Long-term periodontal orthodontic treatment
status after
A. M. Poison,* J. D. Subtelny,** S. W. Meitner,*** A. P. Poison,**** E. W. Sommers,***** H. P. Iker,****** and B. E. Reed******* Rochester, N. Y.
This study evaluated the clinical periodontal status of persons who had completed orthodontic therapy at least 10 years previously (study) and compared the findings to those of adults with untreated malocclusions (control). Subjects in the study (n = 112; 63 female subjects, 49 male subjects; mean age 29.3 ? 4.2 [SD] years) and control (n = 111; 62 female subjects, 49 male subjects; mean age 32.9 + 6.5 years) populations underwent a comprehensive periodontal examination that consisted of measurements taken at six points around the circumference of each tooth: (1) plaque, (2) visual inflammation, (3) bleeding after probing, (4) pocket depth, (5) gingival recession, and (6) loss of connective tissue attachment. Data from the individual measuring points were organized into 14 different combinations of either tooth types or surface locations; each was subjected to a four-way ANOVA partitioned on group (study vs. control), sex, socioeconomic status, and malocclusion type. The results showed that differences in age distribution within the groups were affecting the comparisons between the groups. Consequently, the groups were balanced for age and analyses were done to investigate group differences by means of multiple regression techniques. The comparisons showed no significant differences between the groups for any of the periodontal variables. It was concluded that orthodontic treatment during adolescence had no discernible effect upon later periodontal health. (AM J ORTHOD DENTOFAC ORTHOP 1988;93:51-8.)
I
t is well established that orthodontic therapy can produce a more esthetic dentofacial complex and a superior functional occlusion. However, it remains unclear as to whether long-term periodontal health is better or worse as a consequence of the patient having undergone orthodontic therapy in adolescence. The literature regarding the relationship between crowding of teeth, plaque accumulation, and degree of periodontal disease is conflicting. Several studies report that there is a positive relationship among these factors,lm6while other studies report no relationship.‘-” Clinicians also differ in their opinions regarding relationships between orthodontic treatment and periodontal status; several
From the Departments of Periodontics and orthodontics, Eastman Dental Center. Study supported in part by Grant DE-82413, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland, and Pluta Periodontal Fund. *Chairman, Department of Periodontics. **Chairman, Department of Orthodontics. ***Assistant Professor. Department of Dental Research, University of Rochester. ****Clinical Associate, Department of orthodontics. *****Clinical Associate, Department of orthodontics. ******Professor. Department of Psychiatry, University of Rochester. *******Private practice limited to periodontics, Kingston, Ontario, Canada.
investigators maintain that there is no permanent damage to a healthy periodontium as a result of orthodontic treatment,‘2”3 whereas others believe that orthodontic treatment may initiate the first stage of marginal periodontitis. 14.15In addition, the periodontal remodeling associated with orthodontic therapy may become a significant factor with age.‘6,‘7 A relationship may exist between orthodontic therapy and conversion of gingivitis into periodontitis-for example, orthodontic bands may increase subgingival plaque retention. I’-** Furthermore, orthodontic movement resulting in tooth intrusion may shift supragingival plaque into a subgingival location and predispose toward destructive periodontitis.23 In this respect small but statistically significant loss of connective tissue attachment has been reported shortly after completion of orthodontic therapy.‘9*24 In spite of the differing views on the relationship between orthodontic therapy and periodontal status, scientific data are lacking to provide comprehensive information about this relationship. Consequently, there is an urgent need for studies that evaluate long-term periodontal health after comprehensive orthodontic therapy. Furthermore, it is imperative that the data be obtained from human subjects rather than from animals. 51
52
Poison et ul.
Table I. Distribution of subjects Malocclusion Gr0l4p
Study
Sex
Source*
Female
EDC PVT EDC PVT
13 23 I5 12
10 IS 7 11
1 I 2 2
EDC PVT EDC PVT
22 1s 18 17
16 s 4 7
2 2 I 2
135
75
13
Male
Control
Female Male
Code IOf
TOTAL
*EDC ‘Kode SCode $&de
= 10 21 22
Eastman Dental Center; PVT = Angle’s Class I. = Angle’s Class II, Division = Angle’s Class II, Division
= private
!
