The Experts below are selected from a list of 35085 Experts worldwide ranked by ideXlab platform
Ewa M Roos - One of the best experts on this subject based on the ideXlab platform.
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a pragmatic approach to prevent post traumatic osteoarthritis after sport or exercise related Joint Injury
Best Practice & Research: Clinical Rheumatology, 2019Co-Authors: Jackie L Whittaker, Ewa M RoosAbstract:Lower extremity musculoskeletal injuries are common in sport and exercise, and associated with increased risk of obesity and post-traumatic osteoarthritis (PTOA). Unlike other forms of osteoarthritis, PTOA is common at a younger age and associated with more rapid progression, which may impact career choices, long-term general health and reduce quality of life. Individuals who suffer an activity-related Joint Injury and present with abnormal Joint morphology, elevated adiposity, weak musculature, or become physically inactive are at increased risk of PTOA. Insufficient exercise therapy or incomplete rehabilitation, premature return-to-sport and re-Injury, unrealistic expectations, or poor nutrition may further elevate this risk. Delay in surgical interventions in lieu of exercise therapy to optimize muscle strength and neuromuscular control while addressing fear of movement to guarantee resumption of physical activity, completeness of rehabilitation before return-to-sport, education that promotes realistic expectations and self-management, and nutritional counseling are the best approaches for delaying or preventing PTOA.
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Joint Injury causes knee osteoarthritis in young adults
Current opinion in rheumatology, 2005Co-Authors: Ewa M RoosAbstract:Purpose of reviewThis review presents recent data on Joint Injury as the cause of osteoarthritis development in young adults and proposes and discusses a model that highlights how Joint Injury and other risk factors may contribute to osteoarthritis development through two different pathways: Joint-r
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The Knee Injury and Osteoarthritis Outcome Score (KOOS): From Joint Injury to osteoarthritis
Health and Quality of Life Outcomes, 2003Co-Authors: Ewa M Roos, L. Stefan LohmanderAbstract:The Knee Injury and Osteoarthritis Outcome Score (KOOS) was developed as an extension of the WOMAC Osteoarthritis Index with the purpose of evaluating short-term and long-term symptoms and function in subjects with knee Injury and osteoarthritis. The KOOS holds five separately scored subscales: Pain, other Symptoms, Function in daily living (ADL), Function in Sport and Recreation (Sport/Rec), and knee-related Quality of Life (QOL). The KOOS has been validated for several orthopaedic interventions such as anterior cruciate ligament reconstruction, meniscectomy and total knee replacement. In addition the instrument has been used to evaluate physical therapy, nutritional supplementation and glucosamine supplementation. The effect size is generally largest for the subscale QOL followed by the subscale Pain. The KOOS is a valid, reliable and responsive self-administered instrument that can be used for short-term and long-term follow-up of several types of knee Injury including osteoarthritis. The measure is relatively new and further use of the instrument will add knowledge and suggest areas that need to be further explored and improved.
Joseph A Buckwalter - One of the best experts on this subject based on the ideXlab platform.
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closing the gap between bench and bedside research for early arthritis therapies earth report from the aossm nih u 13 post Joint Injury osteoarthritis conference ii
American Journal of Sports Medicine, 2011Co-Authors: Constance R Chu, Joseph A Buckwalter, Bruce D Beynnon, William E Garrett, Jeffrey N Katz, Scott A Rodeo, Kurt P Spindler, Robert A StantonAbstract:This report summarizes the 2010 AOSSM/NIH (American Orthopaedic Society for Sports Medicine/National Institutes of Health) U13 Post–Joint Injury Osteoarthritis II Conference to include the discussion concerning potential study cohorts, assessment considerations, and research priorities. There was strong consensus and enthusiasm for approaching the development of disease-modifying treatments for osteoarthritis through study of “pre-osteoarthritic” cohorts, particularly human subjects under 30 years of age following acute anterior cruciate ligament injuries. Clinical study of acute treatment strategies initiated within a few days after Injury will need development of recruitment pathways and short-term proof-of-concept outcome measures that are specific to the intervention being studied. For example, measures of Joint inflammation can be used in short-term prospective randomized controlled trials to determine whether an anti-inflammatory intervention was effective in decreasing early inflammation. These sho...
