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The effect on marginal inflammation and tooth mobility of occlusal adjustment by grinding was investigated in 43 occlusally traumatized teeth in 29 subjects with gingivitis and marginal periodontitis. The material consisted of 4 groups with tooth mobility of varying degrees of severity, and bone destruction. In all groups increased tooth mobility decreased subsequent to occlusal adjustment. The latter was without effect on the sulcus fluid flow rate or gingivitis scores in either gingivitis or periodontitis patients.

The oral health of twenth-two patients with a diagnosis of myofascial pain dysfunction syndrome was evaluated. Radiographs, photographs, study casts, visual and digital clinical examinations, hematologic data, blood pressure, and periodontal examinations were used with each patient. A review of the literature indicated a variety of causes for facial pain, including Costen's syndrome, muscle fatique and spasm, occlusion, and psychogenic factors. This study revealed the following trends: (1) The periodontal health of patients with the myofascial pain dysfunction syndrome appears to be better than anticipated. (2) Bruxism accounts for a healthy dental apparatus when other diseases are not present. (3) Groups of muscles, other than the masticatory group, may contribute to the myofascial pain dysfunction syndrome. (4) Patients presented with various ranges of malocclusions and normal occlusions, deep overbites and overjets, complete dentitions, and missing teeth (either equally missing right and left or unequally missing right and left). This article also discusses clinical considerations in the diagnosis of the myofascial pain dysfunction syndrome and offers a practical, physiologic approach to treatment. We conclude that how one uses his mandible is more of a causative factor than the relationships of the teeth.

The unconscious habit of holding the teeth together or clenching, or both, is one of the most dominant factors that leads to mandibular atrophy. This habit causes long periods of mucoperiosteal ischemia due to denture pressure, with inflammation, a lowered PH, and a net bone loss. Pressure resorption is postulated as the primary cause of mandibular atrophy.

Both the inflammatory and noninflammatory types of periodontal diseases begin with an aseptic, traumatic destruction of alveolar bone, caused by traumatizing parafunctions and followed by changes in the gingiva. The latter may or may not have a superimposed infectious inflammatory process. A new concept to fit these facts is proposed: periodontal diseases are autodestructive processes in the masticatory system, with or without superimposed septic inflammation. To confirm the theory of autodestruction, direct evidence as well as indirect but conclusive evidence is given for the existence of traumatizing forces in the masticatory system, for traumatic destruction of alveolar bone, for changes in the gingiva following destruction of alveolar bone, and for the parafunctions by all persons afflicted by periodontal disease. It is concluded that traumatizing parafunctions are the main factor in the etiology of periodontal diseases and that in therapy recurrences are inevitable unless parafunctions have been eliminated.