REVIEW

Australian Dental Journal 2006;51:(4):284-289

Prevention of white spot lesions in orthodontic practice: a contemporary review

TR Sudjalim,* MG Woods, DJ Manton

Abstract The development of white spot demineralization associated with fixed appliance orthodontic treatment is a significant clinical problem. Both established and experimental methods for prevention of such lesions in day-to-day clinical practice are presented and discussed.
Key words: White spot lesions, orthodontics, prevention. Abbreviations and acronyms: ACP = amorphous calcium phosphate; CPP = casein phosphopeptide; CPP-ACP = casein phosphopeptide-amorphous calcium phosphate. (Accepted for publication 28 March 2006.)

Overall management of white spot lesions involves consideration of methods of preventing demineralization and also methods of encouraging remineralization of existing lesions. Preventive measures take precedence, due to the challenging nature of treating patients who do develop significant numbers of white spot lesions. In addition to regular professional oral hygiene visits and the application of appropriate preventive medicaments, successful preventive strategies involve oral health promotion, patient education and patient compliance. This article reviews the relevant historical and contemporary literature regarding methods available to prevent the formation of these white spot lesions during orthodontic treatment. Aetiology of demineralization White spot lesions develop as a result of a dietary carbohydrate and saliva modified bacterial infection, resulting in an imbalance between demineralization and remineralization of the enamel.5 This is an interrupted process, with periods of remineralization and demineralization occurring, depending on the state of the oral environment in terms of the prolonged accumulation and retention of bacterial plaque on the enamel surface, the standard of individual oral hygiene and the inherent resistance of that person.5-7 A white spot lesion is the precursor of frank enamel caries. The white appearance of early enamel caries is due to an optical phenomenon which is caused by mineral loss in the surface or subsurface enamel. Enamel crystal dissolution begins with subsurface demineralization, creating pores between the enamel rods. The resultant alteration of the refractive index in the affected area is then a consequence of both surface roughness and loss of surface shine and alterations in internal reflection, all resulting in greater visual enamel opacity, as porous enamel scatters more light than sound enamel.2,8 The demineralization process may encompass the full thickness of the enamel and some of the dentine before the relatively hypermineralized surface layer is actually lost. It is generally accepted that the insertion of fixed orthodontic appliances creates stagnation areas for plaque and makes tooth cleaning more difficult. The irregular surfaces of brackets, bands, wires and other
Australian Dental Journal 2006;51:4.

INTRODUCTION The demineralization of enamel adjacent to orthodontic brackets is a significant clinical problem. White spot lesions develop as a result of prolonged plaque accumulation on the affected surface, commonly due to inadequate oral hygiene. It has been reported that there is a significant increase in the prevalence and severity of enamel demineralization after orthodontic treatment when compared with untreated control subjects (Fig 1). The overall prevalence of white spot lesions amongst orthodontic patients has been reported as anywhere between 2 and 96 per cent.1-4 Once active orthodontic treatment has been completed, the demineralization process is normally expected to decelerate due to a change in local environmental factors. Some white spot lesions may remineralize and return either to normal or at least to a visually acceptable appearance. However, white spot lesions may also persist, resulting in an aesthetically unacceptable result. In severe cases, restorative treatment may be required.

*Orthodontic graduate student, School of Dental Science, The University of Melbourne. Professor and Chair of Orthodontics, School of Dental Science, The University of Melbourne. Lecturer in Paediatric Dentistry, School of Dental Science, The University of Melbourne.
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Fig 1. Extensive white spot lesion development during active orthodontic treatment.

