Trauma from occlusion refers to pathological changes in the periodontium caused by excessive force from chewing muscles. While excessive force alone does not cause tissue breakdown, it may act as a co-factor in plaque-induced periodontal disease by enhancing the rate of progression. Proper treatment of plaque is important to arrest tissue destruction, even if occlusal trauma persists. Treating occlusal trauma alone through adjustment or splinting may reduce mobility but not stop further breakdown from untreated plaque.

1. Dr. Mohammed Alshehri Dental Implant fellowship program Occlusal Considerations For Implant-Supported Prostheses:Implant-Protectes Occlusion Misch, Chapter 25, Pages 472-507

2. Implant protected occlusion Implant protected occlusion is achieved when the occlusion on the implant restoration provides only a very light drag or resistance to shim-stock in maximum intercuspation with a clenching force applied. definition

33. a

34. Trauma From Occlusion Peri-Implant Tissues (V-1) Lindhe, Chapter 15, Pages 363-370 Dr. Mohammed Alshehri Dental Implant fellowship program

35. Trauma from occlusion is a term used to describe pathologic alterations or adaptive changes which develop in the periodontium as a result of undue force produced by the masticatory muscles. Trauma from occlusion is only one of many terms that have been used to describe such alterations in the periodontium. Other terms often used are: traumatizing occlusion, occlusal trauma, traumatogenic occlusion, periodontal traumatism, overload, etc. In addition to producing damage in the periodontal tissues, excessive occlusal force may also cause injury in, for example, the temporomandibular joint, the masticatory muscles, the pulp tissue. Definitions

36. Glickman (1965, 1967) claimed that the pathway of the spread of a plaque-associated gingival lesion can be changed if forces of an abnormal magnitude are acting on teeth harboring subgingival plaque. This would imply that the character of the progressive tissue destruction of the periodontium at a "traumatized tooth" will be different from that characterizing a “ non-traumatized" tooth. Instead of an even destruction of the periodontium and alveolar bone (suprabony pockets and horizontal bone loss), which according to Glickman occurs at sites with uncomplicated plaque-associated lesions, sites which are also exposed to abnormal occlusal force will develop angular bony defects and infrabony pockets. The interaction between trauma from occlusion and plaque-associated periodontal disease

37. The interaction between trauma from occlusion and plaque-associated periodontal disease

38. The interaction between trauma from occlusion and plaque-associated periodontal disease

39. Zone of irradiation The zone of irritation includes the marginal and interdental gingiva. The soft tissue of this zone is bordered by hard tissue (the tooth) only on one side and is not affected by forces of occlusion. The interaction between trauma from occlusion and plaque-associated periodontal disease

40. The zone of co-destruction includes the periodontal ligament, the root cementum and the alveolar bone and is coronally demarcated by the transseptal (inter-dental) and the dentoalveolar collagen fiber bundles. The interaction between trauma from occlusion and plaque-associated periodontal disease

41. The fiber bundles which separate the zone of co-destruction from the zone of irritation can be affected from two different directions: 1. from the inflammatory lesion maintained by plaque in the zone of irritation 2. from trauma-induced changes in the zone of co-destruction. The interaction between trauma from occlusion and plaque-associated periodontal disease

42. Waerhaug (1979) examined autopsy specimens similar to Glickman's, but measured in addition the distance between the subgingival plaque and (1) the periphery of the associated inflammatory cell infiltrate in the gingiva and (2) the surface of the adjacent alveolar bone. He concluded from his analysis that angular bony defects and infrabony pockets occur equally often at periodontal sites of teeth which are not affected by trauma from occlusion as in traumatized teeth. In other words, he refuted the hypothesis that trauma from occlusion played a role in the spread of a gingival lesion into the "zone of co-destruction". Waerhaug's concept

43. The loss of connective attachment and the resorption of bone around teeth are, according to Waerhaug, exclusively the result of inflammatory lesions associated with subgingival plaque. Waerhaug concluded that angular bony defects and infrabony pockets occur when the subgingival plaque of one tooth has reached a more apical level than the microbiota on the neighboring tooth, and when the volume of the alveolar bone surrounding the roots is comparatively large Waerhaug's concept

46. Since neither analysis of autopsy material nor data from clinical trials can be used to properly determine the role trauma from occlusion may play in periodontal pathology, it is necessary to describe the contributions made by means of animal research in this particular field. Results from such experiments, describing the reactions of the normal and subsequently the diseased periodontium to occlusal forces, are presented below. Conclusion of clinical date

51. Experiments carried out in humans as well as animals, have produced convincing evidence that neither unilateral forces nor jiggling forces, applied to teeth with a healthy periodontium, result in pocket formation or in loss of connective tissue attachment. Trauma from occlusion cannot induce periodontal tissue breakdown. Trauma from occlusion does, however, result in resorption of alveolar bone leading to an increased tooth mobility which can be of a transient or permanent character. This bone resorption with resulting increased tooth mobility should be regarded as a physiologic adaptation of the periodontal ligament and surrounding alveolar bone to the traumatizing forces, i.e. to altered functional demands. CONCLUSIONS

52. In teeth with progressive, plaque-associated periodontal disease, trauma from occlusion may, however, under certain conditions enhance the rate of progression of the disease, i.e. act as a co-factor in the destructive process. From a clinical point of view, this knowledge strengthens the demand for proper treatment of plaque associated with periodontal disease. This treatment will arrest the destruction of the periodontal tissues even if the occlusal trauma persists. A treatment directed towards the trauma alone, however, i.e. occlusal adjustment or splinting, may reduce the mobility of the traumatized teeth and result in some regrowth of bone, but it will not arrest the rate of further breakdown of the supporting apparatus caused by plaque. CONCLUSIONS