[Immune complexes: mediators for the formation of inflammatory granulation tissue? Immunohistologic studies of the hyaline articular cartilage in chronic polyarthritis]
- PMID: 6189306
[Immune complexes: mediators for the formation of inflammatory granulation tissue? Immunohistologic studies of the hyaline articular cartilage in chronic polyarthritis]
Abstract
Previous reports describe the presence of immunoglobulins and complement components within rheumatoid articular cartilage, thereby suggesting an effect of immune complexes on the formation of pannus. This hypothesis is reinvestigated in this paper. As confirmed in our work, the superficial layer of rheumatoid hyaline cartilage may fulfill the immunohistological criteria for the presence of immune complexes. In osteoarthritis, however, a noninflammatory disease not mediated by immunologic mechanisms, similar results can be obtained. The presence of immune-proteins within hyaline cartilage therefore requires a cautious interpretation. Hyaline cartilage in rheumatoid arthritis is replaced by granulation tissue growing not only at its surface (pannus), but also in subchondral bone. We therefore also thoroughly investigated deep layers of hyaline cartilage in the vicinity of such subchondral tissue, but could not obtain any evidence for the presence of immune complexes therein. The growth of subchondral granulation tissue and the accumulation of PMN in the region of its junction with hyaline cartilage therefore appear to be independent of immune complexes within rheumatoid hyaline cartilage. It is suggested on the basis of these data that immune complexes possibly present in hyaline cartilage do not play an essential role in the formation of granulation tissue replacing cartilage in rheumatoid arthritis. It is, however, not entirely excluded that during advanced stages of rheumatic cartilage degradation immune complexes are formed within the matrix or carried into it from the extra-cartilaginous environment, and that they may then contribute to further cartilage destruction by enzyme release during phagocytic processes.
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