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Self-evaluation Questions |
Answers and Explanations 1. A, B, and Ccorrect. Dincorrect. The interproximal starting point is apical to the contact point; for the pit-and-fissure lesion, it usually begins bilaterally at the orifice of the fissure. Eincorrect. The dark and the surface zones are the centers for remineralization; the body of the lesion and the translucent zones are centers for demineralization. 2. A, D, and Ecorrect. Bincorrect. The MS usually precede the lactobacilli. Cincorrect. The bacteria-producing soluble glucans often are noncariogenic because of adherence problems; the insoluble glucans are usually produced by the cariogenic bacteria and facilitate adherence. 3. B, D, and Ecorrect. Aincorrect. The critical pH for enamel demineralization is from 5.5 to 5.0. Cincorrect. The same zones are present but are less clearly defined because of the presence of bacteria, plaque, and debris. 4. A, B, C and Dcorrect. Eincorrect. No studies to date indicate that "deep remineralization" by use of fluoride therapy is or is not an appropriate method of caries control. There is a theoretical basis, much research, and a plethora of hope and enthusiasm for this approach to nonrestorative "repair" of teeth. (What sugar hath rendered asunder, humankind is now laboring to correct!) ^ 1. In 1890, Miller proposed the ________________________ theory for caries, which is still (with many modifications) a basis for our present concept of the dental caries. 2. The beginning and end-points of a carious lesion are the _____________ (initial) lesion, which can be arrested or reversed by remineralization therapy, and the _____________ (end point) lesion, which must be restored. 3. The four zones of an incipient lesion seen with the polarizing microscope (starting from the tooth surface) are the _____________, _____________, _____________, and the _____________ zones. 4. The zone of the incipient lesion that is the best indicator of remineralization is the _____________ zone; the two zones of demineralization are the _____________ and the _____________ zones. 5. As the pH drops in the environment of the HAP, the sa _____________n of calcium and phosphate in the environment must increase in order to protect the crystals. The presence of _____________ (element) will also help to protect the crystal at a lower pH. 6. The critical pH for enamel demineralization is within the generally accepted range of pH _____ to _____. 7. The diagramming of the drop and recovery of pH on a graph is often referred to as the __________ curve for the investigator who first published on the phenomenon. 8. Two possible sources of the calcium and phosphate accounting for the hypermineralized surface of root caries are _____________ and _____________. 9. The four major types (location) of caries are: _____________, _____________, _____________, and _____________. 10. Two causes for rampant caries are _____________ (dietary "food") and _____________ (dry mouth). 11. The pore space in both the translucent and surface zones is 1 percent; dark zone approximately ____ percent, and the body of the lesion ranges up to ____ percent. References 1. Kim, J. W., Jang, K. T., Lee, S. H., et al. (2001). In vivo rehardening of enamel eroded by cola drink. J Dent Child, 68:122-24. 2. Aftin, T., Buchalla, W., Gollner, M., & Hellwig, E. (2000). Use of variable remineralization periods to improve the abrasion resistance of previously eroded enamel. Caries Res, 34:48-52. 