Biological Mechanisms of Tooth Movement. Группа авторов

Figure 2.6 Histologic section from the original article by Oppenheim (1911). Lingual movement; lingual side of the PDL, where it forms compression. The individual newly formed bone spicules (k¹) have arranged themselves in the direction of the force, perpendicular to the long axis of the tooth. The ends of the spicules directed toward the tooth: the ends subjected directly to the pressure show broad, uncalcified zones (cG), which are surrounded by densely arranged rows of osteoblasts (ob). At the ends of the spicules directed from the tooth, occasionally numerous osteoclasts are seen. a, dentine; b, cementum; g, PDL; ok, osteoclasts; nearer to the apex of the root old unchanged bone (k).

      (Source: Oppenheim, 1911. Reproduced with permission of Oxford University Press.)

      Oppenheim substantiated his findings by drawing support from Wolff ’s law, and his investigations could not find any injury in the PDL. He concluded that, in OTM, all mechanical forces applied to a tooth are absorbed by the PDL, and at times he could observe a hypertrophy to withstand the increased demand placed upon it. Unlike Sandstedt, Oppenheim reported on seeing no hyalinization or undermining resorption in his experimental material. He further wrote that “The vitality of the periosteum suffers no injury during the application of “physiological forces,” even on compression of the PDL to a third of its original thickness. It may be exposed to slight hemorrhages, to occasional constriction in the lumen, or disappearance of the vessels, but the staining ability of the cell nuclei is retained, and no disintegration can be demonstrated by any photographs.

      The pressure–tension hypothesis

      Schwarz (1932), working along the same lines as both Sandstedt and Oppenheim, formulated the “pressure–tension hypothesis” of OTM. It is postulated that in sites of compression in the PDL, it displays disorganization and diminution of fiber production. Here, cell replication decreases, seemingly as a result of vascular constriction. In contrast, in PDL tension sites, stimulation produced by stretching of fiber bundles results in an increase in cell replication. Schwarz detailed the concept further by correlating the tissue response to the magnitude of the applied force with the capillary blood pressure and categorized it as four degrees of biologic effect:

       First degree of biologic effect. The force is of such a short duration or so slight that no reaction whatsoever is caused in the periodontium.

       Second degree of biologic effect (Figure 2.8). The force is gentle, speaking biologically; it remains below the pressure in the blood capillaries, i.e., less than 20–26 g for 1 cm2 of root surface, but it is nevertheless sufficient to cause resorption in the alveolar bone at the regions of pressure in the PDL. After the force ceases there will be anatomic and functional resolution of integrity of the PDL and alveolar bone without resorption of dental roots.Figure 2.7 Elongation from the original article by Oppenheim (2011). Apex of the root (a). The spongy bone spicules at the root apex appear as long, thin, buttresses, stretching from the depth toward the root apex (k1), their tops and sides being enclosed by narrow uncalcified zones and strong layers of osteoblasts (ob). ok, osteoclasts.(Source: Oppenheim, 1911. Reproduced with permission of Oxford University Press.)

       Third degree of biologic effect (Figure 2.9). The force is fairly strong; sustaining increased pressure in the blood capillaries of the compressed PDL. At these areas, suffocation of the strangled PDL develops, followed by resorption of the necrotic tissue, including the dental root surfaces. This resorption takes an impetuous course and attacks also those parts of the surface of the root, the vitality of which may be injured by the pressure. After the force ceases, there will be anatomic and functional resolution of integrity of the PDL and alveolar bone, with resorption of roots frequently progressing into the dentin.

       Fourth degree of biologic effect (Figure 2.10). The force is strong, squeezing the strangled PDL, and the tooth touches the bone after the soft tissues are crushed. Alveolar bone resorption occurs in the periphery of the hyalinized PDL zones, as well as in bone marrow cavities near the compressed PDL. However, this situation is associated with a high risk of severe alveolar bone and root resorption, and damage to tissues of the dental pulp. In some cases, ankylosis of the tooth with the alveolar bone may occur.

Figure 2.8 Second degree of biologic effect seen on the (a) marginal side of PDL pressure side of tooth movement as portrayed in Schwarz (1932). Z, tooth; P, periodontium; R, line or resorption; K, old alveolar bone; T, newly formed bone on the outer periosteal surface of the alveolar bone. (b) Apex of the tooth shown. AZ, apical side of pull with newly formed bones; AD, apical side of PDL pressure.

      (Source: Schwarz, 1932. Reproduced with permission of Elsevier.)

Schwarz concluded “that the most favorable treatment is that which works with forces not greater than the pressure of blood capillaries.” He identified this pressure as 15–20 mmHg in man and most mammals, and calculated the optimal force level to be 20–26 g to 1 cm² of root surface area, suggesting that these limits of pressure are critical, capable of generating a continuous resorption of alveolar bone in areas of pressure in the PDL. Schwarz postulated further that the width changes in the PDL alter the cell population and increases cellular activity. There is an apparent disruption of collagen fibers in the PDL, with evidence of cell and tissue damage. If one exceeds this pressure, compression could cause tissue necrosis through “suffocation of the strangulated periodontium.” Application of even greater force levels will result in obliteration of blood vessels, followed by cell death in the ischemic area, which will lead to alteration in the orientation of PDL fibers from horizontal to vertical. This change in orientation will appear as glassy in nature, when observed through the light microscope and is labeled as hyalinization. There will be hyperemia in the area surrounding the necrotic area, which produces tenderness to the tooth. This hyperemia is considered to be essential to the resolution of the problem and speeding up the recovery phenomenon. The resolution of the problem starts when cellular elements such as macrophages, foreign body giant cells, and osteoclasts from adjacent undamaged areas invade the necrotic tissue (Figure 2.10). These cells also resorb the underside of bone immediately adjacent to the necrotic PDL area and remove it together with the necrotic tissue (Schwarz, 1932).