Orthodontics and ABE
Even though the precise process by which alveolar bone exostoses develop after orthodontic treatment is unknown, there is some evidence to support a link to the labial aspect of the alveolar bone thickening brought on by the rapid retraction of the upper incisors. The damage brought on by orthodontic forces, which results in the release of bone morphogenic proteins, which are expressed as exostoses and ossify at the stress points, may be the origin of the formation of buttressing bone. Rapidly retracted anterior teeth cause cortical bone remodeling to stall because it cannot keep up with the movement. It is a well known fact that cortical bone remodeling is influenced by the direction of tooth movement in the horizontal, vertical, and sagittal planes.41,46,47
There have also been reports of alveolar exostosis following the placement of orthodontic mini-implants43,48, although the underlying reason was not identified. The cause may be excessive mechanical stress on the bone, which promotes the growth of osteogenic progenitor cells. Additionally, patients with tori or other bone exostoses are incredibly susceptible to ABE.5
Given this approach, it is logical to assume that tooth movement during orthodontic treatment may also be regarded as a microtrauma and may have a potential role in the emergence of oral exostoses.41,49,50 Yodthong et al. 42 investigated how the thickness of their alveolar bone varied in response to the degree of intrusion, angulation, inclination, and rate of tooth movement . According to the study, when the incisors were retracted, the alveolar bone’s thickness increased. Alveolar bone thickness fluctuations were significantly linked with tooth movement, inclination changes, and intrusion. The proportion of alveolar bone that is altered at the apical level depends on how much intrusion is performed when the upper incisors are retracted. Particularly, the alveolar crestal level labial bone thickness was adversely correlated with the upper incisors in the torque group and strongly positively correlated with the upper incisors in the tipping group.
A comprehensive systematic review47also demonstrated that during en-masse incisor retraction following extractions, alveolar bone thickness significantly increased on the labial side of the central incisors.
The complex etiopathogenesis of ABE may be traced back to the wide range of variables that affect the bone’s capacity to remodel itself during retraction. The 2006 study by Tang et al.,51demonstrated that mechanical strain can generate morphological change and a magnitude-dependent increase in the expression of bone morphogenic protein-2, alkaline phosphatase, and collagen type I mRNA in osteoblast-like cells, which may affect bone remodelling during orthodontic treatment.
We hope to conduct additional research in the near future to determine the correlation of ABE formation on orthodontically treated subjects with a history of TM or TP, as well as to investigate the effects of biomechanical force magnitude, force direction, force type (intermittent, continuous), extent of tooth movement, and individual response on changes in alveolar bone thickness over time.