An experimental study of the effect of orthodontic intrusion and retention on periodontal regeneration

Introduction

The combination of periodontal treatment and orthodontic treatment is frequently performed. The purposes of orthodontic treatment in periodontal treatment include the correcting of crowding (^{Marks, 1980}), infrabony defects ( ^{Ingber, 1974} and ¹⁹⁷⁶), mesially tipped teeth (^{Brown, 1973}) and an improvement of traumatic occlusion (^{Marks, 1980}). Orthodontic treatment has been shown to have a good effects on periodontal tissue in some studies (Alstand and Zachrisson, ¹⁹⁷⁹ ; ^{Polson and Reed, 1984} ; ^{Sadowsky and Begole, 1981} ; ^{Eliasson et al., 1982}), however it has also produced poor effects in other studies (Zachrisson and Alnaes, ¹⁹⁷³ and ¹⁹⁷⁴ ; ^{Dorfmann, 1978} ; ^{Hamp et al., 1982} ; ^{Prichard, 1975} ; ^{Trossello and Gianelly, 1979} ; ^{Kessler, 1976}). This is the reason why the methods and subjects and periodontal conditions tend to differ in individual studies. As a result, no definitive conclusions have yet been made. Basically, orthodontic treatment is thought to have a similar negative effect on periodontal tissue as that of a jiggling force (^{Ericsson and Lindhe, 1982}).

In an animal study (^{Ericsson et al., 1977}), orthodontic tooth movement shifted supragingivally located plaque into a subgingival position, thus resulting in the formation of infrabony pockets on the plaque-infected teeth. That is to say, when orthodontic tooth movement is performed, it is also important to remove any plaque.

Generally, pathologic tooth migration (^{Martinez-Canut et al., 1997} ; ^{Towfighi et al., 1997}) is observed in patients with advanced periodontal disease. After periodontal treatment in facial flaring cases of advanced periodontal disease, tooth malpositioning may remain and the roots may even be exposed. In such cases, orthodontic treatment should be performed, especially intrusion, in order to establish good tooth positioning for both esthetic and maintenance reasons.

Various studies of orthodontic intrusion have been published (^{Ricketts, 1976a} and ^1976b ; ^{Lefkowiz and Wauch, 1945} ; ^{Huettner and Whitman, 1958} ; ^{Dellinger, 1967} ; ^{Bondevik, 1980} ; ^{Ninomia, 1984} ; ^{Melsen et al., 1988} ; ^{Murakami et al., 1989} ; ^{Morimoto, 1993}). However, there have been few reports regarding the effect of orthodontic intrusion on periodontal tissue. In clinical reports, Yokota and Matuda (¹⁹⁸⁰), Melsen et al. (¹⁹⁸⁹), Steffensen et al. (¹⁹⁹³), Aoki et al. (¹⁹⁹⁷), and Someno et al. (¹⁹⁹⁷) reported that the combination of periodontal treatment and orthodontic intrusion improved the condition of periodontal tissue in advanced periodontal disease cases. In animal studies, Melsen et al. (¹⁹⁸⁸) and Morimoto (¹⁹⁹³) studied the effects of orthodontic intrusion on the exposed root surface. They reported that after periodontal surgery, a new attachment was obtained on the experimentally exposed root surface by orthodontic intrusion in combination with plaque control. However, all of these studies covered only a short period of time. As a result, many aspects regarding orthodontic intrusion have yet to be elucidated. In addition Melsen et al. (¹⁹⁸⁸) did not assess any clinical parameters.

As a result, there have been no systematic reports on the clinical and histological changes in periodontal tissue after undergoing orthodontic intrusion during the periodontal treatment period. The purpose of this study is thus to examine the clinical and histological effect of orthodontic intrusion and retention on the experimentally exposed root surface of mongrel dogs.

