Continuing studies of bone destruction associated with periodontal disease have clarified certain questions concerning the nature of local mediators and have directed inquiry to new areas of potential relevance. Radioimmunassay of periodontal tissues at the advancing disease front has demonstrated that prostaglandin E2 is commonly associated with destructive disease but that thomboxane and prostacyclin do not appear to be directly associated with disease. It was found that the prostacyclin metabolite, 6-keto PGE1, is a potent stimulator of bone resorption. The role of this substance in bone metabolism is currently being investigated. Bioassay of human periodontal tissues for bone resorptive activity has revealed that much of this activity is associated with fractions of higher molecular weight than the prostaglandins. Among the agents suspected is osteoclast activating factor (OAF). Following the observation that this substance resorbs bone at a rate comparable to parathyroid hormone, a monoclonal antibody preparation was made against the 1-34 PTH peptide which blocked the bone resorptive activity of OAF. Bacterial products are also being investigated for their potential involvement in periodontal disease. We have found that bone resorptive activity of certain endotoxins can be blocked by polymyxin B, suggesting both a mode of identification and a possible means for control. In addition, the potential of cell wall fragments participating in the bone resorptive lesion of periodontal disease is suggested by the recently reported observation from this laboratory than N-acetyl muramyl dipeptide, a minimal fragment of bacterial peptidoglycan, is a potent stimulator of bone resorption. An important consequence of these studies in the potential of developing diagnostic methods based on mediators of bone resorption which could indicate the presence of an active phase of periodontal destruction. Preliminary studies of a modified radioimmunoassay for PGE2 in gingival crevice fluid appear promising.
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