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Effect of fixed appliances on oral malodor
ORIGINAL ARTICLE
Effect of fixed appliances on oral malodor Hasan Babacan,a Oral Sokucu,b _Ismail Marakoglu,c Hakan Ozdemir,d and Ruhi Nalcacie Sivas, Gaziantep, and Konya, Turkey Introduction: The objective of this study was to evaluate the effect of fixed appliances on oral malodor. Methods: Forty-one patients participated in this study. They were randomized into 2 groups: treated with fixed orthodontic appliances and untreated controls. Oral malodor measurements and the gingival and plaque indexes were recorded in each group by same periodontist. Measurements were taken from the study group before bonding, 1 week after bonding, and 4 weeks after bonding. The control group’s measurements were made at the same time. Results: Oral malodor and the gingival and plaque indexes were significantly increased 1 week after bonding (P \0.05). Oral malodor was increased at 4 weeks after bonding (P .0.05). The comparison of the groups showed differences 1 week and 4 weeks after bonding. Conclusions: The oral malodor reached the critical level during fixed orthodontic treatment. Oral malodor could indicate a need to evaluate oral health and remind patients of the importance of maintaining ideal oral hygiene. (Am J Orthod Dentofacial Orthop 2011;139:351-5)
H
alitosis is a lyrical term derived from the Latin word halitus (breath) and the Greek suffix osis (condition, action of a pathologic process).1 Halitosis (bad breath) is estimated to affect up to 50% of the population with varying degrees of intensity and etiology.2 The consequences of halitosis can be more than social; its presence could reflect serious local or systemic conditions. However, physicians tend to view this as a dental condition, which causes them most often to refer patients with this problem to a dentist.2 When halitosis is a dental problem, the profession should recognize and recommend therapy to address it. Halitosis is caused by several intraoral and extraoral factors, including systemic diseases and disorders of the gastrointestinal or upper respiratory tracts. If halitosis originates from the oral cavity, it is known as oral malodor. This is usually
a Associate professor, Department of Periodontics, Faculty of Dentistry, Cumhuriyet University, Sivas, Turkey. b Assistant professor, Department of Orthodontics, Faculty of Dentistry, Gaziantep University, Gaziantep, Turkey. c Associate professor, Department of Periodontics, Faculty of Dentistry, Selcuk University, Konya, Turkey. d Fellow researcher, Department of Periodontics, Faculty of Dentistry, Cumhuriyet University, Sivas, Turkey. e Fellow researcher, Department of Orthodontics, Faculty of Dentistry, Cumhuriyet University, Sivas, Turkey. The authors report no commercial, proprietary, or financial interest in the products or companies described in this article. Reprint requests to: Hasan Babacan, Cumhuriyet University, Department of Orthodontics, Faculty of Dentistry, 58140 Sivas, Turkey; e-mail, babacanhasan@ yahoo.com. Submitted, January 2009; revised and accepted, March 2009. 0889-5406/$36.00 Copyright Ó 2011 by the American Association of Orthodontists. doi:10.1016/j.ajodo.2009.03.055
caused by microbial metabolism from the tongue, saliva, or dental plaque.3 The prominent elements of oral malodor are volatile sulfide compounds (VSCs) and, in particular, hydrogen sulfide, methyl mercaptan, and dimethyl sulfide. Most of these compounds are metabolized from the proteolytic degradation by oral microorganisms of sulfur-containing peptides and amino acids in saliva, shed epithelium, food debris, gingival crevicular fluid, interdental plaque, postnatal drip, and blood.4 It was shown that the levels of VSCs in the mouth correlate with the depth of periodontal pockets, and that the amount of VSCs in the breath increase with the number, depth, and bleeding tendency of the periodontal pockets.4 Therefore, good plaque control is an important factor in the maintenance of dental health during fixed appliance therapy in orthodontics.5,6 The effects of orthodontic treatment on periodontal health have been investigated in several studies.7,8 Many researchers have observed inflammation of gingival tissues during fixed orthodontic therapy. This condition has been related to oral-hygiene measures hampered by fixed orthodontic appliances with consequent increases in the accumulation of bacterial plaque. Brackets, archwires, and other appliance components are both a focus for plaque accumulation and obstructions to plaque removal, thereby promoting gingivitis.7 Plaque also harbors cariogenic bacteria potentially capable of hard-tissue damage, especially at the bracket margins.6,9 Accordingly, once the fixed appliances are removed after treatment, the inflammation can be expected to resolve.10-12 351
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The aim of this study was to evaluate the effect of fixed orthodontic treatment on oral malodor. MATERIAL AND METHODS
