Biological Mechanisms to Accelerate Tooth Movement

Decreasing the duration of orthodontic treatment by maximizing biological responses is one of the main goals of contemporary orthodontic treatment, but how to achieve this goal is still controversial. There is a general consensus that the rate of tooth movement is controlled by the rate of bone resorption, which in turn is controlled by the rate of osteoclast differentiation and activation. Factors triggering osteoclast differentiation are not clear. Here, we propose that inflammatory markers are the main factors regulating the rate of osteoclast formation. Indeed, in response to orthodontic forces there is a transient up-regulation of inflammatory markers such as interlukine-1 (IL-1), tumor -necrosis factor (TNF-α), interlukine-6 (IL-6), interlukin-8 (IL-8), chemokines CCL2, CCL3, CCL5, and prostaglandins. All these markers together play a key role in the recruitment of osteoclast precursors and their differentiation into active osteoclasts. Therefore, it is logical to assume that one way to accelerate the rate of tooth movement is by mimicking nature by increasing the expression of inflammatory markers, and thus the rate of osteoclastogenesis.In this chapter, we will first review the current understanding of the molecular events taking place after the application of orthodontic forces, and how these events proceed to osteoclastogenesis and finally tooth movement. We will then discuss how these findings can be used as a foundation for developing a new methodology to accelerate tooth movement. In addition, we will discuss other approaches that were proposed to increase the rate of tooth movement and the possible biological principals behind them.