Code 21$
Code 229’
Total
63 - 49 112 h2 49 -ii-i 22.3 --
practice.
1. 2.
In one of the few studies that was addressed to the subject of long-term periodontal status after orthodontic treatment, there were indications of accelerated periodontal breakdown in selected areas of the dentition .25~26 It was the purpose of the present study to provide additional information on this important question.
In the present study of periodontal status after orthodontic therapy, there were 112 subjects who had completed orthodontic treatment at least 10 years previously. These patients were treated at the Department of Orthodontics at the Eastman Dental Center or privately by faculty of the Orthodontic Department. There were comprehensive orthodontic records still available on each patient. The first task was to locate and contact these persons as more than 10 years had passed since they were last examined. The logistic challenge and problems related to tracing and locating persons not seen for more than a decade were considerable. More than 900 contacts had to be initiated before securing a commitment from 112 persons to participate in the study. Once an individual had been successfully contacted and the details of the study explained, the willingness of the patients to participate in the study was 100%. They appeared to be genuinely interested in the goals of the study and, after they had completed the examination, each said they would be very willing to return for reexamination in the future. The mean age of the persons in the study group was 29.3 years (+4.2 SD).
There were 111 persons in the control group; these subjects had untreated malocclusions and a mean age of 32.9 years ( + 6.5 SD). For any subject to participate in the study, there had to be a minimum number of 20 natural teeth present. The number present ranged from 21 to 28 teeth. The mean number of teeth present in the study group was 25.4 ( +- I .9 SD) and in the control group, 27.4 ( + 1.1 SD). The mean number present in the control group was significantly greater than that of the study group.
Each subject underwent a comprehensive periodontal and orthodontic examination. This report will concentrate upon the results of the periodontal examination. During this examination, at six points around the circumference of each tooth, three on the buccal and three on the lingual aspects, the following variables were measured. Bacterial plaque. Plaque was located and scored by means of the system of Silness and Lo~.‘~ Visual injlammation. The gingival margin was examined visually and classified as either noninflamed (paIe pink color) or inflamed (change in color from normaI paIe pink).‘8 Bleeding after probing. The presence or absence of bleeding within 30 seconds after probing with a 25-g force29 was ascertained. An electronic pressuresensitive periodontal probe30 was used to control probing force. Gingivul margin location. The location of the gingival margin was measured as an estimate of recession.
Volume 93 Number I
Long-term periodontal
Table II. Age characteristics of subjects (years) study Mean Median Mode Range
29.3
+ 4.2 28.4 28 23-48
status
after
orthodontic treatment 53
Table Ill. Plaque index
Control 32.9
-+ 6.5 32.1 31 23-52
The distance between the cementoenamel junction and the gingival margin was measured with a conventional periodontal probe. 29 Periodontal pocket depth. Each pocket was probed according to the method described by Ramfjord3’ using the pressure-sensitive probe with a 50-g probing force.29 Loss of connective tissue attachment. The distance from the cementoenamel junction to the depth of probe tip penetration (clinical loss of attachment) was calculated for each pocket by means of pocket depth and gingival margin location measurements. Analysis of data
Table I gives the distribution of subjects. Each person was identified group (study, control) and sex, and classified by source (clinic patients vs. private patients); the latter was used as a possible indication of socioeconomic status. In addition, subjects were classified by type of malocclusion according to Angle. Class I was coded 10; Class II, Division 1 was coded 21; and Class II, Division 2 was coded 22. The broad groupings were fairly well balanced (Table I). For the study group, the female-to-male ratio was 63/49; in the control group, the ratio was 62/49. In malocclusion codes 10 and 21, there were 135 and 75 persons, respectively (Table I). The 13 persons with Class II, Division 2 malocclusion (code 22) were excluded from the study because of the small sample size and because it was not appropriate to include them in the code 21 subgroup. A four-way analysis of variance was performed: group x sex x source x malocclusion. The only significant effect was between groups; on no occasion did “group” interact significantly with either “sex,” “source,” or “malocclusion.” The study group had significantly less loss of connective tissue attachment and gingival recession than the control group. Since there were no differences in plaque levels, the age factor was examined more closely because greater periodontal destruction has been equated with increasing age. There appeared to be close similarities with respect to age characteristics (means, medians, modes, and ranges) in the study and control groups (Table II). How-