Ethical approval was granted by the local ethical committee, and permission was given for this study from the local ethics committee at Cumhuriyet University. All patients met the inclusion criteria: good general health, ages from 12 to 15 years, no previous orthodontic treatment, and no orthognathic surgery required; those with unsatisfactory oral hygiene were excluded from the study. Fifty patients in the permanent dentition were selected for this study from the orthodontic department of the dentistry faculty at Cumhuriyet University. Baseline measurements of plaque and gingival health were recorded for each volunteer by the same researcher (H.O.); if the patients were suitable for inclusion, the study was described in detail to them, and written information was given to them. Six patients were excluded because of poor oral hygiene and unwillingness to participate. Several weeks later, the patients were interviewed again to determine their willingness to participate in this study. After this stage, written consent was obtained, and they were randomly allocated. Forty-four subjects were recruited for this study. They were randomly assigned to the study group or the control group. The blinded periodontist (I.M.) gave formal hygiene instructions to the each patient. The study group included 21 subjects (12 girls, 9 boys) who would have fixed orthodontic treatment. The control group included 20 subjects (11 girls, 9 boys) who did not receive orthodontic treatment. A classic bonding process was used for all patients. All teeth were etched for 20 seconds with 37% phosphoric acid, washed with a spray for 10 seconds, and dried to a chalky white appearance. The tooth surface was thoroughly dried, and a thin layer of Transbond XT sealant (3M Unitek, Monrovia, Calif) was applied. Orthodontic metal brackets (Generus Roth, GAC International, Bohemia, NY) were used in this study. The mouth was fully bonded in 1 session. Nickel-titanium leveling archwires were fixed with elastic ligatures in all teeth. The orthodontic treatments for the patients in the control group started 1 month after the end of this study. Table I shows the distribution and average ages of the subjects. The following were recorded in each group by same periodontist (H.O.): (1) oral malodor measurements, (2) gingival index (GI), and (3) plaque index (PI). Measurements were taken in the study group before bonding (T1), 1 week after bonding (T2), and 4 weeks after bonding (T3). The measurements in the control group were made at the same times. One patient from the study group and 2 patients from the control group did not
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Table I. Distribution and average ages of subjects Girls (n) and Boys (n) and Average age (y) percentage percentage mean 6 SD Study group 12 9 13.05 6 1.48 60% 40% 11 9 13.70 6 1.61 Control group 20 55% 45% n 21
have the measurements and therefore were excluded from the study. All subjects were evaluated at the first appointment to establish their measurements at T1. The participants were asked to carry on their normal oral-hygiene practices. They were instructed to brush their teeth after dinner and to refrain from eating and drinking until coming to the dentistry faculty next morning. They were also requested to avoid spicy foods, onions, and garlic for 48 hours before the appointment. After the first appointment, the study group subjects were bonded immediately. Measurements were taken at T2. Measurements were also taken at T3, after the subjects had conducted their own oral care for 4 weeks. A Halimeter (Interscan, Chatsworth, Calif) was used to evaluate the levels of VSCs in their breath. Oral malodor values were divided into 4 categories and classified as normal (values from 0-100 parts per billion [ppb]), weak (101-150 ppb), strong (151-300 ppb), or very strong ($301 ppb).13 Each subject kept the mouth closed for 60 seconds before sampling. A plastic straw was inserted and positioned above the posterior portion of tongue dorsum, not touching the oral mucosa or the tongue. Breathing was not allowed during sampling. The mouth was kept open by approximately 1.5 cm, and the peak value was recorded. The measurements were duplicated, and the mean value was calculated. The PI was recorded at 4 tooth surfaces (mesial, distal, buccal, and lingual), and the quantity of supragingival plaque on the cervical area was assessed for every tooth. The scores for PI were defined as follows: 0, no plaque in the gingival area; 1, a film of plaque adhering to the free gingival margin and adjacent area of the tooth that could be recognized only by running a probe across the tooth surface; 2, moderate accumulation of soft deposits in the gingival pocket and on the gingival margin or the adjacent tooth surface that could be seen by the naked eye; and 3, abundance of soft matter in the gingival pocket or on the gingival margin and adjacent tooth surface.14 The GI was recorded on the mesial, distal, buccal, and lingual surfaces with a manual periodontal probe (Williams probe, Hu-Friedy, Chicago, Ill). Bleeding was recorded if it occurred within 30 seconds of probing.
