Читать книгу Biological Mechanisms of Tooth Movement - Группа авторов - Страница 31

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).

Figure 2.9 Third degree of biologic effect as portrayed in Schwarz article (1932). (a) Shows MZ, marginal side of pull; MD, marginal side of pressure; 0, tilt axis; AZ, apical side of pull; AD, apical side of pressure. (b) Marginal side of pressure, greatly enlarged: Z, tooth (dentine); C, cementum; H, resorption cavity reaching far into the dentine; P, periodontium; R, line of resorption on the alveolar wall, densely covered by osteoblasts; early stages of regeneration; A, compressed area of the periodontium, no nuclei of cells; U, signs of undermining resorption. (c) Sketch of the spring. The point of application on the tooth is shown at X.

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

Figure 2.10 Fourth degree of biologic effect as portrayed in Schwarz article (1932) depicting osteophytes on the outer surface in the apical region. (a) The influence created by strong force applied in the direction of the arrow: P, pulp; D, dentine; C, cementum; K, old alveolar bone; O, osteophytes; Q, region of compression of the periodontium; R, region of resorption stretching over the newly formed osteophytes. (b) The osteophytes, O, were formed in the lumen of the canalis mandibulae (N, nervus mandibularis). At the region of compression, the old alveolar bone, K, is removed by undermining resorption, R. The young osteophytes were also attacked by the latter. Arrow and also P, C and D as in (a).

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

Through his writings, Schwarz tried to indicate the methodological differences between the approaches made by Sandstedt and Oppenheim (Figure 2.11), and concluded that Oppenheim had euthanized his experimental animals several days after the appliance had been last activated, and Schwarz attributed this fact to the reason why Oppenheim saw only normal adaptation phenomena. Moreover, Oppenheim ignored the acute phase reactions and focused only on the stage of regeneration after the force had been exhausted. It seems more likely that what Oppenheim was describing was the response of cells of the periosteal and endosteal bone surfaces to the bending of the labial alveolar bone plate (Meikle, 2006).

Following Schwarz’s publication, Oppenheim performed additional studies on tissue reactions in mature monkeys (Macaca rhesus) to applications of light and heavy forces (Oppenheim, 1944). He concluded that with light forces, osteoclasts are mobilized at a very fast pace and attack bone by a uniform superficial lacunar resorption. These cells, called “primary osteoclasts,” stayed active in the site for almost 4 days (Figure 2.12). In contrast, the use of heavy forces resulted in crushing of the PDL, with a cutoff in all its nutritional supplies, resulting in undermining resorption. The direction of bone resorption comes from unintended sources, with an inflow of osteoclasts from adjacent unaffected areas. These osteoclasts, called “secondary osteoclasts,” persist until the crushed PDL, bone, and cementum are removed (Figure 2.12). Oppenheim further examined the hemorrhage formed by crushed blood vessels and found that the impaired nourishment along with encroachment of osteophytes and toxins from decomposed red blood cells lead to mobilization of osteoclasts from far off sites, called “tertiary osteoclasts” (Figures 2.13 and 2.14). All these cells were observed by application of higher amounts of force (240–360 g) to teeth. With these findings, Oppenheim advocated the use of intermittent forces, consisting of force application for a short period (1 day) followed by a rest period of longer duration (3 or 4 days). He considered this formula to be a biologic approach, but was later disproved by the evolution of mechanical devices of greater potential. He concluded that primary osteoclasts are the type, which is of great help to the orthodontist, and that only light forces can induce their production in abundance.