Tooth
type
Maxillary Mandibular Molar Premolar Canine Incisor
0.67 0.60 0.74 0.84 0.59 0.57 0.61
0.03 0.03 0.03 0.03 0.03 0.03 0.03
0.64 0.59 0.68 0.83 0.58 0.51 0.56
0.03 0.03 0.04 0.05 0.04 0.03 0.03
Surface location Buccal Lingual Interproximal IP : Lingual IP : Buccal Lingual : Mid Buccal : Mid
0.57 0.77 0.73 0.80 0.64 0.69 0.42
0.03 0.03 0.03 0.03 0.03 0.04 0.03
0.51 0.75 0.69 0.80 0.58 0.67 0.37
0.04 0.04 0.03 0.04 0.04 0.05 0.04
TOTAL
ever, examination of the frequency distribution of ages showed that in the study group there were only two subjects (1.9% of the sample) who were more than 36 years of age. In contrast, there were 28 subjects in the control group (27.5% of the sample) who were more than 36 years old. To equalize the groups for age, both groups were truncated at an upper age of 36 years. This left 104 persons in the study group and 76 in the control group. The mean ages of these groups were 28.9 ( + 3.4 SD) and 29.8 (+ 3.9 SD), respectively, with medians of 28.3 and 30.5 years. Analyses were targeted toward discerning group differences by means of multiple regression techniques. The data were collected and analyzed according to 14 different combinations of tooth types (seven) or surface locations (seven). These various tooth types and locations were examined to explore the possibility that differences between the groups were related to different sites within the mouth. RESULTS
The mean plaque indices are shown in Table III. The overall plaque values for the groups were quite low, 0.67 and 0.64 in the study and control groups, respectively. There was some variation within the groups, dependent upon tooth type and surface location. For example, molar teeth had higher plaque levels than incisor teeth and buccal surfaces showed lower plaque scores than interproximal surfaces. However, there were no differences in any of the corresponding values between study and control groups, indicating that ortho-
Table IV. Percentage of visually inflamed
Table V. Percentage of bleeding gingival sites after probing ___- ..-.--.--_._
gingival sites
Study group Mean Tooth type 51
Maxillary Mandibular Molar Premolar Canine Incisor
41 60
56 48
41 50
2.5 2.6
52 45
3.0 3.1
2.6 2.4 2.6
59 56 51
3.1 2.9 3.0
2.8
49 SO
3.3 3.3
2.9
location
Buccal Lingual Interproximal IP: Lingual IP: Buccal Lingual : Mid Buccal : Mid
SE
Mean
group --. SE
Tooth type
TOTAL
Surface
Control
TOTAL
Maxillary Mandibular Molar Premolar Canine Incisor Sulfate
47 54
2.6 2.6
48 56
60
2.8
62
3.3
62 39
2.9 3.1 2.5
64 60 39
3.4 3.6 3.4
26
2.4
24
2.7
58
3.1 3.2
dontic treatment had no subsequent long-term effect upon plaque levels. Visual inflammation was expressed as the percentage of gingival sites in the mouth exhibiting the presence of inflammatory change (Table IV). Inflammation was present in approximately 50% of the sites examined in both groups and, although there were variations depending upon site in the mouth, there were no differences in any of the comparisons between study and control groups regarding either tooth type or surface location. The results from the bleeding after probing evaluation (Table V) showed the same trends as visual inflammation analysis. Thus, the level of clinically apparent inflammation, as evaluated visually and by bleeding after probing, seemed unrelated to previous orthodontic treatment. Gingival margin location was measured to assess gingival recession (Table VI). All of the mean values for tooth type and surface location were positive, indicating that the gingival margin was coronal to the cementoenamel junction and that recession apical to the cementoenamel junction did not predominate in any region. All of the values for the study group were numerically greater than corresponding values in the control group, suggesting that the gingival margin tended to be more coronal after orthodontic treatment. However, there were no statistical differences in any of the actual comparisons between study and control groups. The mean values for periodontal pocket depth in both the study and control groups for all tooth types
16 13 19
I I 1.0 1.2
16 I5 17
I.2 1.3 12
20
I .4
22
1 .h
16
1.2
17
I :
12
1.1
II
1.3
14
1.2
12
1.2
13
1.2
19 17
1.2
11 21
1 ' t.;,
19 14
1.3 1.2
16 20 13
I .2 1.6 I .?
