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Evaluation of Occlusal Caries after Ozone Treatment

© Dr Julian Holmes
2015


Ozone Information

Evaluation of Occlusal Caries after Ozone Treatment
  • Abstract
  • Introduction
  • Materials and Methods
  • Statistics
  • Results
  • Discussion
  • Conclusion
  • References

  • Evaluation of Occlusal Caries after Ozone Treatment

    Evaluation of Occlusal Caries after Ozone Treatment.
    Authors; Dr. Layla Abu-Naba’, Dr. Hisham Al Shorman BDS, 2003.

    Abstract: Ozone is investigated for the treatment of Primary Occlusal Pit and Fissure Caries (POPFC) in a controlled clinical trial. Purpose: To monitor lesions one month after Ozone treatment or non-treatment. Materials and methods: 258 non-cavitated POPFC lesions (90 patients) were enrolled and detailed locations were recorded. After cleaning using the Prophyflex-2® (KaVo, Germany), the baseline (B) clinical severity scores [Ekstrand KR et al.: Caries Res.1998; 32:247-254], DIAGNOdent® (KaVo, Germany) and ECM® (LODE BV, Netherlands) standard-scale end-value readings were recorded. After randomisation, half the lesions, enrolled for each subject, were treated with Ozone for 10 seconds (HealOzone unit; CurOzone USA) and the other half were reserved as controls. After one month (M), teeth were cleaned and the readings repeated. Univariate analysis of variance (ANOVA) tested the Loge (M/B) ECM and DIAGNOdent readings and Wilcoxon Signed Ranks (WSR) tested the clinical severity score change between groups. Results: ECM showed a significant improvement of the Ozone treated teeth over the control group (ANOVA, f=5.61, p=0.02, n=120) with significant control group worsening from baseline (Student t-test, t=-2.21, df=119, p=0.03) and some treatment group remineralisation (t=+1.09, df=119, p=0.29). There were no significant differences between the treatment and control groups in terms of the DIAGNOdent readings or clinical severity scores change (ANOVA, f=0.15, p=0.70 and WSR, Z=-1.01, p=0.32). Conclusion: ECM readings demonstrated a significant remineralisation difference between Ozone treated and untreated teeth, after one month. This change was not detected using the DIAGNOdent readings or clinical severity scores. Untreated lesions significantly deteriorated.
    Key words: Ozone, Occlusal caries, Remineralisation, ECM, Clinical trial.

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    Introduction:

    Understanding the dynamics of dental caries and applying this knowledge has been associated with a general decline in caries prevalence 1 which was not equally shared by all lesion types. Where approximal surfaces benefited most in fluoridated communities, occlusal pit and fissure caries continued to top prevalence lists 2. Initial occlusal lesions became more prevalent and treatment options were redirected to alter the plaque biofilm activity, preserving healthy as well as repairable tooth structure. Prevention and pharmaceutical measures are aimed at specific individual needs and exclusive tooth surfaces that harness protected plaque activity. Local physical barriers such as intact fissure sealants 3, topical fluorides 4, chlorhexidine varnishes 5, or combinations 6; 7 were recommended to overcome undesirable side effects of general applications of these agents.

    The antimicrobial effect of Ozone has been used in medicine for decades due to its powerful oxidative abilities with no resistant species reported to this agent8. Dental applications for the microbicidal effect were found to be effective against oral microorganisms. Therefore it was suggested for disinfection of dentures 9. C. albicans was significantly reduced after using 10 ppm Ozonated water for variable treatment times 10.

    Cariogenic microorganisms in root carious lesions were significantly reduced when exposed to Ozonised water (0.069 or 0.138 ml Ozone)11. S. mutans and S. sobrinus in inoculated saliva-coated glass beads were also reduced when exposed to a 10-second Ozone gas treatment. Later, root carious lesions became hard after Ozone treatment (n=214, 64.9% treatment group compared to 7.5% in the control group) accompanied with a reduction in DIAGNOdent readings (an occlusal caries diagnostic tool) 12. Sixty-eight point five percent of root sealants applied over Ozone treated root caries lesions were retentive in comparison with only 38.5% in the control group.