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Joint Injury, repair, and remodeling: roles in post-traumatic osteoarthritis
Clinical orthopaedics and related research, 2004Co-Authors: Joseph A Buckwalter, Thomas D. BrownAbstract:Joint injuries, especially intraarticular fractures, frequently lead to progressive Joint degeneration that causes the clinical syndrome of posttraumatic osteoarthritis. Orthopaedists try to prevent this disease by attempting to restore Joint congruity, alignment, and stability; however, many patients have crippling Joint pain and dysfunction develop despite optimal current treatment. The pathophysiology of posttraumatic osteoarthritis has not been explained. It is not simply the magnitude and type of Injury that determines whether an injured articular surface will repair and remodel or undergo progressive degeneration. For these reasons, clinically significant progress in preventing posttraumatic osteoarthritis depends on advances in understanding of the pathogenesis of this disease that will make it possible to decrease the risk of articular surface degeneration and facilitate articular surface repair and remodeling. We examine the relationships between Joint Injury, repair and remodeling, and Joint degeneration; the factors that increase the risk of posttraumatic Joint degeneration; and, the questions that need additional investigation to develop treatments of Joint injuries that will decrease the risk or severity of posttraumatic osteoarthritis.
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Joint Injury, repair, and remodeling: Roles in post-traumatic osteoarthritis : Symposium
Clinical Orthopaedics and Related Research, 2004Co-Authors: Joseph A Buckwalter, Thomas D. BrownAbstract:Joint injuries, especially intraarticular fractures, frequently lead to progressive Joint degeneration that causes the clinical syndrome of posttraumatic osteoarthritis. Orthopaedists try to prevent this disease by attempting to restore Joint congruity, alignment, and stability; however, many patients have crippling Joint pain and dysfunction develop despite optimal current treatment. The pathophysiology of posttraumatic osteoarthritis has not been explained. It is not simply the magnitude and type of Injury that determines whether an injured articular surface will repair and remodel or undergo progressive degeneration. For these reasons, clinically significant progress in preventing posttraumatic osteoarthritis depends on advances in understanding of the pathogenesis of this disease that will make it possible to decrease the risk of articular surface degeneration and facilitate articular surface repair and remodeling. We examine the relationships between Joint Injury, repair and remodeling, and Joint degeneration; the factors that increase the risk of posttraumatic Joint degeneration; and, the questions that need additional investigation to develop treatments of Joint injuries that will decrease the risk or severity of posttraumatic osteoarthritis.
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Sports, Joint Injury, and posttraumatic osteoarthritis.
The Journal of orthopaedic and sports physical therapy, 2003Co-Authors: Joseph A BuckwalterAbstract:Participation in sports increases the risk of Joint injuries that can lead to posttraumatic osteoarthritis, a clinical syndrome caused by trauma-initiated Joint degeneration that results in permanent and often progressive Joint pain and dysfunction. Minimizing the risk of Joint injuries and helping people with osteoarthritis participate in regular physical activity, including some sports, requires understanding of the relationships between Joint use, Joint Injury, and Joint degeneration. Lifelong participation in sports that cause minimal Joint impact and torsional loading by individuals with normal Joints and neuromuscular function does not increase the risk of posttraumatic osteoarthritis. In contrast, participation in sports that subject Joints to high levels of impact and torsional loading increases the risk of Joint Injury and subsequent Joint degeneration. Immediate diagnosis and appropriate treatment and rehabilitation following Joint injuries decrease the risk of subsequent injuries and posttrauma...
Farshid Guilak - One of the best experts on this subject based on the ideXlab platform.