19 12
1.3 1.3
22
I.9
location
Buccal Lingual Interproximal IP : Lingual IP: Buccal Lingual : Mid Buccal : Mid
1.2
9
1.2
and surface locations were less than 3 mm (Table VII). Once again, there were variations in pocket depth, depending upon tooth type (molar tooth values greater than incisors) and surface location (interproximal surface values were greater than midbuccal). However, there were no statistically significant differences between the two groups in any of the comparisons of corresponding tooth types or surface locations. The most significant clinical variable relating to periodontal status is the loss of conaective tissue attachment. This was measured in millimeters and the mean value is shown for tooth type and surface location in Table VIII. It was apparent that there was evidence of loss of attachment distributed around each of the different groups of teeth and surface locations in study and control groups, but the magnitude of loss was small. There were differences within each group relating to tooth type (molars showed a greater loss than incisors) and surface location (midbuccal loss of attachment was greater than the interproximal). However, there were no significant d&&rences between the control and study groups, indicating that orthodontic treatment had no long-term effect upon subsequent connective tissue attachment levels.
Examination of bacterial plaque levels showed that the study and control groups were similar in both the
mean level of plaque present throughout the &n&ion and its distribution in cliffant tooth and surface lo-
Volume 93 Number I
Long-term
Table VI. Distance from the gingival margin to
periodontal
Cow01 SE
Mean
SE
Maxillary Mandibulru Molar Premolar Canine Incisor
1.92 1.91 1.93 2.11 1.96 1.85 1.75
0.04 0.04 0.04 0.04 0.04 0.04 0.04
1.83 1.80 1.85 2.01 1.85 1.78 1.65
0.05 0.05 0.05 0.06 0.05 0.05 0.05
treatment
55
Surface location Buccal Lingual Interproximal IP : Lingual IP : Buccal Lingual : Mid Buccal : Mid
1.86 1.99 2.20 2.20 2.21 1.57 1.15
0.04 0.04 0.04 0.04 0.04 0.04 0.06
1.76 1.90 2.09 2.09 2.09 1.52 1.10
0.05 0.05 0.05 0.05 0.04 0.06 0.07
Control
group
Mean
SE
Mean
SE
Maxillary Mandibular Molar Premolar Canine Incisor
2.16 2.15 2.17 2.42 2.18 2.05 1.94
0.03 0.03 0.03 0.03 0.03 0.03 0.03
2.10 2.12 2.10 2.39 2.11 2.00 1.88
0.03 0.04 0.04 0.05 0.03 0.03 0.03
Surface location Buccal Lingual Interproximal IP: Lingual IP: Buccal Lingual : Mid Buccal : Mid
2.16 2.15 2.40 2.34 2.45 1.76 1.59
0.03 0.03 0.03 0.03 0.03 0.03 0.03
2.10 2.11 2.32 2.29 2.36 1.74 1.54
0.03 0.04 0.04 0.04 0.04 0.04 0.04
Tooth type TOTAL
type
TOTAL
orthodontic
Study group group
Mean Tooth
after
Table VII. Periodontal pocket depth (millimeters)
the cementoenamel junction (millimeters) Study group
status
Table VIII. Loss of attachment (millimeters)
cations (Table III). The distribution of bacterial plaque in relation to tooth type and surface location was consistent with previous reports showing higher plaque levels in the least accessible locations.27’32-36The mean plaque levels were lower than comparable values reported in other studies,27*36*37 suggesting that the populations in our investigation had a high level of “dental awareness.” The control group was derived from persons receiving regular dental care and their willingness to participate in a study pertaining to dental health may have selectively provided a control group conscious of oral hygiene. With regard to the study group, these persons had received oral hygiene instruction and reinforcement during orthodontic treatment. These regimens have been shown to result in improved oral hygiene levels shortly after completion of orthodontic treatment13*183842;however, these differences may not be maintained on a long-term basis.25,26It is unclear whether the lack of difference in plaque levels in our present study reflects long-term oral hygiene relapse by the study group or an increased dental awareness and motivation by the control group. Assessment of clinical inflammation through visual changes and bleeding after probing showed no difference between study and control groups for both the overall level of inflammation and its distribution. As with the plaque levels, the level of existing inflammation was low. The degree of inflammation corresponded with the distribution of plaque and indicated that clinical signs of inflammation (color changes and bleeding) re-
