A cat model for the evaluation of mechanisms of bone resorption: induction of bone loss by simulated immune complexes and inhibition by indomethacin.

Abstract

When simulated immune complexes (SIC) (heat-aggregated IgG) possessing many of the properties of true antigen-antibody complexes were injected via the root canal into the periapical tissues of cat maxillary cuspids, radiographically and histologically evident bone resorption occurred at these sites within 7 days. Bone loss was accompanied in all cases by inflammation of the surrounding collagenous connective tissues and was characterized by the presence of osteoclasts. Bone resorption, but not the accumulation of inflammatory cells, was blocked by the systemic administration of indomethacin, an inhibitor of prostaglandin synthetase. The most likely explanation is that SIC-activated mechanisms such as the complement cascade, prostaglandin synthesis, and neutrophil degranulation were responsible for the bone loss. The minor inflammation and bone loss that followed the repeated injections of BSA and of monomeric IgG can best be explained as a response to trauma. The data presented establish that the cat maxillary cuspid is a useful model in which to explore the mechanism underlying pathological bone resorption.