KEY POINTS
● Occlusal trauma and tooth mobility are associated with periodontal bone and attachment loss. It follows that over many years, this association may lead to enough destruction of peri- odontal support to threaten periodontal longevity. However, strong evidence of cause and effect is lacking.
● Tooth mobility may enhance the probability for further attachment loss during periodontal maintenance therapy, but most mobile teeth can be maintained in function and comfort for many years.
● Control of periodontal inflammation is a key element in minimizing the progression of peri- odontal attachment loss associated with excessive occlusal forces. Reduction of inflam- mation should precede definitive occlusal therapy, and occlusal therapy usually should precede periodontal regenerative surgery when significant mobility exists in the teeth tar- geted for regenerative therapy.
● Occlusal therapy is also important in improving the function and comfort of the dentition, which may also enhance the desire by the patient to retain teeth, thereby increasing tooth longevity
HISTORICAL EVIDENCE
Several articles in Dental Clinics of North America in the late 1990s reviewed the state of knowledge as to the impact of trauma from occlusion and mobility on periodontitis.1–3 Occlusal trauma was defined as an injury (usually a histologically demonstrable lesion) to the attachment apparatus or tooth as a result of excessive occlusal forces.3 Common symptoms of occlusal trauma were described to include pain or discomfort, dental hy- persensitivity, tooth mobility (fremitus), or pathologic migration of teeth.1 Classic animal studies by Lindhe and colleagues4 using a dog model suggested that experimental occlusal trauma alone does not initiate periodontal pockets or periodontal attachment loss, but requires concomitant inflammatory periodontal disease.5,6 Treatment of peri- odontitis and control of inflammation in the presence of experimental occlusal trauma reversed periodontal disease activity.7 However, monkey studies by Polson and col- leagues8,9 found minimal changes in the rate of periodontal attachment loss when experimental occlusal trauma was combined with inflammatory periodontal disease, but no regeneration of bone took place when experimental occlusal trauma was removed in the presence of active inflammation. Osseous regeneration occurred only when both occlusal trauma and periodontal inflammation were eliminated, but with reduced level of periodontal attachment resulting from the previous loss.
Although most tooth mobility is not the result of occlusal trauma, mobility is one of the primary clinical signs of occlusal trauma. However, Ericsson and Lindhe11 concluded that increased tooth mobility did not exacerbate clinical attachment loss caused by plaque-induced periodontitis.
Human clinical studies reviewed in Dental Clinics of North America were sparse, mostly because of the difficulty in performing such investigations. Cross-sectional evaluations or investigations where mobility was noted included the finding that teeth with mobility may have a detrimental effect on postsurgical healing (following curet- tage, modified Widman, or pocket elimination surgery) and do not gain as much attachment.12 More recent evidence that mobility impacts surgical outcomes was re- ported by Cortellini and colleagues13 showing that baseline tooth mobility was signif- icantly associated with reduced clinical attachment gains following procedures to regenerate deep intrabony defects.
Occlusal contacts, even if abnormal, do not necessarily lead to occlusal trauma, but excessive occlusal forces by definition are a needed initiator of the injury of occlusal trauma.3 Early work indicated that abnormal occlusal contacts were associated with increased periodontal bone loss and mobility,14,15 yet later studies were contradic- tory.16 Pihlstrom and coworkers17 found that occlusal contacts (centric relation, work- ing, nonworking, or protrusive) did not lead to more severe periodontitis than in teeth without these contacts. Ismail and colleagues18 reported on a group of 165 subjects who were re-examined for clinical attachment loss following a 28-year evaluation period, and determined that increased age, smoking, and tooth mobility were the fac- tors most closely related to attachment loss. Wang and colleagues19 reported that mobile teeth had significantly more attachment loss during the maintenance years than the nonmobile teeth. Jin and Cao20 found no significant difference in probing depth, clinical attachment level, or bone height loss in teeth with or without abnormal occlusal contact, but teeth with mobility or widened periodontal ligaments had greater probing depths, more attachment loss, and increased alveolar bone loss. McGuire and Nunn21,22 found that parafunctional habits and mobility were correlated with wors- ening prognosis and tooth loss over 5 to 8 years of periodontal maintenance.
