[Immune complexes: mediators for the formation of inflammatory granulation tissue? Immunohistologic studies of the hyaline articular cartilage in chronic polyarthritis]. / Immunkomplexe: Mediatoren für die Bildung von entzündlichem Granulationsgewebe? Immunhistologische Untersuchungen am hyalinen Gelenkknorpel bei chronischer Polyarthritis.

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.

[Proteolytic occurrences in the metabolism of cartilage and their modification by antirheumatics]. / Proteolytische Abläufe im Knorpelstoffwechsel und ihre Beeinflussung durch Antirheumatika.

Rheumatic diseases are characterized by the progressive loss of articular cartilage. According to a well established hypothesis proteolytic enzymes take part in these events. The initial attack in an normal cartilage can be exerted by proteoglycanases originating from either chondrocytes or cells from outside the cartilage like neutrophilic granulocytes or macrophages. In rheumatoid arthritis these latter cells are found in immediate vicinity to cartilage and it is assumed that they release their enzymes directly into the cartilage. Lysosomal elastase from neutrophilic granulocytes is a key enzyme made responsible for the degradation of cartilage, since it is able to soften up this tissue and thereby to deprive it of its normal mechanical properties. Therefore the pharmacological inactivation of elastase bears a therapeutic potential for rheumatic joint disease. The ultimate value of enzyme inhibitory antirheumatic drugs needs, however, further investigation since also enzyme independent variables play an important role in maintaining normal function of cartilage.