Fig. 1.1
A case presentation of a 40-year-old patient who sustains a posterior wall fracture of the acetabulum with subluxation of the femoral head. The patient reported no pre-injury hip symptoms. (a–c) AP, obturator oblique, and iliac oblique radiographs of a patient with a displaced posterior wall acetabular fracture. (d) CT scan demonstrating displacement of the posterior wall fracture and subluxation of the femoral head. (e–g) AP, obturator oblique, and iliac oblique radiographs of postoperative reduction of the acetabulum articular fragment and femoral head with fixation of the posterior wall. (h) CT scans after surgical reduction and fixation. Beginning from the top left the images proceed from left to right. Careful inspection of the image in the top right demonstrates a small gap in the articular surface representing focal cartilage and subchondral bone loss. The remaining images show an otherwise anatomic restoration of the joint surface. (i) AP radiograph taken at 1 year post-injury. There is evidence of joint space loss and sclerosis of the subchondral bone. This is early-onset posttraumatic arthritis (PTA). (j) AP radiograph taken at 4 years after the injury. Essentially complete loss of joint space is now apparent with severe PTA present. (k) AP radiograph taken after total hip replacement performed as treatment for PTA symptoms
Within this text, we have asked contributors to provide in-depth review of several potential mechanisms contributing to the development of arthritis after joint injury. These include cell death, reactive oxygen species available in the joint, direct mechanical overload, and inflammation within the joint after injury. There is some evidence for all of these mechanisms being present in various forms of arthritis that occur after joint injury. It is likely that some forms of arthritis after injury result in a similar clinical endpoint as primary (idiopathic) osteoarthritis. However, it also appears that there are situations in which the response to injury may be more suitable for a focal response such as an anti-inflammatory therapy or other targeted therapy that may not be generally applicable in osteoarthritis per se. In this sense, we believe that both terms, PTA and post-traumatic osteoarthritis (PTOA), are appropriate and they are interspersed throughout this text. These terms are used in an interchangeable manner from chapter to chapter. We thank the many important contributions of the authors, and we hope that this text provides a basis for the next generation of studies on the pathogenesis, diagnosis, and management of this disease.
Acknowledgments
Supported in part by the Arthritis Foundation, Department of Defense, and NIH grant AR50245.
References
1.
CDC. Arthritis: the nation’s most common cause of disability. Chronic disease at a glance reports: arthritis 2011 February 18, 2011 [cited 2011 October 29]; Description of demographics of the burden of disease for arthritis in the United States. Available from: http://www.cdc.gov/chronicdisease/resources/publications/aag/arthritis.htm#chart1.
2.
3.
Key JA. Experimental arthritis: the changes in joints produced by creating defects in the articular cartilage. J Bone Joint Surg Am. 1931;13(4):725–39.
5.
Moskowitz RW, et al. Cartilage proteoglycan alterations in an experimentally induced model of rabbit osteoarthritis. Arthritis Rheum. 1979;22(2):155–63.PubMedCrossRef
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
