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Vibration in the form of High Frequency Acceleration (HFA) is anabolic on the craniofacial skeleton in the absence of inflammation. Orthodontic forces trigger an inflammation-dependent catabolic cascade that is crucial for tooth movement. It is unknown what effect HFA has on alveolar bone if applied during orthodontic treatment. The objectives of this study are to examine the effect of HFA on the rate of tooth movement and alveolar bone, and determine the mechanism by which HFA affects tooth movement. Adult Sprague Dawley rats were divided to control, orthodontic force alone (OTM), and different experimental groups that received the same orthodontic forces and different HFA regimens. Orthodontic tooth movement was assessed when HFA parameters, frequency, acceleration, duration of exposure, and direct or indirect application were varied. We found that HFA treatment significantly enhanced the inflammation-dependent catabolic cascade during orthodontic tooth movement. HFA treatment increased inflammatory mediators and osteoclastogenesis, and decreased alveolar bone density during orthodontic tooth movement. Each of the HFA variables produced significant changes in the rate of tooth movement and the effect was PDL-dependent. This is the first report that HFA enhances inflammation-dependent catabolic cascades in bone. The clinical implications of our study are highly significant, as HFA can be utilized to enhance the rate of orthodontic tooth movement during the catabolic phase of treatment and subsequently be utilized to enhance retention during the anabolic remodeling phase after orthodontic forces are removed.

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Structured Abstract Objectives Investigate the expression and activity of inflammatory markers in response to different magnitudes of orthodontic forces and correlate this response with other molecular and cellular events during orthodontic tooth movement. Setting and Sample Population CTOR Laboratory; 245 Sprague Dawley male rats. Methods and Materials Control, sham, and 5 different experimental groups received different magnitudes of force on the right maxillary first molar using a coil spring. In the sham group, the spring was not activated. Control group did not receive any appliance. At days 1, 3, 7, 14, and 28, the maxillae were collected for RNA and protein analysis, immunohistochemistry, and micro‐CT. Results There was a linear relation between the force and the level of cytokine expression at lower magnitudes of force. Higher magnitudes of force did not increase the expression of cytokines. Activity of CCL2, CCL5, IL‐1, TNF‐α, RANKL, and number of osteoclasts reached a saturation point in response to higher magnitudes of force, with unchanged rate of tooth movement. Conclusion After a certain magnitude of force, there is a saturation in the biological response, and higher forces do not increase inflammatory markers, osteoclasts, nor the amount of tooth movement. Therefore, higher forces to accelerate the rate of tooth movement are not justified.

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