In a rare interventional trial, Burgett and colleagues23 found that occlusal adjustment designed to reduce occlusal trauma resulted in a 0.4-mm improvement in mean probing attachment compared with patients with no occlusal adjustment over a 6-year period. However, there was no significant difference in mobility between those receiving occlusal adjustment and those who did not.
The evidence reported in these manuscripts, written near the turn of the century, is summarized in Box 1. It is the purpose of this current review to analyze subsequent literature to cast new light on the question “Do mobility and occlusal trauma impact periodontal longevity?”
RECENT EVIDENCE: OCCLUSAL TRAUMA AND MOBILITY IMPACT ON PERIODONTITIS PROGRESSION
Support for abnormal occlusal contacts, which may lead to occlusal trauma, as a risk factor in periodontitis progression and eventually tooth longevity was found in a series of retrospective studies by Harrel and Nunn. These authors reported that teeth with occlusal discrepancies had significantly deeper probing depths and worse prognoses and mobility.24 Occlusal discrepancies were defined as differences between retruded position (centric relation) and maximum intercuspation (centric occlusion), and work- ing and balancing contacts in lateral and protrusive movements. After adjusting for other risk factors, such as smoking and poor oral hygiene, occlusal discrepancy continued as an independent contributor to increased probing depths.
Furthermore, teeth with untreated occlusal discrepancies had a significantly greater increase in probing depth per year than teeth without initial occlusal discrepancies or with occlusal treatment designed to correct occlusal discrepancies.25 In fact, only teeth with untreated occlusal discrepancies showed a significant increase in probing depth during periodontal maintenance (0.066 mm/year over an undefined period, at least 1 year). The authors concluded that occlusal treatment reduces the progression of periodontitis.
Finally, characterization of the occlusal discrepancies revealed that deeper probing depths were associated with premature contacts in centric relation (0.89 mm), poste- rior protrusive contact (0.51 mm), balancing contacts (1.01 mm), and combined work- ing and balancing contacts (1.13 mm, all P<.0001).26 Although this series of studies had several major shortcomings, including a small sample size (<100), lack of stan- dardized treatment and appropriate longitudinal evaluation protocols, and not being randomized or blinded, they do suggest that discrepancies potentially leading to occlusal trauma could impact progressive periodontal breakdown, even during peri- odontal maintenance. The importance of nonworking (balancing) side contacts was extended in a large cross-sectional epidemiologic study,27 wherein it was reported that nonworking side contacts only were related to probing depth (P<.0001) and attachment loss (P 5 .001), although it was weak in terms of magnitude and specificity. In another cross-sectional investigation,28 the number of premature and balancing contacts increased with the severity of periodontitis (loss of clinical attachment, P<.001). The authors concluded that secondary trauma from occlusion, which was erroneously defined as premature and balancing contacts, is positively correlated with the severity of attachment loss. The lack of longitudinal data limits determination of the role of occlusal trauma in periodontal longevity.
A recent systematic review of occlusal adjustment in periodontal therapy found no new evidence to encourage the use of routine occlusal adjustment to maintain peri- odontal health. However, it was concluded that it is not detrimental, and occlusal adjustment in conjunction with periodontal therapy may improve patient comfort and function. A similar conclusion was reached in a review article on the biologic effects of occlusal trauma, based on evidence primarily from animal studies.