attachments also limit naturally occurring selfcleansing mechanisms, such as the movement of the oral musculature and saliva.9 This in turn encourages a lower plaque pH in the presence of carbohydrates and accelerates the rate of plaque accumulation and plaque maturation. These changes in the local environment appear to favour colonization of aciduric bacteria such as Streptococcus mutans and lactobacilli. It has been previously reported that S. mutans levels can increase up to fivefold during orthodontic treatment. However, such microbial levels were found to decrease significantly to levels comparable with age-matched controls, 6 to 15 weeks into a retention phase, after the removal of fixed appliances.9 These findings suggest that, while orthodontic treatment may result in temporary elevations in salivary S. mutans levels in some individuals, the use of antimicrobials, such as chlorhexidine, may not be warranted in all orthodontic patients. Prevention of white spot lesions 1. Patient education In the majority of cases, orthodontic treatment will span over a period of some years and the presence of
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fixed orthodontic appliances may reduce the oral hygiene capabilities of orthodontic patients to suboptimal levels. In turn, this may predispose the enamel surfaces, in particular the area between the bracket and gingival margin, to the increased accumulation of bacterial plaque. It has been reported that there is a significant association between poor compliance with home care preventive procedures and the formation of white spot lesions, with no statistically significant differences in the compliance levels of males and females or amongst varying age groups.10 Professional oral hygiene instruction and regular professional cleaning has been shown to be effective in reducing decalcification, especially when the degree of compliance with the recommended home care preventive protocol is poor.10 Unfortunately, this approach is quite labour intensive and may have been impractical in traditional orthodontic practices. More recently however, the integration of dental hygienists and therapists into orthodontic practices has facilitated the provision of regular oral hygiene instruction and professional cleaning. However, whilst such periodic reinforcement by any clinician may help to remotivate a patient, permanently changing patient behaviour is reported to be a difficult process.10 Verbally praising and re-educating the patient regarding the consequences of poor oral hygiene compliance have been found to be very effective methods of improving patient cooperation.11 Twice daily toothbrushing is recommended by many clinicians as an essential part of a daily plaque control programme for all orthodontic patients. Many manual and electric toothbrushes are available, with conflicting reports of the effectiveness of the two types of brushes. Previous studies investigating the relative effectiveness of manual versus electric toothbrushes in orthodontic populations have shown equivocal results.12 More recently, it has been reported that patients who have poor oral hygiene may achieve better results with the use of electric toothbrushes, because plaque removal may be more easily accomplished with the active heads.13 These findings would be consistent with the reports of a recent review in non-orthodontic patients that brushes with a rotation oscillation action can remove plaque and reduce gingivitis more effectively than manual brushes in the short term.14 2. Fluoride administration The fact that fluoride can be integrated into the crystalline lattice of dental enamel resulting in a structure that is more resistant to the onset of dissolution provides the scientific basis for its use in caries prevention.15 Fluoride ions can be incorporated into the hydroxyapatite structure of tooth enamel by the replacement of hydroxy groups or by the redeposition of dissolved hydroxyapatite as less soluble fluoridated forms, such as fluorapatite or fluorhydroxyapatite.16 Calcium fluoride is the major reaction product of topical fluoride treatment of enamel, and it has been found to play a significant role in the cariostatic
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mechanism of fluoride. Calcium fluoride may persist in dental plaque as calcospherites on the enamel surface for several weeks after a topical application, having the potential to be incorporated into the crystal lattice as fluorapatite during pH cycling within the plaque.3,8 During orthodontic treatment, fluoride can be administered to the teeth in various ways, including topical (fluoridated toothpaste, mouthrinse, gel and varnish) and adhesive (fluoride-releasing cements and elastomeric modules and chains) methods. (A) Water fluoridation and community-based fluoride distribution programmes The prevalence of dental caries has been shown to have declined in most industrialized countries over the past 25 years.17,18 Repeated evaluations of the effectiveness and efficiency of fluoride programmes have confirmed that the reduction in the incidence of dental caries would appear to be directly related to the introduction of community-based fluoride distribution programmes and the wide availability of fluoride toothpastes.17 During the early years of water fluoridation (1940s to 1960s), caries levels in fluoridated communities were approximately 50 per cent lower than those in communities without water fluoridation.17,19 The first studies on school-based fluoride rinsing programmes in the 1960s and 1970s also demonstrated a 3050 per cent reduction in caries increment within two to three years of the initial