ABSTRACT
Chronic inflammation is central to tissue destruction in periodontal disease and is also a feature of localized bone destruction by tumors. However, it is most appropriate to relate the role of prostaglandins (PGs) in inflammatory bone destruction to rheumatoid arthritis, where chronic inflammation alone is responsible for the damage to the joint tissues. The phenomenon of “down-regulation” of the receptor-mediated responses to agents such as complement, cytokines, or PGs themselves may regulate resorbing activity, especially in a situation like chronic inflammation where one would expect the levels of these agents to be continuously elevated. The vascular changes which characterize chronic inflammation are central to virtually very aspect of the lesion. In addition to the increase in vascular permeability which enhances migration of leukocytes and transudation of plasma inflammatory mediators into the extra-vascular space, the blood vessels may also act as a depot for inflammatory stimuli and as a source of PGs and lytic enzymes.
