Øgaard B. Prevalence of white spot lesions in 19-year-olds: a study on untreated and orthodontically treated persons 5 years after treatment. Am J Orthod Dentofacial Orthop. 1989; 96:423-427 https://doi.org/10.1016/0889-5406(89)90327-2
Scheie AA, Arneberg P, Krogstad O. Effect of orthodontic treatment on prevalence of Streptococcus mutans in plaque and saliva. Scand J Dent Res. 1984; 92:211-217 https://doi.org/10.1111/j.1600-0722.1984.tb00881.x
Andrucioli MC, Nelson-Filho P, Matsumoto MA Molecular detection of in-vivo microbial contamination of metallic orthodontic brackets by checkerboard DNA-DNA hybridization. Am J Orthod Dentofacial Orthop. 2012; 141:24-29 https://doi.org/10.1016/j.ajodo.2011.06.036
Øgaard B. White spot lesions during orthodontic treatment: mechanisms and fluoride preventive aspects. Semin Orthod. 2008; 14:183-193
Chapman JA, Roberts WE, Eckert GJ Risk factors for incidence and severity of white spot lesions during treatment with fixed orthodontic appliances. Am J Orthod Dentofacial Orthop. 2010; 138:188-194 https://doi.org/10.1016/j.ajodo.2008.10.019
Richter AE, Arruda AO, Peters MC, Sohn W. Incidence of caries lesions among patients treated with comprehensive orthodontics. Am J Orthod Dentofacial Orthop. 2011; 139:657-664 https://doi.org/10.1016/j.ajodo.2009.06.037
Øgaard B, Ten Bosch JJ. Regression of white spot enamel lesions. A new optical method for quantitative longitudinal evaluation in vivo. Am J Orthod Dentofacial Orthop. 1994; 106:238-242 https://doi.org/10.1016/S0889-5406(94)70042-7
Al-Khateeb S, Forsberg CM, de Josselin de Jong E, Angmar-Månsson B. A longitudinal laser fluorescence study of white spot lesions in orthodontic patients. Am J Orthod Dentofacial Orthop. 1998; 113:595-602 https://doi.org/10.1016/s0889-5406(98)70218-5
Artun J, Thylstrup A. Clinical and scanning electron microscopic study of surface changes of incipient caries lesions after debonding. Scand J Dent Res. 1986; 94:193-201 https://doi.org/10.1111/j.1600-0722.1986.tb01753.x
Marinho VC, Higgins JP, Sheiham A, Logan S. Fluoride toothpastes for preventing dental caries in children and adolescents. Cochrane Database Syst Rev. 2003; 2003 https://doi.org/10.1002/14651858.CD002278
Robinson C, Connell S, Kirkham J The effect of fluoride on the developing tooth. Caries Res. 2004; 38:268-276 https://doi.org/10.1159/000077766
Stecksén-Blicks C, Renfors G, Oscarson ND Caries-preventive effectiveness of a fluoride varnish: a randomized controlled trial in adolescents with fixed orthodontic appliances. Caries Res. 2007; 41:455-459 https://doi.org/10.1159/000107932
Jiang H, Hua F, Yao L Effect of 1.23% acidulated phosphate fluoride foam on white spot lesions in orthodontic patients: a randomized trial. Pediatr Dent. 2013; 35:275-278
Sonesson M, Twetman S, Bondemark L. Effectiveness of high-fluoride toothpaste on enamel demineralization during orthodontic treatment – a multicenter randomized controlled trial. Eur J Orthod. 2014; 36:678-282 https://doi.org/10.1093/ejo/cjt096
van der Kaaij NC, van der Veen MH, van der Kaaij MA, ten Cate JM. A prospective, randomized placebo-controlled clinical trial on the effects of a fluoride rinse on white spot lesion development and bleeding in orthodontic patients. Eur J Oral Sci. 2015; 123:186-193 https://doi.org/10.1111/eos.12186
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White spot lesions (WSL) are a commonly reported risk of fixed appliance orthodontic treatment. This article reviews the incidence, aetiology and effectiveness of prevention and management of WSLs with a relevant case report. An adolescent male had fixed-appliance treatment and developed WSLs, despite prevention advice and careful monitoring, the WSLs progressed and ultimately led to the need for early removal of his orthodontic appliances. Removal of appliances prevented further damage and allowed partial resolution of the WSLs.
CPD/Clinical Relevance: Careful monitoring of a patient's dental health during orthodontic treatment is essential; however, if oral health deteriorates, and demineralization occurs, rapid decisive action is necessary to limit irreversible damage.