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dietary fatty acid content regulates wound repair and the pathogenesis of osteoarthritis following Joint Injury
Annals of the Rheumatic Diseases, 2015Co-Authors: Deeptee Jain, Janet L Huebner, Virginia B Kraus, Jenna Mcneill, Dianne Little, John A Anderson, Ramona M Rodriguiz, William C Wetsel, Farshid GuilakAbstract:Objective The mechanisms linking obesity and osteoarthritis (OA) are not fully understood and have been generally attributed to increased weight, rather than metabolic or inflammatory factors. Here, we examined the influence of fatty acids, adipokines, and body weight on OA following Joint Injury in an obese mouse model. Methods Mice were fed high-fat diets rich in various fatty acids (FA) including saturated FAs (SFAs), ω-6 polyunsaturated FAs (PUFAs), and ω-3 PUFAs. OA was induced by destabilising the medial meniscus. Wound healing was evaluated using an ear punch. OA, synovitis and wound healing were determined histologically, while bone changes were measured using microCT. Activity levels and serum cytokines were measured at various time-points. Multivariate models were performed to elucidate the associations of dietary, metabolic and mechanical factors with OA and wound healing. Results Using weight-matched mice and multivariate models, we found that OA was significantly associated with dietary fatty acid content and serum adipokine levels, but not with body weight. Furthermore, spontaneous activity of the mice was independent of OA development. Small amounts of ω-3 PUFAs (8% by kcal) in a high-fat diet were sufficient to mitigate Injury-induced OA, decreasing leptin and resistin levels. ω-3 PUFAs significantly enhanced wound repair, SFAs or ω-6 PUFAs independently increased OA severity, heterotopic ossification and scar tissue formation. Conclusions Our results indicate that with obesity, dietary FA content regulates wound healing and OA severity following Joint Injury, independent of body weight, supporting the need for further studies of dietary FA supplements as a potential therapeutic approach for OA.
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therapeutic opportunities to prevent post traumatic arthritis lessons from the natural history of arthritis after articular fracture
Journal of Orthopaedic Research, 2015Co-Authors: Steven A Olson, Bridgette D Furman, Janet L Huebner, Virginia B Kraus, Farshid GuilakAbstract:An estimated 12% of patients seeking surgical intervention for symptomatic arthritis have an etiology of post-traumatic arthritis (PTA). The onset of PTA is rapid in the setting of articular fracture (AF). The investigation began with development of a murine model of a closed AF that develops PTA. In the process of characterizing this model a technique was developed for assessing quantitative synovial fluid biomarker concentrations. The work began with observations of the natural history of PTA development in the C57BL/6 strain of mice. A species of mice (MRL/MpJ) was found that is protected from PTA after AF. Further work identified key differences between mouse strains that did and did not develop PTA. This knowledge led to an intervention based on anti-cytokine (interleukin 1 receptor antagonist, (IL-1Ra) delivery in the C57BL/6 strain of mice that successfully prevented PTA following AF. This success in preventing PTA in the murine model has elucidated several important clinical implications: 1) Pro-inflammatory cytokines play an important role in the development of PTA after Joint Injury, 2) Pharmacologic intervention can lessen the severity of PTA after an AF, and 3) The murine AF model of Joint Injury provides a novel means of studying mechanisms of PTA development.
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targeting pro inflammatory cytokines following Joint Injury acute intra articular inhibition of interleukin 1 following knee Injury prevents post traumatic arthritis
Arthritis Research & Therapy, 2014Co-Authors: Bridgette D Furman, Daniel S Mangiapani, Evan Zeitler, Karsyn N Bailey, Phillip H Horne, Janet L Huebner, Virginia B Kraus, Farshid Guilak, Steven A OlsonAbstract:Introduction: Post-traumatic arthritis (PTA) is a progressive, degenerative response to Joint Injury, such as articular fracture. The pro-inflammatory cytokines, interleukin 1(IL-1) and tumor necrosis factor alpha (TNF-α), are acutely elevated following Joint Injury and remain elevated for prolonged periods post-Injury. To investigate the role of local and systemic inflammation in the development of post-traumatic arthritis, we targeted both the initial acute local inflammatory response and a prolonged 4 week systemic inflammatory response by inhibiting IL-1 or TNF-α following articular fracture in the mouse knee. Methods: Anti-cytokine agents, IL-1 receptor antagonist (IL-1Ra) or soluble TNF receptor II (sTNFRII), were administered either locally via an acute intra-articular injection or systemically for a prolonged 4 week period following articular fracture of the knee in C57BL/6 mice. The severity of arthritis was then assessed at 8 weeks post-Injury in Joint tissues via histology and micro computed tomography, and systemic and local biomarkers were assessed in serum and synovial fluid. Results: Intra-articular inhibition of IL-1 significantly reduced cartilage degeneration, synovial inflammation, and did not alter bone morphology following articular fracture. However, systemic inhibition of IL-1, and local or systemic inhibition of TNF provided no benefit or conversely led to increased arthritic changes in the Joint tissues. Conclusion: These results show that intra-articular IL-1, rather than TNF-α, plays a critical role in the acute inflammatory phase of Joint Injury and can be inhibited locally to reduce post-traumatic arthritis following a closed articular fracture. Targeted local inhibition of IL-1 following Joint Injury may represent a novel treatment option for PTA.