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Table II. Comparison of the oral malodor scores of the study and control groups Study group mean 6 SD Control group mean 6 SD
n 21
T1 58.55 6 13.77
T2 81.00 6 17.15
T3 94.70 6 12.31
T1-T2 *
T1-T3 *
T2-T3 *
20
58.15 6 14.32
60.85 6 12.05
61.35 6 15.41
NS
NS
NS
0.620 NS
0.000*
0.000*
P value
F 5 56.93 P 5 0.000 P \0.05* F 5 0.66 P 5 0.519 P .0.05
*Significant at the 0.05% level of confidence; NS, not significant.
Table III. Comparison of the plaque index scores of the study and control groups Study group mean 6 SD Control group mean 6 SD
n 21
T1 0.95 6 0.21
T2 1.15 6 0.20
T3 1.17 6 0.14
T1-T2 *
T1-T3 *
T2-T3 NS
20
0.99 6 0.20
1.05 6 0.25
1.05 6 0.19
NS
NS
NS
0.811 NS
0.016*
0.001*
P value
F 5 21.74 P 5 0.000 P \0.05* F 5 1.16 P 5 0.324 P .0.05
*Significant at the 0.05% level of confidence; NS, not significant.
Scores for the GI were defined as follows: 0, normal gingiva; 1, mild inflammation, slight change in color, slight edema, and no bleeding on palpation; 2, moderate inflammation, redness, edema and glazing, and bleeding on probing; and 3, severe inflammation, marked redness and edema, ulceration, and tendency to spontaneous bleeding.15 The group score was subsequently calculated by adding the individual scores and dividing the total by the number of patients included. Statistical analysis
The sample size for each group was calculated and based on a significance level of a 5 0.01 and a power (1-b) of 90%. The sample size calculation showed that 19 patients in each group were sufficient; however, our study group consisted of 21, and the control group consisted of 20 patients. The data were statistically analyzed by using SPSS software (version 15.0, SPSS, Chicago Ill). Multiple comparisons of the data were performed with analysis of variance (ANOVA). If there was evidence of statistically significant differences between the measurements or groups, the Bonferroni test were used. The MannWhitney U test was used to compare the groups. RESULTS
The mean values for oral malodor, the GI, and the PI are shown in Tables II through IV.
In the study group, oral malodor values showed significant differences between T1 and T2, T1 and T3, and T2 and T3) (P \0.05). The control group did not show significant differences between measurements (P .0.05) (Table II). For the PI, the study group showed significant differences between T1 and T2 and T1 and T3 (P \0.05). The control group showed no significant differences among the times (P .0.05) (Table III). For the GI, the study group showed significant differences between T1 and T2 and T1 and T3 (P \0.05). The control group did not show significant differences among the times (P .0.05) (Table IV). The comparison of the parameters (PI, GI, and oral malodor) of both groups showed differences at T2 and T3 (P \0.05) (Tables II-IV). DISCUSSION
The mouth is the cause of more than 90% of cases of oral malodor. The most common cause of oral malodor is elevated levels of VSC, primarily hydrogen sulfide and methyl mercaptan in the breath.16,17 In this study, a portable sulfide monitor was used to measure VSCs. Its advantages include ease of use by nonskilled persons, noninvasiveness, low possibility of cross-infection, portability, relatively low expense, and rapid turnaround time of 1 to 2 minutes between measurements.18,19
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Table IV. Comparison of the gingival index scores of the study and control groups Study group mean 6 SD Control group mean 6 SD P value
n 21
T1 1.03 6 0.19
T2 1.19 6 0.21
T3 1.25 6 0.23
T1-T2 *
T1-T3 *
T2-T3 NS
20
0.98 6 0.10
1.02 6 0.06
0.97 6 0.11
NS
NS
NS
0.341 NS
0.003*
0.000*
F 5 11.84 P 5 0.000 P \0.05* F 5 1.27 P 5 0.292 P .0.05
*Significant at the 0.05% level of confidence; NS, not significant.
