences are provided here courtesy of Wolters Kluwer -- Medknow Publications

RESOURCES