Occlusal forces as a risk factor for periodontal disease

Summary of literature review Most early research on the effects of occlusion on the progression of periodontal disease focused on a cause and effect relationship. Stillman clearly felt that excessive occlusal forces were the cause of periodontal disease and that treatment of the occlusion was the primary method of effective periodontal treatment. As it became evident that bacterial plaque was an integral part of the periodontal disease process, the role of occlusal forces became less clear. Eventually this led to viewing occlusion as a cause of specific types of periodontal destruction. This was described by Glickman as the co‐destructive roles of occlusion and bacterial plaque in the formation of vertical osseous defects and furcation bone loss. Glickman's theory of Co‐Destruction continued to hold to the thesis that occlusion was, in concert with bacterial plaque, a causative factor in periodontal attachment loss and bony destruction. Glickman described an altered pathway of destruction in an attempt to articulate a functional mechanism for the formation of the specific morphology of attachment and bone loss thought to be caused by the co‐destructive action of occlusal forces and bacterial plaque. The altered pathway of destruction still held to the concept that occlusion directly changed the disease process and was thereby, in the presence of bacterial plaque, a causative agent for periodontal destruction. The animal studies on squirrel monkeys and beagle dogs began to shed light on the effect of occlusal forces on the periodontal attachment structures at a cellular level. From these studies it was clear that within these animal models, occlusion had an effect on the periodontium in the form of bone rarefaction, which resulted in the clinical manifestation of mobility. However, it was equally clear that, within the animal models, loss of attachment and thereby periodontal destruction did not occur in the presence of excessive occlusal forces only. Loss of attachment occurred only in the beagle dog model and then only in the presence of excessive occlusal forces and bacterial plaque. While these animal studies gave us an exhaustive insight into the effect of excessive occlusal forces on the periodontal supporting structures of the studied animals, it must be remembered that these studies were performed using animal models that show little or no tendency toward periodontal destruction under natural conditions. The application of the information obtained from these animal models to the periodontal destruction that occurs in humans must be approached with caution. It is probable that these animal studies give us a picture only of the physiologic response of the periodontium to excessive occlusal forces with and without bacterial plaque. It is unlikely that these animal studies give us significant information about the pathophysiology that may occur when excessive occlusal forces are present in humans who may be genetically prone to periodontal destruction and who may also have additional risk factors for periodontal disease beyond occlusal forces and bacterial plaque. Human studies begin to give us some indication of the effect of excessive occlusal forces on the progression of periodontal disease in those patients who show a tendency toward periodontal destruction. While there are many apparently contradictory findings from human studies, there appears to be a trend toward evidence that excessive occlusal forces may play a role in periodontal destruction and the response of the periodontium to periodontal treatment. While the available information suggests a relationship between excessive occlusal forces and progression of periodontal disease, the 1999 International Workshop for Classification of Diseases and Conditions indicated that there was no clear evidence that occlusal forces were a factor in plaque‐induced gingivial disease or connective tissue loss ( 23 ). Since the 1999 Workshop, studies have shown that occlusal interferences have a negative effect on the periodontium and tend to cause more rapid pocket formation and poorer prognosis when compared to teeth that do not have occlusal interference.