Biological basis of orthodontic tooth movement

Nature of orthodontic tooth movement

Orthodontic tooth movement (OTM) is a complex bio-mechanical-humoral and inflammatory process initiated by the clinician that is consequent to force application. The applied force moves the tooth beyond its range of physiological tooth movement, called OTM. A tooth is not static in its environment but in a dynamic state with a limited range of physiological movements. These include tooth movements during various functions of a stomatognathic system, like mastication, lifelong mesial migration and active tooth eruption into the oral cavity. Additionally, tooth migration occurs in diseased conditions such as periodontal diseases, occlusal trauma, and pathologies of the dental, skeletal, and associated tissues. Bones are dynamic organs that undergo a lifelong remodelling process, which takes place by osteoclasts and osteoblasts. Mechanical stimuli are known to alter the remodelling process and are primarily considered ‘osteogenic’. The OTM process involves bone remodelling through the periodontal ligament (PDL), where forces or mechanical stimuli are transmitted through the tooth.

Several factors affect and modify the nature and amount of OTM. The most significant mechanical factors are the magnitude, direction and nature of the force. Biological factors inherent to the body encompass bone density, age, systemic health, hormones, and factors that impact bone turnover.

It is crucial to delve into the intricate biology of tooth movement, as it forms the foundation of orthodontics. Force is the only drug used by the clinician to modify dental and skeletal positions to achieve optimum occlusion. For decades, orthodontists have been on a relentless quest to unravel the biology of tooth movement. This pursuit is driven by the desire to comprehend the effect of orthodontic forces on the surrounding biological milieu, with the goal of achieving the best outcomes in terms of the rate of tooth movement without adverse effects on the dental, periodontal and surrounding tissues.

Therefore, in addition to optimising the force, many surgical and non-surgical approaches have been explored for the acceleration of tooth movement. These include interventions involving micro-perforations, osteotomy, and vibration, which accelerate the inflammatory processes. Besides, photo biomodulation, drugs, vitamins, and proteins have also been used but with limited success.

Orthodontic and orthopaedic force

In general, it is said that forces in the range of 50 and 300 g can induce the movement of a tooth or group of teeth in the alveolus. These are called orthodontic forces.

In comparison, forces usually higher than 300 g (256 g and beyond) are called orthopaedic forces.

Conventionally, in a clinical setting, forces measured in grams are denoted orthodontic forces, and those measured in pounds (256 g and beyond) are orthopaedic.

Orthopaedic forces, capable of altering the bony configuration, play a crucial role in orthodontic treatment. Orthopaedic forces can inhibit or redirect facial growth, providing significant therapeutic benefits in growing children with skeletal class II malocclusion due to prognathic maxilla or skeletal class III malocclusion.

The implications of tooth movement forces in bone have been extensively studied. This research has provided us with a deep understanding of the cellular and biological changes that occur in the periodontium, with a recent focus on the molecular events that control the process.

A traditional pressure-tension hypothesis was put forward to understand the mechanics of tooth translation through bone. The bone gets resorbed in the areas that are subjected to pressure and deposited at sites under tension. The concept of pressure-tension in OTM was evaluated mainly by histologic studies of the periodontium ( Fig. 17.1 ).

Image, AltText currently not available — Figure 17.1

Phases of tooth movement ( Fig. 17.2 )

Burstone suggested three phases of tooth movement by plotting the rates of tooth movement against time: (I) an initial phase, (II) a lag phase and (III) a post-lag phase. A study by Pilon et al. performed on beagles divided the curve of tooth movement into four phases. An additional Vth phase was suggested by the author whereby active force is eliminated yet the process of reorganisation and settling of the tooth in the newly acquired position takes place with minor movements.