3. Ring, M. E., Ed. (1985). Dentistry: An illustrated history. New York: Harry N. Abrams, Inc. 4. A practical treatise on the diseases of the teeth, in which the origine and nature of decay are explained: and a means of prevention pointed out. Ed. William Robertson. Longman, Rees, Brown, Green and Longman. Paternosterrow, and J. Belcha and Son, Birmingham. 1835. 5. Miller, W. D. (1973). The microorganisms of the human mouth. Philadelphia: SS White Dental Manufacturing Company; 1890. Reprinted Basel, Switzerland: Karger. 6. Black, G. V. (1898). Dr. Black's conclusions reviewed again. Dental Cosmos, 40:440-51. 7. Smith, O. E., & Nanci, A. (1995). Overview of morphological changes in enamel organ cells associated with major events in amelogenesis. Int J Dev Biol, 39:153-61. 8. Diekwisch, T. G. (1998). Subunit compartments of secretion of secretory enamel matrix. Connect Tissue Res, 38:101-11; discussion 139-45. 9. Wen, H. B., Finchan, A. G., & Moradian-Oldak, J. (2001). Progressive accretion of amelogenin molecules during nanospheres assembly revealed by atomic force microscopy. Matrix Biol, 20:387-99. 10. Moradian-Oldak, J. (2001). Amelogenins: Assembly, processing and control of crystal morphology. Matrix Biol, 20:293-305. 11. Robinson, E., Brooks, S. J., Shore, R. C., & Kirkham, J. (1998). The developing enamel matrix: nature and function. Eur J Oral Sci, 106:282-91. 12. Simoner, J. P., & Hu, J. C. (2001). Dental enamel formtion and its impact on clinical dentistry. J Dent Educ, 65:896-905. 13. Smith, C. E. (1998). Cellular and chemical events during enamel maturation. Crit Rev Oral Biol Med, 9:128-61. 14. Robinson, C., Kirkham, J., Brooks, S. J., Borass, W. A., & Shore, R. C. (1995). The chemistry of enamel development. Int J Dev Biol, 39:145-52. 15. Moradian-Oldak, J., Leung, W., Tan, J., & Fincham, A. G. (1998). Effect of apatite crystals on the activity of amelogen degrading enzymes in vitro. Conn Tissue Res, 39:131-40. 16. Crabb, H. S. M. (1976). The porous outer enamel of unerupted human premolars. Caries Res, 10:1-7. 17. Dodds, M. W. J. (1993). Dilemmas in caries diagnosisapplications to current practice, and need for research. J Dent Educ, 57:433-38. 18. Silverstone, L. M. (1973). The structure of carious enamel, including the early lesion. Oral Sci Rev, 3:100-60. 19. Konig, K. G. (1963). 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Longitudinal investigation of bacteriology of human fissure decay: Epidemiological studies in molars shortly after eruption. Infect Immun, 46:765-72. 38. Van Houte, J., Sansone, C., Joshipura, K., & Kent, R. (1991). In vitro acidogenic potential and mutans streptococci on human smooth-surface plaque associated with initial caries lesions and sound enamel. J Dent Res, 70:497-502. 39. Edelstein, B., & Tinanoff, N. (1989). Screening preschool children for dental caries using a microbial test. Pediatr Dent, 11:129-32. 40. Geddes, D. A. M. (1975). Acids produced by human dental plaque metabolism in situ. Caries Res, 9:98-109. 41. Gibbons, R. J. (1964). Bacteriology of dental caries. J Dent Res, 43:1021-28. 42. Burne, R. A. (1998). Oral streptococci . . . Products of their environment. J Dent Res, 77:445-52. 43. Quivey, R. G., Kuhnert, W. L., & Hahan, K. (2001). Genetics of acid adaption in oral streptococci. Crit Rev Oral Biol Med, 12:301-14. 44. Brown, L. R., Dreizen, S., & Handler, S. (1976). Effects of elected caries regimens on microbial changes following radiation-induced xerostomia in cancer patients. In Stiles, H. M., Loesche, W. J., & O'Brien, T. C., Eds. Proceedings: Microbial Aspects of Dental Caries. Washington, DC: Information Retrieval, 275-290. 