Offenbacher Steven, Heasman Peter A, Collins John G
J Periodontol. 1993 May;64 Suppl 5S:432-444. doi: 10.1902/jop.1993.64.5s.432.
An increasing body of evidence supports the concept that host-produced PGE mediates much of the tissue destruction that occurs in periodontal disease. PGE 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 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 host response model as a hypothetical framework to discuss new, possible explanations for host susceptibility to periodontal disease. J Periodontol 1993;64:432-444.
越来越多的证据支持这样一种观点，即宿主产生的前列腺素E（PGE）介导了牙周病中发生的大部分组织破坏。龈沟液中的PGE水平可作为对正在进行的疾病活动的静态评估；即附着丧失率和骨吸收情况。对调节PGE合成机制的新见解提供了一种改变的牙周病范式，该范式将重点放在宿主反应而非细菌病因上，将其作为疾病表现的主要决定因素。我们将PGE宿主反应模型描述为一个假设框架，以讨论宿主对牙周病易感性的新的、可能的解释。《牙周病学杂志》1993年；64:432 - 444。