Material and methods

Study animals and teeth

Five adult male mongrel dogs (all about 3 years of age and weighing from 10 to 15 kg) were used in this study. The animals used for this research were provided for use as experimental animals from the City of Kitakyushu Public Health and Welfare Bureau Public Health and Affairs Section Animal Control Center. Then all animals were maintained by Animal Research Center of Kyushu Dental College. The protocol of the present study was approved by the Animal Experiment Committee of Kyushu Dental College. Prior to the start of the experiment, full mouth scaling was performed using pentobarbital sodium (Nembutal^®, Abot Labs) for intravenous anesthesia (25 mg/kg). All treatments during this study were performed under intravenous anesthesia and local anesthesia to prevent any pain. The lower third premolar teeth were used as both the experimental and control teeth.

Procedures of experimental periodontitis and flap operation

Experimental periodontitis was induced on the third premolar by floss ligature, and thereafter a new ligature was placed there every week for 4 weeks. After removing the floss ligature, the deepened periodontal pockets were rinsed with 0,2 % chlorhexidine digluconate two times a week, and this treatment continued up until the end of the study. Five weeks after performing the initial floss ligature, a flap operation was performed. The root surface on the lower third premolar was scaled and planed, and the granulation tissue was removed with a curett. The horizontal bone loss was measured to be about 4 mm from the CEJ and the furcation site was through-and-through (^{fig. 1a}). As a reference for the measurements in the histologic sections, a notch was prepared on the root surface at the level of the marginal alveolar bone with a round bur. Then flaps were replaced in their original position and then were sutured with interrupted sutures. All gingival margins measured about 1 mm below from CEJ at 8 weeks post-surgery. Thereafter, two reference points were prepared with amalgam filling on the buccal surface to measure attachment level and the position of gingival margin (^{fig. 1b}).

After an eight-week healing period following surgical treatment, an orthodontic appliance was inserted in the experimental teeth. Orthodontic intrusion was applied to the experimental teeth at 4 weeks, and retention at 12 weeks under plaque control. In contrast, the control teeth only received plaque control for 16 weeks.

Orthodontic intrusion appliance (fig. 2)

Impressions of the upper and lower jaws were obtained using an alginate impression material. The working models were made of hard plaster. The individual tray of the lower jaws was made of a working model. After preparing the lower canine and fist molar, the final impression for the working model of the appliance was obtained using an individual tray with polyvinylsiloxane. In this model, a waxing-up for the appliance was done and it was thereafter cast with nickelcrom. The appliance consisted of a crown with a bur and crown with an expansion screw (600-010, Dentaurum), and both were connected. The crown with a bur was fixed on the lower canine and first molar. The crown with an expansion screw was fixed on the third lower premolar by a bracket bond (Tomy International).

Experimental procedures (fig. 3)

The experimental subjects were divided into two groups, consisting of :

- the experimental group : experimental periodontitis plus flap operation plus orthodontic intrusion for 4 weeks and retention for 12 weeks plus plaque control ;

- the control group : experimental periodontitis plus flap operation plus plaque control for 16 weeks.

The experimental group underwent orthodontic intrusion and retention after the induction of periodontitis and the flap operation. For intrusion, the expansion screw was rotated 10 times in 4 weeks. Retention was performed for 12 weeks. An orthodontic intrusion appliance was used as the retention appliance. The control group only received plaque control for 16 weeks after the induction of periodontitis and the flap operation.

Observation procedures

Clinical assessment

The clinical parameters below were assessed once a week during the intrusion period, and once every 4 weeks during the retention period :

- probing pocket depth (PPD) ;

- probing attachment level (PAL) ;

- position of gingival margin (GM) ;

- height of keratinized gingiva (KG).

PPD was measured at 12 points including 6 points in the mesial root and 6 points in the distal roots. For PPD, it was the average of 12 values. The PAL and GM were measured from the reference point. Two reference points were prepared in the lower third premolar with an amalgam filling. Two reference points with amalgam filling were used for PAL and GM. These points were prepared at 8 weeks post-surgery. They were located on the buccal surface of the lower third premolar (^{fig. 1b}). For PAL and GM, they were the average of two values. The KG was measured from the buccal gingival margin to the mucogingival junction at 6 points including 3 points in the mesial root and 3 points in the distal root. All measurements were performed with a probe (Hu-Friedy) and one examiner. The clinical changes were calculated by subtracting the baseline value from every weekly value. The statistical analysis was done using Student's t-test ; p = 0,05 was considered to indicate significance.

