Theories of Tooth Movement

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Theories of orthodontic tooth movement

Collected by Riyadh Iskander

(Biological control of orthodontic tooth movement)


- Orthodontic treatment is based on the principle that if prolonged pressure is applied to a tooth, tooth movement will occur as the bone around the tooth remodels. - The tooth moves through the bone carrying its attachment apparatus with it. - Orthodontic tooth movement is a periodontal ligament phenomenon where bone resorption occurs in direction of movement while bone deposition occurs in the opposite direction. Many mechanisms have been considered responsible for the differentiation of cells after the application of an orthodontic force (OF).

The proposed theories are: 1- Pressure-tension theory (Classic theory) 2- Piezoelectric theory - (Bioelectric theory) - (Bone bending theory) 3- Mechano-Chemical theory 4- Chemical and enzymatic theory 5- Biologic pathways of tooth movement 6- Inflammatory reaction hypothesis (Tooth movement mediators) 7- Blood vessel role (Vascular hypothesis) 8- Nerve ending theory

1- Pressure-tension theory (Classic theory) (Oppenheim, Sandstedt and Schwarz)

- It was thought to be generated by alterations in the blood flow through the PL. This hypothesis is based on the movement in PL only: In pressure side of PL there is disorganization of fiber production which leads to bone resorption. In the tension side of PL there is stimulation of fiber production which leads to bone apposition.

Mechanism of tooth movement: Orthodontic pressure Tooth is shifted Compressed / stretched ligament Blood Flow is decreased in compressed while increased or maintained in stretched area Changes in the chemical environment Decrease / increase in oxygen tension Change in proportions of metabolites Act directly or by stimulating the release of biologically active agents Cell differentiation and activity

2- Piezoelectric theory - (Bioelectric theory) - (Bone bending theory)


- Tooth movement is related to changes in bone metabolism controlled by electric signals produced when alveolar bone flexes.

Piezoelectricity a. Definition: It is those charges that are produced as a consequence of distorting any crystalline structure, such as the electrons that are displaced from one part of the crystal lattice to another. i. Areas of concavity: -ve charge. ii. Areas of convexity: +ve charge. As a result of these bioelectric-potential differences, the bone is added to the concave surfaces & resorped from the convex surfaces tooth movement. b. characters: i. Quick decay rate even if force is maintained as the crystalline structure is stable no electric current is generated. ii. Equal but opposite signal when the force is released. This occurs as the crystalline structure returns to its original shape where a reverse charge is generated. iii. Small voltages called streaming potentials. c. Source: Bone and collagen itself are piezoelectric. d. Interaction: Ions in the fluids of the living bone interact with the complex electric field generated when the bone bends, causing: i. Temperature changes. ii. Electric signals. e. Importance:
When a force is applied to a crystalline structure a flow of current is produced that quickly dies away. When the force is released, an opposite current flow is observed. The piezoelectric effect results from migration of electrons within the crystal lattice

i. general maintenance of skeleton (Stress generated signals are essential in the general maintenance of the skeleton & without them bone mineral is lost and skeletal atrophy takes place), e.g. 1. Astronauts (bones no longer flex in weightless environment) 2. Bedridden patients.

ii. Signals produced by the bending of bone during mastication maintain bone around the teeth. N.B. Sustained orthodontic force does not produce stress generated signals so do not explain tooth movement but electric and electromagnetic field induced by magnets can modify bone remodeling on which tooth movement depends through shorten the lag phase of tooth movement.

3- Mechano-Chemical theory
- (Justus & Luft 1970) experiments have suggested that altered physical stress in the bone changes the solubility of the hydroxyapatite crystals.

- This will induce the osteoblastic & osteoclastic activity which results in bone remodeling.

4- Chemical and enzymatic theory


- It suggests that a biochemical process results from mechanical stress by continuously applied forces on the alveolar bone & PL cells both cells and matrix are distorted and extracellular fluids are mobilized. - The extracellular fluid will: i) Flow through the bony fenestrations into the marrow spaces. ii) Move into the contralateral tension side. iii) Rising into the cervicular fluid in the gingival sulcus. - Bone matrix distortion in vivo is associated with phenomenon of reorientation of its proteoglycans that may serve as strain memory because the distorted molecules tend to return slowly to their original configuration. - This phenomenon is also associated with: 1) Appearance of piezoelectric spikes. 2) Slowly dissipating streaming potentials. 3) Alterations in the polarity of plasma membranes of cells.

The cell membrane permits some communication forms (through mechanogated ion channels & receptor sites) that: 1) Carry the electrical charges forming regions of polarity. 2) Act as antennae for communication of signals outside & the inside the cell. - These signals: 1) May be mechanical, electrical, chemical or physical. 2) Result in cell differentiation. 3) Can regulate the influx of Ca & Na alterations in levels of the 2ry messenger cAMP & cGMP differentiation of cells bone remodeling.

N.B. cAMP (Cyclic adenosine monophosphatase) & cGMP (Cyclic guanosine monophosphatase) are nucleotides (that enter in the formation of nucleic acids) responsible for translation of the mechanical orthodontic force into cellular language that cell can understand. - in levels of cAMP & cGMP the osteoclastic activity & vice versa. All of the above chemical processes are done along with enzymes which are:

1) Alkaline phosphatase enzyme (lysosomal enzyme). 2) Lactate dehydrogenase (LDH) enzyme. 3) Collagenase enzyme. in the level of the above enzyme the osteoclastic activity. N.B. Normal value of alkaline phosphatase enzyme is 30-300 IU/L or 0.5-2 kat/L. Normal value of lactate dehydrogenase enzyme is 90-200 IU/L or 0.4-1.7 mol/L.

