Primary Preventive Dentistry 6th Ed. (2004)
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Remineralization of Teeth Answers and Explanations |
Prognostic and Diagnostic Tests Several methods for preventing the onset or progress of caries and periodontal disease have been discussed. Because it is impossible to apply vigorously all the preventive procedures to all the people all the time, it would be desirable to have some tests to indicate the extent of caries and periodontal disease risk of an individual at any given time. This need is highlighted by the fact that an estimated 60% of all carious lesions in schoolchildren occur in 20% of the stu-dents.58 It would save much time to be able to identify this 20% group of high-risk students without having to examine an entire school population. Although no tests are 100% correlated with the extent of caries activity or periodontal disease, several test procedures are sufficiently well correlated with either condition to be of interest. To be successful, such screening tests should be simple to accomplish, valid, economical, require a minimum of equipment, be easy to evaluate, and be compatible with mass-handling techniques. Laboratory methods exist for counting the number of bacteria in the saliva. If the caries-causing mutans streptococci or lactobacilli counts are high, the individual from whom the sample was derived can be presumed to have a higher risk for dental caries, whereas a low count permits the opposite assumption.59 A second general method for estimating caries susceptibility is by use of a refined-carbohydrate dietary analysis to (1) evaluate the patient's overall diet with special attention to food preferences and amounts consumed and (2) to determine if the intake of refined carbohydrates is excessive in quantity or frequency (see Appendix 23-2). A well-balanced diet is assumed to raise host resistance to all disease processes, whereas a frequent and excessive intake of refined carbohydrates (i.e., sugar) has been associated with a high risk of caries development. The dietary analysis is very effective when used as a guide for patient education. The onset of gingivitis is much more visible than the early demineralization that occurs in caries. The sign of impending periodontal disease is an inflammation of the gingiva that can be localized at one site, or generalized around all the teeth. Red, bleeding, swollen, and a sore gingiva are readily apparent to dentist and patient alike. ^ Both demineralization and remineralization occur daily following the cyclic ebb-and-flow of the caries process during and after eating meals and snacks. An eventual caries lesion develops over a period of time when the rate of acid-induced demineralization of teeth exceeds the capability of the saliva to remineralize the damaged enamel components. A negative mineral balance at the enamel-plaque interface, if continually repeated, results in an incipient lesion that eventually can become an overt lesion. It often requires months, or even years, for the overt lesion to develop.60,61 During this time, under proper conditions, remineralization can reverse the progress of the caries front, with the mineral components coming from the saliva. There is a physiological precedent for such a mineralization. Immediately after eruption of the teeth the outer layer of the enamel is not completely mineralized; the maturation (mineralization) of this outer layer requires approximately 1 year, during which time the tooth is continuously bathed in the saliva. The point at which a developing caries lesion is no longer reversible is considered to be when cavitation occurs; clinical experience indicates that as long as the lesion is incipient (i.e., with no cavitation), remineralization is possible.62 The need to exploit this possibility to the benefit of all patients was emphasized by Koulourides's statement many years ago that "there is a wide gap between current practices of many dental clinicians and the potential application of present scientific knowledge to arrest and reverse incipient carious lesions."63 The outstanding electron microscope research contributions of Silverstone several decades ago clearly demonstrated that demineralized tooth structure could be remineralized.64 No longer was a simple interproximal x-ray radiolucency a signal to place an interproximal restoration. Several reports from Scandinavia now indicate that even when the caries