Orthodontics Part 11 Orthodontic tooth movement

D. Roberts-Harry1 and J. Sandy2



Orthodontic tooth movement is dependent on efficient remodelling of bone. The cell-cell interactions are now more fully understood and 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 in bone 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 in every case. Usually this repairs but some root characteristics apparent on radiographs before treatment begins may be indicative of likely root resorption. Some orthodontic procedures (such as fixed appliances) are also known to cause root resorption.



Who needs



Patient assessment and

examination I


Patient assessment and

examination II


Treatment planning


Appliance choices


Risks in orthodontic



Fact and fantasy in



Extractions in



Anchorage control and

distal movement


Impacted teeth


Orthodontic tooth


12. Combined orthodontic


^Consultant Orthodontist, Orthodontic Department, Leeds Dental Institute, Clarendon Way, Leeds LS2 9LU; 2Professor of Orthodontics, Division of Child Dental Health, University of Bristol Dental School, Lower Maudlin Street, Bristol BS1 2LY;

Correspondence to: D. Roberts-Harry E-mail: [email protected]

^Consultant Orthodontist, Orthodontic Department, Leeds Dental Institute, Clarendon Way, Leeds LS2 9LU; 2Professor of Orthodontics, Division of Child Dental Health, University of Bristol Dental School, Lower Maudlin Street, Bristol BS1 2LY;

Correspondence to: D. Roberts-Harry E-mail: [email protected]

Refereed Paper doi:10.1038/sj.bdj.4811129 © British Dental Journal 2004; 196: 391-394

The histological changes which occur when forces are applied to teeth are well documented (Figs 1 and 2). Teeth appear to lie in a position of balance between the tongue and lips or cheeks. This zone is not completely neutral since tongue forces are usually slightly greater than the lips or cheeks. The periodontal ligament is thought to have an intrinsic force which has to be overcome before teeth move. A notable feature of periodontal disease, where this intrinsic force is lost, is splaying, drifting and spacing of teeth. Similarly, if there is excessive tongue activity or destruction of the lips or cheeks (as in cancrum oris) then the teeth will drift.

Very low forces are capable of moving teeth. Classically, ideal forces in orthodontic tooth movement are those which just overcome capillary blood pressure. In this situation bone resorption is seen on the pressure side and bone deposition on the tension side. Teeth rarely move in this ideal way. Usually force is not applied evenly and teeth move by a series of tipping and uprighting movements. In some areas excessive pressure results in hyalanization where the cellular component of the periodontal ligament disappears. The hyalanized zone assumes a ground glass appearance but this returns to normal once the pressure is reduced and the periodontal ligament repopulated with normal cells. In this situation a different type of resorption is seen whereby osteoclasts appear to 'undermine' bone rather than resorbing at the 'frontal' edge (Fig. 3).

Mechanically induced remodelling is not fully understood. The role of the periodontal ligament has been questioned since tooth movement can still occur even where the peri-

odontal ligament is not functioning normally. The ligament itself undergoes remodelling and the role of matrix metalloproteinases (MMPs) together with their natural inhibitors, tissue inhibitors of metalloproteinases (TIMPs) are clearly of importance.1

Osteocytes (osteoblasts incorporated into mineralized bone matrix) are situated in a rigid matrix and are thus ideally positioned to detect changes in mechanical stresses. They could signal to surface lining osteoblasts and thus bone formation and indeed bone resorption may result. There is now good understanding of key mechanisms in bone resorption and formation. Bone is formed by osteoblasts which also have a role in bone resorption. It is the osteoblast which has receptors for many of the hormones and growth factors which stimulate bone turnover.

By contrast, the osteoclast which resorbs mineralised tissue, responds to very few direct hormone actions. Most of the classic agents which have direct effects on osteoclasts have inhibitory actions. For example, Calcitonin and prostaglandin E2 will inhibit osteoclasts from resorbing calcified matrices.

The recruitment and activation of osteo-clasts to sites of resorption comes from the osteoblast when the latter cell is stimulated by various hormones. The signal link from osteoblasts has recently been identified as osteoprotegerin (OPG) and the ligand (OPGL). They both potently inhibit and stimulate respectively, osteoclast differentiation. Furthermore, OPGL appears to have direct effects on stimulating mature osteoclasts into activity. If OPGL is injected into mice there is an

Fig. 1 Pressure side of a tooth being moved. The very vascular periodontal ligament has cementum on one side and bone on the other where frontal resorption is occurring. Osteoclasts can be seen in their lacunae resorbing bone on it's 'frontal edge'
Fig. 2 This is a tension site where the bone adjacent to the periodontal ligament has surface lining osteoblasts and no sign of any osteoclasts. New bone is laid down as the tooth moves

Intermittent forces appear to move teeth and stimulate bone remodelling more efficiently than continuous forces increase in ionised blood calcium within 1 hour. These finding have done much to unravel the final links between bone formation and resorption.

One other role that osteoblasts have in bone resorption is removal of the non-mineralised osteoid layer. In response to bone resorbing hormones, the osteoblast secretes MMPs which are responsible for removal of osteoid. This exposes the mineral layer to osteoclasts for resorption. It has been suggested that the mineral is also chemotactic for osteoclast recruitment and function.

How mechanical forces stimulate bone remodelling remains a mystery but some key facts are known. First, intermittent forces stimulate more bone remodelling than continuous forces. It is likely that during orthodontic tooth movement intermittent forces are generated because of 'jiggling' effects as teeth come into occlusal contact. Second, the key regulatory cell in bone metabolism is the osteoblast. It is therefore relevant to examine what effects mechanical forces have on these cells. The application of a force to a cell membrane triggers off a number of responses inside the cell and this is usually mediated by second messengers. It is known that cyclic AMP, inositol phosphates and intracellular calcium are all elevated by mechanical forces. Indeed the entry of calcium to the cell may come from G-protein controlled ion channels or release of calcium from internal cellular stores. These messengers will evoke a nuclear response which will either result in production of factors responsible for osteoclast recruitment and activation, or bone forming growth factors. An indirect pathway of activation also exists whereby membrane enzymes (phospholipase A2) make substrate (arachidonic acid) available for the generation of prostaglandins and leukotrienes. These compounds have both been implicated in tooth movement.

The main theories of tooth movement are now summarised:

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