POTENTIAL INDICATIONS AND SCIENTIFIC RATIONALE FOR REDUCING OCCLUSAL TRAUMA IN PERIODONTITIS
Although reduction of occlusal trauma by occlusal therapy has not been proved to be a mandatory part of routine periodontal therapy, are there certain comorbidities that accelerate the damage caused by occlusal trauma? Kawamoto and Nagaoka31 found that ovariectomized rats subjected to experimental occlusal trauma demonstrated significantly more bone resorption around the periodontal ligament than sham- treated animals. Nicotine also enhanced bone loss in rats with combined occlusal trauma and ligature-induced periodontitis compared with animals without either nico- tine or both nicotine and occlusal trauma. De Oliveira Diniz and colleagues confirmed that occlusal trauma augmented the bone loss seen with ligature- induced periodontitis in rats, and this effect was further enhanced by diabetes mellitus. These rat studies suggest that attempts to reduce occlusal trauma in certain vulnerable cohorts, such as those with estrogen deficiency, diabetes, or smoking habits, may have merit, or at least deserves further investigation.
The scientific rationale for how occlusal trauma may contribute to increased peri- odontal bone loss has received some attention over the past decade. Central to occlusal trauma-induced (and periodontitis-induced) bone resorption seems to be stimulation of receptor activator of nuclear factor kappa B ligand (RANKL), the primary driver of osteoclast activation. RANKL interacts with RANK receptor on osteoclasts to initiate bone resorption. In a rat model where occlusal trauma was initiated by raising the occlusal surface, immunohistochemistry demonstrated RANKL associated with osteoclasts and osteoblasts.34 A similar occlusal trauma protocol combined with lipopolysaccharide-induced periodontitis extended the length of time that osteoclasts were present on the interproximal bone surface, and the increased expression of RANKL in osteoclasts, endothelial cells, inflammatory cells, and periodontal ligament cells.35 Human periodontal ligament cells exposed to mechanical stress also increased interleukin-6 production, a potent stimulator of RANKL, periodontal inflam- mation, and bone resorption.
The recent evidence for occlusal trauma and mobility impacting tooth longevity is summarized in Box 2.
IMPACT OF OCCLUSAL TRAUMA ON PERI-IMPLANT BONE LOSS
With the surge of dental implant placements over the last 15 years, the role of occlusal trauma or overload in peri-implant bone resorption has been investigated. It was pro- posed that excessive occlusal force may contribute to bone loss around implants.
Monkey studies38,39 found that, as with natural teeth, occlusal overload did not induce peri-implant inflammation but did cause bone resorption around implants. However, when inflammation was added to the occlusal overload by withholding tooth brushing, no acceleration of bone resorption was noted. A subsequent review paper of cellular biomechanics, engineering principles, bone mechanical properties, animal studies, clinical reports, bone physiology, and implant design biomechanics reported that occlusal overload on implants may increase the incidence of marginal bone loss.40 A systematic review of animal studies on the effects of occlusal overload on peri- implant tissue41 revealed only two appropriate controlled trials (in dogs),42,43 which concluded that overload alone is not associated with peri-implant tissue breakdown, but when combined with plaque accumulation is key to increased pocket depths and loss of bone-to-implant contact. A more recent review came to the same conclusion,44 whereas another pointed to the poor level of evidence and conflicting results.45
In a retrospective analysis of 3578 patient records, occlusal trauma was identified as one of several iatrogenic conditions, together responsible for 17.5% of causes for implant loss.46 Sakka and colleagues47 also found that occlusal overload is an impor- tant factor in late implant failure. Despite these pronouncements, well-designed clin- ical trials are lacking.
CLINICAL CONSIDERATIONS
Radiographic changes, such as widened periodontal ligament spaces and alveolar crest density changes, support the clinical evidence of mobility.48 Increased mobility may be an adaptation to short roots, poor crown-to-root ratios, or increased forces in the absence of inflammation, whereas mobility associated with periodontal inflamma- tion or occlusal trauma may contribute to the pathogenesis of disease and require treatment. It could be argued that parafunctional habits or increased occlusal forces in nonperiodontitis patients will eventually result in adaptive mobility and not lead to pathologic consequences.
