Biological Mechanisms of Tooth Movement. Группа авторов
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Figure 1.8 Carl Sandstedt (1860–1904), the father of biology of orthodontic tooth movement.
Figure 1.9 A figure from Carl Sandstedt’s historical article in 1904, presenting a histological picture of a dog premolar in cross section, showing the site of PDL compression, including an osteoclastic front and necrotic (hyalinized) areas.
Oppenheim’s research highlighted common concepts, shared by orthodontists and orthopedists, who were convinced that both specialties should be based upon a thorough knowledge of bone biology, particularly in relation to mechanical forces and their cellular reactions. However, it became evident that in orthodontics the PDL, in addition to bone, is a key tissue with regards to OTM.
Working on Macacus rhesus monkeys in 1926, Johnson, Appleton, and Rittershofer reported the first experiment where they recorded the relationship between the magnitude of the applied force and the distance in which it was active. In 1930, Grubrich reported surface resorptions in teeth subjected to orthodontic forces, a finding confirmed by Gruber in 1931. Even before these histological observations of surface changes were reported, Ketcham (Figure 1.10) (1927, 1929) presented, radiographic evidence that root resorption may result from the application of faulty mechanics and the existence of some unknown systemic factors. Schwarz (1932) conducted extensive experiments on premolars in dogs, using known force levels for each tooth. The effects of orthodontic force magnitude on the dog’s paradental tissue responses were examined with light microscopy. Schwarz classified orthodontic forces into four degrees of biological efficiency:
Figure 1.10 Albert Ketcham (1870–1935), who presented the first radiographic evidence of root resorption. He was also instrumental in forming the American Board of Orthodontics.
(Source: Siersma, 2015. Reproduced with permission of Elsevier.)
below threshold stimulus;
most favorable – about 20 g/cm2 of root surface, where no injury to the PDL is observed;
medium strength, which stops the PDL blood flow, but with no crushing of tissues;
very high forces, capable of crushing the tissues, causing irreparable damage.
He concluded that an optimal force is smaller in magnitude than that capable of occluding PDL capillaries. Occlusion of these blood vessels, he reasoned, would lead to necrosis of surrounding tissues, which would be harmful, and would slow down the velocity of tooth movement.
The proposed optimal orthodontic force concept by Schwartz was supported by Reitan (Figure 1.11), who conducted thorough histological examinations of paradental tissues incidental to tooth movement. Reitan’s studies were conducted on a variety of species, including rodents, canines, primates, and humans, and the results were published during the period from the 1940s to the 1970s. Figure 1.12 displays the appearance of an unstressed PDL of a cat maxillary canine. The cells are equally distributed along the ligament, surrounding small blood vessels. Both the alveolar bone and the canine appear intact. In contrast, the compressed PDL of a cat maxillary canine that had been tipped distally for 28 days, with an 80 g force (Figure 1.13), appears very stormy. The PDL near the root is necrotic, but the alveolar bone and PDL at the edge of the hyalinized zone are being invaded by cells that appear to remove the necrotic tissue, as evidenced by a large area where undermining resorption has taken place. Figure 1.14 shows the mesial side of the same root, where tension prevails in the PDL. Here the cells appear busy producing new trabeculae arising from the alveolar bone surface, in an effort to keep pace with the moving root. To achieve this type of tissue and cellular responses to orthodontic loads, Reitan favored the use of light intermittent forces, because they cause minimal amounts of tissue damage and cell death. He noted that the nature of tissue response differs from species to species, reducing the value of extrapolations.
Figure 1.11 Kaare Reitan (1903–2000), who conducted thorough histological examinations of paradental tissues.
Figure 1.12 A 6 μm sagittal section of a frozen, unfixed, nondemineralized cat maxillary canine, stained with hematoxylin and eosin. This canine was not treated orthodontically (control). The PDL is situated between the canine root (left) and the alveolar bone (right). Most cells appear to have an ovoid shape.
Figure 1.13 A 6 μm sagittal section of a cat maxillary canine, after 28 days of application of 80 g force. The maxilla was fixed and demineralized. The canine root (right) appears to be intact, but the adjacent alveolar bone is undergoing extensive resorption, and the compressed, hyalinized PDL is being invaded by cells from neighboring viable tissues (fibroblasts and immune cells). H & E staining.