front of an incipient lesion extends past the dentino-enamel junction, it can be remineralized. Foster (England) has recommended " that operative intervention (be) considered for approximal lesions which extend deeper that 0.5 mm into the dentine, while preventive treatment and re-assessment may be considered for shallower lesions."65 Missing at the present time is an accurate predictive test for caries that would permit the targeting of individuals who would be candidates for remineralization therapy (see Chapter 23). The conditions for optimum remineralization are the same as for preventing the initiation of a lesion: (1) plaque control to reduce the number of cariogenic bacteria, (2) a strict self-imposed sugar discipline to minimize the number of acidogenic episodes, (3) the use of sealants to interdict bacterial entry into deep pits and fissures, and (4) the use of topical and/or systemic fluoride to inhibit demineralization and to potentiate the remineralization process. Thus, with the same primary preventive dentistry routines using fluoride, an individual can simultaneously protect the tooth into the future by prevention, as well as to compensate for limited past damage through reversal strategies. Question 6 Which of the following statements, if any, are correct? A. Sealants are most effective in preventing smooth-surface caries, whereas fluorides are most effective in preventing caries in the deep occlusal pits and fissures. B. There are enough dentists and dental auxiliaries in the United States to provide approximately 1 hour per year of educational lectures to each of the 250 million citizens of the United States. C. Caries activity indicators (tests) are indicative of a patient's vulnerability at the time of the test. D. Plaque control, sugar restriction, and topical-fluoride therapy not only are effective in preventing demineralization, but they also can enhance remineralization. E. The process of natural mineralization (maturation) of enamel during the first year after eruption is a precedent for man-initiated remineralization (repair) of incipient lesions. Summary Each year more than $60 billion is spent in the United States for dental care, mainly for the treatment of dental caries and periodontal disease or their sequelae. Yet, strategies now exist that with patient knowledge and cooperation, could greatly aid in preventing, arresting, or reversing the onset of caries or periodontal disease. The six general approaches to the control of both caries and periodontal disease involve (1) plaque control, (2) water fluoridation and use of fluoride products for self-care and for professionally initiated remineralization procedures, (3) placement, when indicated, of pit and fissure sealants, and (4) sugar discipline. Supporting these measures are (5) public and private enterprise financed media distributed programs extolling the benefits of oral health and proprietory products for family prevention; and (6) access to a dental facility where diagnosis, comprehensive preventive, restorative treatment, and planned recall and maintenancec programs are available. The zeal and thoroughness with which these preventive measures should be prescribed and used are indicated by the information obtained from the clinical and roentgenographic oral examination, dietary analysis, patient history, and laboratory tests. If at the time of the clinical and roentgenographic examinations, emphasis was placed on searching out the incipient lesions ("white spots") and early periodontal disease (gingivitis), preventive strategies could be applied that would result in a reversal or control of either/or both of the plaque diseases. It is essential that both the profession and the public realize that biologic "repair" of incipient lesions, and "cure" of gingivitis is a preferred alternative to restorations or periodontal treatment. Even if these primary preventive dentistry procedures fail, tooth loss can still be avoided. In practice, the early identification and expeditious treatment of caries and periodontal disease greatly minimizes the loss of teeth. When such routine diagnostic and treatment services are linked with a dynamic preventive-dentistry program that includes an annual dental examination and recall program based on risk assessment, tooth loss can realistically be expected to be reduced to zero or near-zero. This introductory chapter has briefly pointed out some of the problems of dentistry and the means by which the dental profession can make primary preventive dentistry its hallmark. The remaining chapters provide the detailed background that can make this challenge become a reality. cThere is a trend to consolidate the two terms, "recall" and "maintenance", into the word, "recare". ^ 1. A, D, and Ecorrect. Bincorrect. With salaries now escalating, maybe the poor fellow has something to worry about; the true answer is that continued worry is not healthy. Cincorrect. An amalgam restoration is an excellent example of secondary prevention, not tertiary. 