Post-Traumatic Arthritis: Definitions and Burden of Disease

  • Joseph A. Buckwalter
  • David T. Felson


Osteoarthritis, as distinguished from arthritis secondary to inflammatory or neurologic disorders, is the most common form of joint disease and is one of the leading causes of disability in the USA and worldwide. Post-traumatic osteoarthritis (PTOA), the osteoarthritis that develops following joint injury, causes life-long pain and disability for millions of people. Excessive mechanical forces applied to synovial joints as a result of acute joint injury and post-traumatic residual joint abnormalities, primarily instability and articular surface incongruity, lead to progressive loss of articular cartilage, to bone remodeling, and to changes in the joint soft tissues, resulting in PTOA. One of the most important recent advances in understanding of PTOA has been the recognition that while mechanical injury causes direct tissue damage, PTOA is not a direct or inevitable consequence of the initial mechanical damage. Instead, PTOA mechanical joint injury is followed by localized and whole-joint biologic responses, including release of inflammatory mediators, that contribute to progressive tissue destruction as well as repair responses. Increased age significantly increases the risk of OA following joint injury, possibly as a result of an age-related decrease in the ability of chondrocytes, and possibly other cells, to restore and maintain the articular surface. Recent evidence suggests that trivial joint injuries, often unappreciated when they occur, may account for a large percentage of OA, especially in older persons. Unfortunately, current treatments of joint injuries all too often fail to prevent PTOA, although a number of recent research results suggest that inhibiting the biologic mediators of joint destruction initiated by excessive mechanical forces has the potential to prevent or decrease the risk of PTOA.


Joint injury Osteoarthritis Articular cartilage Inflammation Aging 



This research was supported by NIH CORT Grant P50 AR055533 and by NIH MCRC Grant P60 AR47785.

Conflicts of interest: None.


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© Springer Science+Business Media New York 2015

Authors and Affiliations

  1. 1.Department of Orthopedics and RehabilitationUniversity of Iowa HospitalsIowa CityUSA
  2. 2.Iowa City Veterans, Administration Medical CenterIowa CityUSA
  3. 3.Clinical Epidemiology Unit, Department of MedicineBoston University School of MedicineBostonUSA

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