    Ozone is proposed as a pharmaceutical treatment alternative for Primary Occlusal Pit and Fissure Caries (POPFC). This study aimed to monitor POPFC lesions’ remineralisation, arrest or demineralisation with or without Ozone treatment.

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    Materials and Methods:

    Ninety subjects attending the Restorative division (Dental School, Royal Victoria Hospital Belfast) met inclusion criteria by being over 12 years of age and had at least 2 POPFC lesions in permanent dentition. (Tables 1 and 2). A written informed consent was signed. After cleaning (PROPHYflex-2, KaVo, Germany), non-cavitated POPFC lesions were inspected on dry and fully erupted occlusal surfaces, which were illuminated by dental-unit light. DIAGNOdent (KaVo, Germany) detected the most severe part of the inspected lesions that also met the following criteria:

  • Non-cavitated lesions
  • Clinical severity scores 1to 3 (Table 3) 13
  • DIAGNOdent readings equal to or over 10

    Full records of enrolled lesions included:

  • Surface type: a pit or fissure.
  • Location of pit or fissure: Mesial, distal, buccal, lingual or any combination.
  • Baseline clinical severity score.
  • Baseline DIAGNOdent readings and scores (Table 4).
  • Baseline electric caries monitor (ECM IV, LODE BV, Netherlands) site-specific end-value readings (Position 2). Saliva was used for rewetting the teeth between readings for 5 seconds (for detailed description of ECM readings’ protocols 14) (Table 5).

    Lesions within the same subject were randomised using computer random-sampling digit tables.

    Treatment Group: Teeth received Ozone treatment for 10 seconds (HealOzone unit (CurOzone and KaVo, USA and Germany) (2100 ppm O3, 615 ml/min)) and then sprayed by a remineralising mouthwash (Table 6).
    Control Group: Teeth sprayed by the remineralising mouthwash. Subjects received preventive advice, a toothbrush (Brilliant, Brilliant Products, UK) and a toothpaste (Natural White, Natural White Inc., UK; 1,100 ppm F-).

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    Statistics:

    Repeatability of the clinical severity, DIAGNOdent and ECM scores were tested at baseline using Weighed Kappa values. Score changes at the recalls were tested using Wilcoxon’s Signed Ranks Test for the pair (recall visit score, baseline score) and between groups for the pair (recall visit score minus baseline score for the treatment group, recall visit score minus baseline score for the control group). For the raw DIAGNOdent and ECM readings, change from baseline was tested using the Student’s t-test (Loge (baseline value / recall value)). Tests between groups were performed using univariate analysis of variance for Loge ECM and DIAGNOdent readings. Fixed factors included subjects' ID (to exclude subject variability) and lesion treatment group were used. The subject ID was a significant factor determining the effect of treatment, and thus proving such variability (p<0.05).

    End value readings, displayed by the ECM, were chosen for various calculations 14. For each tooth, 4 end-value readings were taken and the average was used to represent the lesion. This average reflected the resistance of the tooth to the applied electric current in standardised clinical conditions. The tooth resistance is expected to be reduced if the mineral content was reduced by the demineralisation activity of cariogenic microorganisms that continues to increase the porosity of decayed lesion. Ion rich saliva fill these porosities and reduce this resistance, thus ECM end-value is the only measured outcome that has an inverse relation to caries severity and activity (Table 7).

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    Results:

    258 Non-cavitated POPFC lesions were included in this study (Table 8).

    Repeatability tests were obtained in-vivo from 32 occlusal pit and fissure surfaces in two visits, one week apart. Weighed Kappa values were 0.74 and 0.62 for the clinical severity and DIAGNOdent scores respectively. For the 4 end-value ECM readings taken from the same lesion, repeatability is defined as that amount, which two measurements could be expected to exceed on just 5% of occasions as dictated in the following equation: Repeatability = ± 1.96 SDev.

    The range in which 95% of the repeated end-value measurements from fissure lesions within one visit occurred was 4.8 times, and 4.3 times for the pit lesions. When the raw end-value readings were transformed to equivalent ECM scores used in this study, mean weighed Kappa value for the four sets of readings were 0.64 and 0.62 for fissure and pit lesions respectively (p<0.001) (Table 9).

