We appreciate Dr. DiBenedetto’s interest in our article. He poses many questions about occlusion and periodontal disease that are impossible to answer, given our present state of understanding. We offer the following responses as partial answers to his questions.
The definition of periodontal disease(s) is a moving target that is difficult to define. This difficulty in defining periodontal diseases has been recognized by the American Academy of Periodontology (AAP). The AAP addressed this concern with the 1999 International Workshop for Classification of Periodontal Diseases and Conditions.
The findings of that workshop, and the most current definitions of periodontal diseases, were published in the Annals of Periodontology.1 Our co-author, William W. Hallmon, was the author of the occlusion section of this publication. These findings were considered in the preparation of our article.
In answer to the question "Is bone loss periodontal disease?", we do not feel that bone loss is synonymous with periodontal disease. Bone loss is closely associated with periodontal disease, but it is not equivalent to periodontal disease. The assumption of equivalency between bone loss and periodontal disease is a common error made by third-party payers, who often view radiographic bone loss as synonymous with periodontal disease. The AAP has stated for many years that radiographic bone loss is not always present with periodontal disease.
As to the Harrel-Nunn articles2–5 referenced in our JADA article, the presence of periodontal disease was diagnosed based on the examiners’ clinical judgment and the presence of deep pockets. All patients included in the study could be considered a periodontal case type III or IV. In reality, all patients included in the study had multiple pockets of at least 6 millimeters. Many patients had pockets of 9 mm. Teeth with or without occlusal discrepancies were evaluated in light of the progression or improvement in pocket depth.
We feel that the definition of normal occlusion is patient-specific. We did not make any attempt to define "normal occlusion." The Harrel-Nunn studies looked specifically at occlusal discrepancies. These are clearly defined in the studies as a slide from a retruded position (nominal centric relation) to the position of maximum intercuspation (nominal centric occlusion) of 1 mm or greater, or the presence of contacts on the non-working side (nominal balancing contacts) during lateral (excursive) movements.
The findings from the Harrel-Nunn articles should be judged in the light of evaluating the relationship of occlusal interferences, as defined above, to the progression of periodontal disease. As was stated in our JADA article, the definition of occlusal trauma must be made at a cellular level, and is defined by the presence of histological evidence of breakdown.
The patients in the Harrel-Nunn studies were undergoing routine periodontal treatment with the aim of retaining their teeth. In fact, almost all of the teeth evaluated in the study were retained for the length of the study. Therefore, the teeth were not extracted, and the tissues could not be evaluated histologically.
Because the definitive diagnosis of occlusal trauma cannot be verified when the tooth is retained, the clinical finding of occlusal discrepancy was used as the study variable. Again, it should be stressed that the Harrel-Nunn studies showed that occlusal discrepancies, not occlusal trauma, appeared to be an independent risk factor for the progression of periodontal disease.
We cannot offer an opinion as to whether the periodontal ligament (PDL) is different from other ligaments in the body. The microscopic picture of the PDL certainly bears similarities to other ligaments in the body. There are many types of ligaments, and these all have some similarities to each other, but there are also many differences. Where the PDL fits in this picture is beyond the scope of our article. It should be pointed out that controversy exists in the medical literature as to the effects of stress and trauma on ligaments.
The "easier" questions posed by Dr. DiBenedetto both refer to the effect of skeletal (Angle’s classification) and tooth position on gingival recession. This has been studied in the orthodontic literature, with mixed results. We refer those with interest in this subject to that literature, so they can make their own decision and, we hope, formulate a study that will give a definitive answer to this question.
As to the Harrel-Nunn study on gingival recession,5 we need to again point out that the effect of occlusal discrepancies, as previously defined, on gingival recession was examined. It was found that occlusal discrepancies did not contribute to increased recession, and that the treatment of occlusal discrepancies did not improve gingival recession.
We would like to express our appreciation again for Dr. DiBenedetto’s interest in our article. He poses many good questions concerning the relationship of occlusion to periodontal disease(s). We hope that our article, the excellent article by Drs. Deas and Mealy, and Dr. DiBenedetto’s questions will stimulate others to study this relationship.
The interface between occlusion and periodontal disease in humans has been extensively evaluated at an opinion and mechanistic level, but has had very little scientific evaluation. We urge all of those interested in this subject to perform and publish scientific research that looks at this interface.
In producing this research, we urge researchers to study this phenomenon at a tooth level (the individual tooth as the unit of study), rather than at a patient level. We feel that research that does not look at tooth-level data will further obscure and confuse the relationship of occlusion to periodontal disease. We continue to perform clinical research in this area, both on natural teeth and on dental implants.
TOP
REFERENCES
