Osteoclastogenesis and Osteogenesis during Tooth Movement.

It is a well-known concept that bone remodeling occurs during orthodontic tooth movement. The orthodontic literature is vastly full of information about the changes occurring on the periodontal ligament level. However, changes occurring in the alveolar bone are being elucidated. The purpose of this chapter is to present some of the studies describing the bone changes associated with orthodontic tooth movement. Initiation of osteoclastogenesis requires inflammation in the adjacent area. Tissue biomarker RANKL responds to the compressive forces. Conversely, an increase in osteoprotegrin biomarker causes a decrease in RANKL and inhibits tooth movement. Osteocyte activity during tooth movement is not well understood. Emerging studies are showing the effect of osteocytes on orthodontic tooth movement. Nitric oxide (NO), produced by osteocytes, is an important regulator of bone response to loading and has been shown to mediate osteoclast activity. iNOS (which produces NO) has been shown to mediate inflammation-induced bone resorption on the compression side. Several molecules have been linked to osteogenesis in tooth movement: TGF-ß, BSP, BMPs and epidermal growth factor. Osteogenesis on the tension side is not well understood. Studies have shown increase in the expression of Runx2 on the tension side. Additionally, eNOS (produces NO) mediates bone formation on the tension side. The concept of osteoclastogenesis and osteogenesis is being unraveled.

Mechanism of action and morphologic changes in the alveolar bone in response to selective alveolar decortication-facilitated tooth movement.

BACKGROUND AND PURPOSE: The aim of this study was to test if corticotomy-induced osteoclastogenesis and bone remodeling underlie orthodontic tooth movement and how selective alveolar decortication enhances the rate of tooth movement. MATERIALS AND METHODS: A total of 114 Sprague-Dawley rats were included in 3 treatment groups: selective alveolar decortication alone (SADc); tooth movement alone (TM); and "combined" therapy (SADc + TM). Surgery was performed around the buccal and palatal aspects of the left maxillary first molar tooth and included 5 decortication dots on each side. Tooth movement was performed on the first molar using a 25-g Sentalloy spring. Measurements were done at baseline (day 0: no treatment rendered) and on days 3, 7, 14, 21, 28 and 42. Microcomputed tomography, Faxitron analyses, and quantitative real-time polymerase chain reaction (q-PCR) of expressed mRNAs were used to assess changes. RESULTS: The combined group showed increased tooth movement (P = 0.04) at 7 days compared with the tooth movement group with significantly decreased bone volume (62%; P = 0.016) and bone mineral content (63%; P = 0.015). RNA markers of osteoclastic cells and key osteoclastic regulators (M-CSF [macrophage colony-stimulating factor], RANKL [receptor activator of nuclear factor kappa-B ligand], OPG [osteoprotegerin], calcitonin receptor [CTR], TRACP-5b [tartrate-resistant acid phosphatase 5b], cathepsin K [Ctsk]) all showed expression indicating increased osteoclastogenesis in the combined group. RNA markers of osteoblastic cells (OPN [osteopontin], BSP [bone sialoprotein], OCN [osteocalcin]) also showed increased anabolic activity in response to the combination of alveolar decortication and tooth movement. CONCLUSIONS: The data suggest that the alveolar decortication enhances the rate of tooth movement during the initial tooth displacement phase; this results in a coupled mechanism of bone resorption and bone formation during the earlier stages of treatment, and this mechanism underlies the rapid orthodontic tooth movement.