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Little has been reported on knee pain after total hip arthroplasty (THA). The purpose of this study was to investigate the incidence and mechanism of knee pain after THA. Two hundred fifty-two patients with hip dysplasia were clinically and radiographically assessed for knee pain before and after THA. Incidences of knee pain and patellofemoral alignment were analyzed with reference to postoperative change in leg length, femoral anteversion, and the femoral offset. Anterior knee pain was present in 16 patients (7.3%). Lateral patellar tilt was increased in all patients with knee pain and significantly larger compared to that seen in patients without knee pain. The increased patellar tilt disappeared within 3 months, but symptoms in 4 patients persisted for more than 3 months. The patellar tilt was significantly related to the amount of leg lengthening. This study demonstrates that THA influences the patellofemoral joint via leg lengthening and causes anterior knee pain.

The main purpose of this study was to examine the relationships among osteonecrosis, steroid-metabolizing hepatic enzyme (cytochrome P450 3A; CYP3A) activity, and steroid dose to determine whether it is possible to prevent osteonecrosis in animals with low hepatic CYP3A activity by reducing exogenous steroid doses.Japanese white rabbits (n = 103) were divided into three groups: a group with CYP3A activity induction (by intramuscular phenobarbital injection, n = 31), a group with CYP3A activity inhibition (by oral itraconazole administration, n = 30), and a control group (n = 42). Three weeks later, all rabbits received a methylprednisolone injection. Each group was divided into two subgroups by dosage of methylprednisolone (5 or 10 mg/kg body weight). Three weeks after methylprednisolone injections, the animals were killed and histological examination was performed to determine the incidences of osteonecrosis in the six subgroups.Incidence in the inhibition subgroup with 5 mg/kg steroid was higher than that in the induction subgroup receiving 10 mg/kg steroid. Thus, suppression of CYP3A activity significantly increased vulnerability to steroid-induced osteonecrosis, while increased CYP3A activity reduced this vulnerability.These findings suggest that low CYP3A activity may be vulnerable to the effect of steroids and increase risk of osteonecrosis, even with a low dose of steroid.

Recombinant human bone morphogenetic protein (rhBMP) is a promising therapeutic cytokine for the induction of bone formation, but a weak response in humans remains a major hurdle in its therapeutic application. We have previously reported an rhBMP-2-induced increase in the bone mass of mice receiving systemic rolipram, a specific inhibitor of phosphodiesterase-4. To overcome the side effects of systemic administration of rolipram, we examined the effects of its local release. Polyethylene glycol discs were used as a delivery system. The discs were impregnated with rhBMP-2 and rolipram and implanted into the dorsal muscle pouches in mice. Bone formation was assessed by measuring the bone mineral content (BMC) of the formed bone. First, to determine the optimal dose of rolipram, we added 0-5000 nmol rolipram and 5 microg rhBMP-2 to the pellets and found that 500 nmol rolipram was the most effective concentration for inducing bone formation after 4 weeks. Second, to examine the time course of bone formation, we implanted 5 microg rhBMP-2 with 0 or 500 nmol rolipram and killed mice 5, 7, 10, 14, or 21 days after implantation. Bone formation was accelerated in the rolipram group. Finally, to determine the rolipram-induced increase in the effect of BMP, BMC obtained after treatment with 5 microg rhBMP-2 and 500 nmol rolipram was compared with that obtained after treatment with 5-9 microg rhBMP-2 without rolipram, 4 weeks after implantation. The results indicated that 500 nmol rolipram enhanced the effect of rhBMP-2 by almost 1.5-fold. In summary, locally released rolipram enhanced the capacity of rhBMP-2 to induce bone formation, an effect previously reported with systemic administration. These findings may decrease the cost and increase the efficacy of rhBMP-2 treatment.

Varus and valgus joint laxity of the normal living knee in flexion was assessed using MRI. Twenty knees were flexed to 90° and were imaged in neutral and under a varus-valgus stress in an open MRI system. The configuration of the tibiofemoral joint gap was studied in slices which crossed the epicondyles of the femur. When a varus stress was applied, the lateral joint gap opened by 6.7 ± 1.9 mm (mean ± sd; 2.1 to 9.2) whereas the medial joint gap opened by only by a mean of 2.1 ± 1.1 mm (0.2 to 4.2). These discrepancies indicate that the tibiofemoral flexion gap in the normal knee is not rectangular and that the lateral joint gap is significantly lax. These results may be useful for adequate soft-tissue balancing and bone resection in total knee arthroplasty and reconstruction surgery on ligaments.