I.
The initial phase, a period of rapid movement immediately following the application of force to the tooth, is a crucial stage in tooth movement. This rapid rate is a result of the tooth’s displacement within the periodontal ligament (PDL) space, a process that is of great interest to orthodontic professionals and researchers.
II.
The lag phase, which follows the initial phase, is a period of relatively low rates of tooth displacement or no displacement. This phase is believed to be caused by the hyalinisation of the PDL in areas of compression.
III.
Post-lag phase. The 3rd phase of tooth movement follows the lag period, during which the rate of movement gradually or suddenly increases. Research on experimental animals supports Burstone’s pattern of tooth movement phases described in humans.
- A study by Pilon et al. performed on beagles divided the curve of tooth movement into four phases. The first phase lasts 24 h to 2 days and represents the initial movement of the tooth inside its bony socket. It is followed by a second phase when the tooth movement stops for 20–30 days.
- IIIrd phase. After the removal of necrotic tissue formed during the second phase, tooth movement is accelerated in the 3rd phase and continues into the 4th linear phase. The 3rd and 4th phases comprise most of the total tooth movement during orthodontic treatment.
- Vth phase of deceleration and reorganisation Kharbanda proposed this phase of the orthodontic life cycle of the tooth, which is not well documented in the literature. Once active orthodontic forces cease, the tooth undergoes micro-adjustments in occlusion and functional adaptation to the surrounding environment and occlusal forces. The alveolar bone (AB), lamina dura, root cementum, and periodontal ligament around the tooth experience a process of reorganisation and healing. Furthermore, the root cementum undergoes healing of the resorption craters. The inflammatory biomarkers in the gingival crevicular fluid (GCF) also gradually trend towards a physiological state. However, the functional forces of the stomatognathic system continue to influence the tooth’s position in the alveolus throughout life.

Optimal orthodontic forces

A threshold of force is required to sustain OTM. The importance of correct force was given very early in the orthodontic history.

According to Schwarz (1932), ‘optimal force is the force leading to a change in tissue pressure that approximated the capillary vessels’ blood pressure, thus preventing their occlusion in the compressed periodontal ligament’ (capillary blood pressure is 20-26 g/cm ² of the root surface area).

Optimum orthodontic force should produce rapid tooth movement without any harmful effects on the tooth and its supporting tissues with the least discomfort to the patient. The optimal force value varies according to the root surface area and the type of tooth movement. For example, tipping of the canine distally requires less force than the one desired for translation. The bone quality, age, sex and growth status of the subject would influence the magnitude of force required and the rate of tooth movement.

Light and heavy forces: Frontal versus rear resorption

The magnitude of force applied for orthodontic mechanotherapy has received significant attention. It is generally accepted that light forces produce favourable tooth displacement by frontal resorption, that is the resorption starting at lamina dura.

Various studies ^, demonstrated that teeth subjected to heavy forces show hyalinisation more often than teeth experiencing light forces. The development of hyalinisation zones in the PDL has a definite relationship to the force magnitude. When heavy forces are applied, PDL cells undergo cellular death, and this zone appears without cells in histological sections, the so-called zone of hyalinisation. The bone resorption within the alveolus starts at a distant site, extending towards the zone of hyalinisation in PDL. This type of bone turnover is called rear resorption. However, it was found that the hyalinisation zones have no relationship to the rate of tooth movement. Once tooth movement has started after the second (arrest) phase, bone remodelling takes place at a certain rate, independent of force magnitude. It was found that force magnitude plays only a subordinate role in OTM. However, maintaining light forces avoids deleterious effects of tooth movement to a large level, with less discomfort for the patient.

Continuous, interrupted and intermittent forces

To produce OTM over a range or distance, applied force should be sustained for a considerable percentage of time. A threshold of force duration of roughly 6 h per day is necessary for effective tooth movement. Force magnitude decreases as the tooth moves, and the desired force level declines between two patient appointments. This is called force decay.

Based on their frequency of expression, orthodontic forces can be grouped as continuous, interrupted and intermittent.

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Continuous force means that the force magnitude is maintained at almost the same level in the period between two activations. The force applied by NiTi coil spring for space closure delivers a constant force between two appointments.
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Interrupted force declines to zero between activations. Fixed appliances produce continuous and interrupted forces. Differentiating between continuous and intermittent movements isn’t always feasible.
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Intermittent force falls to zero when the appliance is removed and shows force decay with tooth movement. For brief intervals, intermittent forces function as an impulse with a succession of disruptions. Examples are removable appliances and headgear.

Light continuous forces produce efficient tooth movement with the least harmful effects. Heavy forces are physiologically acceptable if they act as interrupted ones with a rest period in between. The rest period between appliance activations is the time tissues use for re-organization. This rest can promote favourable cell proliferation for further tissue changes when the appliance is activated again. Light continuous and heavy interrupted forces are clinically acceptable, whereas heavy continuous forces should be avoided.