2. A, B, and Ccorrect. Dincorrect. It is easier to reduce the extraction rate to zero or near-zero by the combined application of treatment and preventive procedures, than to reduce the incidence of disease by preventive procedures alone. Eincorrect. The major income of a dentist is derived from treatment of the plaque diseases and their sequelae. 3. Ecorrect. Aincorrect. Restorations are not a primary preventive-dentistry option; rather they are the mainstay of secondary prevention. Bincorrect. Plaque is found in the pits and fissures of the occlusal surfaces. Cincorrect. Plaque can be removed by use of toothbrush and floss; it is calculus removal that requires instrumentation. Dincorrect. It is not possible to remove oral debris from deep pits and fissures. 4. A and Ccorrect. Bincorrect. Once calculus has formed, professional intervention is required for its removal. Dincorrect. It is vice versathe more often that fluoride is applied topically (dentifrices), the more effective it is. Eincorrect. Remember, brushing with a fluoride dentifrice constitutes a topical application. 5. A, B, C, and Ecorrect. Dincorrect. Bacteria require carbohydrates, fats, proteins, minerals, and water to exist; they need the carbohydrates for their energy needs, which, in turn, results in their acid production and cariogenicity. 6. C, D, and Ecorrect. Aincorrect. Just the opposite. The sealants are used to seal off the convoluted pits and fissures of the occlusal surfaces. Bincorrect. The only means to promote preventive dentistry to a total population is by the use of the schools and the popular media. Self-evaluation Questions 1. Health is defined as ___________________________________________________. 2. If primary prevention fails, the two sequential actions necessary to minimize progression of a disease process are _______ and _______. 3. For planning purposes, oral diseases and abnormalities can be grouped into three general categories: (1) _______, (2) _______, and (3) _______. 4. Five strategies used to attain primary prevention in caries control are: (1) _______ (2) _______, (3) _______, (4) _______, and (5) _______. 5. Of the six general methods for caries control, the two that are also valuable in periodontal disease control are (1) _______ and (2) _______. 6. Plaque control in a home environment requires essential items or devices: (1) _______ and (2) _______ and (3) an irrigator. 7. Caries development depends on four interrelated factors: (1) _______, (2) _______, (3) _______ and (4) time. 8. Fluoride is most effective in preventing caries on (smooth)(occlusal) surfaces of the teeth, whereas plastic sealants are most effective in preventing caries on (smooth)(occlusal) surfaces of the teeth. 9. "Biologic repair" of a tooth results from a positive mineral balance at the enamel surface; the process of replacing the ions lost in demineralization is known as _______. 10. Name three American sugar substitutes and one foreign anticariogenic sugar alcohol used for sweetening: _______, _______, _______ and _______. References 1. U.S. Surgeon General's Report: Part II. (2000). What is the status of oral health in America, 35-39. 2. Evans, C. A., & Kleinman, D. V. (2000). The Surgeon General's report on America's oral health: Opportunities for the dental profession. JADA, 31:1721-28. 3. Milgrom P., & Reisine, S. (2000). Oral health in the United States: The post-fluoride generation. Annu Rev Public Health, 21:403-36. 4. Watt, R., & Sheiham, A. (1999). Inequalities in oral health: A review of the evidence and recommendations for action. Br Dent J, 187:6-12. 5. Locker, D. (2000). Deprivation and oral health. Community Dent Oral Epidemiology, 28:161-9. 6. Marcias, E. P., & Morales, L. S. (2001). Crossing the border for health care. J Health Care Poor Underserved, 12:77-87. 7. Waldman, H. B., & Permah, S. P. (2001). 