Post-traumatic arthritis: overview on pathogenic mechanisms and role of inflammation.

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Abstract

Post-traumatic arthritis (PTA) develops after an acute direct trauma to the joints. PTA causes about 12% of all osteoarthritis cases, and a history of physical trauma may also be found in patients with chronic inflammatory arthritis. Symptoms include swelling, synovial effusion, pain and sometimes intra-articular bleeding. Usually, PTA recoveries spontaneously, but the persistence of symptoms after 6 months may be considered pathological and so-called chronic PTA. A variety of molecular, mechanobiological and cellular events involved in the pathogenesis and the progression of PTA have been identified. The activation of inflammatory mechanisms during the PTA acute phase appears to play a critical role in the chronic disease onset. Human studies and experimental models have revealed that a series of inflammatory mediators are released in synovial fluid immediately after the joint trauma. These molecules have been proposed as markers of disease and as a potential target for the development of specific and preventative interventions. Currently, chronic PTA cannot be prevented, although a large number of agents have been tested in preclinical studies. Given the relevance of inflammatory reaction, anticytokines therapy, in particular the inhibition of interleukin 1 (IL-1), seems to be the most promising strategy. At the present time, intra-articular injection of IL-1 receptor antagonist is the only anticytokine approach that has been used in a human study of PTA. Despite the fact that knowledge in this area has increased in the past years, the identification of more specific disease markers and new therapeutic opportunities are needed.

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Inflammation in joint injury and post-traumatic osteoarthritis.

Jason Lieberthal, Nisha Sambamurthy, Carla R Scanzello (2015)

Inflammation is a variable feature of osteoarthritis (OA), associated with joint symptoms and progression of disease. Signs of inflammation can be observed in joint fluids and tissues from patients with joint injuries at risk for development of post-traumatic osteoarthritis (PTOA). Furthermore, inflammatory mechanisms are hypothesized to contribute to the risk of OA development and progression after injury. Animal models of PTOA have been instrumental in understanding factors and mechanisms involved in chronic progressive cartilage degradation observed after a predisposing injury. Specific aspects of inflammation observed in humans, including cytokine and chemokine production, synovial reaction, cellular infiltration and inflammatory pathway activation, are also observed in models of PTOA. Many of these models are now being utilized to understand the impact of post-injury inflammatory response on PTOA development and progression, including risk of progressive cartilage degeneration and development of chronic symptoms post-injury. As evidenced from these models, a vigorous inflammatory response occurs very early after joint injury but is then sustained at a lower level at the later phases. This early inflammatory response contributes to the development of PTOA features including cartilage erosion and is potentially modifiable, but specific mediators may also play a role in tissue repair. Although the optimal approach and timing of anti-inflammatory interventions after joint injury are yet to be determined, this body of work should provide hope for the future of disease modification tin PTOA.

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Post-traumatic osteoarthritis: improved understanding and opportunities for early intervention.

Donald Anderson, Susan Chubinskaya, Farshid Guilak … (2011)

Even with current treatments of acute joint injuries, more than 40% of people who suffer significant ligament or meniscus tears, or articular surface injuries, will develop osteoarthritis (OA). Correspondingly, 12% or more of all patients with lower extremity OA have a history of joint injury. Recent research suggests that acute joint damage that occurs at the time of an injury initiates a sequence of events that can lead to progressive articular surface damage. New molecular interventions, combined with evolving surgical methods, aim to minimize or prevent progressive tissue damage triggered by joint injury. Seizing the potential for progress in the treatment of joint injuries to forestall OA will depend on advances in (1) quantitative methods of assessing the injury severity, including both structural damage and biologic responses, (2) understanding of the pathogenesis of post-traumatic OA, taking into account potential interactions among the different tissues and the role of post-traumatic incongruity and instability, and (3) application of engineering and molecular research to develop new methods of treating injured joints. This paper highlights recent advances in understanding of the structural damage and the acute biological response following joint injury, and it identifies important directions for future research. Copyright © 2011 Orthopaedic Research Society.

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Epidemiology of ankle arthritis: report of a consecutive series of 639 patients from a tertiary orthopaedic center.

Charles Saltzman, Michael Salamon, G Michael Blanchard … (2005)

The purpose of our study was to identify the cause of symptomatic ankle arthritis in a consecutive series of patients presenting in a tertiary care setting. Between 1991 and 2004, 639 patients with Kellgren grade 3 or 4 ankle arthritis presented to the University of Iowa Orthopaedic Foot and Ankle Surgery service. The cause of the arthritis was determined based on medical history, physical examination, and imaging studies. To get a sense of the relative prevalence of the etiologies of lower extremity arthritis in our setting, we evaluated the cause of arthritis of all new patients presenting to the University of Iowa Orthopaedic Department from 1999-2004 with arthritis of the ankle, to those with arthritis of the hip or knee during one year. Of the 639 arthritic ankles, 445 (70%) were post-traumatic, 76 (12%) were rheumatoid disease and 46 (7%) were idiopathic (primary osteoarthritis). The post-traumatic ankle arthritis patients were most commonly associated with past rotational ankle fractures. The majority of ankle arthritis is associated with previous trauma, whereas the primary cause of knee or hip arthritis is idiopathic. Unique strategies to prevent or treat post-traumatic ankle arthritis are needed.