the cellular, molecular, and genetic levels. The rapid reactions occurring at the initial stage of mechanotherapy, and slower adaptive changes at the later stages of treatment, have attracted increasing attention. This chapter addresses the evolutionary traits of the development of concepts pertaining to the biology of OTM.
Hypotheses about the biological nature of OTM: The conceptual evolution
OTM is the result of a biological response to interference in the physiological equilibrium of the dentofacial complex by an externally applied force (Proffit, 2013). The biological foundation of force‐induced tooth movement, along with some concepts related to it, has been extensively investigated since the onset of the twentieth century. From the classic reports by Sandstedt in 1904 (Figure 2.1), the race was set for exploring the biological foundations of OTM, using histology, radiology, and clinical observations as the main investigative tools. A list of the then prevailing hypotheses aimed at explaining the biological reasons for OTM is presented below:
The old pressure hypothesis of Schwalbe–Flourens, which postulated that pressure moves teeth, preceded the concept that alveolar bone resorption takes place on one side of the dental root, while deposition occurs on the opposite side, until the pressure is eliminated. Hecht (1900), Sandstedt (1904), Pfaff (1906), and Angle (1907) supported this hypothesis (Oppenheim, 1911).
Based on his vast clinical experience, Kingsley (1881) stated that slow OTM is associated with favorable tissue‐remodeling changes (resorption and deposition of alveolar bone), while quick movements displace the entire bony lamellae along with the teeth, while retaining their functional and structural integrity. He attributed these features to the elasticity, compressibility, and flexibility of bone tissue. This report is one of the first written explanations for the biological basis of OTM, although it is not frequently cited (Oppenheim, 1911).
Figure 2.1 Page 1 from Sandstedt’s original article on histological studies of tooth movement published in 1904.
(Source: Sandstedt, 1904, 1905.)
Walkhoff’s hypothesis on the biology of OTM
Soon after Kingsley’s contribution, Walkhoff (1890) stated that “movement of a tooth consists in the creation of different tensions in the bony tissue, its consolidation in the compensation of these tensions.” Walkhoff’s hypothesis was largely based on the elasticity, flexibility, and compressibility of bone, and the transposition of the histological elements (such as the PDL). He also stated that alveolar bone, after all the remodeling changes, maintains its thickness, due to transformation or apposition of bone during the consolidating (retentive) period (Walkhoff, 1891). He emphasized the importance of retention, stating that “osteoid tissue has nothing to do with tooth movement. If we were to remove the retaining devices already after a few weeks from corrected protruding front teeth like from a fractured bone after the formation of a callus, we had only to deal with failures.” The propositions by Walkhoff were based solely on his clinical observations and practical knowledge but lacked the backing of histological evidence.
In 1900, Hecht described a cartilaginous transformation of the bone and rupture of bony spicules surrounding teeth during OTM. He interpreted this situation as an indication of severe changes and leaned upon Schwalbe–Flourens’ pressure hypothesis (Oppenheim, 1911) to substantiate his interpretation. However, Oppenheim argued against this viewpoint, stating that the severe changes, which Hecht had observed, might have been the result of the application of excessive force (Oppenheim, 1911). In any case, Hecht did not support his assumptions with any histological evidence.
Histological examination of paradental tissues during OTM was reported for the first time by Sandstedt (1904), who tipped teeth uncontrollably in dogs, and later studied their tissues by light microscopy (Figures ). In these sections he observed areas of pressure and tension in the PDL, and necrosis or hyalinization zones in the PDL at sites of great compression. Oppenheim (1911), while trying to duplicate those experiments, could not find any thrombosis in vessels or hyalinization in the PDL. He speculated that the lack of necrosis in his own experiment might have been due to the use of light force, in contrast to the heavy forces used by Sandstedt.
Figure 2.2 Plate I from Sandstedt’s original article showing photographs of the control (1) and experimental (2) dogs at sacrifice. The mandibular canines were removed to allow the movement of the maxillary teeth. The appliance consisted of an archwire inserted into tubes attached to bands on the upper canines; distal to the tubes was a screw mechanism, which, when tightened, moved the incisors lingually and the canines mesially.
(Source: Sandstedt, 1904, 1905).
Figure 2.3 Plate III from Sandstedt’s original article showing horizontal sections through the right maxillary canine; the direction of movement is towards the top.
(Source: Sandstedt, 1904, 1905.).
(a) (Sandstedt’s Figure 9.) A section cut in close proximity to the alveolar rim. A. At the site of presumptive compression, the PDL shows the glassy appearance characteristic of hyalinization, with osteoclasts undermining the adjacent alveolar wall. B. On the buccal side of the root, a thin layer of lighter staining new bone is demarcated from the old bone by a von Ebner (reversal) line. At the bottom, new bone takes the form of lighter staining bony trabeculae of woven bone orientated in the direction of pull. C. On the right side, osteoclasts are resorbing the alveolar wall; on the left, the detachment of the PDL from the bone is the result of a tear during sectioning.
(Source: Sandstedt, 1904, 1905.).
(b) (Sandstedt’s Figure 10) A section through the middle third of the same tooth (in dogs, the pulp canal expands towards the middle third of the root before narrowing towards the apex). General remodeling activity at the bone–PDL interface is seen but evidence of the accelerated bone formation and resorption is absent. This area corresponds to the center of rotation of the tooth.
(Source: Sandstedt, 1904, 1905.)
Figure 2.4 Plate IV A from Sandstedt’s original article. These sections show at a higher power the cellular and tissue changes in the
