Posttraumatic arthritis (PTA) is one of the most frequent causes of disability after trauma involving weight-bearing joints and is estimated to be responsible for approximately 10% of the 21 million Americans who have osteoarthritis. Despite a number of similarities in the pathology and end-stage disease of PTA with primary osteoarthritis, the mechanisms involved in the onset and progression of joint degeneration after articular fracture are poorly understood. The largest area of study regarding articular fractures and the development of arthritic changes has focused on the role of adequate surgical reduction of the articular surfaces. However, it is now apparent that a number of complex and interacting biomechanical, biochemical, and, possibly, genetic factors contribute to the development of osteoarthritic changes in the joint after joint trauma, ranging from the cell and molecular level to the joint and systemic level. In this paper, we discuss the potential roles of the initial impact and fracture as well as the subsequent alterations in joint loading, biomechanical and metabolic properties of the cartilage, local and systemic inflammatory cytokines, and viability of chondrocytes in the progression of PTA. An improved understanding of the mechanisms involved in the development of PTA will hopefully lead to the improvement of surgical and nonsurgical therapies for this disease.