    At baseline, and although lesions were randomised into treatment and control groups, there was a tendency for severe lesions to be within the treatment group (p=0.055, Wilcoxon’s Signed Ranks Test). However, this tendency was not supported by the other two diagnostic tools, which showed no severity difference between the two groups (p = 0.240 and 0.130, Wilcoxon’s Signed Ranks Test for baseline DIAGNOdent and ECM scores, respectively) (Table 10).

    ECM score 0 was interpreted clinically as a tooth with mineral contents comparable with healthy tooth structure (ECM manual, 2000). This ECM score was obtained from lesions diagnosed by the clinical severity score and DIAGNOdent readings as being carious. This may indicate that previous activity of these lesions might have been halted or reversed previous to the baseline diagnosis session. This may demonstrate that the DIAGNOdent device and the clinical severity score system may detect severity, size and depth of such activity but would be limited in the detection of mineral change accompanying fluctuating carious activity. Nevertheless, correlations of baseline scores obtained by the three diagnostic methods were significant (p<0.05) (Table 11).

    Changes in the three diagnostic tools were tested in the one-month recall visit (± SE) (33.6 ± 0.48 days). 4 subjects missed visit (12 teeth, 4.7% of enrolled lesions) as one loss of contact with a subject who anticipated a change in her permanent address and unavailability for examination by the other subjects.

    ECM readings and score change analysed showed a significant lesion mineral and thus lesion activity difference between groups (p<0.05). The control group had a significant drop in its ECM readings and thus a significant increase in ECM scores (p<0.05). This difference was enhanced with the treatment group having some increase in ECM readings and a decrease in ECM scores from baseline but that was insignificant (p>0.05) (Table 12).

    If tests were repeated between treatment and control groups, after lesions with ECM baseline score 0 were removed, then only 62 pairs of lesions meet this condition. In this subcategory, the treatment group had a mean change that was significantly higher (better) than baseline (p<0.05), whilst the control group had no significant change (p>0.05) (Table 13).

    The second subcategory (17-pairs) which had baseline ECM score 0 in both treatment and control groups did not experience ECM changes (p>0.05). The third subcategory (38 pairs) had either the treatment or control lesion with a baseline score 0 and was not analysed for changes.

    ECM changes were analysed by co-factors. Those that showed no significant effect on the ECM change included: location of the lesion on the occlusal surface, type of lesion (pit or fissure) and baseline DIAGNOdent and clinical severity scores (p>0.05). The following co-factors had a significant effect; baseline ECM score and tooth number (Figures 1 and 2).

    Fine demineralisation and remineralisation difference between treatment and control groups detected by the ECM seemed not to be detected by clinical severity scores change (Z= -1.005, p= 0.315). DIAGNOdent reading changes were less obvious and both groups had a tendency for readings being higher from baseline (p= 0.06,0.086 for the treatment, control group respectively, difference between groups p>0.05).

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    Discussion:

    When validated diagnostic tools are used for monitoring lesion activity, their ability to discriminate between positive and desirable changes accompanying remineralisation, from those parallel, but clinically insignificant changes (such as staining) should be anticipated. Interference from these parallel changes may be inflicted on the tool. Another limitation would be the sensitivity of tool to fine caries activity changes after a short period beyond the range of repeatability and reproducibility errors. Finally, once occurred, the change measured should be perpetual. Using more than one diagnostic tool would help to overcome each tools limitations by quantifying lesions activity using more than one measured feature, as mineral content, microbial by-products and physical changes in active lesions.

    Ekstrand's clinical severity score system depends on external manifestations to predict the extent of the tooth decay. Being one of the most validated clinical systems for a single diagnosis, it was of high value to detect lesions as they present to the clinics for the first time. Clinical scores correlated with scores using the DIAGNOdent and ECM at baseline. A similar clinical score system had been used to monitor lesions and a significant change was detected in only after 2 years of extensive oral hygiene measures with fluorides 15. No literature was present to monitor changes in teeth subject to Ozone treatment.