After placement of the brackets, the PI and the GI scores began to increase in the study group. The results demonstrated that bonding of brackets enhanced plaque retention. Patients who undergo orthodontic treatment with fixed appliances often have problems cleaning the tooth surfaces effectively around the attachments. Previous studies showed that orthodontic treatment with fixed appliances is accompanied by increased risks of caries and gingivitis.5-7 Our study showed that oral malodor can be added to this list of risks. Immediately after bonding, oral malodor directly increased just like the PI and GI indexes. Tonzetich20 showed a correlation between plaque and oral malodor. However, the mean value of oral malodor during fixed orthodontic treatment is not clinically important (84 ppb). The patients’ orthodontic treatments followed routine oral health procedures. But these procedures could not protect periodontal health ideally. In our study, the PI and GI indexes significantly increased after bonding. Interestingly, 4 weeks after bonding, the PI and the GI were stable. Bacterial dental plaque, like salivary sediment, has a strong potential to form substrates containing cysteine, cystine, methionine, nutrient broth, and salivary sediment to yield similar volatile compounds through salivary putrefaction. The capacity of plaque to use the salivary substrate for odor production was established by the lyophilized fractions of saliva. Another study mentioned that deposits of oral microorganisms of plaque on teeth or in periodontal pockets could contribute to bad breath.21 Eight to 14 hours of maturation are required before plaque deposits produce VSCs. Protected plaque in interproximal sites produced substantial odors and is associated with overall levels of VSCs. Bosy et al22 found that oral malodor in healthy subjects could originate from protected interdental sites. But, interestingly, contrary to our findings, they found no correlation between the PI and oral malodor. Although the comparison of the PI and the GI showed no differences at T3, oral malodor survived and
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increased in our subjects. The last measurements of oral malodor in the study group reached the critical border of the weak stage. The observation of the control group showed no change in any parameter. The parameters were stable for 4 weeks. The presence of dental plaque could cause some oral malodor. Because of the long treatment time of 2 years or more, a rigid plaque-control program is indispensable. Professional tooth cleaning at short intervals must be complemented by efficient oral-hygiene procedures at home. Otherwise, with the aggravation of the PI and the GI, we could be faced with oral malodor in our orthodontic patients. Our study showed that oral malodor can be another way to evaluate oral health. CONCLUSIONS
Oral malodor reached the critical level during fixed orthodontic treatment. The PI and GI scores increased immediately after bonding. Oral malodor could be another indicator to evaluate oral health and to warn patients to achieve ideal oral hygiene. REFERENCES 1. Attia EL, Marshall KG. Halitosis. Can Med Assoc J 1982;126: 1281-5. 2. Meskin LH. A breath of fresh air. J Am Dent Assoc 1996;127: 1282-6. 3. Quirynen M. Management of oral malodour. J Clin Periodontol 2003;30(Supp 5):17-8. 4. Quirynen M, Zhao H, van Steenberghe D. Review of the treatment strategies for oral malodour. Clin Oral Investig 2002;6:1-10. 5. Zachrisson BU. Cause and prevention of injuries to teeth and supporting structures during orthodontic treatment. Am J Orthod 1976;69:285-300. 6. Mitchell L. Decalcification during orthodontic treatment with fixed appliances: an overview. Br J Orthod 1992;19:199-205. 7. Zachrisson S, Zachrisson BU. Gingival condition associated with orthodontic treatment. Angle Orthod 1972;42:26-34. 8. Zachrisson BU, Alnaes L. Periodontal condition in orthodontically treated and untreated individuals. II. Alveolar bone loss: radiographic findings. Angle Orthod 1973;43:402-12.
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9. Atack NE, Sandy JR, Addy M. Periodontal and microbiological changes associated with the placement of orthodontic appliances. A review. J Periodontol 1996;67:78-85. 10. Hamp S, Lundstrom F, Nyman S. Periodontal conditions in adolescents subjected to multiband orthodontic treatment with controlled oral hygiene. Eur J Orthod 1982;4:77-86. 11. Kloehn J, Pfeifer J. The effect of orthodontic treatment on the periodontium. Angle Orthod 1974;44:127-34. 12. Trossello VK, Gianelly AA. Orthodontic treatment and periodontal status. J Periodontol 1979;50:665-71. 13. Monteiro-Amado F, Chinellato LE, Tarzia O, Rezende ML. Evaluation of oral and nasal odor patients with and without cleft lip and palate: preliminary report. Cleft Palate Craniofac J 2004;41:661-3. 14. Sillness P, L€ oe H. Periodontal disease in pregnancy II. Correlation between oral hygiene and periodontal condition. Acta Odontol Scand 1964;22:121-35. 15. L€ oe H. The gingival index, the plaque index and the retention index systems. J Periodontol 1967;38(Supp 6):610-6.
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16. Brunette DM, Proskin HM, Nelson BJ. The effects of dentifrice systems on oral malodor. J Clin Dent 1998;9:76-82. € urk F, Ozdemir € 17. Doruk C, Ozt€ H, Nalc¸aci R. Oral and nasal malodor in patients with and without cleft lip and palate who had undergone orthodontic therapy. Cleft Palate Craniofac J 2008;45:481-4. 18. Astor FC, Hanft KL, Ciocon JO. Xerostomia: a prevalent condition in the elderly. Ear Nose Throat J 1998;94:156-60. 19. Rosenberg M, Kulkarni GV, Bosy A, McCulloch CA. Reproducibility and sensitivity of oral malodor measurements with a portable sulphide monitor. J Dent Res 1991;70:1436-40. 20. Tonzetich J. Production and origin of oral malodor: a review of mechanisms and methods of analysis. J Periodontol 1977;48: 13-20. 21. Neiders M, Ramos B. Operation of bad breath clinics. Quintessence Int 1999;30:295-301. 22. Bosy A, Kulkarni GV, Rosenberg M, McCulloch CAG. Relationship of oral malodor to periodontitis: evidence of independence in discrete subpopulations. J Periodontol 1994;65:37-46.
