salicylates and Atrophy

Topics: Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Arthritis, Rheumatoid; Atrophy; Betamethasone; Drug Interactions; Glucocorticoids; History, 20th Century; Humans; Hydrocortisone; Infections; Injections, Intra-Articular; Joint Diseases; Methylprednisolone; Necrosis; Osteoporosis; Peptic Ulcer; Prednisolone; Prednisone; Rheumatic Diseases; Salicylates; Skin Diseases; Substance Withdrawal Syndrome; Synovitis; Triamcinolone; Vascular Diseases

The effects of salicylate and indomethacin on glycosaminoglycan (GAG) synthesis by atrophic and osteoarthritic (OA) canine cartilage were examined in vitro by transecting distal femora at the metaphysis and incubating the knuckle, with its overlying cap of articular cartilage, in medium containing sodium salicylate or indomethacin, and 35SO4. Atrophic cartilage had an intact articular surface, but its uronic acid content averaged 65% of the control level, and GAG synthesis was decreased to 50% of control values. Both salicylate and indomethacin decreased net GAG synthesis in the atrophic cartilage by an additional 10%. OA cartilage showed surface disruption, a uronic acid content 49% of the control value, and a 49% increase in net GAG synthesis. Salicylate and indomethacin profoundly decreased GAG synthesis in the OA cartilage. However, GAG synthesis and uronic acid content of cartilage which had been lacerated in vitro immediately prior to culture (to stimulate fibrillation) were normal and not affected by either drug. The data emphasize the importance of matrix proteoglycan content in protecting the chondrocyte from the suppressive effects of salicylate and indomethacin on GAG metabolism, and suggest that the lower proteoglycan content of OA cartilage may be more important than fibrillation in rendering it vulnerable to the metabolic effects of these drugs.

Topics: Animals; Atrophy; Cartilage, Articular; Culture Techniques; Dogs; Glycosaminoglycans; Indomethacin; Osteoarthritis; Salicylates; Staining and Labeling; Uronic Acids

According to in vivo experimental data, salicylates and several other nonsteroidal anti-inflammatory agents suppress proteoglycan biosynthesis in normal and degenerating articular cartilage. Therapeutic levels of aspirin in vivo had a similar adverse effect on degenerating cartilage, as noted in two canine models of osteoarthritis and cartilage atrophy. Because the effective daily antirheumatic dose of nonsteroidal anti-inflammatory drugs is lower than that of salicylates, these drugs may have less negative effects on degenerating articular cartilage. However, clinical significance cannot be extrapolated from these experimental data.

Topics: Animals; Anti-Inflammatory Agents; Aspirin; Atrophy; Cartilage, Articular; Dogs; Extracellular Matrix; Glycosaminoglycans; Indomethacin; Osteoarthritis; Prostaglandin Antagonists; Proteoglycans; Salicylates; Sulfur Radioisotopes; Sulindac; Uronic Acids

Topics: Adult; Atrophy; Chloramphenicol; Cycloserine; Female; Humans; Intestinal Absorption; Intestinal Mucosa; Isoniazid; Malabsorption Syndromes; Male; Middle Aged; Quinine; Salicylates; Sulfisoxazole

Topics: Absorption; Aspirin; Atrophy; Cobalt Isotopes; Gastric Mucosa; Gastritis; Humans; Hydrogen-Ion Concentration; Intestinal Absorption; Methods; Salicylates; Time Factors

Topics: Adrenal Glands; Atrophy; Cortisone; Salicylates; Sodium Salicylate