Histological observations

After the experiment, the dogs were sacrificed by means of perfusion with 10 % buffered formalin. The lower jaws were excised and placed in a fixture with 10 % buffered formalin. Following fixture, the tissue block was cut out and decalicified in 10 % formic acid, dehydrated, and embedded in paraffin. The decalcification time was 4 weeks. Sections measuring approximately 8 µm in thickness were cut mesiodistally through each tooth and then were stained with hematoxylin and eosin. Thereafter, they were observed by a microscope.

Histological measurement

Histological measurements were then made on histological sections using a Micrometer (Olympus Japan) and two points (A, B) were determined on the root surface :

- A : the most coronal position of the new cementum ;

- B : the most apical position of the reference notch.

The distance between A and B was considered to be the new cementum (^{fig. 4}). In this manner, the new cementum of the proximal surface and the furcation surface on every root was measured. In all, a total of 30 sections (n = 5) were measured. All values were averaged. The statistical analysis was done using Student's t-test ; p = 0,05 was considered to indicate significance.

Results

Clinical assessment (table I)

Changes in the PPD

The value was 1,8 ± 0,2 at baseline, 1,9 ± 0,3 at 4 weeks, 2,2 ± 0,2 at 16 weeks in the experimental group while it was 1,7 ± 0,2 at baseline, 1,8 ± 0,3 at 4 weeks, 2,0 ± 0,3 at 16 weeks in the control group. No significant difference was seen between the experimental group and the control group. The change in the PPD was 0,4 ± 0,2 mm in the experimental group, and 0,3 ± 0,3 mm in the control group at the end of the experiments.

Changes in the PAL

The value was 3,0 ± 0,2 at baseline, 2,4 ± 0,4 at 4 weeks, 2,1 ± 0,3 at 16 weeks in the experimental group while it was 2,9 ± 0,3 at baseline, 2,9 ± 0,3 at 4 weeks, 2,9 ± 0,3 at 16 weeks in the control group. Between the experimental group and control group, significant differences could be detected from week 2 to week 12. The clinical attachment gain was 0,9 ± 0,3 mm in the experimental group, and 0,0 ± 0,2 mm in the control group at the end of the experiments. In the experimental group, the clinical attachment gain was detected during the retention period, however, the amount was small in comparison to that observed during the intrusion period.

Changes in the gingival margin

The value was 1,5 ± 0,3 at baseline, 0,8 ± 0,3 at 4 weeks, 0,2 ± 0,2 at 16 weeks in the experimental group while it was 1,3 ± 0,6 at baseline, 1,0 ± 0,3 at 4 weeks, 1,0 ± 0,3 at 16 weeks in the control group. Between the experimental group and control group, significant differences could be detected at 2 weeks, 3 weeks, 4 weeks, 8 weeks, 12 weeks, and 16 weeks. The change in the MG was - 1,1 ± 0,4 mm in the experimental group, and - 0,3 ± 0,3 mm in the control group at the end of the experiments. In both groups, the change in the GM still continued even at the end of the experiments.

Changes in the keratinized gingiva

The value was 2,9 ± 1,2 at baseline, 2,9 ± 1,2 at 4 weeks, 3,0 ± 0,9 at 16 weeks in the experimental group while it was 3,1 ± 1,5 at baseline, 3,1 ± 1,3 at 4 weeks, 3,1 ± 1,0 at 16 weeks in the control group. No significant difference was observed between the experimental group and control group. The change in the KG was 0,1 ± 0,4 mm in the experimental group, and 0,3 ± 0,5 mm in the control group at the end of the experiments.

Histological observations (fig. 4, 5a, 5b, 5c et 5d)

On the proximal surface of the experimental group, the reference point was located more apically in relation to the bone than in the control group. The epithelial attachment and cellular cementum were located above the reference point. The transseptal fibers ran obliquely. In addition, the top of the alveolar bone was oblique.