Thomas D. Brown - One of the best experts on this subject based on the ideXlab platform.
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Joint Injury, repair, and remodeling: Roles in post-traumatic osteoarthritis : Symposium
Clinical Orthopaedics and Related Research, 2004Co-Authors: Joseph A Buckwalter, Thomas D. BrownAbstract:Joint injuries, especially intraarticular fractures, frequently lead to progressive Joint degeneration that causes the clinical syndrome of posttraumatic osteoarthritis. Orthopaedists try to prevent this disease by attempting to restore Joint congruity, alignment, and stability; however, many patients have crippling Joint pain and dysfunction develop despite optimal current treatment. The pathophysiology of posttraumatic osteoarthritis has not been explained. It is not simply the magnitude and type of Injury that determines whether an injured articular surface will repair and remodel or undergo progressive degeneration. For these reasons, clinically significant progress in preventing posttraumatic osteoarthritis depends on advances in understanding of the pathogenesis of this disease that will make it possible to decrease the risk of articular surface degeneration and facilitate articular surface repair and remodeling. We examine the relationships between Joint Injury, repair and remodeling, and Joint degeneration; the factors that increase the risk of posttraumatic Joint degeneration; and, the questions that need additional investigation to develop treatments of Joint injuries that will decrease the risk or severity of posttraumatic osteoarthritis.
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Joint Injury, repair, and remodeling: roles in post-traumatic osteoarthritis
Clinical orthopaedics and related research, 2004Co-Authors: Joseph A Buckwalter, Thomas D. BrownAbstract:Joint injuries, especially intraarticular fractures, frequently lead to progressive Joint degeneration that causes the clinical syndrome of posttraumatic osteoarthritis. Orthopaedists try to prevent this disease by attempting to restore Joint congruity, alignment, and stability; however, many patients have crippling Joint pain and dysfunction develop despite optimal current treatment. The pathophysiology of posttraumatic osteoarthritis has not been explained. It is not simply the magnitude and type of Injury that determines whether an injured articular surface will repair and remodel or undergo progressive degeneration. For these reasons, clinically significant progress in preventing posttraumatic osteoarthritis depends on advances in understanding of the pathogenesis of this disease that will make it possible to decrease the risk of articular surface degeneration and facilitate articular surface repair and remodeling. We examine the relationships between Joint Injury, repair and remodeling, and Joint degeneration; the factors that increase the risk of posttraumatic Joint degeneration; and, the questions that need additional investigation to develop treatments of Joint injuries that will decrease the risk or severity of posttraumatic osteoarthritis.
Virginia B Kraus - One of the best experts on this subject based on the ideXlab platform.
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dietary fatty acid content regulates wound repair and the pathogenesis of osteoarthritis following Joint Injury
Annals of the Rheumatic Diseases, 2015Co-Authors: Deeptee Jain, Janet L Huebner, Virginia B Kraus, Jenna Mcneill, Dianne Little, John A Anderson, Ramona M Rodriguiz, William C Wetsel, Farshid GuilakAbstract:Objective The mechanisms linking obesity and osteoarthritis (OA) are not fully understood and have been generally attributed to increased weight, rather than metabolic or inflammatory factors. Here, we examined the influence of fatty acids, adipokines, and body weight on OA following Joint Injury in an obese mouse model. Methods Mice were fed high-fat diets rich in various fatty acids (FA) including saturated FAs (SFAs), ω-6 polyunsaturated FAs (PUFAs), and ω-3 PUFAs. OA was induced by destabilising the medial meniscus. Wound healing was evaluated using an ear punch. OA, synovitis and wound healing were determined histologically, while bone changes were measured using microCT. Activity levels and serum cytokines were measured at various time-points. Multivariate models were performed to elucidate the associations of dietary, metabolic and mechanical factors with OA and wound healing. Results Using weight-matched mice and multivariate models, we found that OA was significantly associated with dietary fatty acid content and serum adipokine levels, but not with body weight. Furthermore, spontaneous activity of the mice was independent of OA development. Small amounts of ω-3 PUFAs (8% by kcal) in a high-fat diet were sufficient to mitigate Injury-induced OA, decreasing leptin and resistin levels. ω-3 PUFAs significantly enhanced wound repair, SFAs or ω-6 PUFAs independently increased OA severity, heterotopic ossification and scar tissue formation. Conclusions Our results indicate that with obesity, dietary FA content regulates wound healing and OA severity following Joint Injury, independent of body weight, supporting the need for further studies of dietary FA supplements as a potential therapeutic approach for OA.
