This article presents a brief review of the literature concerning the relationship between periodontal disease and occlusal forces. Additionally, we will review recent research we have performed and compare it with past research findings. We also will discuss our conclusion that occlusal discrepancies are a significant risk factor for the progression of periodontal disease and our reasoning for suggesting that treatment of occlusal discrepancies should be a routine part of periodontal therapy.

	HISTORICAL STUDIES

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For more than a century, clinicians have postulated that a relationship existed between occlusal forces and the progression of periodontal disease. Karolyi,¹ in the early 20th century, was one of the first to publish on the relationship of occlusion to periodontal disease. He indicated that teeth undergoing excessive occlusal stress seemed to have more periodontal destruction than did teeth not experiencing occlusal stress. Also in the early 20th century, Stillman, one of the early pioneers of periodontal therapy, presented the proposition that excessive occlusal stress was the cause of periodontal disease. Stillman indicated that to treat periodontal disease successfully, the clinician must control occlusal forces.^2,3 Stillman’s comments led to several studies aimed at determining whether occlusion did or did not play a causative role in periodontal disease.^4–6 These studies failed to produce conclusive results, and the controversy continued.

In the 1940s, Weinmann⁷ published one of the first studies to evaluate the relationship of occlusion and periodontal disease at a cellular level. On the basis of his observations of human autopsy material, he felt that periodontal disease was related to progression of an inflammatory process that began at the gingival attachment and spread into the surrounding bone, following the course of blood vessels. Weinmann did not see evidence that occlusion caused or influenced the progression of the inflammatory process.

Two decades later, Glickman and Smulow^8,9 also examined human autopsy material and agreed that inflammation appeared to begin at the gingival attachment and subsequently progressed into the surrounding periodontal supporting tissue. However, they suggested there was evidence that in teeth undergoing occlusal trauma, the inflammation progressed in a different manner than that in teeth that were not undergoing occlusal trauma. They termed this different progression of periodontal disease as an "altered pathway of destruction." They termed the combined effects of occlusal trauma and inflammation as "co-destructive factors" in periodontal disease.^8,9

Other researchers did not agree with this theory of codestruction.^10,11 In the 1970s, Waerhaug,^12,13 again evaluating human autopsy material, felt that there was no evidence that occlusal forces played any role in periodontal destruction. He indicated that no differences in disease progression could be detected between teeth that were undergoing occlusal trauma and teeth that were not. Waerhaug found no evidence for Glickman and Smulow’s "altered pathway of destruction" and indicated that all inflammation and bone loss were associated with the presence of bacterial plaque. Waerhaug showed evidence that bacterial plaque always was present in close proximity to the site of periodontal destruction. He also indicated that there was no evidence of the changes purported to be present in the altered pathway of destruction caused by occlusal trauma. Waerhaug’s conclusion was that occlusal trauma played no part in periodontal destruction and plaque-related inflammation was the only cause of periodontal disease.

Most historical studies of the effect of occlusal forces on the progression of periodontal disease were aimed at showing that occlusion did or did not cause periodontal destruction. The desire to find a single cause of periodontal disease was rooted in the disease concepts of the late 19th century. The idea that a chronic process such as periodontal disease was the result of multiple risk factors did not fit the outlook of the first half of the 20th century. Glickman and Smulow’s view of a codestructive action between bacterial inflammation and occlusal trauma was a step toward the modern concept of multiple risk factors’ affecting the progression and severity of the disease process.

	ANIMAL RESEARCH

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Starting in the 1930s, multiple animal research projects were performed in an attempt to prove or disprove a relationship between occlusion and periodontal disease.^14–16 The most significant animal studies were performed in the 1970s by two research groups, one at Eastman Dental Center in Rochester, N.Y.,^17–21 and the other at the University of Gothenburg in Sweden,^22–25 and they often are referred to as the American and the Scandinavian occlusal studies, respectively. Both evaluated the effect of occlusal trauma and gingival inflammation in animals. The American group used repeated applications of orthodontic-like forces on the teeth of squirrel monkeys, and the Scandinavian group used occlusal forces similar to those of a "high" restoration in beagle dogs. Both groups evaluated the effects of these traumatic occlusal forces in animals: those in which good oral hygiene was maintained with little gingival inflammation and those in which a soft diet allowed the buildup of plaque and subsequent inflammation.

