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      Method for Delivering a Controlled Impact to Articular Cartilage in the Rabbit Knee

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          Abstract

          Objective:

          The authors aimed to develop a mechanical model for delivering controlled impact injuries to an articular cartilage surface, with the ability to control peak contact pressure while maintaining a constant rate of loading across all impact levels.

          Methods:

          A pendulum-style impactor with a direct contact interface was fabricated, based on previously published successful models. This impactor was tested in 2 separate experiments: first with a single analog specimen and next with 15 cadaveric rabbit knee specimens. In both experiments, impacts were performed at 3 pressure levels with multiple repetitions. Peak pressure, rate of pressure application, impulse, and time to peak were evaluated.

          Results:

          There was a significant difference between each of the pressure level groups for both the analog and cadaveric experiments. There was no significant difference between the rates of pressure application for the analog specimen and a statistically significant difference only between the highest and lowest pressure level groups for the cadaveric specimen.

          Conclusions:

          Previous studies have shown that peak pressure and rate of pressure application are both significant contributors to cartilage injury. Previous models have controlled only peak contact pressure, allowing rate of loading to change as a function of peak contact pressure. This model is the first to control both variables, with a rate of pressure application that is typical of an athletic or traumatic injury in humans. Use of this model will enable researchers to investigate the isolated effects of peak pressure on progressive cartilage injuries.

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          Most cited references10

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          Glucosamine sulfate use and delay of progression of knee osteoarthritis: a 3-year, randomized, placebo-controlled, double-blind study.

          Conventional symptomatic treatments for osteoarthritis do not favorably affect disease progression. The aim of this randomized, placebo-controlled trial was to determine whether long-term (3-year) treatment with glucosamine sulfate can modify the progression of joint structure and symptom changes in knee osteoarthritis, as previously suggested. Two hundred two patients with knee osteoarthritis (using American College of Rheumatology criteria) were randomized to receive oral glucosamine sulfate, 1500 mg once a day, or placebo. Changes in radiographic minimum joint space width were measured in the medial compartment of the tibiofemoral joint, and symptoms were assessed using the algo-functional indexes of Lequesne and WOMAC (Western Ontario and McMaster Universities). Osteoarthritis was of mild to moderate severity at enrollment, with average joint space widths of slightly less than 4 mm and a Lequesne index score of less than 9 points. Progressive joint space narrowing with placebo use was -0.19 mm (95% confidence interval, -0.29 to -0.09 mm) after 3 years. Conversely, there was no average change with glucosamine sulfate use (0.04 mm; 95% confidence interval, -0.06 to 0.14 mm), with a significant difference between groups (P =.001). Fewer patients treated with glucosamine sulfate experienced predefined severe narrowings (>0.5 mm): 5% vs 14% (P =.05). Symptoms improved modestly with placebo use but as much as 20% to 25% with glucosamine sulfate use, with significant final differences on the Lequesne index and the WOMAC total index and pain, function, and stiffness subscales. Safety was good and without differences between groups. Long-term treatment with glucosamine sulfate retarded the progression of knee osteoarthritis, possibly determining disease modification.
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            Hyaluronans in the treatment of osteoarthritis of the knee: evidence for disease-modifying activity.

            Although available nonsurgical pharmacotherapies for treatment of osteoarthritis (OA) are considered to be solely symptom-modifying agents, recent advances have been made in the search for agents that may modify disease progression. Intra-articular hyaluronan (HA) therapy is one symptom-modifying approach that has been found to be safe and effective for reducing pain due to OA of the knee. Presented here is a review of the evidence that HAs may also modify the rate of OA disease progression in addition to providing symptomatic efficacy. A review of the literature based on a MEDLINE search through June 2004, using the terms HA, sodium hyaluronate, hyaluronic acid, hylan, hylan G-F 20, OA, disease modification, structure modifying and joint structure. Evidence for disease-modifying activity of HAs stems from 1) the complex biochemical effects of HAs in the synovium and extracellular matrix of the articular cartilage, including interactions between exogenously administered HA and articular cartilage, subchondral bone, matrix proteoglycans, and collagens; 2) the effects of HA administration in animal models of OA, including total or partial meniscectomy and anterior cruciate ligament transectomy; 3) results of clinical trials using one HA, Hyalgan (sodium hyaluronate, molecular weight 500-730 kDa) that evaluated structural outcomes, such as joint-space width, chondrocyte density and vitality, and arthroscopic evaluation of chondropathy. Growing preclinical and clinical evidence supports the notion that, in addition to relieving the symptoms of OA, HAs also modify the structure of the diseased joint and the rate of OA disease progression, at least early in the evolution of the disease process.
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              Survival of articular cartilage after controlled impact.

              Survival characteristics of forty-three specimens of living human bone and articular cartilage from the knees of eight renal-transplant donors were studied, using a drop-tower device. Autoradiography and light and scanning electron microscopy revealed no evidence of chondrocyte death or structural damage until stress levels of twenty-five newtons per square millimeter were reached, corresponding to strains on the order of 20 to 30 per cent and involving energy absorption of one millijoule per cubic millimeter. The data for strain rates of 500 and 1000 s-1 suggest that impact loads sufficient to fracture a femoral shaft of an automobile occupant are nearly sufficient to cause chondrocyte death and fissuring in the articular cartilage of either the knee or the hip if the load-bearing areas measure less than 500 square millimeters.
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                Author and article information

                Journal
                Cartilage
                Cartilage
                CAR
                spcar
                Cartilage
                SAGE Publications (Sage CA: Los Angeles, CA )
                1947-6035
                1947-6043
                July 2010
                July 2010
                : 1
                : 3
                : 211-216
                Affiliations
                [1 ]Department of Orthopaedic Surgery, Orthopaedic and Rheumatologic Institute, Cleveland Clinic, Cleveland, OH, USA
                [2 ]Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA
                [3 ]Department of Orthopaedic Surgery, Henry Ford Health System, Detroit, MI, USA
                [4 ]Premier Orthopaedics and Sports Medicine, Nashville, TN, USA
                Author notes
                [*]Morgan H. Jones, MD, Department of Orthopaedic Surgery, Orthopaedic and Rheumatologic Institute, Cleveland Clinic, 9500 Euclid Ave/ND20, Cleveland, OH 44195, USA Email: jonesm7@ 123456ccf.org
                Article
                10.1177_1947603510363006
                10.1177/1947603510363006
                4297073
                0485bab0-a2bc-4edb-864c-e7da70cafcb7
                © The Author(s) 2010
                History
                Categories
                Original Articles

                animal models,biomechanics,articular cartilage,posttraumatic arthritis,knee

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