MODULATION OF HOST PGE2 SECRETION AS A DETERMINANT OF PERIODONTAL-DISEASE EXPRESSION

AN INCREASING BODY OF EVIDENCE supports the concept that host-produced PGE2 mediates much of the tissue destruction that occurs in periodont al disease. PGE2 levels within the crevicular fluid can serve as a sta tic assessment of ongoing disease activity; i.e., rate of attachment l oss and bone resorption. New insights into the mechanisms that regulat e PGE2 synthesis provide an altered paradigm of periodontal disease wh ich places the emphasis on host response, rather than the bacterial et iology, as the principal determinant of disease expression. We describ e a PGE2 host response model as a hypothetical framework to discuss ne w, possible explanations for host susceptibility to periodontal diseas e.