The objective of this study was to evaluate the effect of fixed appliances on oral malodor.
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.
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.
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.
Halitosis is a lyrical term derived from the Latin word halitus (breath) and the Greek suffix osis (condition, action of a pathologic process). Halitosis (bad breath) is estimated to affect up to 50% of the population with varying degrees of intensity and etiology. 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. 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 caused by microbial metabolism from the tongue, saliva, or dental plaque.
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.
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.
Therefore, good plaque control is an important factor in the maintenance of dental health during fixed appliance therapy in orthodontics. The effects of orthodontic treatment on periodontal health have been investigated in several studies. 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. Plaque also harbors cariogenic bacteria potentially capable of hard-tissue damage, especially at the bracket margins. Accordingly, once the fixed appliances are removed after treatment, the inflammation can be expected to resolve.
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.
|n||Girls (n) and
|Boys (n) and
|Average age (y)
mean ± SD
|13.05 ± 1.48|
|13.70 ± 1.61|
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 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).
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.
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. 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. The group score was subsequently calculated by adding the individual scores and dividing the total by the number of patients included.
The sample size for each group was calculated and based on a significance level of α = 0.01 and a power (1-β) 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 Mann-Whitney U test was used to compare the groups.
The mean values for oral malodor, the GI, and the PI are shown in Tables II through IV .
mean ± SD
|21||58.55 ± 13.77||81.00 ± 17.15||94.70 ± 12.31||∗||∗||∗||F = 56.93
P = 0.000
P <0.05 ∗
mean ± SD
|20||58.15 ± 14.32||60.85 ± 12.05||61.35 ± 15.41||NS||NS||NS||F = 0.66
P = 0.519
|P value||0.620 NS||0.000 ∗||0.000 ∗|