introduction of fluoride into the water supply.20 This significant reduction in the prevalence of dental caries has been widely attributed to the continuous exposure of the dentition to fluoride in saliva and plaque fluid.5,21 The preventive effects of topical fluorides have been found to be greater than their remineralizing effects because of their considerable ability to decrease the solubility of minerals within the crystal lattice.22 (B) Fluoride toothpaste, mouthrinses and gels Whether further benefits can be achieved with the application of topical fluorides (such as fluoride mouthrinses, gels and varnishes), in addition to the measures of fluoride toothpaste and community water fluoridation is questionable, with various clinical trials showing inconsistent results.23-26 In a recent systematic literature review evaluating the effectiveness of fluoride in preventing white spot lesion development during orthodontic treatment, it was shown that the use of daily sodium fluoride mouthrinse or the use of glass ionomer cement for bonding brackets can reduce the severity of enamel demineralization surrounding orthodontic appliances.23 Other fluoride delivery methods which have been reported to reduce the demineralization of enamel surrounding orthodontic brackets include the daily use of toothpastes and/or gels with a high fluoride concentration (15005000ppm) or fluoride toothpaste in combination with chlorhexidine mouthwash.24 Recently, it was suggested that individuals undergoing orthodontic treatment should brush twice
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daily with a 5000ppm fluoride dentrifice. This regime was reported to provide much greater prevention than the daily use of 1000ppm fluoride toothpaste in combination with the daily use of a 500ppm sodium fluoride rinse.25 Other clinical studies evaluating the effectiveness of fluoride programmes in orthodontic patients have shown contrasting results. For instance, in a three-year longitudinal clinical study investigating the combined effects of the daily use of 7600ppm fluoride toothpaste and 500ppm sodium fluoride mouthrinse, it was found that the combined use of these products did not produce any additional benefits to the use of either product alone.26 This result was also confirmed by an in situ study.27 The results of these investigations led to a recommendation that the daily use of a fluoridated mouthrinse might be omitted from orthodontic home care program.26,28 However, caution regarding this recommendation should be taken in the non-compliant patient, who may use the combination of fluoride toothpaste and mouthwash somewhat irregularly. In such patients, the use of any fluoridated product would probably be beneficial. (C) Fluoride varnishes The professional application of fluoride varnish is a preventive method requiring little patient compliance only attendance at the dental practice. In addition to the fluoride mechanisms mentioned previously, the application of a fluoride varnish provides a protective coating over the tooth surface which decreases enamel solubility.29 Fluoride varnish adheres to the enamel surface longer than other topical fluoride products and has been shown to be superior to the use of sodium fluoride and monofluorophosphate toothpastes, weekly acidulated phosphate fluoride gel application and daily sodium fluoride rinses because of its ability to increase fluoride uptake in enamel in vitro.30 Overall, the efficacy of regular application of fluoride varnish appears to reduce lesion formation on bracketed maxillary incisor teeth.29,31 Fluoride varnish also provides additional preventive benefits when brackets have been bonded with composite resin cement (Transbond; 3M Unitek, Monrovia, California, USA). The varnish does not, however, seem to produce any significant additional preventive benefits for brackets that have been bonded with resin modified glass ionomer cement (Fuji Ortho LC; GC Corp., Japan).32 Three monthly re-applications of the varnish are required, however, as the varnish is abraded by toothbrushing and oral function within just a few days.29 (D) Fluoride in orthodontic bonding agents In an attempt to achieve compliance-free, constant exposure to topical fluoride, fluoride-releasing bonding agents were developed. In the late 1980s, glass ionomer cements were proposed as an alternative to the more commonly used composite material for bracket bonding. The proposed benefits of using glass ionomer cements
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included the lack of need for pretreating the enamel with phosphoric acid to create conditions for mechanical bonding, the release of fluoride over several months and the possible development of a modified, less cariogenic microflora.33 However, significant concerns regarding the reduction in both shear and tensile bond strengths of glass ionomer cements when compared with composite resin cements in both in vivo and in vitro studies have limited their clinical use.34 The efficacy of fluoride-releasing cements in inhibiting enamel demineralization has been reported to be localized to the area around the bracket.35 The cariostatic effect is attributed to the fluoride release of both glass ionomer and resin modified glass ionomer cements, and has been reported to occur for longer periods and with greater fluoride release levels than with fluoride-containing composites or compomer cements. Most fluoride-releasing bonding cements show similar fluoride-releasing trends, with the highest levels of fluoride release occurring during the first few days after bonding, then declining to lower but more stable rates thereafter.35-37 