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Community Dent Oral Epidemiol, 24:408-11, 39. Twetman, S., Nederfors, T., & Petersson, L. C. (1998). Fluoride concentrations in whole saliva and separate gland secretions in school children after intake of fluoridated milk. Car Res, 32:412-16. 40. Marino, R. (1995). Should we use milk fluoridation? A review. Bull Pan Am Health Organ, 29:287-98. 41. Bratthall, D., & Barnes, D. E. (1995). Adding fluoride to sugara new avenue to reduce dental caries, or a "dead end"? Adv Dent Res, 9:3-5. 42. Rosan, B., & Lamont, R. J. (2000). Dental plaque formation. Microbes Infect, 2:1599-605. 43. Gustafsson, B. E., Qensel, C. E., Lanke, L. S., Lunqrist, D., Grahnen, H., Bonow, B. E., & Krasse, B. (1954). The Vipehold dental caries study. Acta Odont Scand, 11:232-264. 44. Scheie, A. A., & Fejerskov, O. B. (1998). Xylitol in caries prevention: what is the evidence for clinical efficacy. Oral Dis, 4:226-30. 45. Tanzer, J. M. (1995). Xylitol chewing fums and dental caries. Internat Dent J, 45:65-86. 46. Honkala, S., Honkala, E., Tynjala, K., & Kanas, L. (1999). The use of xylitol chewing gum among Finnish schoolchildren. Acta Odontolog Scand, 57:306-9. 47. Hildebrandt, G. H., & Sparks, B. S. (2000). Maintaining mutans streptococci suppression with xylitol chewing gum. JADA, 131:909-16. 48. Isokanges, P., Soderling, E., Pienihekkinen, K., & Alanen, P. (2000). Occurrence of dental decay in children after maternal consumption of xylitol chewing gum, a follow-up from 0 to 5 years of age. J Dent Res, 29:1885-9. 49. Anasavice, K. J. (1998). Chlorhexidine, fluoride varnish, and xylitol chewing gum: underutilized preventive therapies? Gen Dent, 1:34-8, 40. 50. Mertz-Fairhurst, E. J. (1992). Pit and fissure sealants; a global lack of scientific transfer? [Editorial in] J Dent Res, 71:1543-4. 51. Simonson, R. J. Retention and effectiveness of a single application of white sealant after 10 years (1987). JADA, 115:31-6. 52. Mertz-Fairhurst, E. J., Shuster, G. S., & Fairhurst, C. W. (1986). Arresting caries with sealants: results of a clinical study. JADA, 112:194-323. 53. Qvist, J., Qvist, V., & Mjor, I. A. (1990). Placement and longevity of amalgam restorations in Denmark. J Dent Res [Spec Issue], 69:237 (Abst. 1018). 54. Personal communication, American Dental Association, Chicago, 1997. 55. Personal communication, American Dental Hygienists Association, Chicago 1997. 56. Best, H. A., & Bedi, R. (2001). Is the current access to health care information helping or hindering effective decision-making for dentists and patients? Guidelines for dental practice. Prim Dental Care, 8:77-80. 57. MacKenzie, F. M., & Peterson, M. (1994). The New Zealand School Dental Service. In Harris, N. O., & Christen, A. G., Eds. Primary preventive dentistry, (4th ed.) Norwalk, CT: Appleton & Lange, 601-5. 58. Miller, A. J., & Brunelle, J. (1983). A summary of the NIDR Community Caries Prevention Demonstration Program. JADA, 107:265-9. 59. Krasse, B. (1984). Can microbiological knowledge be applied in dental practice for the treatment and prevention of dental caries? J Can Dent Assoc, 50:221-23. 60. Backer-Dirks, O. (1961). Longitudinal dental caries study in children 9-15 years of age. Arch Oral Biol (Supp.), 6:94;108-27. 61. Foster, L. Y. (1998). Three years in vivo investigating to determine the progression of approximal primary carious lesions extending into dentine. Br Dent J, 185:353-7. 62. Elderton, R. J. (1993). Overtreatment with restorative dentistry: when to intervene. J Internat Dent, 43:20-4. 63. Koulourides, T. I. (1977). To what extent is the incipient lesion of dental caries reversible? In Rowe N. H., Ed. Proceedings of Symposium on Incipient Lesions in Enamel. Ann Arbor, MI; University of Michigan School of Dentistry; November 11-12:51-68. 64. Silverstone, L. M. (1984). Significance of remineraliztion in caries prevention. J Can Dent Assoc, 50:156-166. 65. Foster, L. V. (1998). Three year in vivo investigation to determine the progression of approximal primary carious lesions extending into dentine. Br Dent J, 185:353-57. 0.015625 Copyright © 2004 by Pearson Education, Inc., Pearson Prentice Hall. All rights reserved.  (+/-) Show / Hide Bibliography Working... × Chapter 2. The Development and Structure of Dental Plaque (A Bacterial Biofilm), Calculus, and Other Tooth-adherent Organic Materials - Max A. Listgarten Jonathan Korostoff |
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