Abstract
The aim of this study was to investigate the effect of changes in periodontal tissues caused by trauma from occlusion on the extent of inflammation in experimental periodontitis. Ten Japanese mon-keys were used for the experiment. Trauma from occlusion was applied to the maxillary second premolars (2P2) according to the method described by Kitamura (1990). After removing the cuspid crown, the buccal cusps of 2P2 were intentionally elongated with custom-made casting onlays to receive the induced bruxism force. The monkeys were divided into 3 groups. Group I: For the first 10 weeks trauma from occlusion was applied with the appropriate plaque control, then a silk ligature was placed in the gingival sulcus with trauma from occlusion until week 14. Group II: Trauma from occlusion was applied with the plaque control for the entire 14 weeks. Group III: For the first 10 weeks, plaque control was performed with-out trauma from occlusion, then a silk ligature was placed in the gingival sulcus without trauma from occlusion until week 14. The following clinical parameters were recorded weekly ; probing depth (PD), clinical attachment level (CAL), and tooth mobility (Periotest® value-PT). All monkeys were sacrificed after 14 weeks. The sections were stained with hematoxylin and eosin or Azan-Mal-lory staining, followed by light microscopic observa-tion. The results of the changes in clinical parame-ters were as follows. Clinical attachment level (CAL) : After 14 weeks, Groups I and III showed 1.1 and 1.3 mm, but Group II showed no change during the experimental period (14 weeks). PT value : Group I showed an increase during the experimental period. Group II exhibited an increase in the first 10 weeks, then remained stable until the week 14. Group III remained stable for the first 10 weeks, then increased at week 14. Histological evaluation indicated that in Group I the blood vessels in the supra-alveolar fiber were expanded near the experimental teeth. Numerous inflammatory cells had infiltrated around the expanded blood vessels on the most coronal portion of the periodontal ligament tissues. The crestal area of the alveolar bone was resorbed and several osteoclasts were observed on the resorption lacunae. The coronal portion of marrow space was markedly enlarged. In Group II the blood vessels in the supra-alveolar fiber were observed near the experimental teeth, but the expanded blood 1997 vessels were not observed. The most coronal por-tion of the periodontal ligament space was widened, resembling a funnel. As observed in Group I, this area was occupied by numerous vascular structures. The bone marrow space was slightly enlarged. In Group III there was no evidence of changes in the blood vessels. No inflammatory cells could be found in the most coronal portion of the periodontal ligament tissues and the alveolar crestal area.
These results indicate that the extent of inflam-mation is a consequence of the effect of trauma from occlusion on the periodontal ligament and alveolar bone marrow tissues.
