href="#fb3_img_img_23a420e2-f2fc-59bf-9ffc-cfc706ec636b.jpg" alt="Photo depicts the mesial (PDL tension) side of the tooth shown in Figure 1.13. Here, new trabeculae protrude from the alveolar bone surface, apparently growing towards the distal-moving root."/>
Figure 1.14 The mesial (PDL tension) side of the tooth shown in Figure 1.13. Here, new trabeculae protrude from the alveolar bone surface, apparently growing towards the distal‐moving root. H & E staining.
With experiments on human teeth, Reitan observed that tissue reactions can vary, depending upon the type of force application, the nature of the mechanical design, and the physiological constrains of the individual patient. He observed the appearance of hyalinized areas in the compressed PDL almost immediately after continuous force application and the removal of those hyalinized areas after 2–4 weeks. Furthermore, Reitan reported that in dogs, the PDL of rotated incisors assumes a normal appearance after 28 days of retention, while the supracrestal collagen fibers remain stretched even after a retention period of 232 days. Consequently, he recommended severing the latter fibers surgically. He also called attention to the role of factors such as gender, age, and type of alveolar bone, in determining the nature of the clinical response to orthodontic forces. He also reported that 50 g of force is ideal for movement of human premolars, resulting from direct resorption of the alveolar bone.
Another outlook on differential orthodontic forces was proposed by Storey (1973). Based upon experiments in rodents, he classified orthodontic forces as being bioelastic, bioplastic, and biodisruptive, moving from light to heavy. He also reported that in all categories, some tissue damage must occur in order to promote a cellular response, and that inflammation starts in paradental tissues right after the application of orthodontic forces.
Continuing the legacy of Sandstedt, Kvam and Rygh studied cellular reactions in the compression side of the PDL. Rygh (1974, 1976) reported on ultrastructural changes in blood vessels in both human and rat material as packing of erythrocytes in dilated blood vessels within 30 minutes, fragmentation of erythrocytes after 2–3 hours, and disintegration of blood vessel walls and extravasation of their contents after 1–7 days. He also observed necrotic changes in PDL fibroblasts, including dilatation of the endoplasmic reticulum and mitochondrial swelling within 30 minutes, followed by rupture of the cell membrane and nuclear fragmentation after 2 hours; cellular and nuclear fragments remained within hyalinized zones for several days. Root resorption associated with the removal of the hyalinized tissue was reported by Kvam and Rygh. This occurrence was confirmed by a scanning electron microscopic study of premolar root surfaces after application of a 50 g force in a lateral direction (Kvam, 1972). Using transmission electron microscopy (TEM), the participation of blood‐borne cells in the remodeling of the mechanically stressed PDL was confirmed by Rygh and Selvig (1973), and Rygh (1974, 1976). In rodents, they detected macrophages at the edge of the hyalinized zone, invading the necrotic PDL, phagocytizing its cellular debris and strained matrix.
After direct measurements of teeth subjected to intrusive forces, Bien (1966) hypothesized that there are three distinct but interacting fluid systems involved in the response of the PDL to mechanical loading: the fluids in the vascular network, in the cells and fibers, and the interstitial fluid. Mechanical loading moves fluids into the vascular reservoir of the marrow space through the many minute perforations in the tooth alveolar wall. The hydrodynamic damping coefficient (Figure 1.15) is time dependent, and therefore the damping rate is determined by the size and number of these perforations. As a momentary effect, the fluid that is trapped between the tooth and the socket tends to move to the boundaries of the film at the neck of the tooth and the apex, while acting to cushion the load and is referred to as the “squeeze film effect”. As the squeeze film is depleted, the second damping effect occurs after exhaustion of the extracellular fluid, and the ordinarily slack fibers tighten. When a tooth is intruded, the randomly oriented periodontal fibers, which crisscross the blood vessels, tighten, then compress and constrict the vessels that run between them, causing stenosis and ballooning of the blood vessels, creating a back pressure. Thus, high hydrodynamic pressure heads can be created suddenly in the vessels above the stenosis. At the stenosis, a drop of pressure would occur in the vessel in accordance with Bernoulli’s principle that the pressure in the region of the constriction will be less than elsewhere in the system. Bien also differentiated the varied responses obtained from momentary forces of mastication from that of prolonged forces applied in orthodontic mechanics and suggested that biting forces in the range of 1500 g/cm2 will not crush the PDL or produce bone responses.
Figure 1.15 The constriction of a blood vessel by the periodontal fibers. The flow of blood in the vessels is occluded by the entwining periodontal fibers. Below the stenosis, the pressure drop gives rise to the formation of minute gas bubbles, which can diffuse through the vessel walls. Above the stenosis, fluid diffuses through the walls of the cirsoid aneurysms formed by the build‐up of pressure.
(Source: Bien, 1966. Reproduced with permission of SAGE Publications.)
Pointing out a conceptual flaw in the pressure tension hypothesis proposed by Schwarz (1932), Baumrind (1969) concluded from an experiment on rodents that the PDL is a continuous hydrodynamic system, and any force applied to it will be transmitted equally to all regions, in accordance with Pascal’s law. He stated that OTM cannot be considered as a PDL phenomenon alone, but that bending of the alveolar bone, PDL, and tooth is also essential. This report renewed interest in the role of bone bending in OTM, as reflected by Picton (1965) and Grimm (1972). The measurement of stress‐generated electrical signals from dog mandibles after mechanical force application by Gillooly et al. (1968), and measurements of electrical potentials, revealed that increasing bone concavity is associated with electronegativity and bone formation, whereas increasing convexity is associated with electropositivity and bone resorption (Bassett and Becker, 1962). These findings led Zengo et al. (1973) to suggest that electrical potentials are responsible for bone formation as well as resorption after orthodontic force application. This hypothesis gained initial wide attention but its importance diminished subsequently, along with the expansion of new knowledge about cell–cell and cell–matrix interactions, and the role of a variety of molecules, such as cytokines and growth factors in the cellular response to physical stimuli, like mechanical forces, heat, light, and electrical currents.
Histochemical evaluation of the tissue response to applied mechanical loads
Identification of cellular and matrix changes in paradental tissues following the application of orthodontic forces led to histochemical studies aimed at elucidating enzymes that might participate in this remodeling process. In 1983, Lilja, Lindskog, and Hammarström reported on the detection of various enzymes in mechanically strained paradental tissues of rodents, including acid and alkaline phosphatases, β‐galactosidase, aryl transferase, and prostaglandin synthetase. Meikle et al. (1989) stretched rabbit coronal sutures in vitro, and recorded increases in the tissue concentrations of metalloproteinases, such as collagenase and elastase, and a concomitant decrease in the levels of tissue inhibitors of this class of enzymes. Davidovitch et al. (1976, 1978, 1980a, b, c, 1992, 1996) used immunohistochemistry to identify a variety of first and second messengers in cats’ mechanically stressed paradental tissues in vivo. These molecules included cyclic nucleotides, prostaglandins, neurotransmitters, cytokines, and growth factors. Computer‐aided
