Effect of piroxicam on structure and function of joint cartilage

Mohr, W.; Kirkpatrick, Charles James; Wildfeuer, A; Leitold, M

doi:10.1007/bf00915722

Cited by 10 publications

(4 citation statements)

References 19 publications

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“…For instance, indomethacin has been reported to induce and aggravate degenerative changes in the joints of chicken (15), mice (10) and Man (13-14) but seems not to affect the cartilage cells of dogs (12). Piroxicam has been found to reduce the prevalence of spontaneous osteoarthritis in Cs7-Black mice (10) and increased chondrocyte metabolism in Wistar rats (17), but apparently had no effect on canine (12), porcine (8) or rabbit cartilage (16).…”

Section: Introductionmentioning

confidence: 99%

Proteoglycan Metabolism in Tissue-cultured Human Articular Cartilage: Influence of Niflumic Acid

Verbruggen

Veys

Malfait

et al. 1990

Scandinavian Journal of Rheumatology

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Proteoglycan metabolism was investigated in tissue-cultured human cartilage. Normal cartilage obtained from a normal joint showed improving accumulation rates for 35S-labelled proteoglycans over a 3-6 weeks' period. The loss of newly synthesized molecules in the nutrient media was low and constant throughout culture. A decrease in accumulation of 35S-proteoglycan was observed in visually intact cartilage from joints showing foci of osteoarthrosis. This decrease was more pronounced in fibrillated cartilage. No clear effect on proteoglycan metabolism was observed when normal cartilage samples from the normal joint were incubated for several weeks in a nutrient medium containing niflumic acid. However, the cartilage samples from this donor tended to retain more proteoglycan aggregates in the intercellular matrix after a 6-weeks culture period in the presence of this NSAID. When niflumic acid was added to the incubation media of visually intact samples from pathological joints, significantly more newly synthesized proteoglycans were retained in the intercellular matrix. The effect was also observed and was more pronounced in the fibrillated cartilage samples.

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Section: Introductionmentioning

confidence: 99%

Proteoglycan Metabolism in Tissue-cultured Human Articular Cartilage: Influence of Niflumic Acid

Verbruggen

Veys

Malfait

et al. 1990

Scandinavian Journal of Rheumatology

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“…Experimental in vivo studies, examining the effects of NSAID on cartilage, demonstrated differences in cartilage structure and metabolism after exposure to the drug from between four and eight weeks (19,21,24,27,28,30). The patients in our study were treated with carprofen for an average of three months with a median treatment time of two months and a minimum of one month.…”

Section: Discussionmentioning

confidence: 75%

Histological features of osteoarthritic canine cartilage after prolonged administration of carprofen

Dassler

Griffey

Vasseur

2003

Vet Comp Orthop Traumatol

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SummaryThe objective of this study was to determine whether the non-steroidal anti-inflammatory drug (NSAID) carprofen causes adverse histological changes to cartilage after prolonged administration for treatment of naturally acquired osteoarthritis.Dogs diagnosed with cranial cruciate ligament rupture and secondary osteoarthritis of their stifle joints were divided into two groups: those who had received a standard dose of carprofen for a minimum of four weeks and those who had not received a NSAID for a minimum of one month. Cartilage from the intercondylar notch was obtained when the patients underwent surgical procedures to stabilize the stifle joint. The samples were processed and evaluated for histological differences using haematoxylin and eosin and safranin-O-fast green-iron haematoxylin stains and were graded according to a Mankin scale (graded 0-14) for osteoarthritis.The histopathological findings were variable and included loss of matrix staining, irregularities to the cartilage surface, matrix fragmentation, chondrocyte clustering, matrix degeneration and vascular and synovial invasion (pannus) and were not specific to either group. There was not any significant difference between study groups (p = 0.2721) according to the Wilcoxan rank sum test.

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“…Furthermore, long-term (2-year) in vivo stud ies conducted in OA in rats and mice have classified meloxicam aschondroneutral [29], Studies conducted on other NSAIDs have shown variable effects on chondroformation and PGEt formation that seem to be in fluenced by the animal species and experi mental models used [26, 30. 31], Piroxicam, which, like meloxicam, is derived from enolic acid, had no effect on proteoglycan synthesis in chondrocytes isolated from rabbit shoulder cartilage [12,32], or in porcine [32] or dog articular cartilage [26], Similarly, piroxicam did not affect proteoglycan metabolism in iso lated and monolayer cultured chondrocytes, and the synthetic activity or quality of proteo glycans was unaffected by the presence of piroxicam in the test system [33], However, other studies have shown that NSAIDs, such as acetylsalicylatc [ 10,28.32] and indomethacin [34], may depress proteoglycan synthesis in articular cartilage of OA patients. Further more, it has been observed that indomethacin adversely affects disease progression in pa tients with OA hip joints [31,[35][36][37], Others, such as piroxicam [26], have shown no appre ciable effect on proteoglycan synthesis in nor mal cartilage [ 13,32,33].…”

Section: Discussionmentioning

confidence: 99%

“…In addition to gastrointestinal and renal tolerability problems, often associated with NSAID use, some NSAIDs have also been shown to affect cartilage synthesis negatively [9][10][11][12]. In particular, the effect of NSAIDs on proteoglycan synthesis by chondrocytes has been investigated.…”

Section: Introductionmentioning

confidence: 99%

Effects of Meloxicam Compared to Acetylsalicylic Acid in Human Articular Chondrocytes

Bassleer

J²,

Geenen³

et al. 1997

Pharmacology

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Meloxicam is a new nonsteroidal anti-inflammatory drug (NSAID) derived from enolic acid, which has displayed potent anti-inflammatory properties in animal studies combined with low gastrointestinal toxicity. Other NSAIDs have been shown, in vitro, to have a variety of effects on cartilage repair processes in diseased articular cartilage. The aim of this study was to ascertain the effects of meloxicam on some of these processes using in vitro models. Acetylsalicylic acid, a NSAID whose characteristics have been previously elucidated in the models, was used as an active comparator. The effects of meloxicam were different from those of acetylsalicylic acid on chondrocyte clusters. At pharmacologically active concentrations, meloxicam was a potent inhibitor of prostaglandin-E₂ production. However, all chondroformative processes were unaffected by meloxicam as indicated by a lack of effect on DNA synthesis and on type-II collagen and proteoglycan levels in chondrocyte culture medium and clusters, while acetylsalicylic acid decreased proteoglycan production and cell proliferation. Consequently, these in vitro findings suggest that meloxicam does not adversely affect the reparative processes active within the cartilage matrix of a diseased joint. This study represents a sound basis for future studies to establish the effects of meloxicam on osteoarthritis disease progression.

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Effect of piroxicam on structure and function of joint cartilage

Cited by 10 publications

References 19 publications

Proteoglycan Metabolism in Tissue-cultured Human Articular Cartilage: Influence of Niflumic Acid

Proteoglycan Metabolism in Tissue-cultured Human Articular Cartilage: Influence of Niflumic Acid

Histological features of osteoarthritic canine cartilage after prolonged administration of carprofen

Effects of Meloxicam Compared to Acetylsalicylic Acid in Human Articular Chondrocytes

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