Despite major differences in the animal models and the types of excessive occlusal forces applied, the results of these two studies were similar in many respects. Within both animal models, researchers found that if oral hygiene was maintained and inflammation controlled, occlusal trauma resulted in increased mobility and loss of bone density, but no loss of attachment, during the length of the study. In no case in which inflammation was controlled was there any attachment loss or pocket formation. Furthermore, if the occlusal forces were removed, there was a return to pretreatment stability and bone volume. In animals in which plaque was allowed to accumulate and gingival inflammation was present, there was greater loss of bone volume and increased mobility, but still no attachment loss. Only in cases in which the bone support of beagle dogs was surgically decreased, inflammation was allowed to develop and occlusal stress was applied was there any evidence of attachment loss. The conclusion of both research groups was that without inflammation, occlusal trauma does not cause irreversible bone loss or loss of attachment. On the basis of the collective results of these studies, it appears that in animals, occlusal trauma is not a causative agent of periodontal disease.

The cited animal research seems to suggest that occlusal forces are not a factor in the progression of periodontal destruction. However, several questions remain concerning the application of these results to humans. Naturally occurring periodontal disease is virtually unknown in monkeys, and it usually occurs only in much older dogs than those used in these studies. Furthermore, in humans, most periodontal destruction resulting in attachment and bone loss occurs relatively slowly over a much longer period than that used in the animal studies. Both the use of animal models and the relatively short duration of the studies leave questions concerning the application of these results to periodontal destruction occurring in humans.

	HUMAN STUDIES

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Human research on occlusion has yielded mixed results. One study evaluated teeth with balancing or nonworking contacts in relation to teeth without balancing contacts.²⁶ Teeth with non-working contacts showed greater periodontal destruction and pocket depths. Another similar study showed no difference between the two groups. ²⁷ The researchers conducting these studies used existing records such as periodontal charting and study models to determine which teeth were undergoing occlusal trauma, and they did not conduct direct patient examinations. Other human studies have yielded similar conflicting results.^28,29 Furthermore, these studies were epidemiologic in nature and looked at a general population rather than patients with periodontal disease.

Burgett and colleagues³⁰ used a controlled clinical trial to evaluate the effect of treating the occlusion on healing outcomes after periodontal treatment. In this trial, one-half of the patients received occlusal adjustment by means of selective grinding before undergoing surgical and non-surgical periodontal therapy. The other one-half did not receive occlusal adjustment. After an extended healing period, the group that received occlusal adjustment before periodontal treatment showed consistently and statistically significantly better healing, in the form of improvements in attachment levels, when compared with patients who did not receive occlusal adjustment. This well-controlled study demonstrated that in a group of patients with existing periodontal disease, there was improved healing if occlusal trauma was minimized by occlusal adjustment.

As part of a large study on prognosis, McGuire and Nunn^31,32 reviewed the change in prognosis and in the number of teeth lost by patients with periodontal disease who had parafunctional habits. In patients with parafunctional habits that had not been treated with an occlusal appliance, there was no improvement in prognosis despite periodontal therapy. Also, more teeth were lost in the untreated group than in a group that received occlusal appliances. This study indicated that for patients with periodontal disease, the treatment of occlusal trauma improved treatment outcomes and that the lack of treatment resulted in greater tooth loss.

The consensus of the 1996 World Workshop in Periodontics indicated that there was inadequate information to determine whether a relationship exists between occlusion and the progression of periodontal disease.³³ Another review article published in the mid-1990s stated a similar viewpoint.³⁴ More recently, the 1999 Consensus Report on Periodontal Disease Classification agreed that occlusal trauma represented injury resulting in tissue changes within the attachment apparatus as a result of occlusal force(s). This report also agreed that excessive occlusal forces alone do not initiate plaque-induced gingival disease or loss of connective tissue associated with periodontitis.³⁵

