Experimentally induced corticosteroid arthropathy

Moskowitz, Roland W.; Davis, Wirt; Sammarco, James; Mast, William A.; Chase, Samuel W.

doi:10.1002/art.1780130304

Cited by 106 publications

(42 citation statements)

References 8 publications

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“…Such ulceration, when seen, consisted of loss of superficial layers of cartilage over a small area. Fissure formation was seen primarily on the medial tibial plateau and did not exceed that described previously in the normal rabbit knee (6).…”

Section: Histologic Examinationsupporting

confidence: 64%

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Experimentally Induced Degenerative Joint Lesions Following Partial Meniscectomy in the Rabbit

Moskowitz

Davis

Sammarco

et al. 1973

Arthritis & Rheumatism

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212

111

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Degenerative lesions characterized by osteochondrophyte spur formation and cartilage degeneration were induced by partial meniscectomy in the rabbit knee. Cartilage degenerative lesions included ulceration, fissure and cyst formation, and diminished concentration of matrix proteinpolysaccharide. Proliferation of chondrocytes represented efforts at repair. Osteophytes increased in size with time. Changes resembled certain components of degenerative joint disease. The partial meniscectorny animal may be useful in studies of osteoarthritis pathogenesis, pathology and treatment.Degenerative joint changes frequently follow meniscus injury in the human (1,2). In the present study degenerative lesions characterized by osteochondrophyte spur formation and cartilage degeneration were induced by partial meniscectomy in the rabbit knee. Since the pathologic changes observed resemble certain components of degenerative joint disease, the partial meniscectomy animal may be useful in studies of osteoarthritis pathogenesis, pathology and treatment. MATERIALS AND METHODSNew Zealand white rabbits were divided into three groups for study. The animals in the three groups were of relatively similar characteristics with respect to range of weight and to average and median weights (Table 1). Group 1, 82 rabbits, comprised the experimental meniscus surgery model. The rabbits were anesthetized with IV sodium pentothal (Diabutalm, E.L. Squibb and Sons, New York, NY) after which, under sterile surgical conditions, an anteromedial incision was made in the right knee. The soft tissue and retinaculum were incised and reflected medially and laterally. The joint capsule was then incised and the medial compartment of the knee exposed. Using iris scissors, the peripheral attachment of the anterior one-half of the medial meniscus was released and the anterior one-third of the meniscus excised (Figure 1). The capsule and medial retinaculum were closed with three 5-0 catgut sutures and the skin closed with 4-0 silk suture. The operated extremity was placed in a long-leg plaster cylinder cast with the knee and ankle joints maintained at angles of approximately 9W. After 1 week the cast and skin sutures were removed and the animals allowed to move freely in their cages. Sacrifice using intravenous injection of Diabutal was carried out at periodic intervals of 2, 5, 8 and 12 weeks postoperatively ( Table 1). The largest number of animals in the series comprised those sacrificed at 12 weeks, since this became the standard model being used in ongoing experimental studies. The operated knees were carefully dissected and examined for gross changes, Particular note was made of the presence of osteophyte-like spur formation, pitting and ulcerative erosions. Severity of spur formation was graded as follows: mild-spur present and less than 2 mm in maximal width; moderate-spur 2 mm in maximal width: and severespur exceeding 2 mm in maximal width. Ulcers were graded

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Section: Histologic Examinationsupporting

confidence: 64%

“…As in the partial meniscectomy series, changes were noted in femoral cartilage only. Fissure formation on both the femoral and tibial surface did not exceed that seen in normal rabbit knees (6). Diminished Safranin 0 stain was observed on the medial femoral condyle in 2 animals.…”

Section: Proliferation Of Chondrocytes In Clones (mentioning

confidence: 66%

Experimentally Induced Degenerative Joint Lesions Following Partial Meniscectomy in the Rabbit

Moskowitz

Davis

Sammarco

et al. 1973

Arthritis & Rheumatism

Self Cite

212

111

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“…The use of corticosteroids in OA remains controversial due to reports of a possible deleterious effect on cartilage (13)(14)(15). Further studies using an OA model that closely mimics the changes observed in the human disease are needed.…”