Tooth
type
Maxillary Mandibular Molar Premolar Canine Incisor
0.36 0.35 0.36 0.43 0.35 0.32 0.30
0.03 0.03 0.03 0.04 0.03 0.03 0.03
0.38 0.40 0.36 0.50 0.36 0.30 0.33
0.04 0.05 0.04 0.06 0.04 0.04 0.04
Surface location Buccal Lingual Interproximal IP : Lingual IP: Buccal Lingual : Mid Buccal : Mid
0.41 0.30 0.32 0.28 0.35 0.32 0.54
0.04 0.03 0.03 0.03 0.03 0.03 0.05
0.43 0.33 0.35 0.33 0.38 0.35 0.55
0.05 0.04 0.04 0.05 0.04 0.04 0.06
TOTAL
lated to the presence or absence of plaque, rather than a history of orthodontic treatment. 13*42,43 Gingival margin location was measured as an indication of gingival recession. The lack of differences between study and control groups does not implicate orthodontic treatment during adolescence as a contributing factor for gingival recession in adulthood. These long-term findings agree with earlier reports that evaluated gingival margin location during, or shortly after, orthodontic treatment.‘3,‘9@ Contrary to expectations, the orthodontically treated group consistently
56
Polson et al.
showed a more coronal gingival margin location than the control group. Although the difference was not statistically significant, this trend was present for all tooth types and surface locations. There are two possibilities that may be responsible for the more coronal gingival margin in the orthodontically treated group. First, orthodontic appliances result in gingival inflammation and enlargement,38~45independent of the presence of supragingival plaque. ‘x.46 Generally, however, the gingiva returns to normal after bands have been removed. ‘* The second possibility relates to the gingival bunching that may occur with orthodontic relocation of the teeth. The incidence of gingival bunching and clefting has been reported primarily in association with orthodontic closure of extraction spaces.‘8,47-49 It is reasonable, however, to consider that gingival tissue bunching could also occur in other locations where tooth position is changed by orthodontic movement. ‘Rs” Although studies have indicated that tissue bunching is transient and resolves with time, 47,49~5’~s2 the tendency for a more coronal gingival margin location has been reported on a long-term basis after tooth movement into extraction spaces.” A similar generalized effect throughout the dentition would result in a tendency toward the more coronal gingival margin in the orthodontically treated group in our present study. Examination of pocket depths showed no statistical difference between study and control groups; however, the pocket depth values for all tooth types and surface locations were always greater in the orthodontically treated group. Although one tends to associate deeper periodontal pockets with destructive periodontal disease, this is not necessarily the case since the critical clinical variable relating to periodontal destruction is the loss of connective tissue attachment .54,55The lack of difference between the groups regarding loss of attachment (Table VIII) means that the increased pocket depth tendency in the study group did not represent greater periodontal destruction. Consequently, the tendency for deeper pocket depths in the study group resulted from a more coronally positioned gingival margin, rather than from increased periodontal destruction at the base of the pocket. Residual tissue bunching would result in coronal positioning of the gingival margin and an associated increase in pocket depth, and may have been responsible for the greater pocket depth tendencies in the study group. It was of interest that loss of connective tissue attachment was prevalent around all areas of the dentition, although the magnitude of loss was small (Table VIII). These values and the distribution of ranges around different tooth types and surface locations were similar to
