Role of chondrocytes in the development of osteoarthritis.

The chondrocyte holds a key position in the development of osteoarthritis. As the only living element of the articular cartilage, it produces the components of the matrix, i.e., collagens and proteoglycans. In the course of its life, the chondrocyte is susceptible to nutrient and toxic dangers. This leads to a qualitative and quantitative jeopardy of the matrix production. Collagens and proteoglycans are also subject to metabolic influences. Whatever the cause(s), osteoarthritis results in deficient masking of the collagen fibers and in roughening of the cartilaginous surface. Thus, the phase of "wear and tear" is initiated, which is characteristic of osteoarthritis. This process may provoke a total loss of cartilage and opening of the subchondral medullary spaces. However, osteoarthritis probably only becomes clinically manifest when a secondary synovitis supervenes, which is caused by mediators developing from degradation products of the cartilaginous matrix. Thus, osteoarthritis can be considered to develop from a disproportion between the quality of the matrix and load to the cartilage. Aside from avoiding non-physiologic overload to the articular cartilage, therapy must influence the secondary synovitis. Furthermore, an attempt should be made to interfere effectively with the chondrocytic metabolism by means of "chondroprotective substances."

Detection of sarcolectin-specific receptors like the cytokine macrophage migration inhibitory factor in rheumatoid nodules.

The objective of this study was the evaluation of the relation between the N-acetyl-neuraminic acid-binding endogenous lectin sarcolectin and the cytokine macrophage migration inhibitory factor (MIF) during development of rheumatoid nodules (RN) in seropositive rheumatoid arthritis (RA). Sarcolectin was purified and biotinylated. The binding patterns of this probe were analyzed in RN from patients with RA (n = 23) and compared with the distribution of antibodies with specificity for MIF, fibrin, fibronectin. In early RN, all areas of the inflammatory tissue displayed presence of receptors for sarcolectin. Macrophages were especially positive. In mature rheumatoid nodules binding of sarcolectin was restricted to the periphery of necrotic areas, to endothelial cells and perivascular connective tissue of marginal zones. Distribution patterns of MIF were similar but not identical. The histological staining characteristics demonstrate sarcolectin-binding receptors in RN that are altered upon disease progression. The finding suggests that specific interactions between this endogenous lectin and MIF may be involved in the course of RA.

Current understanding of rheumatoid arthritis.

A full understanding of rheumatoid arthritis depends on the appreciation of clinical, radiological, immunological, genetic, biochemical, and structural mechanisms. Rheumatoid arthritis is characterized by the destruction of tissue structures such as articular cartilage and bone, but may also involve tendonous tissue, artery walls, cardial structures, and sclera of the eye. Structural analysis of tissue obtained by biopsy and operation in rheumatoid arthritis patients reveals a complicated mosaic of different components, which are together responsible for the clinical symptoms and destructive nature of the disease.

Recurring synovitis as a possible reason for aseptic loosening of knee endoprostheses in patients with rheumatoid arthritis.

We evaluated histologically samples of synovial tissue from the knees of 50 patients with rheumatoid arthritis (RA). The samples were taken during revision for aseptic loosening. The findings were compared with those in 64 knees with osteoarthritis (OA) and aseptic loosening and in 18 knees with RA without loosening. The last group had been revised because of failure of the inlay or the coupling system of a constrained prosthesis. All the patients had had a total ventral synovectomy before implantation of the primary prosthesis. In all three groups a foreign-body reaction and lymphocellular infiltration were seen in more than 80% of the tissue samples. Deposits of fibrin were observed in about one-third to one-half of the knees in all groups. Typical signs of the reactivation of RA such as rheumatoid necrosis and/or proliferation of synovial stromal cells were found in 26% of knees with RA and loosening, but not in those with OA and loosening and in those with RA without loosening. Our findings show that reactivation of rheumatoid synovitis occurs after total knee replacement and may be a cofactor in aseptic loosening in patients with RA.

[Osteoarthritis in the light of current research findings]. / Die Osteoarthrose im Licht neuer Forschungsergebnisse.

Chondrocyte and cartilage matrix can in the course of time lose in quality due to nutritive, toxic and enzymatic influences but also due to excessive mechanical usage so that the hyaline articular cartilage can no longer fulfill its function as a hydro-elastic bumper. This results in progressive mechanical cartilage destruction and sclerosing reconstruction of the subchondral bone. The parts of the matrix that are freed by the mechanical abrasion can function as inflammatory mediators and set an accompanying synovitis going. It is this secondary synovitis that then leads to a painful manifestation of osteoarthritis. In this case, an antiphlogistic therapy is necessary, because during a secondary synovitis cytokines are set free that endanger the yet intact articular cartilage.

[Osteoarthritis in light of the results of new research]. / Osteoartroza u svjetlu rezultata novih istrazivanja.

Chondrocyte and cartilage matrix can in the course of time lose in quality due to nutritive, toxic and enzymatic influences, but also due to excessive mechanical usage so that the hyaline articular cartilage can no longer fulfill its function as a hydroelastic bumper. The results are progressive mechanical cartilage destruction and sklerosing reconstruction of the subchondral bone. The parts of the matrix that are freed by the mechanical abrasion can function as inflammatory mediators and set an accompanying synovitis going. It is this secondary synovitis that then leads to a painful manifestation of osteoarthritis. In this case, an antiphlogistic therapy is necessary, because during a secondary synovitis cytokines are set free that endanger the yet intact articular cartilage.