Fifty-four patients with anterior cruciate ligament tears that were arthroscopically reconstructed within 3 months of initial injury were prospectively evaluated. Patients with grade 3 medial collateral ligament, lateral collateral ligament, or posterior cruciate ligament tears were excluded. Eighty percent of our patients had a bone bruise present on the magnetic resonance image, with 68% in the lateral femoral condyle. Two of the latter findings--an abnormal articular cartilage signal (P = 0.02) and a thin and impacted subchondral bone (P = 0.03)--had a significant relationship with injury to the overlying articular cartilage. Meniscal tears were found in 56% of the lateral menisci and 37% of the medial menisci. A significant association was present between bone bruising on the lateral femoral condyle and the lateral tibial plateau (P = 0.02). Results of our study support the concept that the common mechanism of injury to the anterior cruciate ligament involves severe anterior subluxation with impaction of the posterior tibia on the anterior femur. Determination of the significance of bone bruising, articular cartilage injury, or meniscal tears will require a long-term followup that includes evaluation for arthritis, stability, and function. These 54 patients represent the first cohort evaluated in this ongoing prospective clinical study.

T1-weighted FS 3D FLASH imaging is accurate for the detection and grading of articular cartilage abnormalities of the patellofemoral joint.

Although the clinical results of total joint arthroplasty are usually excellent, some implants develop loosening and require revision. Implants usually fail by a combination of mechanisms, but different basic designs tend to show different dominant mechanisms of failure. Infection causes failure of about 1-5% of cases of primary arthroplasty. Clues to the presence of infection include clinical signs, a periosteal reaction, a positive culture of aspirated joint fluid, and acute inflammation identified in tissue around the implant. There are several different mechanisms and modes of implant wear, and perhaps the most important cause of aseptic loosening is an inflammatory reaction to particles of wear debris. Abrasive, adhesive, and fatigue wear of polyethylene, metal and bone cement produces debris particles that induce bone resorption and implant loosening. Particles can cause linear, geographic, or erosive patterns of bone resorption (osteolysis), the distributions of which are influenced by the implant design. Micromotion of implants that did not achieve adequate initial fixation is another important mechanism of loosening. Fatigue failure at the bone/cement and bone/implant interface may cause aseptic loosening, and may be especially important for implants with relatively smooth surfaces. Stress shielding can influence local bone density, but is rarely an isolated cause of implant loosening. Elevated hydrodynamic pressure has been associated with bone resorption in the absence of implants, and may also play a role in implant loosening.

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Early tendon retraction, but not the total magnitude, correlates with formation of a recurrent tendon defect and worse clinical outcomes. "Failure with continuity" (tendon retraction without a recurrent defect) appears to be a common phenomenon after rotator cuff repair. These data suggest that repairs should be protected in the early postoperative period and repair strategies should endeavor to mechanically and biologically augment the repair during this critical early period.