When compared with glass ionomer and resin modified glass ionomer cements, fluoride-releasing composite resin cements have been reported to release smaller concentrations of fluoride over time, with fluoride release rates varying significantly between different commercial products.38 The reduction in white spot lesion formation with the use of glass ionomer cement for bonding in orthodontics can be significant, with an average 16.5 per cent reduction having been achieved when compared with the use of composite resin cements in one longitudinal study of 60 patients.38 An equivalent level of protection against enamel demineralization has also been reported with the use of either a resin modified glass ionomer cement alone, or a composite resin cement in combination with daily topical fluoride application.37 It has been suggested, however, that a high caries susceptibility might still be expected to overcome these local protective effects of fluoride released from glass ionomer and resin modified glass ionomer cements.35 (E) Fluoride in elastomeric modules and ligature ties The use of elastomeric modules and chains to deliver forces for space closure and controlled tooth movement is common in contemporary orthodontic practice. Fluoride-releasing elastomeric auxiliaries have not been popular, however, largely due to apparent compromised force delivery and inconsistent fluoride release.39,40 The commonly reported in vitro pattern of fluoride release from such elastomeric products includes an initial burst of fluoride release during the first 24 to 48 hours. The amount of fluoride release then appears to decrease in a logarithmic pattern.39,40 In an in vitro study, it was shown that more than 85 per cent of the total fluoride content of elastomeric chains or modules may have leached out as early as 14 days after placement, requiring the elastomeric auxiliary to be replaced regularly to obtain optimum clinical benefit.40 The use
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of such elastomeric auxiliaries would have to be questioned in the current climate with a move towards widespread use of so-called self-ligating bracket systems. 3. Casein phosphopeptide-amorphous calcium phosphate The role of casein phosphopeptide-amorphous calcium phosphate (CPP-ACP) in decreasing the incidence of dental caries in the community is anticipated to be additive to the beneficial effects of topical fluoride.41 The topical anticariogenic effect of dairy products in both animal and human in situ caries models has led to the production of casein phosphopeptides (CPP) and their accepted ability to stabilize calcium and phosphate in an amorphous state.41-44 The CPP molecules contain a cluster of phosphoseryl residues which markedly increase the apparent solubility of calcium phosphate by stabilizing amorphous calcium phosphate (ACP) under neutral and alkaline conditions. The multiple phosphoseryl residues of the CPP bind to nanoclusters of ACP in supersaturated solutions, thereby preventing growth to the critical size required for phase transformations.41,45 The proposed anticariogenic mechanism of CPPACP involves the incorporation of the nanocomplexes into dental plaque and onto the tooth surface, thereby acting as a calcium and phosphate reservoir. Studies have shown that CPP-ACP incorporated into dental plaque can significantly increase the levels of plaque calcium and phosphate ions.43,44,46 This mechanism is ideal for the prevention of enamel demineralization as there appears to be an inverse association between plaque calcium and phosphate levels and measured caries experience.46 The localized CPP-ACP nanocomplexes subsequently act to buffer free calcium and phosphate ions in the plaque fluid, in order to maintain a state of supersaturation of ACP with respect to enamel mineral, thereby limiting enamel demineralization and enhancing remineralization.43,46 In addition, immunolocalization studies have revealed that CPPACP can be incorporated into supragingival dental plaque by binding to the surfaces of bacterial cells, to components of the intercellular plaque matrix and to adsorbed macromolecules on the tooth surface. All these interactions may then lead to the formation of a less cariogenic plaque.47 CPP-ACP has been incorporated into various products in order to exert a topical effect. These products include commercially available sugar-free chewing gum (Recaldent; GC Corp., Japan and Trident White; Cadbury Adams USA, Parsippany, New Jersey, USA), mints (Recaldent Mints; Cadbury Japan Ltd., Japan), topical gels (Tooth Mousse; GC Corp., Japan) and experimentally-tested sports drinks and glass ionomer cements.44,46,48,49 In CPP-ACP containing sugar-free chewing gum and mint in-situ trials, it was demonstrated that daily topical exposure to CPP-ACP resulted in a dose-related increase in enamel