Reactivating orthodontic appliances more frequently than every 3 weeks is not recommended. In a clinical practice, an appointment cycle of 4 weeks is more common.

However, newer material wires such as Cu-NiTi and heat-activated nickel-titanium wires have a long range of action and can last for a few months. The patient may require a review and not necessarily activation.

Tissue reactions to orthodontic forces

Tissue reactions to orthodontic forces were first described by Sandstedt (1904, 1905 ), and later by Oppenheim (1911, 1930, 1935, 1936 ).

Sandstedt’s work was on dogs, where he applied force through an appliance for a period of 3 weeks, moving the crowns of incisors by 3 mm.

He demonstrated that both heavy and light forces were used to deposit bone on the tooth’s tension side, while light forces were used to resorb AB directly by multinucleate osteoclast cells on the pressure side. He also demonstrated that the application of heavy forces compresses the periodontal tissues, resulting in a cell-free zone known as the hyalinised tissue due to thrombosis of vessels and cell death. This zone resembles hyaline connective tissue on histological sections, hence the term hyalinisation. In hyalinised areas, resorption of the alveolus takes place far from the cell-free zone in the bone marrow spaces and is called ‘undermining resorption’ or ‘rear resorption’.

Oppenheim studied bone transformation following the application of force in primary teeth of monkeys several days after the force was last activated. He continued to work in this field, including root resorption (1930, 1935, 1936 ). Kaare Reitan, a Norwegian orthodontist, did extensive work on tissue response to OTM. He researched human models (1957, 1964 ) and dogs (1959 ). His classical work on human premolars that were destined for orthodontic extraction demonstrated that continuous forces as low as 30 g can produce some degree of hyalinisation, particularly when tipping movements are attempted in contrast to translation where forces get evenly distributed on a wide area of tooth/bone surface. It takes about 2–4 weeks to remove this hyalinised tissue by the phagocytes. It has been shown that the patency of the blood vessels is required for direct resorption to be initiated.

Later, Per Rygh (1972), based on ultrastructural cellular reactions and vascular changes in pressure zones in rat molars, demonstrated events that take place after the application of a force on a tooth.

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First 30 min: Erythrocyte packing occurs in dilated blood vessels; necrotic alterations in PDL fibroblasts, including endoplasmic reticulum dilatation and mitochondrial enlargements
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2–3 h (2–3 days in humans): Fragmentation of erythrocytes, cell membrane rupture and nuclear fragmentation occurs.
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1–7 days: Disintegration of the blood vessel walls and extravasations of their contents.

These events are followed by the removal of the necrotic hyalinised tissue by multinucleated giant cells. It has been shown by Brudvik and Rygh (1994) that tartrate resistant acid phosphatase (TRAP)-positive macrophages and multinucleated giant cells have a role in the removal of hyalinised tissues. Resorption lacunae are created on the root surface when TRAP-positive cells continue to remove the cementum and neighbouring dentine after reaching the adjacent root surface.

PDL remodelling—histological findings

Sandstedt, Oppenheim and Schwarz’s classic histologic studies on tooth movement produced the theory that a tooth moves in the periodontal space by producing two sides: a ‘pressure side’ and a ‘tension side’. Later, ultrastructural studies by Rygh (1972) and Brudvik, and Rygh (1994) , gave a very detailed description of events. The above research findings have been meticulously summarised ( Figs 17.3–17.4 ) by Krishnan and Davidovitch (2006).

On the tension side

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The PDL is seen to be getting wider. Along with an increase in connective tissue cells and vascularity, the stretched PDL appears to activate a number of cellular processes. The vascular supply to the PDL diminishes after a certain amount of stress, and cell death takes place in the spaces between stretched fibres.
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There is distension of blood vessels on the tension side in the PDL, and there is cellular infiltration of the tissue by macrophages and leucocytes along with proteins and fluids, which migrate from the adjacent PDL capillaries and evoke an inflammatory response.
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Fibroblasts are rearranged in the direction of strain. These fibroblasts release new Sharpey’s collagen fibres into the PDL; some of these collagen fibres are integrated into the newly formed osteoid, while the remainder is embedded in the PDL at the same time that a new matrix is deposited on the wall of the AB socket.

