From Articular Fracture to Posttraumatic Arthritis: A Black Box That Needs to Be Opened

Posttraumatic arthritis (PTA) is a painful and debilitating condition that represents a commonly recognized sequela following intraarticular fractures.1,2 However, very little is known about the etiology, pathogenesis, or mechanisms of PTA as a disease. This issue is most clearly illustrated when contrasting the amount of investigation on cartilage degeneration after fracture with those on idiopathic osteoarthritis or rheumatoid arthritis.3,4 The biomechanical and cellular mechanisms that begin with joint trauma and articular fracture and ultimately result in PTA are poorly understood. Such voids in knowledge are occasionally described as a "black box." The goal of obtaining an anatomic articular reduction at the time of surgical repair is a tenet of modern fracture care.5 Important questions concerning the role of articular alignment in the development of PTA remain unanswered, however.6 Why are small amounts of articular malreduction tolerated better by some joints than others? Why does the magnitude of articular malreduction not consistently correlate with the extent of posttraumatic arthritis that develops after injury? In general, trauma surgeons have focused on the clinical techniques and outcomes of articular reduction and fixation without seeking a deeper understanding of basic mechanisms leading to PTA.5,7 There has been little basic science investigation of this disease, however, partly as a result of the lack of epidemiologic data on the socioeconomic impact of PTA as a separate entity from generalized osteoarthritis. The diagnosis of PTA is made using a combination of clinical and radiographic findings.1 Serum biomarkers and other blood or joint fluid analyses are generally not used in the diagnosis because of lack of specificity or validity of current methods. However, unlike most forms of arthritis, there is often an identifiable event, the fracture itself, that can lead to the onset of disease. Clinical manifestations can vary widely, with some patients presenting with severe joint degeneration within a year of traumatic injury and others with only mild changes after many years. There is no clear time limit after injury when arthritis is no longer considered "posttraumatic" and is simply "osteoarthritis." Trauma as an etiology of arthritis is considered a secondary form of arthritis in the field of rheumatology.3 Indeed, some rheumatology texts do not mention trauma or fracture as an etiology of arthritis at all.4 Once the disease is established, the predominant management options for PTA are osteotomy, arthroplasty, or arthrodesis.8 Why do we know so little about how articular fractures contribute to the development of posttraumatic arthritis? There are many reasons. First, the primary intervention available for the treatment of articular fractures is reduction of the articular surface and surgical fixation with early restoration of motion.2 Second, although there are cartilage repair therapies for articular cartilage defects, these techniques have not been used widely for articular fractures.9,10 Third, for many patients fracture care and arthritis management are provided by orthopedic surgeons with differing practice specialties. For the traumatologist, who treats the fracture but not the PTA, and the arthroplasty surgeon, who treats the PTA many years after the fracture, there is a disconnect between the articular fracture and the development of degenerative joint changes. Social factors such as change in employment or insurance status that result from effects of the injury may contribute to this disconnect between articular fracture and subsequent PTA. Fourth, there is a lack of prospective, evidence-based studies in this area resulting in treatment driven by dogma for clinical care of articular fractures that has remained virtually unchanged for decades. For example, it has simply been assumed that an anatomic reduction is a dominant factor required for significantly improved outcomes for all articular fractures, yet several investigations report equivalent long-term outcomes with slight articular malreductions in specific injuries.2,11,12 Finally, from a research perspective, PTA is a difficult topic to study. Articular fractures are multifactorial conditions that involve complex sequences of biomechanical and biological events.1,13 Because many of the factors that potentially contribute to PTA following articular fractures occur simultaneously, it is difficult to isolate the effects of specific events from numerous, potentially confounding variables in any articular fracture. For example, joint trauma may involve impact of the cartilage, fracture of the articular surface, fracture of the bone, and damage to other surrounding soft tissues. Joint trauma is often accompanied by "polytrauma" to other sites in the body. To fully understand the contributions of different factors, and the subsequent molecular and biomechanical pathways that lead to PTA, new methods and experimental models for both clinical and basic science research will be needed to sort through this complex area. The priorities for surgical treatment of an articular fracture consist of obtaining and maintaining an accurate reduction of the articular surface, obtaining appropriate axial alignment of the limb, and providing enough fracture stability to allow early range of motion and return to function of the injured extremity.6 Yet the links between the basic science knowledge of articular fractures and these treatment priorities are rudimentary at best. Numerous aspects of articular fractures may contribute to PTA. At the tissue level, articular fracture may include alteration of the mechanical environment following malreduction, blunt impaction injury to the articular surface, instability of the articular surface, and exposure of the articular surface to marrow contents and blood products with resultant inflammation.13 In this symposium, the works of Borrelli et al, McKinley et al, and Furman et al address many of these important aspects of articular fractures. Demographic analysis of the incidence of PTA has not been reported. In this symposium Brown et al reports the incidence of patients presenting to an orthopedist for symptomatic treatment of arthritis with a history of antecedent trauma in the involved joint. These data are critical to the understanding of PTA because they begin to quantify the tremendous socioeconomic impact and burden of this disease in the United States. The goal of this symposium is to stimulate interest and research in this area. By opening this "black box," we aspire to develop therapies to improve the outcomes of patients with articular fractures and reduce the burden of PTA on society.