Biological Mechanisms of Tooth Movement. Группа авторов
stages of treatment, have attracted increasing attention. This chapter addresses the evolutionary traits of the development of concepts pertaining to the biology of orthodontic tooth movement.
Introduction
Orthodontic tooth movement (OTM) is facilitated by remodeling of the dental and paradental tissues which, when exposed to varying degrees of magnitude, frequency, and duration of mechanical loading, express extensive physical and chemical changes that differ from the processes of physiological dental drift, or tooth eruption. In OTM, a tooth moves as a result of mechanical forces derived from external devices, while forces leading to mesial migration of teeth are derived from the individual’s own musculature, and tooth eruption results from complex interactions between dental and paradental cells. The common denominator of all these phenomena is the generation of mechanical forces, either physiologically or therapeutically. OTM resembles tooth eruption because both processes depend on remodeling of the periodontal ligament (PDL) and the alveolar bone, but the two processes present different models of bone remodeling (Davidovitch, 1991; Wise and King, 2008). The status of bone metabolism determines the specific characteristics of tissue remodeling associated with tooth eruption and OTM. In both cases mechanical forces are applied to the teeth, which are transmitted through the PDL to the alveolar bone, followed by an instantaneous cellular reaction. The details of this reaction have been the main target of investigation since the end of the nineteenth century. However, since orthodontic forces are usually greater than the forces of eruption, the tissue reaction during OTM may include iatrogenic injury to teeth and their surrounding tissues. OTM can occur rapidly or slowly, depending on the physical characteristics of the applied force, and the size and biological response of the PDL. Typically, when a tooth is tipped by mechanical forces, the root movement within the PDL develops areas of compression and of tension. When optimal forces are applied, alveolar bone resorption occurs in PDL compression sites, while new bone apposition takes place on the alveolar bone surfaces facing the stretched PDL (Sandstedt, 1904, 1905; Oppenheim, 1911; Schwarz, 1932). However, when the applied force exceeds a threshold, cells in the compressed PDL may die, and the orientation of the collagenous PDL fibers may change from horizontal to vertical. This change in PDL fiber orientation causes the necrotic area to appear opaque in the microscope, resembling the appearance of hyaline cartilage (Reitan, 1960). Tooth movement will resume only after these hyalinized tissues and the adjacent alveolar bone are removed by invading cells from the adjacent viable PDL or alveolar bone marrow spaces. Some of these cells coalesce to form multinucleated osteoclasts, targeting the alveolar bone, while macrophages that are attracted to the site remove the necrotic PDL, thus enabling the tooth to move.
During OTM, cellular activities in sites of PDL tension are meant to narrow the widened space created by the movement of the dental root away from the alveolar bone. This stretching of the PDL affects both the cells and their extracellular matrix (ECM). The stretched cells detach themselves from their surrounding ECM, then reattach, and engage in a variety of functions commensurate with returning the width of the PDL to its original dimensions. These functions include proliferation, differentiation, synthesis and secretion of autocrine and paracrine molecules, and new ECM components. Some of these components are mineralizable and will eventually become the new layer of bone that covers the alveolar surface that faces the stretched PDL. The new bone first appears as fingerlike projections, which grow along the stretched PDL fibers, perpendicular to the surface of the old alveolar bone. The force‐induced strains alter the PDL’s nervous network, vascularity, and blood flow, resulting in local synthesis and/or release of various key molecules, such as vasoactive neurotransmitters, cytokines, growth factors, colony‐stimulating factors, and arachidonic acid metabolites. These molecules evoke a plethora of cellular responses by many cell types in and around teeth, providing a favorable microenvironment for tissue deposition or resorption (Davidovitch, 1991; Krishnan and Davidovitch, 2006).
The studies performed in the early years of the twentieth century were mainly directed towards analyzing the histological changes in paradental tissues following short‐term and long‐term OTM. Those studies revealed extensive cellular activities in the mechanically stressed PDL, involving neurons, immune cells, fibroblasts, endothelial cells, osteoblasts, osteoclasts, osteocytes, and endosteal cells. Moreover, mechanical stresses were found to alter the structural properties of tissues at 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