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of artificially demineralized remineralization subsurface enamel lesions, with an increase in enamel mineralization of 78 to 176 per cent compared with control samples.46,48 In addition, the consumption of chewing gum and mints has been demonstrated to result in the increased production of stimulated saliva. Such stimulated saliva has been shown to contain increased calcium and phosphate ionic concentrations when compared with non-stimulated saliva.50 Enamel lesions which have been remineralized with topical exposure to CPP-ACP have been shown to be more resistant to subsequent acid challenge compared with normal remineralized enamel as CPP-ACP is able to promote the remineralization of enamel subsurface lesions with hydroxyapatite. In addition, the relatively low carbonate environment of the CPP-ACP treated subsurface lesion may also exhibit both improved crystallinity and lower microstrain than might be found in normal tooth enamel.51 4. Argon-laser enamel surface attenuation The results of recent studies would suggest that argon laser may be used to prevent enamel decalcification by altering the crystalline structure of enamel.52-54 It has been reported that enamel exposure to argon laser irradiation results in the alteration of the surface characteristics of the enamel by creating microspaces that stabilize ions during an acid attack rather than allowing them to be lost from the enamel.53 The available calcium, phosphate and fluoride ions in saliva may then precipitate into these microspaces, increasing the resistance of the enamel to demineralization and increasing the uptake of minerals from saliva.53,54 Further in vivo and in vitro studies are required in order to establish the optimal fluence (energy density) for argon laser administration in order to simultaneously prevent enamel decalcification and achieve curing of bonding cements.53 CONCLUSIONS The development of white spot lesions during fixed appliance orthodontic treatment is preventable. The chosen method or methods for prevention will be largely dependent on the individual needs of each patient and the opinion of the clinician. White spot lesions are generally considered to be the precursors of frank enamel carious lesions. It is therefore necessary to universally promote the need to maintain a high standard of oral hygiene and to reduce daily exposure to refined carbohydrates throughout the treatment period. In addition, the continuous presence of fluoride in both saliva and plaque, even in low concentrations, is necessary for maximum caries inhibition. This would, at first, involve daily exposure to fluoridated water (where available) and the use of a fluoride containing toothpaste. The need to prescribe an additional topical fluoride will be dependent upon the needs of the individual patient and clinical judgment. The performance of currently available fluoride-releasing
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bonding cements and elastomeric modules and chains makes their use both difficult and impractical. Studies of the effects of CPP-ACP have so far shown promising dose-related increases in enamel remineralization within already demineralized enamel lesions. The ability of CPP-ACP to prevent white spot lesion formation has not, as yet, been proven. REFERENCES
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22. OReilly MM, Featherstone JD. Demineralization and remineralization around orthodontic appliances: an in vivo study. Am J Orthod Dentofacial Orthop 1987;92:33-40. 23. Benson PE, Shah AA, Millett DT, Dyer F, Parkin N, Vine RS. Fluorides, orthodontics and demineralization: a systematic review. J Orthod 2005;32:102-114. 24. Derks A, Katsaros C, Frencken JE, vant Hof MA, KuijpersJagtman AM. Caries-inhibiting effect of preventive measures during orthodontic treatment with fixed appliances. A systematic review. Caries Res 2004;38:413-420. 25. Alexander SA, Ripa LW. Effects of self-applied topical fluoride preparations in orthodontic patients. Angle Orthod 2000;70:424-430. 26. Blinkhorn AS, Holloway PJ, Davies TG. Combined effects of a fluoride dentifrice and mouthrinse on the incidence of dental caries. Community Dent Oral Epidemiol 1983;11:7-11. 27. al-Khateeb S, ten Cate JM, Angmar-Mansson B, et al. Quantification of formation and remineralization of artificial enamel lesions with a new portable fluorescence device. Adv Dent Res 1997;11:502-506. 28. Bergstrand F, Twetman S. Evidence for the efficacy of various methods of treating white-spot lesions after debonding of fixed orthodontic appliances. J Clin Orthod 2003;37:19-21. 29. Demito CF, Vivaldi-Rodrigues G, Ramos AL, Bowman SJ. The efficacy of a fluoride varnish in reducing enamel demineralization adjacent to orthodontic brackets: an in vitro study. Orthod Craniofac Res 2004;7:205-210. 30. Arends J, Lodding A, Petersson LG. Fluoride uptake in enamel. In vitro comparison of topical agents. Caries Res 1980;14:403413. 31. Ogaard B, Larsson E, Henriksson T, et al. Effects of combined application of antimicrobial and fluoride varnishes in orthodontic patients. Am J Orthod Dentofacial Orthop 2001;120:28-35. 32. Schmit JL, Staley RN, Wefel JS, Kanellis M, Jakobsen JR, Keenan PJ. Effect of fluoride varnish on demineralization adjacent to brackets bonded with RMGI cement. Am J Orthod Dentofacial Orthop 2002;122:125-134. 33. Matalon S, Slutzky H, Weiss EI. Antibacterial properties of 4 orthodontic cements. Am J Orthod Dentofacial Orthop 2005;127:56-63. 34. Graf I, Jacobi BE. Bond strength of various fluoride-releasing orthodontic bonding systems. Experimental study. J Orofac Orthop 2000;61:191-198. 35. Gorton J, Featherstone JD. In vivo inhibition of demineralization around orthodontic brackets. Am J Orthod Dentofacial Orthop 2003;123:10-14. 36. McNeill CJ, Wiltshire WA, Dawes C, Lavelle CL. Fluoride release from new light-cured orthodontic bonding agents. Am J Orthod Dentofacial Orthop 2001;120:392-397. 37. Corry A, Millett DT, Creanor SL, Foye RH, Gilmour WH. Effect of fluoride exposure on cariostatic potential of orthodontic bonding agents: an in vitro evaluation. J Orthod 2003;30:323329. 38. Marcusson A, Norevall LI, Persson M. White spot reduction when using glass ionomer cement for bonding in orthodontics: a longitudinal and comparative study. Eur J Orthod 1997;19:233242. 39. Storie DJ, Regennitter F, von Fraunhofer JA. Characteristics of a fluoride-releasing elastomeric chain. Angle Orthod 1994;64:199209.

