RESUMEN
OBJECTIVES: To create an orthodontic anchor screw (OAS)-loosening model and to investigate whether filling the bone hole with beta-tricalcium phosphate (ß-TCP) can fix the OAS against orthodontic force. MATERIALS AND METHODS: Bone holes with different diameters (1.6, 2.1, or 2.5 mm) were drilled in the tibias of 11-week-old male Wistar rats, and an OAS (3.0 mm in length and 1.2 mm in diameter) was inserted. After a healing period of 2 or 4 weeks, orthodontic force was applied, and the diameter of the bone hole appropriate for the loosening model was determined. Subsequently, under the loosening model, the bone hole was filled with ß-TCP, orthodontic force was applied, and movement of the OAS and surrounding tissue changes were evaluated by micro-computed tomography images and histological specimen analysis. RESULTS: The bone hole of 1.6 mm in diameter was employed as the OAS-loosening model. When ß-TCP was inserted into the bone hole, the linear distance and mesial tipping angle of the OAS movement decreased markedly. Furthermore, the values of bone morphometry significantly increased with ß-TCP filling. CONCLUSIONS: An OAS-loosening model was established in rats and demonstrated that the loosening OAS was stabilized by ß-TCP filling through bone formation. ß-TCP may be useful for fixation of a loosening OAS.
RESUMEN
BACKGROUND: Previous clinical observational studies have suggested that orthodontic tooth movement (OTM) is related, at least partly, to the mass and/or capabilities of the masticatory muscles. OBJECTIVES: Our study aimed to examine the influence of masticatory muscle mass on the OTM in an animal experimental model in which the masseter muscle was modulated by botulinum neurotoxin type A (BTX) injection. METHODS: Eighteen Wistar rats were equally divided into two groups: BTX injection and control. BTX was injected bilaterally into the masseter muscles. Three days after the injection, the maxillary left first molars were orthodontically moved for 14 days. At the end of the experiment, micro-computed tomography was performed to evaluate the rate of OTM and bone morphometry. The masseter muscles were weighed and prepared for histological analyses. RESULTS: The masseter muscle mass in the BTX group was less than that in the control group, and histological findings showed atrophy of muscle fibres. The rate of OTM was significantly higher in the BTX group than in the control group. Furthermore, a negative correlation was detected between masseter muscle mass and OTM in the BTX group. Bone morphometry showed no difference between the control and BTX groups. CONCLUSION: Decreased masseter muscle mass was found to be closely related to an increase in the rate of OTM in rats using BTX injection to modify the masseter muscle mass. Masseter muscle mass could be a predictive factor for OTM in rats injected with BTX.