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Orthodontics. Part 11: Orthodontic tooth movementD. Roberts-Harry1 and J. Sandy2

Orthodontic tooth movement is dependent on efficient remodelling of bone. The cell-cell interactions are now more fully understoodand the links between osteoblasts and osteoclasts appear to be governed by the production and responses of osteoprotegerin ligand.The theories of orthodontic tooth movement remain speculative but the histological documentation is unequivocal. A periodontal ligament placed under pressure will result in bone resorption whereas a periodontal ligament under tension results inbone formation. This phenomenon may be applicable to the generation of new bone in relation to limb lengthening and cranial-suture distraction. It must be remembered that orthodontic tooth movement will result in root resorption at the microscopic level inevery case. Usually this repairs but some root characteristics apparent on radiographs before treatment begins may be indicative oflikely root resorption. Some orthodontic procedures (such as fixed appliances) are also known to cause root resorption.

1*Consultant Orthodontist, OrthodonticDepartment, Leeds Dental Institute,Clarendon Way, Leeds LS2 9LU; 2Professor of Orthodontics, Division ofChild Dental Health, University of BristolDental School, Lower Maudlin Street,Bristol BS1 2LY; *Correspondence to: D. Roberts-HarryE-mail: robertsharry@btinternet.com

Refereed Paperdoi:10.1038/sj.bdj.4811129© British Dental Journal 2004; 196:391–394

● The osteoblast is the pivotal cell in bone remodelling and the link between the osteoblast andosteoclast recruitment and activation is now established

● Excessive orthodontic forces cause inefficient tooth movement and adverse tissue reactions● The mechanisms which prevent root resorption are not fully understood but it remains a

consequence of any orthodontic treatment. The extent and degree of root resorption cannotbe predicted but some indicators are available

I N B R I E F

The histological changes which occur whenforces are applied to teeth are well documented(Figs 1 and 2). Teeth appear to lie in a position ofbalance between the tongue and lips or cheeks.This zone is not completely neutral since tongueforces are usually slightly greater than the lips orcheeks. The periodontal ligament is thought tohave an intrinsic force which has to be overcomebefore teeth move. A notable feature of peri-odontal disease, where this intrinsic force is lost,is splaying, drifting and spacing of teeth. Simi-larly, if there is excessive tongue activity ordestruction of the lips or cheeks (as in cancrumoris) then the teeth will drift.

Very low forces are capable of moving teeth.Classically, ideal forces in orthodontic toothmovement are those which just overcome capil-lary blood pressure. In this situation boneresorption is seen on the pressure side and bonedeposition on the tension side. Teeth rarelymove in this ideal way. Usually force is notapplied evenly and teeth move by a series of tip-ping and uprighting movements. In some areasexcessive pressure results in hyalanizationwhere the cellular component of the periodontalligament disappears. The hyalanized zoneassumes a ground glass appearance but thisreturns to normal once the pressure is reducedand the periodontal ligament repopulated withnormal cells. In this situation a different type ofresorption is seen whereby osteoclasts appear to‘undermine’ bone rather than resorbing at the‘frontal’ edge (Fig. 3).

Mechanically induced remodelling is notfully understood. The role of the periodontalligament has been questioned since toothmovement can still occur even where the peri-

odontal ligament is not functioning normally.The ligament itself undergoes remodelling andthe role of matrix metalloproteinases (MMPs)together with their natural inhibitors, tissueinhibitors of metalloproteinases (TIMPs) areclearly of importance.1

Osteocytes (osteoblasts incorporated intomineralized bone matrix) are situated in a rigidmatrix and are thus ideally positioned to detectchanges in mechanical stresses. They could signal to surface lining osteoblasts and thusbone formation and indeed bone resorptionmay result. There is now good understanding ofkey mechanisms in bone resorption and forma-tion. Bone is formed by osteoblasts which alsohave a role in bone resorption. It is theosteoblast which has receptors for many of thehormones and growth factors which stimulatebone turnover.

By contrast, the osteoclast which resorbsmineralised tissue, responds to very few directhormone actions. Most of the classic agentswhich have direct effects on osteoclasts haveinhibitory actions. For example, Calcitonin andprostaglandin E2 will inhibit osteoclasts fromresorbing calcified matrices.

The recruitment and activation of osteo-clasts to sites of resorption comes from theosteoblast when the latter cell is stimulatedby various hormones. The signal link fromosteoblasts has recently been identified asosteoprotegerin (OPG) and the ligand (OPGL).They both potently inhibit and stimulaterespectively, osteoclast differentiation. Fur-thermore, OPGL appears to have direct effectson stimulating mature osteoclasts into activi-ty. If OPGL is injected into mice there is an

11

ORTHODONTICS1. Who needs

orthodontics?2. Patient assessment and

examination I3. Patient assessment and

examination II4. Treatment planning5. Appliance choices6. Risks in orthodontic

treatment7. Fact and fantasy in

orthodontics8. Extractions in

orthodontics9. Anchorage control and

distal movement10. Impacted teeth11. Orthodontic tooth

movement12. Combined orthodontic

treatment

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increase in ionised blood calcium within 1 hour. These finding have done much tounravel the final links between bone forma-tion and resorption.