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therapeutic opportunities to prevent post traumatic arthritis lessons from the natural history of arthritis after articular fracture
Journal of Orthopaedic Research, 2015Co-Authors: Steven A Olson, Bridgette D Furman, Janet L Huebner, Virginia B Kraus, Farshid GuilakAbstract:An estimated 12% of patients seeking surgical intervention for symptomatic arthritis have an etiology of post-traumatic arthritis (PTA). The onset of PTA is rapid in the setting of articular fracture (AF). The investigation began with development of a murine model of a closed AF that develops PTA. In the process of characterizing this model a technique was developed for assessing quantitative synovial fluid biomarker concentrations. The work began with observations of the natural history of PTA development in the C57BL/6 strain of mice. A species of mice (MRL/MpJ) was found that is protected from PTA after AF. Further work identified key differences between mouse strains that did and did not develop PTA. This knowledge led to an intervention based on anti-cytokine (interleukin 1 receptor antagonist, (IL-1Ra) delivery in the C57BL/6 strain of mice that successfully prevented PTA following AF. This success in preventing PTA in the murine model has elucidated several important clinical implications: 1) Pro-inflammatory cytokines play an important role in the development of PTA after Joint Injury, 2) Pharmacologic intervention can lessen the severity of PTA after an AF, and 3) The murine AF model of Joint Injury provides a novel means of studying mechanisms of PTA development.
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targeting pro inflammatory cytokines following Joint Injury acute intra articular inhibition of interleukin 1 following knee Injury prevents post traumatic arthritis
Arthritis Research & Therapy, 2014Co-Authors: Bridgette D Furman, Daniel S Mangiapani, Evan Zeitler, Karsyn N Bailey, Phillip H Horne, Janet L Huebner, Virginia B Kraus, Farshid Guilak, Steven A OlsonAbstract:Introduction: Post-traumatic arthritis (PTA) is a progressive, degenerative response to Joint Injury, such as articular fracture. The pro-inflammatory cytokines, interleukin 1(IL-1) and tumor necrosis factor alpha (TNF-α), are acutely elevated following Joint Injury and remain elevated for prolonged periods post-Injury. To investigate the role of local and systemic inflammation in the development of post-traumatic arthritis, we targeted both the initial acute local inflammatory response and a prolonged 4 week systemic inflammatory response by inhibiting IL-1 or TNF-α following articular fracture in the mouse knee. Methods: Anti-cytokine agents, IL-1 receptor antagonist (IL-1Ra) or soluble TNF receptor II (sTNFRII), were administered either locally via an acute intra-articular injection or systemically for a prolonged 4 week period following articular fracture of the knee in C57BL/6 mice. The severity of arthritis was then assessed at 8 weeks post-Injury in Joint tissues via histology and micro computed tomography, and systemic and local biomarkers were assessed in serum and synovial fluid. Results: Intra-articular inhibition of IL-1 significantly reduced cartilage degeneration, synovial inflammation, and did not alter bone morphology following articular fracture. However, systemic inhibition of IL-1, and local or systemic inhibition of TNF provided no benefit or conversely led to increased arthritic changes in the Joint tissues. Conclusion: These results show that intra-articular IL-1, rather than TNF-α, plays a critical role in the acute inflammatory phase of Joint Injury and can be inhibited locally to reduce post-traumatic arthritis following a closed articular fracture. Targeted local inhibition of IL-1 following Joint Injury may represent a novel treatment option for PTA.