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Effect of fixed appliances on oral malodor Hasan Babacan,a Oral Sokucu,b _Ismail Marakoglu,c Hakan Ozdemir,d and Ruhi Nalcacie Sivas, Gaziantep, and Konya, Turkey Introduction: The objective of this study was to evaluate the effect of fixed appliances on oral malodor. Methods: Forty-one patients participated in this study. They were randomized into 2 groups: treated with fixed orthodontic appliances and untreated controls. Oral malodor measurements and the gingival and plaque indexes were recorded in each group by same periodontist. Measurements were taken from the study group before bonding, 1 week after bonding, and 4 weeks after bonding. The control group’s measurements were made at the same time. Results: Oral malodor and the gingival and plaque indexes were significantly increased 1 week after bonding (P \0.05). Oral malodor was increased at 4 weeks after bonding (P .0.05). The comparison of the groups showed differences 1 week and 4 weeks after bonding. Conclusions: The oral malodor reached the critical level during fixed orthodontic treatment. Oral malodor could indicate a need to evaluate oral health and remind patients of the importance of maintaining ideal oral hygiene. (Am J Orthod Dentofacial Orthop 2011;139:351-5)
H
alitosis is a lyrical term derived from the Latin word halitus (breath) and the Greek suffix osis (condition, action of a pathologic process).1 Halitosis (bad breath) is estimated to affect up to 50% of the population with varying degrees of intensity and etiology.2 The consequences of halitosis can be more than social; its presence could reflect serious local or systemic conditions. However, physicians tend to view this as a dental condition, which causes them most often to refer patients with this problem to a dentist.2 When halitosis is a dental problem, the profession should recognize and recommend therapy to address it. Halitosis is caused by several intraoral and extraoral factors, including systemic diseases and disorders of the gastrointestinal or upper respiratory tracts. If halitosis originates from the oral cavity, it is known as oral malodor. This is usually
a Associate professor, Department of Periodontics, Faculty of Dentistry, Cumhuriyet University, Sivas, Turkey. b Assistant professor, Department of Orthodontics, Faculty of Dentistry, Gaziantep University, Gaziantep, Turkey. c Associate professor, Department of Periodontics, Faculty of Dentistry, Selcuk University, Konya, Turkey. d Fellow researcher, Department of Periodontics, Faculty of Dentistry, Cumhuriyet University, Sivas, Turkey. e Fellow researcher, Department of Orthodontics, Faculty of Dentistry, Cumhuriyet University, Sivas, Turkey. The authors report no commercial, proprietary, or financial interest in the products or companies described in this article. Reprint requests to: Hasan Babacan, Cumhuriyet University, Department of Orthodontics, Faculty of Dentistry, 58140 Sivas, Turkey; e-mail, babacanhasan@ yahoo.com. Submitted, January 2009; revised and accepted, March 2009. 0889-5406/$36.00 Copyright Ó 2011 by the American Association of Orthodontists. doi:10.1016/j.ajodo.2009.03.055
caused by microbial metabolism from the tongue, saliva, or dental plaque.3 The prominent elements of oral malodor are volatile sulfide compounds (VSCs) and, in particular, hydrogen sulfide, methyl mercaptan, and dimethyl sulfide. Most of these compounds are metabolized from the proteolytic degradation by oral microorganisms of sulfur-containing peptides and amino acids in saliva, shed epithelium, food debris, gingival crevicular fluid, interdental plaque, postnatal drip, and blood.4 It was shown that the levels of VSCs in the mouth correlate with the depth of periodontal pockets, and that the amount of VSCs in the breath increase with the number, depth, and bleeding tendency of the periodontal pockets.4 Therefore, good plaque control is an important factor in the maintenance of dental health during fixed appliance therapy in orthodontics.5,6 The effects of orthodontic treatment on periodontal health have been investigated in several studies.7,8 Many researchers have observed inflammation of gingival tissues during fixed orthodontic therapy. This condition has been related to oral-hygiene measures hampered by fixed orthodontic appliances with consequent increases in the accumulation of bacterial plaque. Brackets, archwires, and other appliance components are both a focus for plaque accumulation and obstructions to plaque removal, thereby promoting gingivitis.7 Plaque also harbors cariogenic bacteria potentially capable of hard-tissue damage, especially at the bracket margins.6,9 Accordingly, once the fixed appliances are removed after treatment, the inflammation can be expected to resolve.10-12 351
Babacan et al
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The aim of this study was to evaluate the effect of fixed orthodontic treatment on oral malodor. MATERIAL AND METHODS
