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.