Bone remodeling is the continual process to renew the adult skeleton through the sequential action of osteoblasts and osteoclasts. Nuclear factor RANK, an osteoclast receptor, and its ligand RANKL, expressed on the surface of osteoblasts, result in coordinated control of bone remodeling. Inflammation, a feature of illness and injury, plays a distinct role in skewing this process toward resorption. It does so via the interaction of inflammatory mediators and their related peptides with osteoblasts and osteoclasts, as well as other immune cells, to alter the expression of RANK and RANKL. Such chemical mediators include TNFα, glucocorticoids, histamine, bradykinin, PGE2, systemic RANKL from immune cells, and interleukins 1 and 6. Conditions, such as periodontal disease and alveolar bone erosion, aseptic prosthetic loosening, rheumatoid arthritis, and some sports related injuries are characterized by the result of this process. A thorough understanding of bone response to injury and disease, and ability to detect such biomarkers, as well as imaging to identify early structural and mechanical property changes in bone architecture, is important in improving management and outcomes of bone related pathology. While gut health and vitamin and mineral availability appear vitally important, nutraceuticals also have an impact on bone health. To date most pharmaceutical intervention targets inflammatory cytokines, although strategies to favorably alter inflammation induced bone pathology are currently limited. Further research is required in this field to advance early detection and treatments.

Jumper's knee is not synonymous with patellar tendinopathy. The term includes patellar tendinopathy and quadriceps tendinopathy. Although the patellar and quadriceps tendons work in tandem as part of the extensor mechanism of the knee, they have distinct anatomy and functional roles. As a result, there are probable differences in risk factors, etiology, and response to treatment. It is time to clinically separate patellar tendinopathy and quadriceps tendinopathy and design more specific rehabilitation programs. In this Viewpoint, the authors will (1) provide a rationale for distinguishing the 2 clinical entities—patellar tendinopathy and quadriceps tendinopathy—for treatment decision making, and (2) identify areas of research priority in quadriceps tendinopathy. J Orthop Sports Phys Ther 2019;49(9):627–630. doi:10.2519/jospt.2019.0611

A systematic search was performed of online databases for any Achilles tendon (AT) injuries occurring within the National Basketball Association (NBA). Video was obtained of injuries occurring during competition and downloaded for analysis in Dartfish. NBA athletes (n = 27) were identified with AT rupture over a 30-year period (1991–2021). Of the 27 NBA athletes found to have AT ruptures (mean age: 29.3 [3.3] y; average time in the NBA: 8.5 [3.8] y), 15 in-game videos were obtained for analysis. Noncontact rupture was presumed to have occurred in 12/13 cases. Eight of the 13 athletes had possession of the ball during time of injury. The ankle joint of the injured limb for all 13 athletes was in a dorsiflexed position during the time of injury (47.9° [6.5°]). All 13 athletes performed a false-step mechanism at time of injury where they initiated the movement by taking a rearward step posterior to their center of mass with the injured limb before translating forward. NBA basketball players that suffered AT ruptures appeared to present with a distinct sequence of events, including initiating a false step with ankle dorsiflexion of the injured limb at the time of injury.

In recent years, the use of diagnostic imaging in physical therapist practice in the United States (US) has gained considerable interest. In several countries around the world and in the US military, patient direct referral for diagnostic imaging has been considered normative practice for decades. US physical therapy program accreditation standards now stipulate that diagnostic imaging content must be included in physical therapist educational curricula. The American Physical Therapy Association (APTA) has made efforts to pursue practice authority for imaging referral. A recent review of state practice acts and other statutory language concluded that many states have no prohibitions against physical therapists referring for imaging studies. Additionally, physical therapists can now pursue certification as musculoskeletal sonographers. In light of these advances, and with a growing number of PTs serving patients who have not yet seen another healthcare provider, it may be helpful for those who have been actively involved in the use of imaging in PT practice to provide their collective recommendations to serve as a guideline to those interested in incorporating this practice privilege. The purpose of this perspective article is to provide an overview of the key elements necessary for effective implementation of referral for imaging in physical therapist practice while emphasizing the cornerstone of effective communication.

A systematic search was performed of online databases for any anterior cruciate ligament (ACL) injuries within the NBA. Video was obtained of injuries occurring during competition and downloaded for 2-dimensional video analysis. Thirty-five in-game videos were obtained for analysis. Of the reviewed cases, 19% were noncontact ACL injuries where there was no player-to-player contact from an opposing player. Three injury mechanism categories were found based on the events at the point of initial ground contact of the foot of the injured limb: single-leg casting (mean dorsiflexion angle 18.9° (14.4°); mean knee flexion angle 15.6° (7.8°); and mean trunk lateral flexion 18.2° (8.4°)); bilateral hop (mean dorsiflexion angle 18.2° (15.2°), mean knee flexion angle 21° (14.5°), mean trunk extension angle 6.9° (11.4°), and landing angle from the athlete’s center of mass 47.9° (10.1°)); and single-leg landing after contact (mean abduction angle of the swing leg 105.4° (18.1°), mean knee flexion angle of the injured limb 34.2° (8.0°), and mean trunk ipsilateral flexion angle 22.2° (7.0°)).