Article
Decalcification, or demineralization, is the first clinically recognizable stage of enamel caries. The co-existence of plaque bacteria (mutans streptococci and lactobacilli), substrate, susceptible tooth surface and time are necessary for decalcification.1 Its incidence among patients undergoing fixed-appliance treatment varies greatly with sociodemographic areas and individual risk factors, but a commonly accepted incidence is that WSLs occur in up to half of orthodontic patients.2 The labio-gingival aspect of the maxillary lateral incisors has the highest incidence followed by mandibular buccal segment teeth, and the lowest is in the maxillary posterior region.3 These sites are most likely to be affected due to reduced salivary flow to these regions.4 They may also have an number of attachments which, along with the length of orthodontic treatment, are risk factors.5,6 WSLs are commonly graded via the index of Gorelick et al (Figure 1).1
The opaque appearance is due to subsurface mineral loss with increased porosity and optical changes in the enamel. The lesion is developed through repeated mineral loss during the dynamic process of repair and destruction. The pH and fluoride concentration of the oral environment directly affects diffusion of calcium and phosphate ions. Salivary flow rate may explain why, in some patients, there is minimal decalcification despite high plaque scores.8,9 While the surface is unchanged, arrest and reversal is still possible, however, if there is continued mineral loss then a point will be reached where the surface can no longer be reconstituted by remineralization, and cavitation may occur. Forceful probing may also take over cavitation.10
Lesions that develop in a highly fluoridated environment can become ‘sealed’ with fluoro-apatite on the surface. This arrests the lesion, but does not reverse it, because repair of the subsurface does not occur: the surface layer is well mineralized while the subsurface is hypomineralized and the opaque lesion remains. These lesions can persist for years after treatment and are an aesthetic concern.3,10 Therefore, the opacity of an advanced lesion will not respond to fluoride supplements. Initial surface lesions can, however, remineralize, and the opaque surface can regress completely once the main cause of decalcification, the fixed appliance, is removed and good oral hygiene practised.11,12 Regression of the lesion is primarily from surface abrasion along with some re-deposition of minerals.13
Prevention
First, any patient commencing fixed orthodontic appliance treatment must have an up-to-date assessment with their dentist, with excellent oral hygiene a prerequisite.14 Oral hygiene and anti-cariogenic dietary habits are necessary to prevent WSLs, and the evidence on this are covered comprehensively elsewhere.14,15 Fluoride supplements can also be used as an adjunct.
Fluoride
Fluoride ions adsorb onto the surface of enamel and stop dissolution, as well as increasing remineralization of the enamel. Fluoride is most effective when applied topically and is present at low concentrations in the mouth.16 Side-effects include skeletal and dental fluorosis caused by excessive fluoride intake. Skeletal fluorosis is a rare bone disease resulting in joint and bone pain, and may occur where fluoride concentration is unusually high in the drinking water (8 mg/L), or where there are very high levels of toothpaste consumption. Dental fluorosis occurs as opaque white areas to stained yellow dark brown pitted surfaces. There is no threshold dose, but its greatest risk is at early maturation while the dentition is developing. Patients who are over the age of 6 years are not generally at risk of dental fluorosis.17
There are numerous means of fluoride application, with evidence for WSL reduction summarized in Table 1. It is important to remember that fluoride supplements can only act as an adjunct, and the emphasis should be on good oral hygiene and dietary habits.
10,000ppm fluoride varnish applied to the teeth every 6 weeks at the fixed appliance adjustment appointment can have a significant reduction in WSL incidence
Guidance advises high-strength fluoride toothpaste for those in fixed appliances: 2800ppm for those over the age of 10 years and 5000ppm for those over 16 years
Mouth rinse (0.05%/225ppm) may be prescribed although, compared with a placebo, there is no significant difference in WSL incidenceIf it is prescribed as an additive measure, it must be used at a different time to brushing because the rinsing will clear away the toothpaste, which has a higher level of fluoride content (1450ppm)
May be used for bonding orthodontic brackets however a multi-centre RCT has found no difference in WSL incidence between standard composite bonding and resin modified glass ionomer cement (RMGIC) in orthodontic patients
In this Cochrane review, it was found overall, that there is not enough evidence to support a significant difference from: amine fluoride and stannous fluoride, fluoride-releasing materials, fluoride mouth rinse or varnish applicationThere is a low level of certainty that 12,300ppm fluoride foam or high fluoridated tooth paste 5000ppm may reduce WSL incidence
Treatment of WSLs
Treatment of WSLs involves a step-wise approach, that is the treatment of choice should be the least invasive that satisfies the aesthetic and functional needs of the patient. This will range from no treatment to more invasive restorative methods, such as composite restorations and veneers. It should be remembered that bleaching of teeth is well established for management of non-carious enamel defects; however, bleaching decalcification will only improve the shade of the surrounding tooth and not the lesion itself, making it appear worse.
No treatment
Most lesions undergo at least partial regression following the removal of fixed appliances and appropriate oral hygiene instruction.26 Therefore, a 3–6-month watch and wait approach before any intervention is a sound approach.
