American Journal of Orthodontics and Dentofacial Orthopedics
Special articleAccelerated orthodontic tooth movement: Molecular mechanisms
Section snippets
Bone modeling, remodeling, and orthodontic tooth movement
Bone modeling is the uncoupled process of activation-resorption (catabolic) or activation-formation (anabolic) on bone surfaces, resulting in changes of the shape, size, or position of the bone.20 Bone remodeling or turnover, on the other hand, is a tightly coupled local process, which starts with bone resorption, followed by reversal and bone formation phases, resulting in the replacement of old bone with new bone.21, 22 Both bone modeling and remodeling are determinants for the rate of
Osteoclast formation and bone resorption
The rate-limiting step in orthodontic tooth movement is considered to be bone resorption at the leading (compression) side. Histologic studies show that the formation of osteoclasts is induced at the compression side during orthodontic tooth movement.32, 33, 34, 35 Alveolar corticotomy and nonsurgical interventions that accelerate tooth movement significantly increase the numbers and functions of osteoclasts.14, 15, 16, 17, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45 The formation of
Osteoblast formation and bone apposition
Osteoblast proliferation, differentiation, survival, and function are regulated by a number of extracellular factors including growth factors, cytokines, and hormones, as well as by interactions with osteoclastic cells. Transforming growth factor (TGF)-β1 is a secreted protein that enhances bone formation by chemotactic effects on osteoblastic cells, promoting osteoblast proliferation and differentiation at early stages while inhibiting osteoclast formation by reducing RANKL and increasing OPG
Role of osteocytes
Osteocytes are terminally differentiated osteoblasts that are embedded in the bone matrix during bone formation. They are stellate cells that form a functional network with other osteocytes, bone surface cells, bone marrow cells, and endothelial cells via long cytoplasmic extensions, or dendrites. This network of osteocytes occupies the lacunae-canaliculi system within the bone matrix, where the cell bodies and dendrites reside, respectively. Cell-to-cell signaling and material exchanges take
Clinical and experimental methods to accelerate orthodontic tooth movement
Direct injury to the alveolar or basal bones of the maxilla and mandible accelerates orthodontic tooth movement by inducing RAP as a wound-healing process, which is the basis for clinical procedures such as corticotomy-assisted orthodontics, piezocision-aided orthodontics, and surgery-first orthodontics.24, 33 The wound-healing process after trauma is similar, if not identical, as reviewed above. Nonsurgical methods, such as various physical and pharmacologic approaches, also enhance bone
Conclusions
The rate of orthodontic tooth movement depends on the modeling and remodeling of the alveolar process while adapting to the new biomechanical environment. The rate of alveolar modeling and remodeling is determined by the level of activity of bone cells (osteoclasts, osteoblasts, and osteocytes), which are under the control of mechanical and biochemical factors, most notably PGs and cytokines. Osteoclast activation is crucial for elevated bone modeling and remodeling required for accelerated
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All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest, and none were reported.