Increased signal in the proximal patellar tendon: normal or pathologic?

OBJECTIVE: To determine the clinical significance of T2 signal hyperintensity in the proximal patellar tendon seen on MRI of the knee. MATERIALS AND METHODS: MRIs of 100 patients who underwent MRI of the knee between 1 May 2018 and 15 July 2018 were retrospectively evaluated. All examinations were performed on 3-Tesla MRI scanners with a dedicated knee coil and in accordance with our institution's standard knee MRI protocol. The presence of increased T2 signal was assessed on both sagittal and axial T2-weighted fat-saturated images. The amount of increased signal in the proximal patellar tendon on T2-weighted images was characterized as: none, mild, moderate, or severe. A corresponding chart review of the referring physicians' notes was performed to determine the presence of clinical symptoms of patellar tendinopathy. Patellar tendinopathy was considered present if the clinical notes described tenderness on palpation of the inferior patellar pole, infrapatellar tenderness, or patellar tendinosis/tendinitis. RESULTS: The majority (66%) of knee MRIs demonstrated the presence of increased T2 signal in the proximal patellar tendon. Only 4.5% of these patients had associated clinical findings of patellar tendinopathy. CONCLUSION: Although increased T2 signal in the proximal patellar tendon is a common finding, only in rare cases are there associated clinical symptoms. Thus, increased T2 signal in the proximal patellar tendon may not be a pathological finding in the absence of clinical findings of patellar tendinopathy.

Orthopedic wear debris mediated inflammatory osteolysis is mediated in part by NALP3 inflammasome activation.

Activation of myeloid cells by orthopedic particulate debris is a key event in the pathogenesis of periprosthetic osteolysis and implant loosening after total joint replacement (TJR). Several lines of evidence implicate NACHT, LRR, and PYD domains-containing protein 3 (NALP3) inflammasome-mediated production of interleukin 1 beta (IL-1ß) in the pathogenesis of clinical disorders ascribable to foreign particulate materials, including asbestos, silica, and urate crystals. Recent reports indicate that orthopedic polymer products and metallic particulates and ions may activate the same pathway. Here, we investigated the contribution of the NALP3 inflammasome to the pathogenesis of peri-implant osteolysis. Pharmaceutical and genetic perturbations of caspase-1 and inflammasome components were used to assess the role of the NALP3 inflammasome in IL-1ß production and osteoclast formation by human monocytes and mouse macrophages in response to polymethylmethacrylate (PMMA) particle phagocytosis. The role of caspase-1 in a mouse calvarial model of particle-mediated osteolysis was assessed using µCT. Phagocytosis of PMMA particles induces caspase-1 dependent release of IL-1ß from human monocytes and mouse macrophages. Importantly, using macrophages from mice deficient in components of the NALP3 inflammasome, we show PMMA-induced IL-1ß production is strictly dependent on these components. Mice lacking caspase-1, the sole effector of the NALP3 inflammasome, show reduced orthopedic wear particle-induced calvarial osteolysis compared to wild-type controls. Absence of NALP3 inflammasome components fails to alter osteoclast formation in vitro. Our findings identify the NALP3 inflammasome as a critical mediator of orthopedic wear-induced osteolysis and as a viable therapeutic target for the treatment of periprosthetic osteolysis.

Early detection and treatment of wear particle-induced inflammation and bone loss in a mouse calvarial osteolysis model using HPMA copolymer conjugates.

Wear particle-induced inflammation is considered to be the major cause of aseptic implant loosening and clinical failure after total joint replacement. Due to the frequent absence of symptoms, early detection and intervention prior to implant failure presents a significant challenge. To address this issue, a N-(2-hydroxypropyl)methacrylamide (HPMA) copolymer-based optical imaging contrast agent (P-IRDye) was developed and used for the detection of wear particle-induced inflammation employing a murine calvaria osteolysis model. The particle-induced osteolysis of calvaria was evaluated by H&E, tartrate-resistant acid phosphatase (TRAP) staining and µ-CT after necropsy. One-day post particle implantation, P-IRDye was administrated to the mice via tail vein injection. Live imaging of the animals 6 days after implantation revealed the preferential distribution and sustained retention of the macromolecular contrast agent at the site of particle implantation. Immunohistochemical staining and FACS analyses of the calvaria-associated soft tissue revealed extensive uptake of the HPMA copolymer by F4/80, Ly-6G (Gr1) and CD11c positive cells, which accounts for the retention of the macromolecular probes at the inflammatory sites. To test the potential of the system for therapeutic intervention, an acid-labile HPMA copolymer-dexamethasone conjugate (P-Dex) was prepared and shown to prevent the particle-induced inflammation and bone damage in the calvaria osteolysis model.

Pullout strength and load to failure properties of self-tapping cortical screws in synthetic and cadaveric environments representative of healthy and osteoporotic bone.

BACKGROUND: The parameters of self-tapping screw (STS) performance in normal and osteoporotic bone have been defined in representative environments, but the question remains as to the clinical application of such findings. The goal of this study was to analyze the biomechanical performance of STSs in cadaveric and synthetic environments representative of healthy and osteoporotic bone. METHODS: Ninety-six Synthes STSs were inserted into cadaveric and synthetic models representative of osteoporotic and healthy bone. Screws were inserted to depths of 1 mm short of the far cortex, flush and 1 mm and 2 mm beyond the far cortex. Screws were tested with an Instron 8511 material testing system utilizing axial pullout forces. A SAS procedure was used to conduct analysis of variance for unbalanced datasets. RESULTS: Substantial differences were appreciated with respect to screw performance between osteoporotic and healthy bone specimens. Although a similar pattern of increased pullout strength and loading energy with increasing depth of insertion was demonstrated, absolute values were lower in osteoporotic specimens. Although performance trends were similar in cadaveric and synthetic testing models for both osteoporotic and healthy bone, values obtained during testing were different. Incomplete insertion of STSs resulted in a 21.5% and 37% reduction of biomechanical properties in osteoporotic and normal bone, respectively. CONCLUSIONS: These results indicate that previously published findings on the performance of STSs in synthetic models cannot reasonably be applied to the clinical realm. Although trends may be similar, screw performance in synthetic, as compared with cadaveric, models is markedly different.