corresponding values obtained from a population 01 30- to 40-year-old persons who had received “regulat dental visits” throughout their lives.37,56Although loss of periodontal support was present, the magnitude indicates a slow overall rate of progression in these populations over that decade. In making this generalization, however, it is necessary to exercise caution since progressive periodontal destruction seems to be a sitespecific condition that advances in a few unpredictable sites and is not a generalized phenomenon.57,5” It is probable that the connective tissue attachment level is the single most important variable when assessing the progression of marginal periodontitis .“,55 The lack of difference in attachment levels between study and control groups in the present study implies no adverse long-term effect after orthodontic treatment in adolescence. These findings are consistent with the results from an analysis of the radiographic alveolar bone levels from these two groups in an earlier investigation . 59 Although current information on the effect of orthodontic therapy on attachment levels is conflicti%,‘9,24 most of these studies were relatively short term. If clinical probing measurements are made shortly after completion of orthodontic therapy, errors relating to depth assessment may occur because of probe tip penetration into the inflamed connective tissue associated with orthodontic bands.” In addition, it is not known whether the small differences found in attachment levels in these studies persisted at long-term observation periods . In the only other long-term study,‘” it was reported that overall periodontal status did not differ between study and control groups. There was some evidence, however, for increased periodontal breakdown in the maxillary posterior regions of orthodontically treated persons. Although similar trends were not observed in our investigation, the orthodontically treated subjects in the other study25 were approximately 9 years older and it is possible that detrimental periodontal consequences may become apparent in later years when patients become more “susceptible” to periodontal breakdown. In this respect it would be intriguing and meaningful to conduct similar comparisons between our study and control populations several years hence. These longitudinal evaluations would ascertain the future patterns and rate of periodontitis progression, and whether or not orthodontically treated persons become more susceptible to periodontal breakdown. In summary, analyses of the data obtained from the comprehensive clinical variables failed to demonstrate any major differences in long-ten-n periodontal status between tooth surfaces that had been subjected to ortho-
Volume 93 Number 1
dontic treatment and corresponding surfaces that had not received orthodontic tooth movement. Although the study was limited in that it was retrospective rather than prospective, it was concluded that orthodontic treatment during adolescence had no discernible effect upon later periodontal health. However, the upper age limit in each group was 36 years and periodontal differences may, or may not, become manifest in later years.
REFERENCES
1. Pot&on DR, Aaronson SA. The relationship between occlusion and periodontal status. AM J ORTHOD 1961;47:690-9. 2. Bilimoria KF. Malocclusion, its role in the causation of periodontal disease. J Indian Dent Assoc 1963;35:293-300. 3. Suomi JD. Periodontal disease and oral hygiene in a institutionalized population; report of an epidemiological study. J Periodontol 1969;40:5-10. 4. Alexander AG, Tipnis AK. The effect of irregularity of teeth and the degree of overbite and overjet on the gingival health. Br Dent J 1970; 128539-47. 5. Buckley IA. The relationship between malocclusion and periodontal disease. J Periodontol 1972;43:415-7. 6. Ainamo J. Relationship between malalignment of the teeth and periodontal disease. Stand J Dent Res 1972;80:104-IO. 7. Beagrie GS, James GA. The association of posterior tooth irregularity and periodontal disease. Br Dent J 1962;113:239-43. 8. Geiger AM. Occlusal studies in 188 consecutive cases of periodontal disease. AM J ORTHOD 1962;48:330-60. 9. Gould MSF, Picton DCA. The relation between irregularities of the teeth and periodontal disease. Br Dent J 1966;121:20-3. 10. Razsan DP, Shawla TN. Malocclusion-its association with periodontal disease. J Indian Dent Assoc 1970;42:39-43. 11. Geiger AM, Wasserman BH, Turgeon LR. Relation of occlusion and periodontal disease. Part VIII. Relationship of crowding and spacing to periodontal destruction and gingival inflammation. J Periodontol 1974;45:43-9. 12. Rateitschak KH. Orthodontics and periodontology. Int Dent J 1968;18:108. 13. Kloehn JS, Pfeifer JS. The effect of orthodontic treatment on the periodontium. Angle Orthod 1974;44:127-34. 14. Kessler M Interrelationships between orthodontics and periodontics. AM 3 ORTHOD 1976;70:154-72. 