Intra-articular fracture is one of the leading contributors to the development of secondary osteoarthritis. Articular fractures not only cause focal necrotic death to mechanically disrupted chondrocytes, but also induce a cascade of chondrocyte apoptosis.(20,21,22) Chondrocyte apoptosis exacerbates articular damage and correlates with the severity of secondary osteoarthritic changes. Principles of anatomic reduction of the involved articular surfaces must be followed to reduce the incidence of post traumatic arthrosis. Any residual step-off in the articular surface will lead to rapid joint deterioration. While operative fracture care has progressed enormously over the last fifty years, we still do not understand the many molecular pathways responsible for the process of programmed cell death, nor how to augment articular repair in an attempt to mitigate against post-traumatic arthritis. Interestingly, humoral factors like IGF-1 (insulin like growth factor-1) have been shown to stop chondrocyte apoptosis in vitro. (24,25) Limiting acutely-triggered programmed cell death, and the resulting joint destruction may limit long term osteoarthrosis and improve prognosis of patients who suffer intra-articular injury. Like all other forms of DJD, the progression of post traumatic arthritis is followed clinically and radiographically. Post traumatic OA presents with symptoms of pain and decreased range of motion. Radiographic evidence similar to those seen in primary OA are coupled with deformities induced by the original injury. Because of the natural alignment of the lower extremity mechanical axis, fractures ankles and hips tend to fail in varus resulting in increased wear of the adjacent joints. Prior to arthroplasty, reconstructive osteotomies may be attempted in an attempt to restore the normal angular alignment of a limb. However, once a joint has been fractured it is at increased risk of deterioration with a pattern similar to what accelerated primary OA would look like.