On the pressure side

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The PDL space is getting smaller, and the alveolar crest bone is getting deformed. This location reacts differently depending on the amount of force applied; direct bone resorption is produced by light pressure, while hyalinisation is produced by heavy forces.
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Oedema, progressive blood vessel obliteration, vein wall degradation and blood constituent leaking into the extravascular environment are characteristics of changes in the compressed PDL.
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The endoplasmic reticulum moderately swells, vacuoles develop, rupture, and cytoplasm is lost in fibroblasts at certain locations. The separated nuclei that remain after this disintegration undergo lysis over a few weeks, and the powdered substance that is preserved gives the surface a glossy look. Products of erythrocyte breakdown that accumulate in pressure areas may crystallise.
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After the removal of necrotic tissue in 3–5 weeks, the tooth movement occurs. The PDL post-hyalinisation is broader than before the start of treatment, so it may withstand higher mechanical insults or forces.

Orthodontic literature has traditionally elaborated much on the pressure tension theory, and our thinking has remained within the confines of this theory. Baumrind believed that the periodontal membrane, enclosed in a space surrounded by the tight boundaries of cementum and bone, serves like a fluid, a hydrostatic system. Therefore, as per Pascal’s law, similar force should be distributed to all areas of the PDL. We know that the PDL contains several types of collagen fibres, cells, blood vessels and tissue fluids, and the lamina dura is not a closed wall. The analogy of ‘fluid in a closed vessel’ is not correct. The evidence from tooth movement experiments has shown that within the PDL, ‘differential pressure’ is generated. Hence, distinct compression and tension areas are created around tooth surfaces. The variable morphology of the root form, surface, and lamina dura, alongside the direction of the force, also determines the resultant differential pressures from orthodontic forces.

Pathways of tooth movement

Various hypotheses were put forward to understand the biological process of tooth movement. Mostafa et al. in 1983 came up with a broad outline of various modes of cellular changes bringing about tooth movement. They proposed an integrated model for the mechanism of tooth movement ( Fig. 17.5 ). According to this model, there are two pathways, and both of them work concurrently to cause efficient tooth movement.

Pathway 1

It is the major biological response to orthodontic force. It represents a physiologic response and may be associated with normal bone growth and remodelling. When orthodontic force is applied, bone bending occurs, and it can lead to the production of inflammatory mediator prostaglandins and also the creation of positive and negative charges on bone due to charge polarisation of its matrix, which is due to the phenomenon of ‘piezoelectric response’. The formation of bioelectric signals following force application to bone is well-known in the current scientific literature.

Electric effects on bone due to force can be:

Piezoelectric (dry bone) ( Fig. 17.6 )

Streaming potentials (wet bone).

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Piezoelectricity. It is a phenomenon found in numerous crystalline materials when a current of electricity is created when the crystal structure deforms because electrons are dispersed across different parts of the crystal lattice. Piezoelectric signals have two characteristics: (1) quick decay rate and (2) production of equivalent signal opposite in direction when force is released. Sources of piezoelectric current are hydroxyapatite-collagen and collagen-hydroxyapatite interface.
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Streaming potentials.
- When live bone bends, a complex electric field is created that interacts with ions in the fluid surrounding it to produce electric signals and temperature changes. The streaming potential is the name given to the tiny voltage that is seen. Such potentials may develop in bone as a result of blood flow and interstitial fluid movement in the structure’s vascular channels, haversian networks, canaliculi and microporosities. These voltages, like piezoelectric signals, have rapid onset and alterations.

According to Mostafa et al., piezoelectric response acts by itself and by producing prostaglandins. The electric response gave directional control to bone remodelling by the bone formation in negative charge areas and resorption in positive charge areas. It also described the action of prostaglandins through cell membranes and cyclic adenosine monophosphate (cAMP). They described a diffusible product secreted by osteoblasts, which is believed to synchronise bone resorption and formation, and named it the coupling factor.

Pathway 2

It illustrates the tissue inflammatory response by orthodontic force and how it affects bone remodelling directly as well as through the formation of prostaglandins.

