Modulation of Host PGE₂ Secretion as a Determinant of Periodontal Disease Expression

TLDR

Host‑produced PGE2 drives most periodontal tissue destruction, and recent insights shift focus to host response rather than bacterial etiology as the main determinant of disease. The study proposes a PGE2 host response model to explain host susceptibility to periodontal disease. The authors develop a hypothetical PGE2 host response model to explore mechanisms underlying host susceptibility. PGE2 levels in crevicular fluid reflect disease activity, indicating rates of attachment loss and bone resorption. J Periodontol 1993;64:432–444.

Abstract

A n increasing body of evidence supports the concept that host‐produced PGE 2 mediates much of the tissue destruction that occurs in periodontal disease. PGE 2 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 PGE 2 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 PGE 2 host response model as a hypothetical framework to discuss new, possible explanations for host susceptibility to periodontal disease. J Periodontol 1993;64:432–444.