The ortho–endo interface
Orthodontics is the speciality of dentistry concerned with the growth and development of the dentofacial complex, and the diagnosis, prevention and correction of dental and facial irregularities and/or abnormalities. Orthodontic treatment is commonly undertaken for the management of malocclusion, which refers to any deviation from normal or “ideal” occlusion. As well as the management of malocclusion, orthodontic treatment is increasingly being undertaken to enhance the results of other forms of dental and surgical treatment, with a multidisciplinary approach. These include the management of severe skeletal discrepancies in combination with corrective jaw surgery, termed orthognathic surgery, the management of clefts of the lip and palate, severe craniofacial deformities, hypodontia and obstructive sleep apnoea. In addition, with greater numbers of adults with more compromised dentitions requesting orthodontic treatment, the orthodontic–restorative dentistry interface is more important than ever. As such, it is imperative for endodontists and orthodontists to have an understanding of each others’ specialities, as well as recognizing the situations when they must rely on one another’s expertise.
The application of a continuous force to a tooth results in remodelling of alveolar bone, reorganization of the periodontal ligament and tooth movement. Orthodontic tooth movement is a complex process involving the coordinated activity of many cell types and numerous chemical mediators. The application of a continuous force to a tooth surface results in the development of areas of compression and tension within the periodontal ligament. Tipping forces, resulting from single point contact on a tooth surface, such as those resulting from springs on removable orthodontic appliances, produce loads that are greatest at the alveolar crest and root apex on diagonally opposing sides. Bodily tooth movement results from even compressive loads along one side of the periodontal ligament, resulting from a force couple from a fixed orthodontic appliance. The magnitude of the force delivered is important in determining the tissue response. Ideally, orthodontic forces should not exceed the capillary pressure within the periodontal ligament, in order to prevent ischaemia and tissue necrosis. The optimal force for tooth movement also depends on the type of tooth movement required and the root surface area of the teeth to be moved (Table 13.1); teeth with smaller roots require reduced forces for movement. The forces for intrusion are the lightest as the forces are concentrated at the root apices, which have a small surface area.
|Type of tooth movement||Force level (g)|
Light orthodontic forces that do not exceed capillary pressure result in frontal bone resorption in areas of periodontal ligament compression and bone deposition in areas of periodontal ligament tension. Forces that exceed capillary pressure result in sterile necrosis in the area of the periodontal ligament affected. As such, tooth movement is delayed and bone resorption commences from beneath the area of necrosis within a few days. This is termed undermining resorption because the cellular response occurs by cell populations derived from the marrow spaces of the alveolar bone on the undersurface of the area of necrosis. Resorption of the necrotic tissue also leads to resorption of root surface cementum adjacent to these areas, by cells termed “cementoclasts”. This may be the mechanism causing orthodontically-related root resorption. Areas of resorbed cementum may undergo repair if the defects are small. With prolonged heavy forces, root resorption may outstrip deposition resulting in significant root shortening.
On the whole, the orthodontic discipline does not perceive that well-managed movement of teeth compromises the pulp–dentine complex or tooth roots. This perception may either be generally true or the effects are such that they do not manifest until they are beyond the care of the orthodontist.
Orthodontic tooth movement by virtue of direct interruption and interference with the neurovascular supply and, to a lesser extent, indirectly by tooth flexure, may affect the pulp physiology and status. Although the literature is relatively restricted, studies have been performed on animal and human teeth, which were thoroughly reviewed by Hamilton & Gutmann (1999). The nature, direction and extent of forces exerted (type of orthodontic technique and its execution) during tooth movement, their intermittent or continuous nature, the apical root maturity and age of patient may all influence pulp changes. A variety of outcome measures have been used to determine the effect of orthodontic tooth movement on the pulp, including effects at a tissue level (pulpal inflammation, pulpal degeneration, cellularity, fibrotic changes, predentine width, reparative dentine formation, pulpal space obliteration, Hertwig’s epithelial root sheath), cellular level (pulp cell metabolism and cell respiration rate, survival or degeneration of odontoblasts), vascular level (vascularity, blood flow, circulatory disturbances, angiogenesis), neural level (neuronal cell density, distribution of myelinated versus non-myelinated cells), molecular level (expression of various molecular factors including calcitonin-gene-related neuropeptide [CGRP], methionine encephalin, β-endorphin, substance P, neurokinin A, vasoactive intestinal polypeptide, neuropeptide Y) and clinical level (pulp response to pulp testing, signs and symptoms, discoloration, pulpitis, pulp necrosis).
Although the results were sometimes conflicting and contradictory, the overall findings suggest that orthodontic tooth movement can cause neurovascular disturbances, which result first in inflammatory and then degenerative changes in the pulp, particularly in teeth with mature root apices. The effects are likely to be mediated through variations in the expression of a variety of controlling molecular signalling systems, which would exert their effects at vascular, neural, metabolic, cellular, and tissue levels. The rate and pattern of dentinogenic activity may be altered or affected resulting in tertiary dentine and, rarely, even pulp obliteration (Fig. 13.1). The prevalence and severity of the effects may be affected by the magnitude, direction, continuous or intermittent nature and duration of forces exerted, as well as any previous history of pulpal stimulation, such as through caries, restorations, trauma or periodontal disease. Teeth with immature roots are likely to be less affected because of a richer, thicker and less constrained (apical foramen size) neurovascular bundle.
Clinically evident effects are generally minimal and may include altered sensations to stimuli, such as pulp tests, pulpitis, dentinal pain due to distortions caused by uneven cementing resin polymerization during bracket attachment, pulpal haemorrhage and pulp necrosis. Sensation originating from the pulp may be blended with or masked by those emerging from the stressed periodontal ligament.
Resorption of roots associated with orthodontic tooth movement is well established and has a logical biological basis. Yet it does not occur consistently and may be affected by pulpal status, root morphology and nature and magnitude of orthodontic forces. Small amounts of root resorption, up to 1–2 mm, occur in the majority of patients undergoing fixed appliance orthodontic treatment, with little known long-term implications. Approximately 15% of patients may be affected by greater than 2.5 mm loss of root length, which may have long-term implications, particularly if it occurs in conjunction with periodontal bone loss. Potential risk factors for orthodontically-induced root resorption are listed in Table 13.2.