We developed a new tensor to measure the joint gap throughout knee flexion during total knee arthroplasty (TKA). This tensor has the same articular shape as that of the tibial liner, including the post structure and the curvature of femorotibial articular surface, to measure the gap intraoperatively under the same conditions as after TKA. The present study aimed to examine the precision of the new tensor for gap measurement after implantation. We performed TKA using the modified gap technique in four cadaveric knees and measured the gaps using the new tensor. The intra-observer and inter-observer error of the tensor was analyzed using 168 measurements of the gaps as determined at least twice by two surgeons. In addition, the gaps in rotating-platform posterior-stabilized TKA were measured at seven positions with the knee bending from extension to full flexion. The inter-observer and intra-observer errors were 0.8 and 0.3 mm, respectively, indicating precise and reproducible gap measurement. The gaps before implantation in reduced patellar position were 12.1 mm at extension and 12.5 mm at 90° flexion. The gaps after implantation were 9.1, 12.9, 13.1, 13.5, 13.8, 13.3, and 10.1 mm at 0°, 30°, 45°, 60°, 90°, 120°, and full flexion, respectively. The new tensor provides precise and reproducible measurements. Although the joint gap before implantation was parallel and equal at extension and 90° flexion, the joint gap after implantation was variable throughout knee flexion. This feature of the gap should be considered during the operation.

Effective therapies for the regeneration of large osteochondral defects are still lacking; however, various approaches have been used. We evaluated the efficacy of Escherichia coli-derived dimeric recombinant human BMP-2 (E-rhBMP-2) for the repair of large osteochondral defects in a rabbit model. Osteochondral defects made in the femoral patellar groove of the knee were treated by transplanting gelatin sponges onto which no or various doses of E-rhBMP-2 were loaded. The outcomes were compared with those of an untreated control group four, 12 and 24 weeks after transplantation. At early time points, the cartilage tissue was repaired in a dose-dependent manner, and bone repair was accelerated in the defects treated with high doses of E-rhBMP-2. At 24 weeks, the repair of cartilage tissue was better with E-rhBMP-2 treatment, even at low doses, than without E-rhBMP-2 treatment. Our findings suggest that the use of E-rhBMP-2 improves and accelerates the repair of osteochondral defects in a rabbit model.

Articular cartilage defects are a major clinical problem for orthopedic surgeons. About 10 years ago, autologous chondrocyte implantation (ACI) was explored [1], approved by the U.S. Food and Drug Administration (FDA), and performed in more than 20 000 patients worldwide. However, the effectiveness of ACI remains controversial because of the lack of evidence of effi cacy from randomized controlled trials. There is currently no satisfactory clinical technique that is widely accepted for the regenerative repair of these lesions. Current clinical practice usually involves a bone marrow stimulation technique, which involves subchondral bone breaking to facilitate cartilage repair from bone marrow-derived cells and cytokines. However, with this procedure, cartilage defects are repaired with fi brocartilage [2]. Almost 15 years ago, mosaicplasty [3,4] was explored in addition to ACI. Using this technique, we can repair small articular cartilage defects with hyaline cartilage, but there are still a number of problems that remain unsolved, such as donor site morbidity. In attempts to develop better methods, different cell sources and delivery vehicles, the addition of growth factors, and transduction of some genes have all been investigated. We have been interested in the use of bone marrow mesenchymal cells (BMMC) because they have a number of suitable properties [5–8]. First, it is easy to obtain autologous cells: this can be achieved by aspiration of blood from the bone marrow using local anesthesia, without major side effects. Another reason for our interest in using these cells is that because we can cause them to proliferate without their capacity for differentiation being lost, this technique can be applied in large articular cartilage defects. Therefore, this procedure can be performed clinically with relative ease. Thus, we performed BMMC transplantation in human articular cartilage defects in knee joints. In this article, we explain the articular cartilage repair procedure with cell transplantation, mainly focusing on those with BMMC transplantation.