One other role that osteoblasts have in boneresorption is removal of the non-mineralisedosteoid layer. In response to bone resorbing hor-mones, the osteoblast secretes MMPs which areresponsible for removal of osteoid. This exposesthe mineral layer to osteoclasts for resorption. Ithas been suggested that the mineral is alsochemotactic for osteoclast recruitment andfunction.

How mechanical forces stimulate boneremodelling remains a mystery but some keyfacts are known. First, intermittent forcesstimulate more bone remodelling than contin-uous forces. It is likely that during orthodontictooth movement intermittent forces are gener-ated because of ‘jiggling’ effects as teeth comeinto occlusal contact. Second, the key regula-tory cell in bone metabolism is the osteoblast.It is therefore relevant to examine what effectsmechanical forces have on these cells. Theapplication of a force to a cell membrane trig-gers off a number of responses inside the celland this is usually mediated by second mes-sengers. It is known that cyclic AMP, inositolphosphates and intracellular calcium are allelevated by mechanical forces. Indeed theentry of calcium to the cell may come from G-protein controlled ion channels or releaseof calcium from internal cellular stores. Thesemessengers will evoke a nuclear responsewhich will either result in production of fac-tors responsible for osteoclast recruitment andactivation, or bone forming growth factors.An indirect pathway of activation also existswhereby membrane enzymes (phospholipaseA2) make substrate (arachidonic acid) avail-able for the generation of prostaglandins andleukotrienes. These compounds have bothbeen implicated in tooth movement.

The main theories of tooth movement arenow summarised:

BIOMECHANCIAL ORTHODONTIC TOOTHMOVEMENTThis theory simply states that mechanically dis-torting a cell membrane activates PLA2 makingarachidonic acid available for the action of cycloand lipoxygenase enzymes. This producesprostaglandins which feed back onto the cellmembrane binding to receptors which thenstimulate second messengers and elicit a cellresponse. Ultimately, these responses willinclude bone being laid down in tension sitesand bone being resorbed at pressure sites. It isnot clear how tissues discriminate between ten-sion and pressure. It is worth remembering thatcells which are rounded up show catabolicchanges whereas flattened cells (? under tension)have anabolic effects.

BONE BENDING, PIEZOELECTRIC ANDMAGNETIC FORCESThere was considerable interest in piezoelectricityas a stimulus for bone remodelling during the1960s. This arose because it was noted that distor-tion of crystalline structures generated small elec-trical charges, which potentially may have beenresponsible for signalling bone changes associat-ed with mechanical forces. The interest thereforein ‘electricity’ and bone was considerable.

Magnets have been used to provide the forceneeded for orthodontic tooth movement. Classi-cally an unerupted tooth has a magnet attachedto it and a second magnet is placed on an ortho-dontic appliance with the poles orientated toprovide an attractive force. It is unlikely that themagnetic forces alone have any actions on tis-sues. If magnetic fields are broken (as in pulsedelectromagnetic fields) then there is some evi-dence that tissues will respond. It is worth mak-ing the following points about the effects ofmagnetic and electric fields on tooth movement:

• The periodontal ligament is unlikely to trans-fer forces to bone. If the periodontal ligamentis disrupted, orthodontic tooth movement stilloccurs

Intermittent forcesappear to move teethand stimulate boneremodelling moreefficiently than continuous forces

Fig. 1 Pressure side of a tooth being moved. The very vascularperiodontal ligament has cementum on one side and bone on theother where frontal resorption is occurring. Osteoclasts can be seenin their lacunae resorbing bone on it's ‘frontal edge’

Fig. 2 This is a tension site where the bone adjacent to theperiodontal ligament has surface lining osteoblasts and no sign ofany osteoclasts. New bone is laid down as the tooth moves

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• Magnetic fields alone have little, if any, effecton tissues

• Pulsed magnetic fields (which induce electricfields) can increase the rate and amount oftooth movement

• When an orthodontic force is applied, thetooth is displaced many times more than theperiodontal ligament width. Bone bendingmust therefore occur in order to account forthe tooth movement over and above the widthof the periodontal ligament

• Physically distorting dry bone producespiezoelectric forces which have been implicat-ed in tooth movement. Piezoelectric forces arethose charges which develop as a consequenceof distorting any crystalline structure. Themagnitude of the charges is very small andthere is some doubt whether they are suffi-cient to induce cellular change.

• It must also be remembered that in hydratedtissues, streaming potential and nerve impuls-es produce larger electrical fields and thus it isunlikely that piezoelectric forces alone areresponsible for tooth movement.2

A wider application of the phenomenon ofmechanically induced bone remodelling isseen where sutures are stretched. In youngorthodontic patients the midline palatalsuture can be split using rapid maxillaryexpansion techniques. The resulting tensiongenerates new bone which fills in between thedistracted maxillary shelves. A similar tech-nique is also used to lengthen limbs. This

method, known as distraction osteogenesis,can be used in any situation where it is hopedthat new bone will be generated. Originallythis was described in Russia where many sol-diers returning from war faced the problem ofnon-union limb fractures. Initially attemptswere made to induce new bone formation bycompressing bone ends. It was only when apatient inadvertently turned the screw forcompression of bone ends in the wrong direc-tion that it was noted excessive new bone for-mation was seen where bone ends were dis-tracted rather than compressed.