On the proximal surface of the control group, the reference point was located in a slightly apical direction from the bone. The epithelial attachment and cellular cementum were located above the reference point. The transseptal fibers ran parallel to the top of the alveolar bone. The top of the alveolar bone was flat. The most apical side of the epithelial attachment and the most coronal side of the new cementum both terminated at the same position.

Regardingly furcation, the experimental group and control group were both similar. The reference point was located a little apicaly to the bone. The epithelial attachment and cellular cementum were located above the reference point.

Measurements of histologic section (table II)

The new cementum of the proximal surface was 1 483,52 ± 450,40 µm in the experimental group, and 1 148,83 ± 409,61 µm in the control group, thus indicating a significant gain in the experimental group. The new cementum of the furcation was 748,20 ± 274,60 µm in the experimental group, and 766,88 ± 411,25 µm in the control group. There was also no significant difference between the experimental group and the control group. However, there was a significant gain in the proximal surface in both groups.

Discussion

So far few studies have been made regarding orthodontic intrusion including the clinical parameters. ^Melsen reported that a new attachment was histologically observed by orthodontic intrusion on the exposed root surface under plaque control, but no clinical parameters were assessed. The present study was not only histologically assessed, but four clinical parameters were also assessed. In addition, a retention period and histological assessment of furcation were included as well.

^Murakami reported that the gingival sulcus was deepened by orthodontic intrusion under normal periodontal conditions. However, no significant difference was observed between the experimental groups and the control group in the present study. Our results might thus be attributable to good plaque control, but the depth of the PPD tended to be a little too deep. Regarding the clinical attachment gain, ^{Morimoto (1993)} considered the reason for the clinical attachment gain under reduced periodontal conditions to be due to the effect of the long junctional epithelium following the flap operation and the effect of the orthodontic intrusion. In the present study, the experimental group also showed a significant clinical attachment gain in comparison to the control group. It was extremely interesting to note that a clinical attachment gain was shown not only during the intrusion period but also during the retention period. Unfortunately, we could not elucidate the reason for this in this study. Further studies are thus called for to clarify this mechanism. Nevertheless we believe the complete action of intrusion requires a long period of time and the retention of the intruded tooth could be successfully performed.

The gingival margin showed a significant change in a coronal direction in the experimental group. These results suggest that orthodontic intrusion does not cause a recession of the gingival margin.

^Coatoam and ^{Dorfman (1978)} reported that after orthodontic therapy, the height of the keratinized gingiva changed, but no differences between the groups were observed in the present study. Vertical movement did not affect the height of the keratinized gingiva. The reason for this might be that the movement was within the alveolar ridge.

Regarding the histological results, new cementum was significantly observed on the proximal surface of the experimental group while both the transseptal fibers ran in an oblique direction and the alveolar bone crest was oblique in comparison to the control group. As a result, the stress of intrusion was thus considered to activate the cementblasts and osteoblasts, thereby affecting both the transseptal fibers and the alveolar bone.

^Melsen and ^{Morimoto (1993)} reported that a new attachment could be formed by orthodontic intrusion under plaque control. However, their study made no mention of the furcation site. The present study showed that the gain of new cementum on the proximal surface was significant in comparison to the furcation. The reason for this is thought to be due to the fact that plaque control was difficult at the furcation site and the action of intrusion is considered to be the strongest on the epithelium.

We consider that the results obtained by this study were satisfactory, however, we could not elucidate why orthodontic intrusion and retention caused a greater clinical attachment gain, a coronal shift of gingival margin and new cementum formation. As a result, further study is called for to clarify this mechanism. We conclude that orthodontic intrusion and retention, when combined with plaque control, may thus be a useful modality for periodontal treatment within the limit of this study in an animal model (dog).

Acknowledgement

The authors would like to thank Drs Philippe Bouchard, Paul Mattout and other reviewers for critical reading of this manuscript. This study was supported in part by grants-in-aid A-08771718, A-09771633 from the Ministry of Education, Science, Sports and Culture of Japan.

Demande de tirés à part :

Dr Yoshiyuki TASHIRO, Department of Periodontology and Endodontology, Kyushu Dental College, 2-6-1, Manazuru, Kokurakitaku, Kitakyushu City, Fukuoka, 803-8580 - JAPON.

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