15. Norton L. Periodontal considerations in orthodontic treatment. Dent Clin North Am 1981;25:117-30. 16. Burkett L. The effects of orthodontic treatment on the soft periodontal tissues. AM J ORTHOD 1963;49:660-71. 17. Schluger S. The periodontist and the postorthodontic patient. Dent Clin N Am 1968:515-27. 18. Zachrisson S, Zachrisson BU. Gingival condition associated with orthodontic treatment. Angle Orthod 1972;42:26-34. 19. Zachrisson B, Alnaes L. Periodontal condition in orthodontically treated and untreated individuals. I. Loss of attachment, gingival pocket depth and clinical crown height. Angle Orthod 1973; 43:402- 11. 20. Zachrisson B, Alnaes L. Periodontal condition in orthodontically treated and untreated individuals. II. Alveolar bone loss: radiographic findings. Angle Orthod 1974;44:48-55. 21. Tersin J. Studies of gingival conditions in relation to orthodontic treatment. I. The relationship between amounts of gingival exudate and gingival scores, plaque scores and gingival pocket
Long-term
22.
23.
24.
25. 26.
27.
28. 29.
30.
31. 32. 33.
34.
35.
36.
37.
38.
39.
40.
41. 42.
periodontal
status after orthodontic
treatment
57
depths in children undergoing orthodontic treatment. Swed Dent J 1973;66:165-75. Tersin J. Studies of gingival conditions in relation to orthodontic treatment. II. Changes in amounts of gingival exudate in relation to orthodontic treatment. Swed Dent J 1975;68:102-210. Ericsson IB, Thilander B, Lindhe J, Okamoto H. The effect of orthodontic tilting movements on the periodontal tissues of infected and non-infected dentitions in dogs. J Clin Periodontol 1977;4:278-93. 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. Sadowsky C, Begole E. Long-term effects of orthodontic treatment on periodontal health. AM J ORTHOD 1981;80:156-72. Sadowsky C. Long-term effects of orthodontic treatment on the periodontium during adolescence. In: MacNamara JA Jr, Ribbens KA, eds. Malocclusion and the periodontium. Monograph 15, Craniofacial Growth Series. Ann Arbor: 1984:77-87. Center for Human Growth and Development, The University of Michigan. Silness J, Lee H. Periodontal disease in pregnancy. II. Correlation between oral hygiene and periodontal condition. Acta Odontol Stand 1964;22:121-35. Meitner S, Zander H, Iker H, Polson A. Identification of inflamed gingival surfaces. J Clin Periodontol 1979;6:93-7. Proye M, Caton J, Polson A. Initial healing of periodontal pockets after a single episode of root planing monitored by controlled probing forces. J Periodontol 1982;53:296-301. Polson A, Caton J, Yeaple R, Zander H. Histological determination of probe tip penetration into the gingival sulcus of humans using an electronic pressure-sensitive probe. J Clin Periodontol 1980;7:479-88. Ramfjord S. The periodontal disease index. J Periodontol 1967;38:602-20. Lilienthal B, Amerena V, Gregory G. An epidemiological study of chronic periodontal disease. Arch Oral Biol 1965;10:553-66. Alexander A. A study of the distribution of supra and subgingival calculus, bacterial plaque and gingival inflammation in the mouths of 400 individuals. J Periodontol 1971;42:21-8. Cumming B, Loe H. Consistency of plaque distribution in individuals without special home care instruction. J Periodont Res 1973;8:94-100. Lang N, Cumming B, Lee H. Oral hygiene and gingival health in Danish dental students and faculty. Community Dent Oral Epidemiol 1977;5:237-42. Loe H, Anerud A, Boysen H, Smith M. The natural history of periodontal disease in man. Study design and baseline data. J Periodont Res 1978;13:550-62. Anerud A, Loe H, Boysen H, Smith M. The natural history of periodontal disease in man. Changes in gingival health and oral hygiene before 40 years of age. J Periodont Res 1979;14: 526-40. Zachrisson B, Zachrisson S. Gingival condition associated with partial orthodontic treatment. Acta Odontol Stand 1972;30: 127-36. Alstad S, Zachrisson B. Longitudinal study of periodontal condition associated with orthodontic treatment in adolescents. AM J ORTHOD 1979;76:277-86. Lundstrom F, Hamp S, Nyman S. Systematic plaque control in children undergoing long-term orthodontic treatment. Eur J Orthod 1980;2:27-39. Feliu J. Long-term benefits of orthodontic treatment on oral hygiene. AM J ORTHOD 1982;82:473-7. Boyd R. Longitudinal evaluation of a system for self-monitoring
58
43.