The source of the occlusal force becomes much less important than the interaction of the resultant tooth movement and periodontal inflammation, which may lead to accelerated loss of bone and periodontal attachment. This may be analogous to ortho- dontic tooth movement through inflamed tissue in a periodontitis-susceptible indivi- dual. Careful inflammation reduction and management is important for successful active orthodontic therapy, and similar inflammation control is important when mobility from excessive occlusal forces is superimposed on periodontitis. Pathogenic mobility becomes more problematic when it increases over time, suggesting that widening of the periodontal ligament space or possible attachment loss is occurring.
The degree of tooth mobility can be difficult to determine because of varying sys- tems that have been proposed, and operator subjectivity. The most common manual measure of tooth mobility is the Miller Index (Box 3) based on the amount of tooth movement. Other mobility classification schemes have much more subjective criteria, such as grade II as moderately more than normal and grade III as severe mobility facio- lingually and mesiodistally, combined with vertical displacement.
Even though the Miller system uses definitive distances of movement, the ability of the clinician to judge 1 mm of horizontal movement is questionable.51 Subjectivity and lack of reliability in using the Miller technique for the measurement of mobility have been demonstrated.52 Various instruments have been developed to rule out “operator subjectivity” in determining tooth mobility. Historically, the most prominent and objec- tive of these instruments is the Periotest (Fig. 1). The Periotest (Medizintechnik Gul- den, Modautal, Germany) instrument uses an electromagnetically retracting tapping head that automatically makes contact with the tooth or implant 16 times (four times per second). The contact time on impact with the tooth is less in teeth with greater periodontal support and, therefore, less mobility. It has been shown53 that a strong as- sociation exists between Periotest values and bone loss, but adaptation of the instru- ment to posterior teeth is difficult and use of the instrument in clinical practice has not become common. Modification of standard mirror handles to allow calibration of hor- izontal movement may be simpler and more helpful (Fig. 2). This would allow easier measurement of mobility during routine periodontal examinations, which then should be recorded and evaluated against previous findings to reveal increasing mobility.
Determining the prognosis of a tooth based on mobility is questionable.48 However, mobility can affect prognosis and, therefore, subsequent treatment options. Patients considered “high risk” (those with aggressive periodontitis, smoking habit, estrogen deficiency, diabetes) are especially vulnerable to generalized periodontal breakdown and mobile teeth may have an even worse prognosis. Miller class II1 mobile teeth should be assigned “questionable prognosis” according to McGuire.54 Teeth in frem- itus during centric or excursive contacts may be removed from occlusion early in treat- ment. However, it is prudent to perform definitive occlusal therapy following completion of the inflammation control stage of therapy, specifically scaling and root planing. It is not uncommon for periodontally mobile teeth to tighten or shift po- sition following scaling and root planing (Fig. 3), and adjusting occlusion at a subse- quent visit will likely yield more appropriate results. However, occlusal therapy before surgical pocket reduction or regenerative treatment may enhance healing and clinical outcomes.
The positive effect of routine, quality supportive periodontal maintenance therapy has been established many times, but the impact of mobility on outcomes remains un- clear. However, it is reasonable that special attention should be directed toward pa- tients with increasing mobility and sustained inflammation, and then focusing on inflammation reduction and controlling forces in these mobile teeth.
As was emphasized in the point-counterpoint discussion in 2006,55,56 the clinician should recognize that occlusal discrepancies are not the pathology, but rather the pathology is the potential resulting lesion of occlusal trauma, the symptom of which is mobility. Not all occlusal discrepancies cause mobility.
Overall, the periodontal literature has weak evidence that mobility and occlusal trauma impact periodontal longevity. However, a prudent approach may dictate that focused occlusal therapy (following inflammation reduction) be directed toward teeth with mobility associated with parafunctional habits or increasing severity. Further- more, occlusal therapy should be considered if it could result in improved patient com- fort and function. A suggested algorithm is presented in Fig. 4.
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