CPP-ACP
Casein phosphopeptide–amorphous calcium phosphate (GC Tooth Mousse, GC Corp, Japan) is derived from dairy products and can remineralize demineralized lesions.27
However, exposing white spot lesions to fluoride can create a hypermineralized surface layer of fluoro-apatite that prevents ionic ingress of calcium and phosphate into the body of the lesion, and so the opacity persists.28
CPP-ACP can deliver high concentrations of calcium and phosphate ions to promote remineralization and eliminate the opacity.29 It is available as a tooth mousse and is often administered via vacuum-formed retainers. The evidence is still equivocal, and further studies are required before remineralization agents can be routinely recommended for the treatment of white spot lesions.30
Micro-abrasion
Micro-abrasion involves removal of the superficial layer of enamel by applying an acid slurry to the tooth, and repeating this until the opacity has improved. In orthodontics, 18% hydrochloric acid is normally used, but 37% phosphoric acid has similar results.31
Aesthetics are improved via surface abrasion of the discoloured enamel and the creation of a lustrous sheen that significantly improves the white spot lesion.32,33 After micro-abrasion, vital bleaching may be performed if there is a yellow shine-through from the underlying dentine.
Resin infiltration
Resin infiltration is a minimally invasive process for treating white spots by optical manipulation and little, if any, tooth removal. The ICON (Infiltration CONcept, DMG, Germany) kit is commonly used.34 It involves applying 15% hydrochloric acid gel for 2 minutes, washing and drying, applying ethanol, and air drying for 30 seconds – this may be repeated until the patient is satisfied, and finally unfilled resin is applied, light cured and polished. It is effective in treating WSLs,35,36 as well as other white spots caused by fluorosis, hypomineralization and amelogenesis imperfecta (Figure 2).
Case report
A 14-year-old boy presented with a Class II division 1 incisor relationship on a Class II skeletal base. This was associated with restored firstt molars, supernumeraries palatal to UR1 and UL1, severe upper arch crowding, upper centreline shift to the left and mesially impacted LR7 and LL7 (Figures 3 and 4).
The patient underwent a general anaesthetic for surgical removal of supernumeraries, LR8 and LL8, and extraction of UR6 and UL6. This was followed by orthodontic treatment that included a transpalatal arch and upper and lower fixed appliances.
Oral hygiene at the commencement of treatment was excellent; however, 15 months and 12 visits into fixed-appliance treatment, it was noted that oral hygiene had deteriorated and early signs of decalcification were evident. This was despite reinforcement of diet and oral hygiene instruction at every visit, which included tooth brushing and interdental brushing instructions, the use of 1450ppm fluoride toothpaste and a fluoride mouth rinse 225ppm. Additionally, the patient attended his general dentist regularly for check ups. The patient and his parents were advised of the clinical findings and the consequences if oral hygiene did not improve including the risk of irreversible damage to the dentition and the requirement to remove appliances to prevent further damage. Patient-specific diet and oral hygiene advice was provided. A diet diary was not used, but may have been beneficial. Photographs were taken to act as a baseline and to monitor the decalcification progression (Figure 5). The patient's social history was also updated at this stage to investigate any potential child safeguarding issues.
At the following visit, decalcification had progressed and was severely affecting the labial surfaces of the maxillary incisors, predominately on the gingival aspects. These findings were discussed with the patient and his parents. It was noted that there was still spacing in the upper right quadrant; however, the patient was happy with the appearance and function of his dentition. Clinically, it was felt that the risks of further treatment would outweigh the benefits. Both the patient, and his parents, agreed to have his appliances removed early, and he was consented for ‘early removal of braces’. The consent form explained the aspects of malocclusion still uncorrected and the reasons for early removal of appliances. The appliances were removed and thermoplastic retainers provided for wear on a night-time basis (Figure 6). Oral hygiene instruction was reinforced again at this stage, and an update of the orthodontic treatment was written to the GDP.
The patient was reviewed 12 weeks after removal of the appliances, and it was noted that the oral hygiene, WSLs and gingivitis had improved significantly (Figure 7).
Discussion
Prevention of WSLs is naturally better than the cure, and to this end, it is essential that patients have an up-to-date dental assessment prior to orthodontic treatment, and the oral health is deemed suitable to support orthodontic treatment. Past caries experience is the biggest predictor of future caries,14 and therefore it is important to identify patients as high risk for WSLs and provide appropriate tailored advice. The use of fluoride supplements is often prescribed; however, compliance with oral hygiene and diet control is of paramount importance. If WSLs become established and advanced, fluoride supplements may arrest the lesion, but will not improve the appearance of the opacity.
When advanced decalcification occurs, the benefits of continuing orthodontic treatment must be considered against the potential risks. Communication of this to the patient is important to ensure informed consent is gained for the early removal of appliances.
WSLs may regress on their own accord. Failing that, there are minimally invasive methods to improve the appearance of affected teeth as outlined in this article.