44.
45.
46.
47. 48.
49.
50. 51. 52.
Poison
et al.
plaque control effectiveness in orthodontic patients. J Clin Periodont 1983;10:380-8. Alexander A. Dental calculus and bacterial plaque and their relationship to gingival disease in 400 individuals. Br Dent J 1970;129:116-22. Hollender L, Ronnerman A, Thilander B. Root resorption, marginal bone support and clinical crown length in orthodontically treated patients. Eur J Orthod 1980;2: 197-205. Huettner R. Experimental histologic study of the effects of orthodontic movement on the gingiva and periodontal membrane in the Macnca rhesus monkey. AH J ORTHOD 1960;46:929. Kobayashi L, Ash M. A clinical evaluation of an electric toothbrush used by orthodontic patients. Angle Orthod 1964;34: 209-19. Atherton J. The gingival response to orthodontic tooth movement. AM J ORTHOD 1970;58:179-86. Robertson P, Schultz L, Levy B. Occurrence and distribution of interdental gingival clefts following orthodontic movement into bicuspid extraction sites. J Periodontol 1977;48:232-5. Rivera Circuns AL, Tulloch JF. Gingival invagination in extraction sites of orthodontic patients: their incidence, effects on periodontal health, and orthodontic treatment. AM J ORTHOD 1983;83:469-76. Trossello V, Gianelly A. Orthodontic treatment and periodontal status. J Periodontol 1979;50:665-71. Atherton J, Kerr N. Effect of orthodontic tooth movement upon the gingivae. Br Dent J 1%8;124:5.55-60. Kurol J, Ronnerman A, Heyden G. Long-term gingival conditions after orthodontic closure of extraction sites. Histological and histochemical studies. Eur J Orthod 1982;4:87-92.
53. Reed BE, Polson AM, Subtelny JD. Long-term periodontai amtus of teeth moved into extraction sites. AM J ORTHOD 1985;88:203-8. 54. Ramfjord S. Surgical pocket therapy. Int Dent J lY’?7:27, 263-9. 55. Polson A. Nonsurgical treatment of periodontal disease. in. NH Rowe, ed. Proceedings of symposium on trends in the prevention and treatment of periodontal disease. Ann Arbor: 1981: 17-27. The University of Michigan School of Dentistry. The Dental Research Institute. 56. toe H, Anerud A, Boysen H, Smith M. The natural history ot periodontal disease in man. The rate of periodontal destruction before 40 years of age. J Periodontol 1978;49:607-20. 57. Lindhe J, Haffajee A, Socransky S. Progression of periodontal disease in adult subjects in the absence of periodontal therapy. J Clin Periodontol 1983;10:433-42. 58. Lindhe J, Nyman S. Long-term maintenance of patients treated for advanced periodontal disease. J CIin Periodontol 1984: 11:504-14, 59. Poison A, Reed BE. Long-term effect of orthodontic treatment on crestal alveolar bone levels. J Periodontol 1984;55:28-34. Reprint requests to: Dr. Alan M. Polson Department of Periodontics Eastman Dental Center 625 Elmwood Ave. Rochester. NY 14620