Joint trauma leads to acute posttraumatic arthritis and in the majority of individuals, as a long-term complication, to osteoarthritis (OA) [1
]. There are an estimated 900,000 cases of knee injuries annually in the United States, and posttraumatic OA accounts for 12% of all cases of OA [2
]. In some joints, such as the ankle, OA predominantly develops after joint trauma [2
]. As posttraumatic OA primarily affects younger individuals [3
], it leads to reduced physical activity and to deconditioning of the musculoskeletal system. Joint replacement in this young patient group is complicated by the limited lifespan of the implants.
OA risk increases with patient age at the time of injury and with time from the onset of injury [4
]. The presence of additional OA risk factors, such as obesity, joint malalignment or genetic risk factors, leads to a more severe outcome. Between 60 and 80% of patients with magnetic resonance imaging or arthroscopically documented cartilage injury developed cartilage degeneration within 5 years [6
]. Patients with anterior cruciate ligament (ACL)-deficient knees, with or without a concomitant meniscus injury, are at high risk for posttraumatic OA [5
]. Previous concepts that residual joint instability after ACL reconstruction is the cause of OA have not been confirmed as OA develops in joints with ACL injuries even if reconstructive surgery successfully normalizes joint biomechanics. These observations emphasize the role of events in the time period after the initial joint trauma.
Joint trauma affects all joint tissues to some degree but the damage to articular cartilage appears most significant, as it is largely irreversible and may be the major determinant for the subsequent development of OA. There is a certain degree of immediate or irreversible damage, but the days and weeks after injury represent the phase where damage progresses most rapidly. The acute symptoms following joint injury include joint pain and swelling due to intraarticular bleeding, synovial effusion and inflammatory cell infiltration. Patients typically undergo surgical treatment of the ligament and meniscus lesions within 3 months after the initial injury [2
]. Currently there are no approved therapies to address acute posttraumatic arthritis. Corticosteroids have potent anti-inflammatory activity but potential benefits or adverse effects of corticosteroids in a restricted dose and frequency of administration for traumatic joint injury have not been resolved and remain to be studied.
Furthermore, measures to prevent OA are not available, although patients with posttraumatic arthritis represent a readily identified population at risk for developing OA and thus are ideal to test preventive and therapeutic measures. Interventions early during the most dynamic postinjury phase have the potential to limit the degree of acute joint damage and to delay the onset and reduce the severity of OA. The prolonged posttraumatic inflammatory insult also significantly increases the risk of arthro-fibrosis for which satisfactory management remains to be developed. The present review addresses pathogenetic mechanisms and mediators involved in the acute and chronic consequences of joint trauma and candidates for pharmacological intervention.