45. Gibbons, R. J. (1989). Bacterial adhesion to oral tissues: A model for infectious diseases. J Dent Res, 668:750-760. 46. Jenkinson, H. F. (1994). Adherence and accumulation of oral streptococci. Trends Microbiol, 2:209-12. 47. Murchison, H., Larrimore, S., & Curtiss, R. (1985). In vitro inhibition of adherence of Streptococcus mutans strains by nonadherent mutants of S. mutans 6715. Infect Immun, 50:826-32. 48. Littleton, N. W., McCabe, R. M., & Carter, C. H. (1967). Studies of oral health in persons nourished by stomach tube. II. Acidogenic properties and selected bacterial components of plaque material. Arch Oral Biol, 12:601-9. 49. De Stoppelar, S. D., van Houte, J. S., & Backer-Dirks, O. (1970). The effect of carbohydrate restriction on the presence of Streptococcus mutans, Streptococcus sanguis and iodophilic polysaccharide-producing bacteria in human dental plaque. Caries Res, 4:114-23. 50. Dodds, M. W. J., & Edgar, W. M. (1986). Effects of dietary sucrose levels on pH fall and acid-anion profile in human dental plaque after a starch mouthrinse. Arch Oral Biol, 31:509-12. 51. Sgan-Cohen, H. D., Newbrun, E., Huber, R., Tenebaum, G., & Sela, M. N. (1988). The effect of previous diet on plaque pH response to different foods. J Dent Res, 67:1434-37. 52. Zickert, I., Emilson, C-G, & Krasse, B. (1982). Effect of caries preventive measures in children highly infected with the bacterium Streptococcus mutans. Arch Oral Biol, 27:861-68. 53. Carlsson, J., Grahnen, H., & Jonsson, G. (1975). Lactobacilli and streptococci in the mouth of children. Caries Res, 9:333-9. 54. Suhonen, J. (1992). Mutans streptococci and their specific oral target: New implications to prevent dental caries. Schweiz Monafsschr Zahnmed, 102:286-91. 55. Alalluusia, S. (1991). Transmission of mutans streptocci. Proc Finn Dent Soc, 87:443-7. 56. Kohler, B., & Bratthall, D. (1978). Intrafamilial levels of Streptococcus mutans and some aspects of the bacterial transmission. Scand J Dent Res, 86:35-42. 57. Zickert, I., Emilson, C-G., & Krasse, B. (1983). Correlation of level and duration of Streptococcus mutans infection with incidence of dental caries. Infect Immun, 39:982-85. 58. Carlsson, J., Soderholm, G., & Almfedt, I. (1969). Prevalence of Streptococcus sanguis and Streptococcus mutans in the mouth of persons wearing full-dentures. Arch Oral Biol, 14:243-49. 59. Avery, J. K. (2000). Essentials of oral histology and embryology: A clinical approach (2nd ed.) St Louis, MO: Mosby, Inc., 94-106. 60. Silverstone, L. M., & Hicks, M. J. (1985). The structure and ultra structure of the carious lesion in human dentin. Gerodontics, 1:185-93. 61. Pashley, D. H., & Matthews, W. G. (1993). The affects of outward forced convective flow on inward diffusion in human dentine in vitro. Arch Oral Biol, 38:577-82. 62. Ciucchi, B., Bouillaguet, S., Holz, J., & Pashley, D. (1995). Dentinal fluid dynamics in human teeth, in vivo. J Endod, 21:919-4. 63. Heyeraas, K. J., & Berggreen, E. (1999). Insterstitial fluid pressure in normal and inflamed puls. Crit Rev Oral Biol Med, 10:328-36. 64. Hahn, C. L., & Overton, B. (1997). The effects of immunoglobulins on the convective permeability of human dentine in vitro. Arch Oal Biol Med, 42:835-43. 65. Pashley, D. H. (1996). Dynamics of the pulpo-dentin complex. Crit Rev Oral Biol Med, 7:104-33. 66. Pashley, D. H. (1992). Dentin permeability and dentine sensitivity. Proc Finn Dent Soc, 88: Suppl. 1;31:13-7. 67. Pashley, D. H. (1991). Clinical correlations of dentin structure and function. J Prosthet Dent, 66:777-81. 