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."/>
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.)
The fluid dynamic hypothesis
Bien (1966), through his research on the effect of intrusive forces on mandibular incisors, recorded an oscillation of the force inside the dental socket, and named it the hydraulic damping effect. He identified three distinct but interactive fluid systems present in paradental tissues: the vascular system, interstitial fluids, and cellular fluids. All three are presumably involved in damping oscillations of the tooth. He used Reynold’s numbers to measure tooth oscillation and concluded that the low Reynold’s number observed for the tooth subjected to oscillations is due to predominance of viscous forces acting within the system. He observed an escape of extracellular fluids from the PDL to the marrow spaces through the minute perforations in the alveolar wall (Figure 2.17). This phenomenon, occurring in the first stage of OTM, when PDL fibers are slack, depends mainly on size and number of alveolar bone perforations. The slack fibers become tightened once the extracellular fluids are exhausted. Owing to the presence of interstitial fluid or ground substance throughout the PDL, and the fact that the PDL is extremely thin, when compared with the sizes of the dental root and alveolus, he related the behavior of the PDL to that of the “squeeze film effect” proposed by Hays (1961). The presence of this film enables the tooth to withstand the heavy forces applied as part of orthodontic treatment or masticatory efforts. Masticatory forces, which are momentary in nature, will displace the fluid in the PDL space to its boundaries of the squeeze film (towards the apex and cervical areas of the dental root). Once the force is released, replenishment of fluid occurs through recirculation of interstitial fluid and diffusion through capillary walls, restoring the equilibrium. Likewise, a similar chain of events may occur following the application of low, sustained orthodontic forces.
Figure 2.17 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.)
With application of high sustained forces, as was the practice in the early era of orthodontics, capillary pressure will not be sufficient enough to counteract the effect and thus to replenish the fluid back to equilibrium. In this stage, the randomly running PDL fibers, which crisscross the blood vessels, tighten‐up, leading to compression, constriction of blood vessels, and leading to stenosis. This constriction point creates ballooning of the vessel wall above it, creating hydrodynamic pressure heads. Drawing support from Bernoulli’s principle, Bien explained the creation of a pressure drop in areas of stenosed blood vessels, leading to gas formation and sub‐atmospheric pressure. The gas bubbles formed might escape out of the capillaries and become lodged between bone spicules to create a favorable area for bone resorption. Bien attributed the large vacuoles seen in histologic sections of bone to be the escaped gas bubbles lodged there (Figure 2.18). Furthermore, he associated the lack of cementum resorption with its smooth nature, containing fewer small radii of curvature, producing unfavorable areas for gas lodgment.
Figure 2.18 The lodgment of minute gas bubbles at small radii of curvature. The minute bubbles of gas, which diffuse through the blood vessel walls below the stenosis, lodge against the solid boundaries of tooth root and bone. Since there are many more areas of small radii of curvature in the bone, a greater number of gas bubbles may accumulate on the bone surface rather than on the root surface.
(Source: Bien, 1966. Reproduced with permission of SAGE Publications.)
The bone‐bending hypothesis
Baumrind (1969) explored the assumption that orthodontic forces bend the alveolar bone. He measured changes in PDL cell dimensions, metabolic activity, and fiber synthesis with the help of radioisotopes (tritiated thymine, uridine, and proline). While discussing the findings of his research, he highlighted a conceptual flaw in Schwarz’s pressure–tension hypothesis. He described the PDL as a continuous hydrostatic system, which, in accordance with Pascal’s law, dictates that force applied to this system is distributed equally to all regions of the PDL. He emphasized that the presence of fibers in the PDL does not modify the operation of this law, because of the concomitant existence of a continuous body of liquefied ground substance. He recognized that only part of the PDL, where differential pressures exist, as mentioned in the pressure–tension hypothesis, can be developed, is actually solid, i.e., bone, tooth, and discrete solid fractures of the PDL.
Kingsley (1881) and Farrar (1888) were the first to be credited for proposing the concept of bone bending as being an integral part of OTM. Farrar wrote in favor of this hypothesis: “Teeth move by one of two kinds of tissue changes in the alveolus … by the reduction of the alveolus through what is called absorption on one side of the tooth, followed by the growth of new supporting tissue on the other and by bending of the alveolar bone.” Kingsley and Farrar increased the force levels to such an extent that visible bending of alveolar bone could be observed, but several authors who followed this approach complained that their patients had experienced alveolar fractures. Because of this problem, and the influence of Oppenheim and his lectures in the Angle School, the pressure–tension hypothesis