Figure 2.11 Comparative diagram of the theories put forward by Sandstedt (1904) and Oppenheim (1911) as drawn by Schwarz (1932). In (a), which depicts the theory of pressure (Sandstedt), the tooth moved by the force, P, tilts around an axis, O, lying a little apically from the center of the root. By this means two regions of pressure and pull arise, lying diametrically opposite. In the regions of pressure in the PDL, the old alveolar bone is resorbed (jagged line) and in the regions of pull, new bone is added (horizontal shading). Gray shading, alveolar bone without transformation. (b) This depicts the theory of transformation (Oppenheim, 1911, 1944). There is only one side of pressure and one side of pull. On both sides the alveolar bone opens into a transitional spongy bone, whose elements are arranged vertically to the surface of the tooth (horizontal shading). On the side of pressure, this newly formed transitional bone is resorbed (jagged line). On the side of pull, new bone is added. Gray shading indicates the old untransformed alveolar bone at a greater distance from the moved tooth,

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

Figure 2.12 Higher magnification image from Oppenheim’s article (1944) showing labial alveolar crest. The aplastic zone facing the periodontium has for the greatest part disappeared, as has the crest itself. Where some aplastic bone is still present (ab), the secondary osteoclasts (Occ) are still at work removing it. No osteoclastic activity whatsoever is found at the periosteal smooth bone surface. The still remaining but decreased pressure caused the appearance of primary osteoclasts (Oc) and will be present for 2 days after force discontinuation. D, dentine; C, cementum; Pd, periodontal membrane; Po, formation of smooth periosteal bone surface; Opk, scarce osteophyte. ac, acellular cementum.

(Source: Oppenheim, 1944. Reproduced with permission of Elsevier.)

Figure 2.13 Higher magnification image of hemorrhage as portrayed in Oppenheim (1944).

(Source: Oppenheim, 1944. Reproduced with permission of Elsevier.)

In short, all three major researchers (Sandstedt, 1904, 1905; Oppenheim, 1911, 1944; Schwarz, 1932) exploring tissue reactions during OTM, agreed that there is a creation of pressure and tension sites in the PDL during OTM. Furthermore, it appears that cell replication is decreased in pressure sites owing to a decrease in vascular supply, whereas it is increased in tension sites due to PDL fiber stretching.

Figure 2.14 Hyalinization reaction as portrayed in Oppenheim (1944). The osteocytes are mostly normal; the osteophytic bone formation (Oph) is quite poor; no sign of any periosteal osteoclastic activity was found. The cementum within the compression area is aplastic, and again displays its signs of vitality (cementoblasts, cementoid seam) above the compression area (C). Within this area, we see a cementum resorption with cementoclasts (Cc) still present 4 days after force discontinuation. A proof that the lowering of the crest has really taken place is found in the presence of another small cementum resorption (r) in a region opposite which bone is no longer present. The larger resorption, though not deep, is already quite extended buccolingually. Above the crest we find the effect of the relapse movement of 4 days, the formation of an osteoid seam (Ost). C, Aplastic cementum; D, dentine; Pd, periodontal membrane; ca, crushed periodontal tissue with hyaline degeneration and debris; Occ, secondary osteoclasts: Oph, osteophytic apposition; r, small cementum resorption: cc, greater cementum resorption with cementoclasts still present; Ost, osteoid.

(Source: Oppenheim, 1944. Reproduced with permission of Elsevier.)

Reitan (1957, 1960), in his classic papers on histological changes during OTM, reported that hyalinization refers to cell‐free areas within the PDL, in which the normal tissue architecture and staining characteristics of collagen in the processed histological material have been lost (Figures 2.15 and 2.16). He observed that:

 hyalinization occurred within the PDL following the application of even minimal force, meant to bring about a tipping movement;

 a greater degree of hyalinization occurred following application of force, if a tooth had a short root;

 during tooth translation, very little hyalinization was observed.

Reitan (1960) concluded that the tissue changes observed were those of degeneration related to force per unit area, and that attempts should be made to minimize these changes.

Figure 2.15 Cell free areas as shown by Reitan (1960). The figure shows pressure in the PDL during tooth movement, where cells gradually disappear in a circumscribed area. A, Root surface: B, compressed cell free fibers; C, border line between bone and hyalinized tissue: D, undermining bone resorption; E, small marrow space in dense, compact lamina dura.

(Source: Reitan, 1960. Reproduced with permission of Elsevier.)

Figure 2.16 (A) Formation of cells and capillaries in hyalinized tissue after the force was released as shown by Reitan (1960). B, Root surface; C, direct resorption; D, undermining resorption.

(Source: Reitan, 1960. Reproduced with permission of Elsevier.)