	RECENT HUMAN STUDIES

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The results of a large retrospective study performed by two of the authors (S.K.H. and M.E.N.) that evaluated the effects of occlusal discrepancies on the progress of periodontal disease have refocused attention on this area of periodontal therapy.^36–38 In that study, the authors evaluated a group of private practice patients referred for the treatment of active periodontal disease. All patients had advanced periodontal disease with clinically detectable bone loss. For inclusion in the study, the patients had to have been recommended to receive both nonsurgical and surgical periodontal treatment. All cases could be classified as periodontal case type III or IV. All patients had to have complete initial periodontal records, including a full occlusal analysis consisting of a recording of an initial contact point, measurement of any slide existing between a retruded position (centric relation) and maximum intercuspation (centric occlusion), lateral working and balancing contacts, and protrusive contacts. Furthermore, to be included, the patients had to undergo a second examination at least one year after the initial examination, at which time another complete periodontal evaluation was performed and the results recorded. We recorded other pertinent data such as pocket depth, mobility (according to the Miller³⁹ index), fremitus, width of gingiva and treatment performed. For this study, we defined occlusal discrepancies as teeth with a slide between centric relation and centric occlusion of 1 millimeter or greater or the presence of non-working contacts. We placed all data in a database so that we could use general estimating equations to analyze the data.

We need to make clear that our study evaluated the effects of occlusal discrepancies on the progression of periodontal disease. We did not attempt to make a diagnosis of "occlusal trauma." The diagnosis of occlusal trauma can be made only by the histologic evaluation of the periodontium. This makes it impossible to verify the diagnosis of "occlusal trauma" for a tooth that is to be retained. Proposed surrogate markers of occlusal trauma, such as mobility or tooth wear, are problematic because of inconsistencies in presentation. Some teeth with severe wear facets may have no detectable mobility, while very mobile teeth may have no detectable occlusal wear. It even is possible to find mobile teeth that are not in occlusal function. We studied occlusal discrepancies because they can be consistently identified clinically without extraction of the tooth. The teeth identified as having an occlusal discrepancy may or may not have received a histologic diagnosis of "occlusal trauma." All data from these studies should be interpreted as demonstrating the effects of occlusal discrepancies and not necessarily the effects of "occlusal trauma."

We recorded all data on an individual-tooth basis. Recording and analyzing data in this manner allowed the comparison of teeth that had occlusal discrepancies with teeth that did not. Analysis of individual teeth according to occlusal discrepancy sets this study apart from most previous studies that have made comparisons between patients with and without occlusal trauma. While making such comparisons enables one to use traditional statistical tools for analysis, the "all-or-none" measure for describing each patient is a crude instrument for making comparisons. In addition, success or failure at individual sites is the measure by which patients and practitioners most often judge the outcome of periodontal therapy, and by using the measure of individual teeth for assessing occlusal discrepancy, each patient’s occlusion can be put on a continuum—something that normally is not possible when patients are simply classified as having or not having an occlusal problem.

We entered data regarding 89 patients and 2,147 teeth into the database. The patients fell into three groups based on the type of treatment performed. In all groups, patients were selected randomly for inclusion and had self-selected the treatment that was performed.

– The first group was seen for a periodontal examination but elected to not receive any of the recommended treatment. The patients in this group voluntarily returned for another complete periodontal examination at least one year after the initial collection of data. We designated this group the "untreated" group and felt they represented how occlusal interferences could affect the progression of untreated periodontal disease.

– The second group completed the initial nonsurgical phase of the recommended treatment but did not complete the recommended surgical treatment. All patients in this group received at least root planing and oral hygiene instructions. Some patients in this group had occlusal adjustment performed. We designated this group the "nonsurgically treated" group.

– The third group was selected randomly from patients who had completed all recommended periodontal therapy, including surgery, and were in a periodontal maintenance program. In evaluating the initial data of all patients within the study, we found that teeth with an occlusal discrepancy had pocket depths approximately 1 mm deeper than those of teeth with no occlusal discrepancy. This difference was highly statistically significant (P .0001) and was true regardless of age, sex, smoking status or other risk factors. In addition to having deeper probing depth, teeth with occlusal discrepancies had statistically greater mobility, as well as a prognosis statistically worse than that for teeth without occlusal discrepancies. The presence of occlusal discrepancies was a statistically significant predictor of deeper pocket depths, greater mobility and a poorer prognosis. When we evaluated only patients with good oral hygiene, occlusal discrepancies were a better predictor of pocket depths, mobility and poor prognosis than were any other risk factors evaluated, including smoking. These data are shown in the table.