This may also have application in patientswhose sutures fuse prematurely (craniosynos-toses such as Crouzon's or Aperts Syndrome).In this situation continued growth of the brainresults in a characteristic appearance of thecranium but more importantly the eyesbecome protuberant with possible damage tothe optic nerve. Treatment involves surgicallyopening the prematurely fused sutures andburring out to enable normal brain growth. Ifdistraction forces are applied prior to this earlyfusion then bony infill could occur at a con-trolled rate. The phenomenon of pressureresulting in bone loss is also seen in pathologi-cal lesions. Much work was done to examinepressures within cystic lesions and to equatethis with the rate of bone destruction. It is nowrecognised that cytokines and bone resorbingfactors produced by cystic and malignantlesions are more likely to be responsible for theassociated bone resorption.

Tension results inbone formation, thiscan be used to generate new bonefor digit lengtheningor suture distraction

Fig. 3 This is an area of excessive pressurewhere the periodontal ligament has beencrushed or ‘hylanized’ and the periodontalligament has lost its structure. There is a largecell lying in a lacunae behind the frontal edgewhich is probably an area of underminingresorption

Fig. 4 Area of root resorption associated withorthodontic tooth movement. The apex ofthe tooth has a large excavation of the rootsurface and this is typical of excessivetipping forces that are placed on the apicesof the teeth

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ROOT RESORPTIONThe ability to move teeth through bone isdependent on bone being resorbed and toothroots remaining intact. It is highly probable thatall teeth which have undergone orthodontictooth movement exhibit some degree of micro-scopic root resorption (Fig. 4). Excessive rootresorption is found in 3–5% of orthodonticpatients. Some teeth are more susceptible thanothers, upper lateral incisors can, on average,lose 2 mm of root length during a course of fixedorthodontic treatment. There are specific fea-tures of appliances which can increase the risk ofroot resorption. The following are consideredrisk factors:

• Fixed appliances • Class II elastics• Rectangular wires• Orthognathic surgery

There is also some evidence that the use offunctional appliances appears to cause lessresorption than fixed appliances and may beused to reduce increased overjet where there arerecognised risks of root resorption which includepre-existing features such as:

• Short roots• Blunt root apices• Thin conical roots• Root filled teeth• Teeth which have been previously traumatised

What prevents roots from resorbing is notknown but the following have been suggested:

• Cementum has anti-angiogenic properties.This means blood vessels are inhibited fromforming adjacent to cementum and osteo-clasts have less access for resorption.

• Periodontal ligament fibres are inserted moredensely in cementum than alveolar bone andthus osteoclasts have less access to the cemen-tal layer.

• Cementum is harder than bone and moredensely mineralised.

• Cemental repair may be by a material which isintermediate between bone and cementum.These semi-bone like cells may be moreresponsive to systemic factors such as parathy-roid hormone and thus where roots are alreadyshort (and repaired with a bone/cementum likematerial) the teeth are more susceptible to fur-ther root resorption.

The exact reason why roots generally do notresorb is not known but without this property itwould not be possible to move teeth orthodonti-cally. A number of reviews are available whichcover bone remodelling and tooth movement ingreater depth.3,4

1. Waddington R J, Embery G, Samuels R H. Characterization ofproteoglycan metabolites in human gingival fluid duringorthodontic tooth movement. Arch Oral Biol 1994; 39: 361-368.

2. McDonald F. Electrical effects at the bone surface. Eur JOrthod 1993; 15: 175-183.

3. Hill P A. Bone remodelling. Br J Orthod 1998; 25: 101-107.4. Sandy J R, Farndale R W, Meikle M C. Recent advances in

understanding mechanically-induced bone remodelling andtheir relevance to orthodontic theory and practice. Am JOrthod Dento-fac Orthop 1993; 103: 212-222.

The British Dental Association Research Foundationinvites applications for awards from the Shirley GlasstoneHughes Memorial Prize Fund.

The Prize may be awarded as a single three year projectgrant commencing in 2004, to a maximum of £16,000including all salary ‘on costs' and running expenses.Alternatively, smaller grants may be made to more projects, to the same total. Applications will be considered from dentists in all fields of practice.

Where applications are made by dentists who are not in university employment, the Foundation advises thatapplications should include appropriate supervisoryarrangements involving an independent experiencedresearcher.

The Foundation will favour projects, which will yieldresults of direct clinical relevance.

Shirley Glasstone Hughes Memorial Prize for Dental Research

Application formsand further information areavailable from:

BDA Awards Officer,Members’ Services DepartmentBritish Dental Association, 64 Wimpole Street, London W1G 8YSTel: 020 7563 4174Email: awards@bda.org

The closing date for applications is Friday 30th April 2004.

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