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In 1991, Kenneth D. Brandt, MD, one of the main researchers on NSAIDs’ effect on cartilage wrote, “No clinical evidence exists today, however, to support the contention that NSAIDs favorably influence the progression of joint degeneration in man.”⁷⁰ While this author will not refute this statement, an addition to it is warranted …but much evidence exists that NSAID use accelerates articular cartilage degeneration. This issue is extremely important since 30 billion over-the-counter doses of NSAIDs are sold annually in the United States.⁷¹
 
While the condition known as osteoarthritis has other names, including degenerative joint disease, the name is actually misleading; the words do not accurately describe the pathophysiology of the condition. The term osteoarthritis literally means inflammation of a bony joint but the most common clinical presentation of the condition is one of articular cartilage breakdown without joint swelling, heat, or any other markers of inflammation. The more appropriate term for osteoarthrosis or degenerative joint disease is understood as a non-inflammatory degenerative process. The notion of treating a non-inflammatory condition with an anti-inflammatory medication is bound to have long-term detrimental effects.

At present no quantitative non-invasive method for determining the anabolic (building up) and catabolic (breaking down) activity of NSAIDs on human cartilage in vivo exists.

Most information on the effects of NSAIDs on the turnover of extra-cellular matrix macromolecules comes from short-term organ culture studies. Initial evaluations into the pathophysiology of osteoarthritis concentrated on the effects of NSAIDs on glycosaminoglycan synthesis. It was established that in all but the most severe cases of osteoarthritis, the chondrocyte response to proteoglycan depletion was an increase in glycosaminoglycan synthesis.^{72, 73} One of the first to show that NSAIDs diminished glycosaminoglycan synthesis in aged human cartilage cells (taken during hip surgery) in vitro was a research group from the University of Sydney in 1976.⁷⁴ J.T. Dingle, led several of the follow-up studies on the effects of NSAIDs on human cartilage metabolism. The initial studies revealed significant declines in glycosaminoglycan synthesis in both normal and osteoarthritic human cartilages.⁷⁵ (See Figure 11.) In a follow-up study, the same research group, took femoral head articular cartilage from non-arthritic and osteoarthritic patients post-operatively after total hip replacement. The relative human cartilage metabolism was measured on 245 osteoarthritic patients and 80 normal patients’ cartilage organ cultures subjected to various NSAIDs. The commonly used NSAIDs indomethacin, ibuprofen, and naproxen were shown to significantly inhibit (from 40 to 70%) glycosaminoglycan synthesis in patients’ cartilage.⁷⁶ (See Figure 12.) Notice that paracetamol (acetaminophen or Tylenol) did not inhibit GAG synthesis. The researchers noted that caution must be exercised in extrapolation from in-vitro (lab) to in-vivo (person) effects of NSAIDs, but it seems possible that some highly effective anti-inflammatory agents may produce adverse effects on cartilage integrity when employed during long-term treatment.⁷⁷ Other researchers have confirmed NSAIDs’ inhibitory effect on proteoglycan synthesis and have commented that “…any drug that suppresses proteoglycan synthesis and impairs the ability of the chondrocyte to repair its damaged extracellular matrix, could potentially accelerate the breakdown of the articular tissue.”^{78, 79}