5- Biologic pathways of tooth movement (Mostafa et al 1983)


- Force applied to a tooth produces two main effects 1. Pathway I: - It has a major biologic response. - It induces tooth movement through: Bone bending

a. Piezoelectric response i. Areas of concavity: -ve charge bone deposition ii. Areas of convexity: +ve charge bone resorption Bone remodeling

b. Local production of PG cAMP release Initiate osteoprogenitor cells proliferation & differentiation Osteoclasts & osteoblasts Bone remodeling

2. Pathway II: - It has a 2ry effect. - It induces tooth movement through: Periodontal tissue injury Inflammation Cellular & vascular infiltration Hydrolytic reaction activates collagenase enzyme Bone remodeling

6- Inflammatory reaction hypothesis (Tooth movement mediators) (Sandy & Harris 1984)

- The inflammatory reaction due to orthodontic tooth movement vascular permeability of the PL stimulate the migration of lymphocytes (inflammatory cells) to site of orthodontic force. - The activated Lymphocytes release lymphokines resulting in: 1) Direct bone resorption by synthesize of osteoclastic-activating factor. 2) Chemotactic & stimulate macrophages that: i) Stimulate osteoclasts formation. ii) Release collagenase enzyme & prostaglandin where collagenase enzyme & prostaglandin bone resorption. Mediators responsible for tooth movement are: I) Cytokines (Lymphokines): Act once at a time to alter the physiology of the cell like: 1. Cell proliferation. 2. Cell differentiation. 3. Fabrication of cell products. 4. Changes in cytoskeletal proteins. 5. Changes in cell shape. 6. Cell migration (chemotaxis). 7. Cell apoptosis. 8. Changes in cell surface adhesion. II) Prostaglandin (PG): - Lipid soluble hormone like substances release from many cells (phospholipids of cell membrane arachidonic acid PG) that bind to surface receptor & act as local mediators). - Found at sites of tissue injury in response to inflammatory process. - Function: 1. Prostaglandin promotes bone remodeling, but its main effect is osteoclastic activity. 2. Activates cyclase enzyme responsible for production of cAMP & cGMP. 3. Change the influx of Ca alterations in levels of cAMP & cGMP. 4. Act as vasodilator. - PG inhibitors the rate of tooth movement. - Injection of PG will double the rate of tooth movement.

III) cAMP: 1. Act as 2ry messenger.

2. Controls the proliferation of osteoprogenitor cells. IV) Coupling factor: - Diffusible substance produced by osteoblasts. - It regulates both osteoblastic & osteoclastic activity so that bone formation equals resorption. Role of Piezoelectricity in production of the mediators: 1. Promotes the release of prostaglandins. 2. Controls the changes in the levels of cAMP. N.B. Electric polarization provides directional control with orthodontic bone remodeling.

7- Blood vessel role (Vascular hypothesis) (Gianelli 1969)


- He suggests that, the vasculature may act as a hydraulic pressure system transmitting the applied force to the attachment apparatus distortion in crystal structure of the bone. - Intact vascular perfusion system in the PL seems to be necessary for frontal resorption of bone, i.e. the bone resorbed is the alveolar bone immediately adjacent to the PL. - When the vessels are occluded undermining resorption occurs, i.e. the PL is deprived of its nutritional supply hyalinization (acellular area with amorphous PL) no bone resorption in the frontal area of alveolar bone but below area of hyalinized area undermining of the alveolar bone.

8- Nerve ending theory

- The applied orthodontic force gradual shift in PL fluids distortion of the nerve ending of PL release of neuropeptides from the nerve ending which are: i) Substance P. ii) Vasoactive intestinal polypeptide (VIP). iii) Calcitonin gene related peptide (CGRP). - Substance P & VIP are vasodilators extravasation of plasma migration of leukocytes from the capillaries to the extravascular spaces of the PL. -The migratory leukocytes synthesize & secrete cytokines (Interleukin & interferon) that are small molecules involved in local inflammation which can stimulate the following cells: i) Endothelial cells. ii) Fibroblasts. iii) Alveolar bone cells. i) Endothelial cells: - The endothelial cells are characterized by the presence of chemical messengers (nitric oxide synthase NOS) that are capable of translating the mechanical force into a vascular activity. - A study was made to identify the presence of NOS in PL reveals the following: 1) The presence of endothelial nitric oxide synthase (eNOS) & inducible nitric oxide synthase (iNOS) in stationary teeth which upon movement of the tooth. 2) The presence of eNOS and iNOS in the odontoblast layer of the pulp chambers in stationary teeth which upon movement of the tooth. 3) Possible role of NO in periodontal remodeling during tooth movement. ii) Fibroblasts: - Function: 1- Formation of new matrix components. 2- Degrade the necrotic PL. 3- Regulate the osteoclasts & PGE2 which play important role in bone remodeling. iii) Alveolar bone cells: - Growth factor regulate local bone metabolism. - Growth factors include: a. Growth hormone (GH) b. Insulin like growth factor 1 (1GF-1) c. Epidermal growth factor (EGF) d. Interleukin -1 alpha (IL-) - Osteoclasts function may be affected by the above factors. - Osteoblasts produce vascular endothelial growth factor (VEGF) which enhances tooth movement.

Factors affecting orthodontic tooth movement

The transmission of orthodontic forces to the teeth will depend on the following factors: I. General Factors (methods of transmitting force): 1. Magnitude of force. 2. Distribution of force (Type of orthodontic tooth movement according to direction of force). 3. Duration of force. 4. Decay of force (type of orthodontic force). II. Factors related to local (individual) variations: 1. Drugs effect 2. Variability in various tissue reactions 3. Individual variations. 4. Anchorage. 5. Rate of tooth movement. 6. Growth changes.

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