Section: Protective Effects O F Corticosteroids On Cartilage Lesions mentioning

confidence: 99%

Protective effects of corticosteroids on cartilage lesions and osteophyte formation in the pond‐nuki dog model of osteoarthritis

Pelletier

Martel‐Pelletier

1989

Arthritis & Rheumatism

147

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The in vivo effects of corticosteroids on osteoarthritic (OA) lesions were examined in 12 dogs in which the anterior cruciate ligament had been sectioned. Six were treated with oral prednisone and 6 were treated with intraarticular (IA) injections of triamciaolone hexacetonide (TH), at surgery and 4 weeks later. Twelve other operated dogs received no treatment. All dogs were killed 8 weeks postsurgery. Four of 15 normal control dogs received IA TH injections. Operated untreated dogs developed significant cartilage lesions on the femoral condyles and tibial plateaus with prominent osteophytes. Operated dogs treated orally or with IA injections had a significant reduction in osteophyte size.Cartilage erosions on femoral condyles were observed in 25% of the untreated dogs, 8% of the dogs receiving oral prednisone, and none of the dogs receiving IA TH. In both groups of treated dogs, the size of the tibial plateau lesions was significantly reduced compared with the operated untreated dogs. Histologically, corticosteroids significantly reduced the severity of OA structural changes of the cartilage on both medial and lateral femoral condyles and tibial plateaus in operated animals, with the exception of the lateral plateaus of those

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“…Clinicians have also used intra-and periarticular corticosteroids for managing inflammation associated with both acute and chronic arthritic diseases [4143]. While these agents reduce expression of matrix metalloproteinases and are clearly helpful in relieving the symptoms of joint inflammation, experimental evidence suggests that corticosteroids damage articular cartilage independent of the disease process [27,35,39,45]. Pathological changes de-* Corresponding author.…”

Section: Introductionmentioning

confidence: 99%

Corticosteroids alter the differentiated phenotype of articular chondrocytes

Fubini

Todhunter

Burton‐Wurster

et al. 2001

Journal Orthopaedic Research

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Experimental evidence suggests that recommended dosages of some corticosteroids used clinically as antiinflammatory agents for treating arthropathies damage articular cartilage, but low dosages may be chondroprotective. The purpose of this study was to evaluate how different concentrations of methylprednisolone affect chondrocyte function and viability. Articular cartilage and chondrocytes were obtained from young adult horses, 1 5 3 . 5 years of age. Corticosteroid-induced changes in collagen expression were studied at the transcriptional level by Northern blot analyses and at the translational level by measuring [3H]-proline incorporation into [3H]-hydroxyproline. Fibronectin mRNA splicing patterns were evaluated with ribonuclease protection assays. Cytotoxicity was studied using erythrosin B dye exclusion. Steady-state levels of type I1 procollagen mRNA decreased without concurrent changes in type I procollagen expression as the medium methylprednisolone concentrations were increased from 1 x lo1 to 1 x 10' pg/ml, dropping below 10% of control values by 1 Y lo5 pg/ml. Cytotoxicity occurred as methylprednisolone levels were increased further from 1 x loR to 1 A lo9 pg/ml. Changes in total collagen (protein) synthesis were less pronounced, but also demonstrated significant suppression between 1 x lo4 and 1 x lo8 pg/ml. Corticosteroid-induced changes in fibronectin isoform levels were evaluated in articular cartilage samples without in vitro culture. The cartilage-specific (V + C)-isoform was suppressed in both normal and inflamed joints by a single intraarticular injection (0.1 mg/kg) of methylprednisolone. Combined, these data indicate that methylprednisolone suppresses matrix protein markers of chondrocytic differentiation. Decreased and altered chondrocyte expression of matrix proteins likely contributes to the pathogenesis of corticosteroid-induced cartilage degeneration.

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Experimentally induced corticosteroid arthropathy

Cited by 106 publications

References 8 publications

Experimentally Induced Degenerative Joint Lesions Following Partial Meniscectomy in the Rabbit

Experimentally Induced Degenerative Joint Lesions Following Partial Meniscectomy in the Rabbit

Protective effects of corticosteroids on cartilage lesions and osteophyte formation in the pond‐nuki dog model of osteoarthritis

Corticosteroids alter the differentiated phenotype of articular chondrocytes

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