    Although DIAGNOdent was recommended for lesion monitoring, no published data monitored occlusal lesions in-vivo. Continuous deposition of proteins (porphyrins) at various amounts and depths within the demineralised tissue was reflected by the increase in lesion fluorescence. Theory is that remineralisation might shuffle the protein distribution by continuous washing of saliva and less protein production by biofilms, then DIAGNOdent readings may significantly decline. Stains or calculus may be part of the change occurring in lesions with slow progression and repeated cycles of demineralisation and remineralisation. DIAGNOdent may pick these parallel changes as a higher reading and might not reflect the reduced protein production as previously proposed. A total significant reduction of DIAGNOdent readings was reported when root lesions were treated with Ozone 12 but these results could not be equated to occlusal caries lesions, as the structures involved in the attack are different as well as the environment to which lesions are subjected, including the microbial environment and composition 12.

    ECM is known to be highly sensitive to the mineral content of the tooth. Natural changes, as enamel maturation, were monitored by more than one study 16 17 18. Approximate maturation periods were suggested. Minor differences in the mineral content of the sound mature surfaces, as fine cracks and hypomineralised areas, were also detected using the ECM 19. Furthermore, ECM readings at baseline were suggested as a predictor of future lesion behaviour by calculating survival rates 20.

    Lesions incorporated in the study covered the spectrum of lesions’ presentations without frank cavitation. Using inclusion criteria, lesions were enrolled in all age groups within both genders. This might be a reflection that age was no longer a factor deterring any caries attack 21.

    Lesions were also distributed between all posterior teeth as well as between various types of surface topographies (pits and fissures) where teeth were in the mouth of subjects for more than a year and had full eruption status. However, this didn’t mean that all teeth were in full occlusion.

    Each lesion within the treatment group had a control within the same subject. This served to reduce the number of various factors, which might affect different subjects to various degrees, such as fermentable carbohydrate intake, oral hygiene habits, possible age related factors, salivary bacterial counts, social and racial variables as well as gender. Such variables may explain the mineralisation variability detected when the subject ID was used as fixed factor for group analysis and accounted for by adjusting for any block effect.

    A significant mineral activity difference occurred between lesions treated with ozone in comparison with the control group lesions. Although further recall visits would be needed to monitor and follow up this trend, it could be claimed that the mechanism for these early changes is different. As there was no significant interfering factor in the control group, then it might be natural to propose that the change was a steady deterioration of the health status of the lesions if left untreated. However, the changes in the treatment group could only be explained by the effect of Ozone treatment. This should be followed up further and assess the clinical presentations and DIAGNOdent reading accompanying such remineralisation shift.

    Further analysis of subgroups divided by ECM baseline score showed that demineralised lesions within the treatment group (Scores 1-3) had significant remineralisation, while this mineral change was not parallel in treatment group lesions that most probably had previous remineralisation before baseline visit (ECM score 0). This would support that the effect of Ozone was directed to demineralised lesions while already remineralised lesions, Ozone might help to stabilise it. The control group lesions that had a baseline ECM score 0 had no significant mineral change which may prove the previous conclusion that remineralised lesions may have a more stable mineral content that could be more resistant to further demineralisation from natural tooth minerals due to the accumulation of stronger mineral enamel crystals 22. Further recalls would be needed to follow up this conclusion.

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    Conclusion:

    Ozone treatment of primary occlusal pit and fissure caries produced an early remineralisation shift in demineralised lesions after one month while demineralisation of control lesions continued regardless of lesion type and location within the occlusal surface or tooth sequence. Additional monitoring is planned for this study.

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    Reference List:

  • 1. Bratthall D, Hansel-Petersson G, Sundberg H. Reasons for the caries decline: what do the experts believe? Eur J Oral Sci 1996; 104 (4): 416-422.
  • 2. Anderson M. Risk assessment and epidemiology of dental caries: review of the literature. Pediatr Dent 2002; (24): 377-385.
  • 3. Weintraub J A. Pit and fissure sealants in high-caries-risk individuals. J Dent Educ 2001; 65(10): 1084-1090.
  • 4. ten Cate J M. Current concepts on the theories of the mechanism of action of fluoride. Acta Odontol Scand 1999; 57 (6): 325-329.
  • 5. Matthijs S, Adriaens P A. Chlorhexidine varnishes: a review. J Clin Periodontol 2002; 29 (1): 1-8.
  • 6. Whelton H, O'Mullane D. The use of combinations of caries preventive procedures. J Dent Educ 2001; 65 (10): 1110-1113.
  • 7. Bader J D, Shugars D A, Bonito A J. A systematic review of selected caries prevention and management methods. Community Dent Oral Epidemiol 2001; 29 (6): 399-411.
  • 8. Bocci V. Biological and clinical effects of ozone. Has ozone therapy a future in medicine? Br J Biomed Sci 1999; 56 (4): 270-279.
  • 9. Oizumi M, Suzuki T, Uchida M, Furuya J, Okamoto Y. In vitro testing of a denture cleaning method using ozone. J Med Dent Sci 1998; 45 (2): 135-139.
  • 10. Murakami H, Sakuma S, Nakamura K, Ito Y, Hattori M, Asai A, and others. Disinfection of removable dentures using ozone. Dent Mater J 1996; 15 (2): 220-225.
  • 11. Baysan A, Whiley R A, Lynch E. Antimicrobial effect of a novel ozone- generating device on micro-organisms associated with primary root carious lesions in vitro. Caries Res 2000; 34 (6): 498-501.
  • 12. Baysan A. Management Of Primary Root Caries Using Fluoride or Ozone Therapies. University of London 2002.
  • 13. Ekstrand K R, Ricketts D N, Kidd E A, Qvist V, Schou S. Detection, diagnosing, monitoring and logical treatment of occlusal caries in relation to lesion activity and severity: an in vivo examination with histological validation. Caries Res 1998; 32 (4): 247-254.
  • 14. Abu-Naba'a L. Management of primary occlusal pit and fissure caries using Ozone. Queen's University Belfast 2003.
  • 15. Carvalho J C, Thylstrup A, Ekstrand K R. Results after 3 years of non-operative occlusal caries treatment of erupting permanent first molars. Community Dent Oral Epidemiol 1992; 20 (4): 187-192.
  • 16. Ie Y L, Verdonschot E H, Schaeken M J, van't Hof M A. Electrical conductance of fissure enamel in recently erupted molar teeth as related to caries status. Caries Res 1995; 29 (2): 94-99.
  • 17. Schulte A, Gente M, Pieper K. Posteruptive changes of electrical resistance values in fissure enamel of premolars. Caries Res 1999; 33 (3): 242-247.
  • 18. ten Bosch J J, Fennis-le Y, Verdonschot E H. Time-dependent decrease and seasonal variation of the porosity of recently erupted sound dental enamel in vivo. J Dent Res 2000; 79 (8): 1556-1559.
  • 19. Huysmans M C, Longbottom C, Hintze H, Verdonschot E H. Surface-specific electrical occlusal caries diagnosis: reproducibility, correlation with histological lesion depth, and tooth type dependence. Caries Res 1998; 32 (5): 330-336.
  • 20. Fennis-Ie Y L, Verdonschot E H, van't Hof M A. Performance of some diagnostic systems in the prediction of occlusal caries in permanent molars in 6- and 11-year-old children. J Dent 1998; 26 (5): 403-408.
  • 21. ten Cate J M. What dental diseases are we facing in the new millennium: some aspects of the research agenda. Caries Res 2001; 35 (Suppl 1): 2-5.
  • 22. Robinson C, Shore R C, Brookes S J, Strafford S, Wood S R, Kirkham J. The chemistry of enamel caries. Crit Rev Oral Biol Med 2000; 11 (4): 481-495.

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    Tables

    Age group Range Number Percentage 1 12-21 40 44.4 2 22-31 39 43.3 3 32-41 8 8.9 4 >41 3 3.3 Total 90 100%

    Table 1: Distribution of subjects enrolled in the main study according to age.

    Gender Numbers Percentage Male 35 38.9 Female 55 61.1 Total 90 100%

    Table 2: Distribution of subjects enrolled in the study according to gender.

    Score Description 0 No or slight change in enamel translucency after prolonged air drying (>5s) 1 1a Opacity (white) hardly visible on the wet surface, but distinctly visible after air-drying (>5s). Opacity (brown) hardly visible on the wet surface, but distinctly visible after air-drying (>5s) 2 2a Opacity (white) distinctly visible with out air-drying. Opacity (brown) distinctly visible with out air-drying. 3 Localised enamel breakdown in opaque or discoloured enamel and or greyish discolouration from the underlying dentine. 4 Cavitation in opaque or discoloured enamel exposing the dentine beneath.