40. Wiltshire WA. Determination of fluoride from fluoride-releasing elastomeric ligature ties. Am J Orthod Dentofacial Orthop 1996;110:383-387. 41. Rose RK. Effects of an anticariogenic casein phosphopeptide on calcium diffusion in streptococcal model dental plaques. Arch Oral Biol 2000;45:569-575. 42. Reynolds EC, Johnson IH. Effect of milk on caries incidence and bacterial composition of dental plaque in the rat. Arch Oral Biol 1981;26:445-451. 43. Reynolds EC. Remineralization of enamel subsurface lesions by casein phosphopeptide-stabilized calcium phosphate solutions. J Dent Res 1997;76:1587-1595. 44. Shen P, Cai F, Nowicki A, Vincent J, Reynolds EC. Remineralization of enamel subsurface lesions by sugar-free chewing gum containing casein phosphopeptide-amorphous calcium phosphate. J Dent Res 2001;80:2066-2070. 45. Shaw L, Murray JJ, Burchell CK, Best JS. Calcium and phosphorus content of plaque and saliva in relation to dental caries. Caries Res 1983;17:543-548. 46. Reynolds EC, Cai F, Shen P, Walker GD. Retention in plaque and remineralization of enamel lesions by various forms of calcium in a mouthrinse or sugar-free chewing gum. J Dent Res 2003;82:206-211. 47. Rose RK. Binding characteristics of streptococcus mutans for calcium and casein phosphopeptide. Caries Res 2000;34:427-431. 48. Cai F, Shen P, Morgan MV, Reynolds EC. Remineralization of enamel subsurface lesions in situ by sugar-free lozenges containing casein phosphopeptide-amorphous calcium phosphate. Aust Dent J 2003;48:240-243. 49. Ramalingam L, Messer LB, Reynolds EC. Adding casein phosphopeptide-amorphous calcium phosphate to sports drinks to eliminate in vitro erosion. Pediatr Dent 2005;27:61-67. 50. Dawes C, Macpherson LM. Effects of nine different chewinggums and lozenges on salivary flow rate and pH. Caries Res 1992;26:176-182. 51. Iijima Y, Cai F, Shen P, Walker G, Reynolds C, Reynolds EC. Acid resistance of enamel subsurface lesions remineralized by a sugarfree chewing gum containing casein phosphopeptide-amorphous calcium phosphate. Caries Res 2004;38:551-556. 52. Oho T, Morioka T. A possible mechanism of acquired acid resistance of human dental enamel by laser irradiation. Caries Res 1990;24:86-92. 53. Elaut J, Wehrbein H. The effects of argon laser curing of a resin adhesive on bracket retention and enamel decalcification: a prospective clinical trial. Eur J Orthod 2004;26:553-560. 54. Anderson AM, Kao E, Gladwin M, Benli O, Ngan P. The effects of argon laser irradiation on enamel decalcification: An in vivo study. Am J Orthod Dentofacial Orthop 2002;122:251-259.

Address for correspondence/reprints: Professor Michael Woods School of Dental Science The University of Melbourne 720 Swanston Street Carlton, Victoria 3010 Email: mgwoods@unimelb.edu.au

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