68. ten Cate, J. M. (2001). Remineralization of caries lesions extending into dentin. J Dent Res, 80:1407-11. 69. Tugnait, A., & Clerehugh, V. (2001). Gingival recessionits significance and management. J Dent, 29:381-94. 70. Katz, R. V., Hazen, S. P., Chilton, N. W., & Mumm, R. D. Jr. (1982). Prevalence and intraoral distribution of root caries in an adult population. Caries Res, 16:265-71. 71. Winn, D. M., Brunelle, J. A., Selwitz, R. H., Oblakowski, R. J., Kingmon, A. & Brown, L. J. (1996). Coronal and root caries in the dentition of adults in the United States, 1988-1991 J Dent Res, 75:642-51. 72. Locker, D., Slade, G. D., & Leake, J. L. (1989). Prevalence of and factors associated with root decay in older adults in Canada. J Dent Res, 68:768-72. 73. Vehkalahti, M. M., & Paunlo, I. K. (1988). Occurrence of root caries in relation to dental health behavior. J Dent Res, 67:911-14. 74. Banting, D. W. (1986). Epidemiology of root caries. Gerodontology, 5:5-11. 75. Jordan, H. V., & Hammond, B. F. (1972). Filamentous bacteria isolated from human root surface caries. Arch Oral Biol, 17:1333-42. 76. Sumney, D., & Jordan, H. (1974). Characterization of bacteria isolated from human root surface carious lesions. J Dent Res, 63:343-51. 77. Van Houte, J., Jordan, H. V., Laraway, R., Kent, R., Sopark, P. M., & DePaula P. F. (1990). Association of the microbial flora of dental plaque and saliva with human root-surface caries. J Dent Res, 69:1463-68. 78. Bowden, G. H. W. (1990). Microbiology of root surface caries in humans. J Dent Res, 69:1205-10. 79. Dung, S. Z. (1999). Effects of mutans streptococci, Actinomyces species and Porphyromona gingivalis on collagen degenerations. Chung Hua I, Hsueh Tsa Chihi (Taipai). 62:764-74. 80. Mellberg, J. R. (1986). Demineralization and remineralization of root surface caries. Gerodontology, 5:25-31. 81. Nyvad, B., & Fejerskov, O. (1986). Active root surface caries converted into inactive caries as a response to oral hygiene. Scand J Dent Res, 94:281-84. 82. Schupbach, P., Lutz, F., & Guggenheim, B. (1992). 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The relationship between plaque pH, plaque acid anion profiles and oral carbohydrate retention after ingestion of several 'reference foods' by human subjects. J Dent Res, 67:861-65. 96. ten Cate, J. M. (1992). Saliva a physiological medium. Ned Tijdschr Tandheelkr, 99:82-4. 97. ten Cate, J. M. (2001). Remineralization of caries lesions extending into dentin. J Dent Res, 80:1407-11. 98. Ogaard, B. (1999). The cariostatic mechanism of fluoride. Comp Contin Educ Dent, 20 (1 Suppl):10-17. 99. ten Cate, J. M., & Loveren, van Cor (1999). Fluoride mechanisms. Dent Clinics Nor Amer, 43:713-42. 100. Rosin-Grget, K., & Lincir, J. (2001). Current concept on the anticaries fluoride mechanism of the action. Coll Antropol, 25:703-12. 101. Gaffar, A. (1998). Treating hypersensitivity with fluoride varnishes. Comp Cont Edu Dent, 19:1088-90. 102. Beltran-Aguilar, E. D., Goldstein, J. W., & Lockwood, S. A. (2000). Fluoride varnishes. A review of their clinical use, cariostatic mechanisms, efficacy and safety. JADA, 131:589-96. 103. Seppa, L. (1991). Studies of fluoride varnishes in Finland. Proc Finn Dent Soc, 87:541-47. 104. Autio-Gold, J. T., & Courts, F. (2000). Assessing the effect of fluoride varnish on early enamel carious lesions in the primary dentition. JADA, 132:1247-53. 0.125 Copyright © 2004 by Pearson Education, Inc., Pearson Prentice Hall. All rights reserved. ![]() ![]() ![]() ![]() ![]() |
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