    Table 3: Clinical severity index scores 12.

    Score D value Description 0 <10 Sound 1 10-14 Enamel caries in the outer half 2 15-20 Caries in enamel up to DEJ 3 21-30 Caries in enamel reaching DEJ with some dentine demineralisation 4 ?31 Deep dentinal caries.

    Table 4: Recommended DIAGNOdent cut-off points as stated by the manufacturer.

    ECM Score Corresponding ECM end value Possible clinical inferences 0 > 10.00 MO Sound enamel 1 10.00 to 2.50MO Lesions up to DEJ 2 2.5 to 0.151 MO Lesions in dentine 3 Equal or less than 0.150 MO Deep dentinal lesions

    Table 5: ECM scores, corresponding end values and possible clinical inferences (ECM Manual, 2000).

    Active ingredients in the reductant were as follows: % wt/wt Water To make up 100% Sodium Benzoate NF 0.50000 Sodium tripolyphosphate 3.00000 Sodium fluoride 1100 ppm F Xylitol 1.00000 Zinc Chloride 0.75000 Sodium Citrate USP 2.60000 Methyl paraben 0.12000 Sodium Methyl Cocoyl Taurate 0.60000 Riboflavin 0.00010 Flavour (Noville AN114153) 1.00000

    Table 6: Active ingredients of the remineralising solution used after Ozone treatment.

    Outcome measurement Range included in the study Relation with carious activity Clinical severity score 1-3 Parallel DIAGNOdent reading 10-99 Parallel DIAGNOdent score 1-4 Parallel ECM reading 0.05-5000 MW Inverse ECM score 0-3 Parallel

    Table 7: Relationship of measurements taken by three diagnostic tools to quantify carious activity in POPFC lesions.

    Location Tooth number Total 1st premolars 2nd premolars 1st molars 2nd molars 3rd molars Mesial 12 7 1 11 2 33 Central 6 19 36 56 14 131 Distal 25 16 26 27 0 94 Total 43 42 63 94 16 258

    Table 8: Distribution of POPFC lesions within the treatment and control groups according to lesion location.

    Paired comparisons Weighed Kappa value Fissures Pits Severity set 1&2 0.685* 0.645* Severity set 1&3 0.639* 0.671* Severity set 1&4 0.635* 0.610* Severity set 2&3 0.614* 0.570* Severity set 2&4 0.610* 0.600* Severity set 3&4 0.650* 0.640* Mean 0.639* 0.622*

    Table 9: Weighed Kappa values for the ECM scores in the four sets of readings taken for the teeth within one visit (*p<0.001).

    Clinical severity scores Treatment group Control group Number % Number % 1 63 49.6 79 62.2 2 53 41.7 39 30.7 3 11 8.7 9 7.1 Total 127 100.0 127 100.0 DIAGNOdent scores DIAGNOdent ranges Treatment group Control group Number % Number % 1 10-14 8 6.4 13 10.3 2 15-20 20 16.0 24 18.8 3 21-30 36 28.8 34 26.6 4 ?31 61 48.8 57 44.5 ECM score Corresponding end values MO Treatment group Control group Number % Number % 0 > 10.00 36 28.1 45 35.2 1 10.00 to 2.50 39 30.5 37 28.9 2 2.5 to 0.151 47 36.7 42 32.8 3 = 0.150 6 4.7 4 3.1

    Table10: Distribution of POPFC lesions within the treatment and control groups (p values between groups are 0.055, 0.240, 0.130 for the clinical severity, DIAGNOdent and ECM scores respectively).

    DIAGNOdent score Clinical severity score Scores Total Pits Fissures Total Pits Fissures ECM score 0.20** 0.25** 0.17** 0.31** 0.28** 0.33** DIAGNOdent score 1.00 1.00 1.00 0.24** 0.18* 0.28** * (p<0.05) ** (p<0.01)

    Table 11: Spearmen’s correlation values between scores obtained from the diagnostic tools at baseline.

