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-β, 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.