Ethical approval was granted by the local ethical committee, and permission was given for this study from the local ethics committee at Cumhuriyet University. All patients met the inclusion criteria: good general health, ages from 12 to 15 years, no previous orthodontic treatment, and no orthognathic surgery required; those with unsatisfactory oral hygiene were excluded from the study. Fifty patients in the permanent dentition were selected for this study from the orthodontic department of the dentistry faculty at Cumhuriyet University. Baseline measurements of plaque and gingival health were recorded for each volunteer by the same researcher (H.O.); if the patients were suitable for inclusion, the study was described in detail to them, and written information was given to them. Six patients were excluded because of poor oral hygiene and unwillingness to participate. Several weeks later, the patients were interviewed again to determine their willingness to participate in this study. After this stage, written consent was obtained, and they were randomly allocated. Forty-four subjects were recruited for this study. They were randomly assigned to the study group or the control group. The blinded periodontist (I.M.) gave formal hygiene instructions to the each patient. The study group included 21 subjects (12 girls, 9 boys) who would have fixed orthodontic treatment. The control group included 20 subjects (11 girls, 9 boys) who did not receive orthodontic treatment. A classic bonding process was used for all patients. All teeth were etched for 20 seconds with 37% phosphoric acid, washed with a spray for 10 seconds, and dried to a chalky white appearance. The tooth surface was thoroughly dried, and a thin layer of Transbond XT sealant (3M Unitek, Monrovia, Calif) was applied. Orthodontic metal brackets (Generus Roth, GAC International, Bohemia, NY) were used in this study. The mouth was fully bonded in 1 session. Nickel-titanium leveling archwires were fixed with elastic ligatures in all teeth. The orthodontic treatments for the patients in the control group started 1 month after the end of this study. Table I shows the distribution and average ages of the subjects. The following were recorded in each group by same periodontist (H.O.): (1) oral malodor measurements, (2) gingival index (GI), and (3) plaque index (PI). Measurements were taken in the study group before bonding (T1), 1 week after bonding (T2), and 4 weeks after bonding (T3). The measurements in the control group were made at the same times. One patient from the study group and 2 patients from the control group did not
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Table I. Distribution and average ages of subjects Girls (n) and Boys (n) and Average age (y) percentage percentage mean 6 SD Study group 12 9 13.05 6 1.48 60% 40% 11 9 13.70 6 1.61 Control group 20 55% 45% n 21
have the measurements and therefore were excluded from the study. All subjects were evaluated at the first appointment to establish their measurements at T1. The participants were asked to carry on their normal oral-hygiene practices. They were instructed to brush their teeth after dinner and to refrain from eating and drinking until coming to the dentistry faculty next morning. They were also requested to avoid spicy foods, onions, and garlic for 48 hours before the appointment. After the first appointment, the study group subjects were bonded immediately. Measurements were taken at T2. Measurements were also taken at T3, after the subjects had conducted their own oral care for 4 weeks. A Halimeter (Interscan, Chatsworth, Calif) was used to evaluate the levels of VSCs in their breath. Oral malodor values were divided into 4 categories and classified as normal (values from 0-100 parts per billion [ppb]), weak (101-150 ppb), strong (151-300 ppb), or very strong ($301 ppb).13 Each subject kept the mouth closed for 60 seconds before sampling. A plastic straw was inserted and positioned above the posterior portion of tongue dorsum, not touching the oral mucosa or the tongue. Breathing was not allowed during sampling. The mouth was kept open by approximately 1.5 cm, and the peak value was recorded. The measurements were duplicated, and the mean value was calculated. The PI was recorded at 4 tooth surfaces (mesial, distal, buccal, and lingual), and the quantity of supragingival plaque on the cervical area was assessed for every tooth. The scores for PI were defined as follows: 0, no plaque in the gingival area; 1, a film of plaque adhering to the free gingival margin and adjacent area of the tooth that could be recognized only by running a probe across the tooth surface; 2, moderate accumulation of soft deposits in the gingival pocket and on the gingival margin or the adjacent tooth surface that could be seen by the naked eye; and 3, abundance of soft matter in the gingival pocket or on the gingival margin and adjacent tooth surface.14 The GI was recorded on the mesial, distal, buccal, and lingual surfaces with a manual periodontal probe (Williams probe, Hu-Friedy, Chicago, Ill). Bleeding was recorded if it occurred within 30 seconds of probing.
