2. Orthodontic tooth movement models

Several models have been proposed for mechanism of initiation of orthodontic tooth movement as below.


afferent nerve endings [11]. A report showed that the nerve ending released the neuropeptides after periodontal ligament had been strained by the force applied to the tooth [12].

biologic mediators and inflammatory cytokines, osteoclast differentiation factors and ECM proteins such as collagen I, III, V and their modifying enzymes and proteases. These biomolecules, in turn, initiate the activation of fibroblasts, osteoblasts, osteocytes and recruitment and differentiation of osteoclasts leading to anabolic activities on the tension side and increased osteoclastic activity and low bone density on the compression side of tooth movement. These cellular and molecular events are strictly controlled at transcriptional, posttranscriptional and translational levels and the interference of these events affects the rate of tooth movement. Therefore, understanding the mechanism of cellular and molecular events of tooth movement will allow us to apply the cutting edge knowledge to improve clinical orthodontic practice

Several models have been proposed for mechanism of initiation of orthodontic tooth move-

1. Pressure-tension model: it was derived from the observation of experiments from animal models, in which a force of a given direction was applied to a tooth to create the tension and compression areas in periodontal tissues [1–4]. The histological studies demonstrated that bone was deposited on the alveolar wall on the tension side of the tooth in the presence of both heavy and light forces, with newly formed bone spicules followed the orientation of the periodontal fiber bundles. On the compression side, with the light forces, alveolar bone was resorbed directly by numerous multinucleated osteoclasts in Howship's lacunae (frontal resorption). In contrast, the periodontal tissues were compressed with heavy forces, leading to capillary thrombosis, cell death and the production of localized cell-free areas (hyalinization). Hyalinization phenomenon was later supported by several investigators [5–7]. At the hyalinization sites, osteoclastic resorption of the adjacent alveolar wall did not take place directly, but was initiated from the neighboring marrow spaces

2. Bone bending/piezoelectric current model: it was observed that the deformation that occurred when an external load was applied to a long bone produced electrical current in the surface curvature of the bone. Increased bone concavity was shown to be associated with electronegativity and bone formation; while increased bone convexity was associated with electropositivity and bone resorption [9]. This model has major flaws given the fact that piezoelectricity does not require the presence of living cells. Dead bone produces the same effects, which appear to be generated by shearing forces acting on the collagen fibers of the bone matrix. Therefore, the stress-generated electrical potentials could be a byproduct of deformation. In addition, the magnitude of the current is small and may not

3. Neurogenic inflammation model: it was based on the assumption that orthodontic tooth movement was the result of inflammatory processes triggered by peripheral nerve fibers referred as neurogenic inflammation. This inflammation is characterized by the release of neuropeptides such as calcitonin gene-related peptide (CGRP) and substance P upon the stimulation of

using gene therapy or molecular biology approaches.

2. Orthodontic tooth movement models

referred as 'undermining resorption' [8].

be sufficient to induce cellular changes [8, 10].

ment as below.

52 Current Approaches in Orthodontics

4. Fluid flow shear stress model: it was based on the concept that osteocytes respond to mechanical forces. Locally strain derived from the displacement of fluid in bony canaliculi of osteocytes is very important [13]. When loading occurs, interstitial fluid squeezes through the thin layer of the non-mineralized matrix surrounding the cell bodies and cell processes, resulting in local strain at the cell membrane and activation of the affected osteocytes [14]. With regard to orthodontic force, the force on the side of the tooth receiving orthodontic pressure creates shear stress and activates responses on osteocytes [15]. The shear stress on the osteocytes induces increased secretion of biological mediators from the osteocytes leading to activation of osteoclasts [16, 17]. At the same time, on the tension side, the increased pulling force on the periodontal ligament is transferred to the bone. The resulting deformation drives the fluid flow shear stress on the network of osteocytes. This shear stress induces osteocyte activation, and osteocytes respond by secreting signaling molecules that contribute to osteoclast recruitment and differentiation.

In addition, it has been shown that compressive force induces bone matrix deformation and microcracks; and the accumulation of microscopic cracks in the bone matrix may induce additional damage to osteocytes in the microcrack region [18]. Microcracks are more prevalent on the pressure-side than on the tension-side of the tooth, and it has been hypothesized that microcracks were the first damage induced by the orthodontic force to induce osteocyte apoptosis and bone remodeling. Osteocyte apoptosis has been observed at the pressure side in an experimental tooth movement model in animal models, which may be associated with the subsequent bone resorption [19, 20]. Therefore, the microcracks may play a role in the initiation of bone resorption on the pressure side of the tooth under the compressive force of orthodontic loading [21].
