'Chondroprotection' by non-steroidal anti-inflammatory drugs

Article Abstract:

Osteoarthritis, a chronic disease of the joints, is characterized by destruction of the cartilage, and overgrowth, malformation, and impaired function of the bone. Studies suggest that non-steroidal anti-inflammatory drugs (NSAIDs) may influence the disease processes of osteoarthritis by affecting the metabolism of cartilage. The mechanism of NSAID action on cartilage metabolism does not appear to involve inhibition of prostaglandins, fatty acid compounds that may contribute to the disease process. NSAIDs have more effect on osteoarthritic cartilage than normal cartilage, because of better access to the tissue due to increased blood flow and tissue surface area in the osteoarthritic joint. Chondrocytes, or cartilage cells, of the osteoarthritic joint are also more sensitive than cells of the normal joint. Some NSAIDs have been shown to decrease the production of glycosaminoglycans, protein and carbohydrate compounds that contribute to connective tissue structure. Other studies show that NSAIDs can cause specific types of arthropathy or joint disease, characterized by the wearing away of cartilage and bone, a decreased number of osteophytes or bony outgrowths, and retention of joint space. These effects may result from direct toxicity of NSAIDs on osteoarthritic joints. Several studies examining NSAID effects in osteoarthritis have produced inconsistent results, were poorly conducted, and tended to extend data from animal models to human conditions. Thus, well-designed human studies are needed to assess the effectiveness and possible toxicity of NSAIDs in treating osteoarthritis. (Consumer Summary produced by Reliance Medical Information, Inc.)

Joints, Joints (Anatomy), Physiological aspects, Drug therapy, Nonsteroidal anti-inflammatory drugs, Nonsteroidal anti-inflammatory agents, Osteoarthritis, Cartilage

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Rapid development of a tophus following ipsilateral hemiparesis

Article Abstract:

The development of a neurological deficit may cause other types of complications in patients suffering from gout. Gout is an inherited metabolic disorder characterized by recurrent episodes of arthritis and deposition of crystalline sodium urate in different types of tissue. A 85-year-old man with a long history of gout was admitted to the hospital with slight paralysis affecting only the left side of his body. He subsequently developed a large tophus, or a deposit of sodium urate, on his left heel. The development of the tophus occurred over a six-week period and was not accompanied by any type of inflammation. The patient had no prior history of tophi. Tissue damage or trauma associated with the development of paralysis may have triggered the formation of the tophus on the patient's heel.

Complications and side effects, Gout, Paralysis

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Calcium pyrophosphate crystal deposition is not always 'wear and tear' or aging

Article Abstract:

Underlying metabolic and possibly hereditary conditions may cause calcium pyrophosphate dihydrate (CPPD) deposits to develop in joint cartilage giving the appearance of an arthritic condition. CPPD deposits were discovered in two middle-aged patients experiencing joint pain over a period of years. Analysis of liver tissue samples on the 54-year-old male patient revealed an underlying iron imbalance also later found in the patient's sister. Joint fluid tests in the 55-year-old female patient revealed abnormally low magnesium levels. This condition was not identified in any other family members.

Case studies, Joint diseases, Chondrocalcinosis

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