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Table II. Comparison of the oral malodor scores of the study and control groups Study group mean 6 SD Control group mean 6 SD
n 21
T1 58.55 6 13.77
T2 81.00 6 17.15
T3 94.70 6 12.31
T1-T2 *
T1-T3 *
T2-T3 *
20
58.15 6 14.32
60.85 6 12.05
61.35 6 15.41
NS
NS
NS
0.620 NS
0.000*
0.000*
P value
F 5 56.93 P 5 0.000 P \0.05* F 5 0.66 P 5 0.519 P .0.05
*Significant at the 0.05% level of confidence; NS, not significant.
Table III. Comparison of the plaque index scores of the study and control groups Study group mean 6 SD Control group mean 6 SD
n 21
T1 0.95 6 0.21
T2 1.15 6 0.20
T3 1.17 6 0.14
T1-T2 *
T1-T3 *
T2-T3 NS
20
0.99 6 0.20
1.05 6 0.25
1.05 6 0.19
NS
NS
NS
0.811 NS
0.016*
0.001*
P value
F 5 21.74 P 5 0.000 P \0.05* F 5 1.16 P 5 0.324 P .0.05
*Significant at the 0.05% level of confidence; NS, not significant.
Scores for the GI were defined as follows: 0, normal gingiva; 1, mild inflammation, slight change in color, slight edema, and no bleeding on palpation; 2, moderate inflammation, redness, edema and glazing, and bleeding on probing; and 3, severe inflammation, marked redness and edema, ulceration, and tendency to spontaneous bleeding.15 The group score was subsequently calculated by adding the individual scores and dividing the total by the number of patients included. Statistical analysis
The sample size for each group was calculated and based on a significance level of a 5 0.01 and a power (1-b) of 90%. The sample size calculation showed that 19 patients in each group were sufficient; however, our study group consisted of 21, and the control group consisted of 20 patients. The data were statistically analyzed by using SPSS software (version 15.0, SPSS, Chicago Ill). Multiple comparisons of the data were performed with analysis of variance (ANOVA). If there was evidence of statistically significant differences between the measurements or groups, the Bonferroni test were used. The MannWhitney U test was used to compare the groups. RESULTS
The mean values for oral malodor, the GI, and the PI are shown in Tables II through IV.
In the study group, oral malodor values showed significant differences between T1 and T2, T1 and T3, and T2 and T3) (P \0.05). The control group did not show significant differences between measurements (P .0.05) (Table II). For the PI, the study group showed significant differences between T1 and T2 and T1 and T3 (P \0.05). The control group showed no significant differences among the times (P .0.05) (Table III). For the GI, the study group showed significant differences between T1 and T2 and T1 and T3 (P \0.05). The control group did not show significant differences among the times (P .0.05) (Table IV). The comparison of the parameters (PI, GI, and oral malodor) of both groups showed differences at T2 and T3 (P \0.05) (Tables II-IV). DISCUSSION
The mouth is the cause of more than 90% of cases of oral malodor. The most common cause of oral malodor is elevated levels of VSC, primarily hydrogen sulfide and methyl mercaptan in the breath.16,17 In this study, a portable sulfide monitor was used to measure VSCs. Its advantages include ease of use by nonskilled persons, noninvasiveness, low possibility of cross-infection, portability, relatively low expense, and rapid turnaround time of 1 to 2 minutes between measurements.18,19
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Table IV. Comparison of the gingival index scores of the study and control groups Study group mean 6 SD Control group mean 6 SD P value
n 21
T1 1.03 6 0.19
T2 1.19 6 0.21
T3 1.25 6 0.23
T1-T2 *
T1-T3 *
T2-T3 NS
20
0.98 6 0.10
1.02 6 0.06
0.97 6 0.11
NS
NS
NS
0.341 NS
0.003*
0.000*
F 5 11.84 P 5 0.000 P \0.05* F 5 1.27 P 5 0.292 P .0.05
*Significant at the 0.05% level of confidence; NS, not significant.
