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 periodontal disease. PGE₂ levels within the crevicular fluid can serve as a static assessment of ongoing disease activity; i.e., rate of attachment loss and bone resorption. New insights into the mechanisms that regulate PGE₂ synthesis provide an altered paradigm of periodontal disease which places the emphasis on host response, rather than the bacterial etiology, as the principal determinant of disease expression. We describe a PGE₂ host response model as a hypothetical framework to discuss new, possible explanations for host susceptibility to periodontal disease. J Periodontol 1993;64:432-444.