The clinical relevance of post-traumatic arthritis (PTA) has emerged over the past decade [1]. PTA has gone from a footnote in discussions of the burden of disease of arthritis to the level of being recognized in recent years as a cause of a significant proportion of the overall incidence of joint disease, as well as the most common cause of soldiers being unfit for active duty [2, 3]. Important advances in elucidating the pathophysiology of PTA have been made. The current focus on PTA research provides an important stimulus to find ways to translate these advances into clinical interventions to lessen the impact of PTA after joint injury. In many ways, arthritis after joint injury provides important advantages as a system of study [4]. For example, the time of joint injury is frequently known, and the mechanism and severity of injury can often be assessed. The time for PTA to develop after joint injury is much faster than traditional osteoarthritis, particularly PTA after intra-articular fracture, making interventional studies more feasible [3, 5]. Yet the numbers of published peer-reviewed investigations on PTA are significantly fewer in comparison to peer-reviewed investigations focusing on rheumatoid arthritis or osteoarthritis [5].

It is appropriate to consider why there are so many fewer investigations focused on PTA relative to other forms of arthritis. To provide perspective on the variation in numbers of peer-reviewed investigations in PTA as compared with other forms of arthritis a PubMed search in November 2014 gave the following numbers of published citations for the subject terms “Rheumatoid Arthritis”—119,704, “Osteoarthritis”—58,213, and “Post-Traumatic Arthritis”—950 [5]. A majority of our understanding of arthritic conditions comes from the work of rheumatologists and musculoskeletal basic science researchers; much of this work focuses on mechanisms and outcomes of medical therapy for various forms of arthritis. However, joint injury is unique among causes of arthritis in that the primary management is often surgical and is provided almost exclusively by orthopedic surgeons [6]. There are several aspects in the practice of orthopedic surgery that affect the ability to have an insight into the development of PTA [2]. Surgeons are trained to restore anatomy (reduction/fixation) or soft tissue function (reconstruction of the ACL or repair of the meniscus) following injury—this is the case with treatment of joint injuries. Orthopedic surgeons have used surgical management as the primary (and often only) form of treatment to prevent PTA after joint injury. In part this is because not only are the mechanisms that cause PTA incompletely understood, but there are no pharmacologic therapies currently available to limit PTA development after joint injury. With increasing specialization in practice, often-care for a patient’s acute joint injury and care for the PTA that develops later are provided by different orthopedic surgeons. This lack of continuity of care has limited observation of the process of development of PTA.

The treatment of major joint injury is primarily evaluated and treated by orthopedic surgeons. For this reason, the primary onus for prevention and treatment of PTA should also belong to orthopedic surgeons [3, 6]. This important clinical area of PTA development is relatively unexplored. As with traumatic injury in general, PTA tends to occur in a younger population [7]. These patients are at risk for lifelong disability secondary to the effects of joint injury [7]. The impact on both the patients and on society is significant. Taking a leadership role in calling for an increased understanding of the effects of joint injury and encouraging development of therapies to prevent PTA is an important role for the Orthopedic Surgery community.

The traditional paradigm with which most orthopedic surgeons approach treatment of a joint injury can be paraphrased as “biomechanics trumps biology” [8]. This is reflected in the approach of surgical restoration of anatomy following joint injury. The observations highlighted in Chaps. 8 and 18 that increasing the magnitude of articular mal-alignment leads to higher contact stresses affecting a progressively smaller are a of the joint surface-points to one of the conundrums of PTA development. Why does a focal area of mal-alignment and its resultant localized cartilage damage lead to global arthritis throughout the entire involved joint? The work of Loeser, Goldring, and coworkers provides direction to begin to address this question [9]. They highlight the intra-articular response to joint injury as an organ system response within this local environment. Increasing numbers of investigators have begun to recognize the importance of the interactions between biological and biomechanical factors among the many cell and tissue types within the intra-articular environment in the pathophysiology of various forms of arthritis [10]. Orthopedic surgeons have classically focused on the effects of joint injury on articular cartilage and chondrocytes in isolation until recently. There is a paucity of data, both acute and chronic, regarding the intra-articular response to joint injury in humans. The focus of this text is to expand that understanding of the various aspects of joint injury and the intra-articular injury response.

The importance of understanding molecular mechanisms that are active in the intra-articular environment after joint injury that may lead to novel therapies has only recently been appreciated. The role of cytokines in PTA has recently been highlighted in the literature. Chapters 4–10 detail experimental models of cartilage and whole joint injury. The sophistication of articular injury models has increased significantly. Standardized models of joint injury in mice that progress to PTA have been developed in the past 10 years (see Chaps. 5–10). These models provide opportunity to identify molecular mechanisms and assess novel therapies in response to specific types of joint injury. The use of genetically modified or inbred strains of mice is beginning to lead to novel therapies that may prove clinically useful. It is likely that different mechanisms of joint injury may result in detectable differences in injury response within the joint.