It is well known that inflammatory and proinflammatory mediators play a significant role in response to tissue injury in OTM. These include prostaglandins, cytokines, leukotrienes, neurotransmitters, nitric oxide (NO) and hormones ( Fig. 17.7 ).

1. Arachidonic acid metabolites—prostaglandins and leukotrienes

Von Euler (1934) first discovered the compound in the prostate fluid, hence the name. Prostaglandins are important mediators of inflammation and are synthesised from arachidonic acid by cyclo-oxygenase (COX) pathway, whereas leukotrienes are synthesised by lipo-oxygenase (LOX) pathway. The formation of various prostaglandins and leukotrienes from cell membranes is a complex process and it happens through various stages. Various clinical and animal studies suggested that prostaglandins are important mediators of mechanical stress, and they have an important role in stimulating bone resorption during tooth movement.

An experimental animal study on rats by Mohammed et al used PG inhibitor, leukotriene inhinitor and both, and performed tooth movement. A comparison of tooth movement rates with controls suggested that tooth movement was most decreased when prostaglandins (PGs) leukotrienes were inhibited together, and tooth movement was also decreased when prostaglandins and leukotrienes were individually inhibited. This gives evidence to the role of PGs and leukotrienes in tooth movement. Among PGs, PGE has the most important role to play. The binding of these molecules to the cell membrane can activate second messengers.

2. Neurotransmitters

Neuropeptides have been demonstrated to either directly impact bone cells or indirectly impact through their effects on the vascular system. These include substance P, vasoactive intestinal polypeptide (VIP), and calcitonin gene-related peptide (CGRP). The mechanical strain produced by tooth movement may trigger their release.

Neurotransmitters can also act centrally, which elicits pain sensation. Direct action is on cells, causing intracellular signalling. Substance P’s in vitro incubation with human PDL fibroblasts markedly raised the cells’ cAMP concentration and the medium’s PGE2 content in just 1 min. On the vascular system, they produce vasodilatation and cause the leucocytes to migrate out of the capillaries, further creating the formation of inflammatory substances. All these can produce intracellular signalling by the production of second messengers, that is cAMP.

3. Cytokines

Cytokines are small proteins with either paracrine or endocrine functions involved in local inflammation or immune regulation. Cytokines exhibit overlapping biological activities and have multiple biological effects. An initial inflammatory response marked by leucocyte migration takes place during the early stages of OTM. This reaction raises the possibility that some chemotactic signals are present and could be involved in bone remodelling, specifically resorption. Cytokines that were found to affect bone metabolism and, thereby OTM, include interleukin-1 (IL-1), interleukin-2 (IL-2), interleukin-3 (IL-3), interleukin-6 (IL-6), interleukin-8 (IL-8), tumour necrosis factor alpha (TNF-α), gamma interferon and osteoclast differentiation factor (ODF).

IL-1 is the most powerful of them. In order to encourage bone resorption and prevent bone formation, it attracts leucocytes and stimulates fibroblasts, endothelial cells, osteoclasts and osteoblasts. On the application of orthodontic force, IL-1 is released, which activates the release of prostaglandins. Prostaglandins act on cells, initiating second messengers, followed by gene expression. Interleukins (ILs) play a significant role in the differentiation and function of osteoclasts under the influence of various regulatory genes ( Fig. 17.8 ).

4. Nitric oxide ^,

It was discovered that nitric oxide synthase (NOS), which is abundant in endothelial cells and other organs, converts the amino acid L-arginine into nitric oxide (NO). There are three different kinds of NOS: inducible (iNOS), endothelial (eNOS), and neuronal (nNOS). Both nNOS and eNOS are constitutively produced and collectively called constitutive NOS enzymes (cNOS). It was discovered that iNOS influences how rats’ periodontal tissue reacts to orthodontic force.

1.
The production of NO by PDL fibroblasts may be increased by orthodontic forces, which in turn may activate guanylyl cyclase in the fibroblasts, resulting in an increase in cGMP. This second messenger in the cell cytoplasm increases the permeability of the lysosome membrane, which causes the exocytosis of lysosome content and the resorption of organic and mineral components of bone.
2.
NO synthesises prostaglandins by direct activation of cyclo-oxygenase.
3.
NO influences the function of osteoclastic differentiation and osteoblast function.

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