Orthodontic tooth movement

5 Orthodontic tooth movement

If a force is applied to a tooth it will elicit a response within the periodontium, resulting in remodelling of the periodontal ligament and alveolar bone, and ultimately tooth movement. The physical and biological principles that underlie this process form the basis of orthodontic practice and are discussed in this chapter.

Biological basis of tooth movement

It was first noted in the nineteenth century that a mechanical stimulus applied to bone could lead to remodelling and this is the basic principle, which facilitates orthodontic tooth movement.

Physiology of bone

Bone is a hard tissue composed of a collagen matrix impregnated with mineral salts. As well as providing the foundation of the musculoskeletal system in most vertebrates, it serves as a storage site for many important elements, especially calcium. Bone consists of three principle components:

• An extracellular matrix, consisting predominantly of type I collagen and a variety of proteoglycans and bone-specific proteins;
• Inorganic mineral, which makes up approximately 67% of bone by weight and consists mainly of calcium and phosphate in the form of hydroxyapatite crystals; and
• Cells, which include osteoblasts responsible for laying down and mineralizing the bone matrix; osteocytes, which are osteoblasts that have become enveloped by bone as it mineralizes, and osteoclasts, which are large multinucleate cells derived from haematopoetic precursors within the circulation that resorb bone.

There is close intercellular communication between osteoblasts and osteocytes, the main function of this osteoblast–osteocyte complex being to maintain integrity of the bone matrix.

Bone remodelling

Bone is a dynamic tissue, with resorption and deposition continually occurring and being closely linked and regulated. This process produces remodelling of the skeleton, in simple terms by osteoblastic deposition and osteoclastic resorption. However, the situation is complex and in addition to their direct role in bony deposition, several osteoblastic responses have been identified that indirectly facilitate osteoclastic resorption:

• Osteoblasts lining the bone represent a physical barrier to resorption and their retraction provides access for bone-resorbing osteoclasts;
• Osteoblasts remove unmineralized collagen or osteoid that lines the bone surface, which also acts as a physical barrier to osteoclasts; and
• Osteoblasts release a soluble activating factor, which has a direct action on osteoclasts.

Regulation of bony deposition and resorption is important for normal maintenance of the skeleton and when these mechanisms break down, pathological change can occur. Numerous systemic and local factors have been implicated in bone remodelling (Table 5.1).

Table 5.1 Factors affecting bone remodelling and maintenance of the periodontal space

Systemic factors Local factors
Parathyroid hormone Cytokines and growth factors
Vitamin D metabolites Prostaglandins
Calcitonin Leukotrienes

Biomechanics of tooth movement

Early research into tooth movement investigated the histological response of tissues using animal models, whilst more recent work has focused on cellular activity following mechanical stimulation (Box 5.1).

Box 5.1 How has orthodontic tooth movement been investigated?

Early investigations into orthodontic tooth movement examined the histological effect within the periodontal ligament and alveolar bone of loading a tooth. Later experimental models were developed, both in vitro and in vivo, to study the effect that these forces had in greater detail. Numerous animal models have been used, including rats, cats and primates. Usually an orthodontic appliance is attached to the teeth and force applied over a given period of time, samples of cervicular fluid are collected for assay during the experimental period and then the animal is sacrificed for histological examination. Organ culture systems have also been used. As the periodontal ligament is similar to sutural joints, in both anatomy and function, one model involves placing mechanical stress across cranial sutures taken from newborn rabbits. Animal models tell us much about the histological and biochemical changes that occur during mechanical stress; however, the major drawback of such experiments is the difficulty in determining the individual cellular response. To examine this, a single cell type is cultured on a substrate that is mechanically deformed. Petri dishes with flexible bases are available, and these can be deformed by placing them over a convex template or applying a vacuum. Different cell types can be examined in this way and the size and periods of the deformation can be varied. Samples are taken periodically from the cell culture medium in which the cells are immersed for subsequent biochemical assay.

Pressure–tension theory

Histological studies carried out independently by Carl Sandstedt and Albin Oppenheim at the turn of the past century provided the foundation for current understanding of orthodontic tooth movement. When a force is placed on a tooth, bone is laid down on the tension side of the periodontal ligament and resorbed on the pressure side (Fig. 5.1). On the pressure side, when the force is light, multinucleate cells resorb bone directly. However, if the forces are higher and exceed capillary blood pressure, cell death can occur and a cell-free area forms. This is described as hyalinization, due to the glass-like appearance of these regions when viewed with light microscopy resembling hyaline cartilage. Resorption of these areas proceeds at a much-reduced rate. This process is described as undermining resorption and will result in slower tooth movement and greater pain and discomfort for the patient. Later work showed that even forces as light as 30g will produce some areas of hyalinization, and this tends to occur more with tipping than bodily movement of teeth, presumably because the force is dissipated more evenly through the periodontal ligament during bodily movement (Reitan, 1964).

image

Figure 5.1 Histological appearance of the periodontium during orthodontic tooth movement.