    Clinical severity scores DIAGNOdent scores ECM scores Score change Treatment Number % Control Number % Treatment Number % Control Number % Treatment Number % Control Number % -3 - - - - 0 0.0 0 0.0 0 0.0 0 0.0 -2 1 0.9 0 0.0 2 1.6 5 4.2 5 4.2 0 0.0 -1 12 10.5 6 5.3 14 10.9 16 13.4 24 20.0 17 14.2 0 85 74.6 93 81.6 71 61.7 63 52.9 71 59.2 71 59.2 1 16 14.0 15 13.3 23 20.0 27 22.7 17 14.2 23 19.2 2 0 0.0 0 0.0 3 2.6 7 5.9 3 2.5 9 7.5 3 - - - - 2 1.7 1 0.8 0 0.0 0 0.0 P =* 0.724 0.050 0.060 0.086 0.210 0.005 P=** 0.315 0.978 0.001 -not possible. Only a 2 score difference is present. *from baseline **between groups

    Table 12: The number and percentage of teeth experiencing a change in the diagnostic scores after one month, in the treatment and the control groups.

    Group p value Mean Lesion no. SD SE Loge DIAGNOdent change Treatment 0.016* 0.0783 116 0.34 0.03 Control 0.016* 0.0865 119 0.39 0.04 Change 0.701** -0.001 115 0.46 0.04 Loge ECM change Treatment 0.278* 0.116 120 1.37 0.13 Control 0.029* -0.255 120 1.37 0.12 Change 0.019** 0.410 120 1.51 0.14 Loge ECM change after excluding baseline ECM score 0 (62 pairs) Treatment 0.008* 0.391 120 1.34 0.14 Control 0.491* 0.096 120 1.22 0.14 Change 0.021** 0.451 62 1.50 0.19 Loge ECM change for lesions with baseline ECM score 0 (17 pairs) Treatment 0.013* -0.5630 32 1.22 0.21 Control 0.000* -0.960 42 1.34 0.21 Change 0.645** 0.1491 17 1.31 0.32 *from baseline **between groups after adjusting for block effect

    Table 13: Change in ECM readings after one month.

    Figures

    Figure 1: Mean (± SE) ECM change after 1 month in the Ozone treatment and control groups categorised by the tooth sequence from midline.

    Figure 2: Mean (± SE) ECM change after 1 month in the Ozone treatment and control groups categorised by baseline ECM scores.

    Legends • Table 1: Distribution of subjects enrolled in the main study according to age. • Table 2: Distribution of subjects enrolled in the study according to gender. • Table 3: Clinical severity index scores 12. • Table 4: Recommended DIAGNOdent cut-off points as stated by the manufacturer. • Table 5: ECM scores, corresponding end values and possible clinical inferences (ECM Manual, 2000). • Table 6: Active ingredients of the remineralising solution used after Ozone treatment. • Table 7: Relationship of measurements taken by three diagnostic tools to quantify carious activity in POPFC lesions. • Table 8: Distribution of POPFC lesions within the treatment and control groups according to lesion location. • Table 9: Weighed Kappa values for the ECM scores in the four sets of readings taken for the teeth within one visit (*p<0.001). • Table10: Distribution of POPFC lesions within the treatment and control groups (p values between groups are 0.055, 0.240, 0.130 for the clinical severity, DIAGNOdent and ECM scores respectively). Table 11: Spearmen’s correlation values between scores obtained from the diagnostic tools at baseline. • Table 12: The number and percentage of teeth experiencing a change in the diagnostic scores after one month, in the treatment and the control groups. • Table 13: Change in ECM readings after one month. • Figure 1: Mean (± SE) ECM change after 1 month in the Ozone treatment and control groups categorised by the tooth sequence from midline. • Figure 2: Mean (± SE) ECM changes after 1 month in the Ozone treatment and control groups categorised by baseline ECM scores.

    Acknowledgement

    Authors would like to thank Dr. Mike Stevenson for his expert statistical advice. Also we would like to thank all the participants who gave from their time and effort to make this study possible.

    Source of fund: The PhD was an award from Jordan University of Science and Technology, Irbid Jordan.

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    January 2015
    The-O-Zone © Dr Julian Holmes