View larger version (68K): [in this window] [in a new window]   Figure 1. Change in probing depth over time for all subjects. General estimating equation regression model with median follow-up of 2.7 to 8.7 years; range of follow-up, 0.8 to 21.2 years. mm: Millimeters. Adapted with permission of the American Academy of Periodontology from Harrel and Nunn.38

View larger version (68K): [in this window] [in a new window]   Figure 2. Change in probing depth over time for untreated subjects. General estimating equation regression model with median follow-up of 2.7 to 8.7 years; range of follow-up, 0.8 to 21.2 years. mm: Millimeters. Adapted with permission of the American Academy of Periodontology from Harrel and Nunn.38

View larger version (70K): [in this window] [in a new window]   Figure 3. Change in probing depth over time for subjects who received nonsurgical treatment. General estimating equation regression model with median follow-up of 2.7 to 8.7 years; range of follow-up, 0.8 to 21.2 years. mm: Millimeters. Adapted with permission of the American Academy of Periodontology from Harrel and Nunn.38

Our study should be viewed in the context of its design. It does not meet the level of what is considered the gold standard of clinical research: the controlled clinical trial. Ideal research is prospective in nature, with a double-blind design in which neither the patients nor the evaluators know what treatment the patients did or did not receive. Our study was retrospective in nature, a single practitioner performed all treatment and the same practitioner performed all evaluations and data gathering. Furthermore, the patients’ oral hygiene and maintenance compliance was not standardized. All of these are significant concerns regarding our research design.

However, we need to point out that the only way to fulfill the parameters of a controlled clinical trial would be to first diagnose periodontal disease and evaluate the patients for occlusal discrepancies, then follow the patients’ status for many years without performing any treatment for their diagnosed periodontal disease. This clearly is unethical and would violate all standards for human research. We feel that our research, with its admitted flaws, represents the most valid and complete evaluation of the relationship between periodontal disease and occlusal forces published to date. The results of our studies demonstrate very strong statistical evidence that occlusal discrepancies are a significant risk factor in the progression of periodontal disease. We feel that the strong statistical relationship between occlusal discrepancies and the progression of periodontal disease is clinically valid, and that this positive correlation may be independent of the classic histologic diagnosis of "occlusal trauma."

	SUMMARY

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The exact effect of occlusal discrepancies/occlusal trauma on the progression of human periodontal disease remains unknown. However, all studies performed to date strongly indicate that occlusion is not a causative factor in periodontal disease. On the basis of this finding, we should state categorically that there is no justification in the literature for prophylactic adjustment of the occlusion to prevent periodontal disease. It also can be stated that research involving humans has shown that occlusal discrepancies may be a significant risk factor for the progression of existing periodontal disease and that the treatment of occlusal discrepancies significantly improves the outcome achieved with periodontal treatment.

Periodontal disease is a multifactorial disease that affects only a limited number of people within a population. Our current understanding of periodontal disease is that it occurs in these susceptible people in the presence of multiple risk factors, such as bacterial plaque and smoking. Periodontal disease does not appear to be due to a single cause such as a specific bacterial species, but rather to be a result of multiple risk factors. This disease model is relevant to many chronic inflammatory diseases. Just as smoking does not cause periodontal disease but is a significant risk factor in the progression of periodontal disease, occlusal discrepancies do not cause periodontal disease but may be a significant risk factor in the progression of periodontal disease.^41,42 Removing the risk factor of occlusal discrepancies through selective grinding and/or occlusal appliances during periodontal therapy has been shown to produce significant changes in the progression of the disease and improve the results from treatment of the inflammatory component of the disease. On this basis, we feel there is evidence that the treatment of occlusal discrepancies should be considered as an integral part of the overall treatment of periodontal disease and should be included in the comprehensive treatment of this disease.