Osteoblastic bone deposition (arrowed) on the tension side. Osteoclastic frontal resorption (arrowed) on the pressure side. Hyalinization occurs in areas of excess pressure and is characterized by a glass-like appearance in regions of the periodontal ligament (*) and areas of undermining resorption (arrowed). AB, alveolar bone; PL, periodontal ligament; T, tooth.

Courtesy of Professor Jonathan Sandy.

From histological and clinical studies there appears to be a range of force effective for tooth movement (Storey & Smith, 1952) although the optimum force magnitude for orthodontic tooth movement has yet to be described (Ren et al, 2003). Light continuous forces are thought to be more effective than heavy forces as these will increase the risk of hyalinization, with no increase in the desired tooth movement but with greater potential anchorage loss (Fig. 5.2). However, large variation does exist between individuals and more important than the absolute force is the stress generated in the periodontal ligament. Stress is force per unit area and depending on the type of tooth movement, stress distribution within the periodontium will vary. Therefore, different force levels are recommended for different types of tooth movement (Table 5.2). Tipping teeth requires less force than bodily movement, whilst intrusive forces need to be light as these are dissipated through the apices of the teeth, increasing the risk of root resorption.

image

Figure 5.2 Graph of force applied to the periodontal ligament and subsequent tooth movement.

Up to a certain threshold, tooth movement increases with force. However, once this force exceeds a certain level, no additional movement is obtained. Indeed, extreme forces can even cause a reduction in movement.

Table 5.2 Range of forces for different tooth movements

Tipping 30–60 g
Bodily movements 100–150 g
Rotational movements 50–75 g
Extrusion 50–75 g
Intrusion 15–25 g

Bone deflection and piezoelectricity

Orthodontic forces are transmitted within the periodontal ligament of the tooth and traditionally this has been thought to be via principle fibres of the periodontal ligament itself. However, when cross-linking of collagen is disrupted, the histological response of bone to orthodontic tooth movement appears normal (Heller & Nanda, 1979). Therefore, it has been proposed that the periodontal ligament represents a continuous hydrostatic system that distributes forces equally to all its regions (Baumrind, 1969). However, this would mean differential forces could not be distributed within the ligament, which is clearly not the case.

Teeth will displace a greater amount than the width of the periodontal ligament when force is initially applied to them, which implies that some deflection of alveolar bone also occurs. This might explain why differential forces can develop at the bone surfaces of the periodontal ligament. Bone deflection also produces stress-generated electrical potentials at the bone surface, which at one time were thought to be involved in bone remodelling. However, these are short-lived and very small and as such, unlikely to play an active role (McDonald, 1993).

Cellular shape change and signal transduction

When an external force is applied to a tooth, this stimulus generates an intracellular response, which ultimately leads to a change in function of affected and adjacent cells by production of local bone remodelling mediators.

A relationship appears to exist between cell shape and metabolic activity. Cell shape is controlled by the cytoskeleton, which terminates in specialized sites at the cell membrane, which form junctional complexes with the extracellular matrix. At these focal adhesion integrins, a family of proteins that span the cell membrane link the cytoskeleton to the extracellular matrix. They act as intracellular signalling receptors and are involved in numerous signalling pathways. Mechanical stress on cells within the periodontal ligament initiates both the cyclic AMP and phosphoinositide pathways, which results in an increase in production of secondary messengers. This produces an increase in intracellular calcium levels, which mediates further cellular events, including a stimulation of DNA synthesis (Harell et al, 1977).

Production of arachidonic acid metabolites

Arachidonic acid is an unsaturated fatty acid produced from membrane phospholipids, which is metabolized into prostaglandins, leukotrienes and thromboxanes (Fig. 5.3). These molecules are potent mediators of inflammation and numerous in vitro and in vivo experiments have shown a relationship between mechanical stimulation and prostaglandin production in bone. Based on this work, prostaglandins have been used clinically via local administration in the gingivae to increase the efficiency of orthodontic tooth movement (Yamasaki et al, 1984). The other principle products of arachidonic acid metabolism, leukotrienes, have also been shown to increase around teeth moved orthodontically. This may explain the observation that on administration of a non-steroidal anti-inflammatory drug in an animal model, there is a decrease in osteoclast numbers, but not tooth movement (Sandy & Harris, 1984). This suggests some overlap between the pathways and a degree of redundancy within the system. Inhibition of leukotriene production itself results in inhibition of tooth movement (Mohammed et al, 1989).

image

Figure 5.3 The arachidonic acid pathway producing prostaglandins, leukotrienes and thromboxanes.

Production of cytokines

Cytokines are low-molecular-weight proteins that regulate or modify the action of cells. These protein groups are diverse and complex, and include some potent stimulators of bone resorption. It appears that osteoclast activity is dependent on soluble factors produced by osteoblasts and stromal cells in the periodontal ligament, so-called osteoclast-stimulating factors. On mechanical stimulation, t/>

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  2. Development of the dentition
  3. The orthodontic patient: treatment planning
  4. Management of the developing dentition
  5. Adult orthodontics
  6. The orthodontic patient: examination and diagnosis

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Jan 1, 2015 | Posted by in Orthodontics | Comments Off on Orthodontic tooth movement

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