Biological Mechanisms of Tooth Movement

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This new edition continues to be an authoritative reference to the scientific foundations underpinning clinical orthodontics The newly and thoroughly revised Third Edition of
delivers a comprehensive reference for orthodontic trainees and specialists.
It is fully updated to include new chapters on personalized orthodontics as well as the inflammatory process occurring in the dental and paradental tissues. It is heavily illustrated throughout, making it easier for readers to understand and retain the information discussed within. The topics covered range from bone biology, the effects of mechanical loading on tissues and cells, genetics, tissue remodeling, and the effects of diet, drugs, and systemic diseases.
The Third Edition of
features seven sections that cover subjects such as:
The development of biological concepts in orthodontics, including the cellular and molecular biology behind orthodontic tooth movement Mechanics meets biology, including the effects of mechanical loading on hard and soft tissues and cells, and biological reactions to temporary anchorage devices Inflammation and orthodontics, including markers for tissue remodeling in the gingival crevicular fluid and saliva Personalized diagnosis and treatment based on genomic criteria, including the genetic influences on orthodontic tooth movement Rapid orthodontics, including methods to accelerate or decelerate orthodontic tooth movement Perfect for residents and PhD students of orthodontic and periodontal programs,
is also useful to academics, clinicians, bone biologists, and researchers with an interest in the mechanics and biology of tooth movement.

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35 Pavlin, D., Zadro, R. and Gluhak‐Heinrich, J. (2001) Temporal pattern of osteoblast associated genes during mechanically induced osteogenesis in vivo: early responses of osteocalcin and type I collagen. Connective Tissue Research 42, 135–148.

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CHAPTER 2 Biology of Orthodontic Tooth Movement: The Evolution of Hypotheses and Concepts

Vinod Krishnan and Ze’ev Davidovitch

Summary

Orthodontic treatment has been practiced for 2000–3000 years, but the last century‐and‐a‐half has witnessed major advances in the accumulation of meaningful biological information, which facilitates the formulation of hypotheses that help in the design, explanation, and improvement of clinical procedures. These hypotheses focus on the biological nature of the physical and biochemical events, which occur in teeth and their surrounding tissues following the administration of mechanical forces. Among the chief hypotheses are those related to creation of tissue strain and electrical signals that stimulate the cells in the regions affected by these forces. These studies revealed extensive cellular activities in the mechanically stressed periodontal ligament, 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 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.

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