After placement of the brackets, the PI and the GI scores began to increase in the study group. The results demonstrated that bonding of brackets enhanced plaque retention. Patients who undergo orthodontic treatment with fixed appliances often have problems cleaning the tooth surfaces effectively around the attachments. Previous studies showed that orthodontic treatment with fixed appliances is accompanied by increased risks of caries and gingivitis.5-7 Our study showed that oral malodor can be added to this list of risks. Immediately after bonding, oral malodor directly increased just like the PI and GI indexes. Tonzetich20 showed a correlation between plaque and oral malodor. However, the mean value of oral malodor during fixed orthodontic treatment is not clinically important (84 ppb). The patients’ orthodontic treatments followed routine oral health procedures. But these procedures could not protect periodontal health ideally. In our study, the PI and GI indexes significantly increased after bonding. Interestingly, 4 weeks after bonding, the PI and the GI were stable. Bacterial dental plaque, like salivary sediment, has a strong potential to form substrates containing cysteine, cystine, methionine, nutrient broth, and salivary sediment to yield similar volatile compounds through salivary putrefaction. The capacity of plaque to use the salivary substrate for odor production was established by the lyophilized fractions of saliva. Another study mentioned that deposits of oral microorganisms of plaque on teeth or in periodontal pockets could contribute to bad breath.21 Eight to 14 hours of maturation are required before plaque deposits produce VSCs. Protected plaque in interproximal sites produced substantial odors and is associated with overall levels of VSCs. Bosy et al22 found that oral malodor in healthy subjects could originate from protected interdental sites. But, interestingly, contrary to our findings, they found no correlation between the PI and oral malodor. Although the comparison of the PI and the GI showed no differences at T3, oral malodor survived and
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increased in our subjects. The last measurements of oral malodor in the study group reached the critical border of the weak stage. The observation of the control group showed no change in any parameter. The parameters were stable for 4 weeks. The presence of dental plaque could cause some oral malodor. Because of the long treatment time of 2 years or more, a rigid plaque-control program is indispensable. Professional tooth cleaning at short intervals must be complemented by efficient oral-hygiene procedures at home. Otherwise, with the aggravation of the PI and the GI, we could be faced with oral malodor in our orthodontic patients. Our study showed that oral malodor can be another way to evaluate oral health. CONCLUSIONS
Oral malodor reached the critical level during fixed orthodontic treatment. The PI and GI scores increased immediately after bonding. Oral malodor could be another indicator to evaluate oral health and to warn patients to achieve ideal oral hygiene. REFERENCES 1. Attia EL, Marshall KG. Halitosis. Can Med Assoc J 1982;126: 1281-5. 2. Meskin LH. A breath of fresh air. J Am Dent Assoc 1996;127: 1282-6. 3. Quirynen M. Management of oral malodour. J Clin Periodontol 2003;30(Supp 5):17-8. 4. Quirynen M, Zhao H, van Steenberghe D. Review of the treatment strategies for oral malodour. Clin Oral Investig 2002;6:1-10. 5. Zachrisson BU. Cause and prevention of injuries to teeth and supporting structures during orthodontic treatment. Am J Orthod 1976;69:285-300. 6. Mitchell L. Decalcification during orthodontic treatment with fixed appliances: an overview. Br J Orthod 1992;19:199-205. 7. Zachrisson S, Zachrisson BU. Gingival condition associated with orthodontic treatment. Angle Orthod 1972;42:26-34. 8. Zachrisson BU, Alnaes L. Periodontal condition in orthodontically treated and untreated individuals. II. Alveolar bone loss: radiographic findings. Angle Orthod 1973;43:402-12.
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16. Brunette DM, Proskin HM, Nelson BJ. The effects of dentifrice systems on oral malodor. J Clin Dent 1998;9:76-82. € urk F, Ozdemir € 17. Doruk C, Ozt€ H, Nalc¸aci R. Oral and nasal malodor in patients with and without cleft lip and palate who had undergone orthodontic therapy. Cleft Palate Craniofac J 2008;45:481-4. 18. Astor FC, Hanft KL, Ciocon JO. Xerostomia: a prevalent condition in the elderly. Ear Nose Throat J 1998;94:156-60. 19. Rosenberg M, Kulkarni GV, Bosy A, McCulloch CA. Reproducibility and sensitivity of oral malodor measurements with a portable sulphide monitor. J Dent Res 1991;70:1436-40. 20. Tonzetich J. Production and origin of oral malodor: a review of mechanisms and methods of analysis. J Periodontol 1977;48: 13-20. 21. Neiders M, Ramos B. Operation of bad breath clinics. Quintessence Int 1999;30:295-301. 22. Bosy A, Kulkarni GV, Rosenberg M, McCulloch CAG. Relationship of oral malodor to periodontitis: evidence of independence in discrete subpopulations. J Periodontol 1994;65:37-46.
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