Bone quality, and the combination and penetration of cement-bone interface: A comparative micro-CT study of osteoarthritis and rheumatoid arthritis.

To compare the microstructure, bone quality, and the combination and penetration of cement-bone interface in tissue specimens from patients with osteoarthritis (OA) and rheumatoid arthritis (RA).A total of 80 femoral condyle tissue specimens from 20 OA patients (40 condyles) and 20 RA patients (40 condyles) who underwent total knee arthroplasty at the Department of Orthopaedics in Tengzhou Central People's Hospital were collected between January 2017 and September 2017. According to the random number table method, 20 specimens from the OA group were defined as group A, and 20 specimens in the RA group were defined as group B. The bone quality parameters were measured by micro-CT. The remaining 20 specimens in the OA group and the remaining 20 specimens in the RA group were defined as group C and group D, the cement-bone interfaces were established by the self-made bone cement compression device, and were analyzed by micro-CT.Micro-CT measurement revealed that the bone volume fraction (BV/TV), trabecular thickness (Tb.Th), and trabecular number (Tb.N) in group A were significantly higher than those in group B (all P < .05). The bone surface/bone volume (BS/BV), structure model index (SMI), trabecular separation (Tb.Sp), and degree of anisotropy (DA) in group A were significantly lower than those in group B (all P < .05). The penetration depth of bone cement in group D was significantly greater than those in group C via x-ray detection.The bone quality of OA patients is better than that of RA patients, but the combination and penetration of cement-bone interface of RA patients are better than that of OA patients. The findings advance our understanding of knee prosthesis and have important clinical implications, but they require validations in future studies with larger sample sizes.

TWEAK/Fn14 signaling: a promising target in intervertebral disc degeneration.

Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) is a potent chemoattractant cytokine with various biological functions, such as stimulation of angiogenesis, induction of proinflammatory cytokines, regulation of cellular proliferation and apoptosis. Therefore, it has also been implicated in several pathological processes, from cancer to inflammatory diseases. Remarkably, TWEAK and its receptors, fibroblast growth factor inducible 14 (Fn14), are also present in intervertebral disc (IVD) tissue, where they play a role in the pathogenesis of IVD degeneration. The interaction of TWEAK with Fn14 is involved in physiological and pathological activities of IVD degeneration patients, which includes apoptosis of endplate chondrocytes, extracellular matrix degradation, reduction in proteoglycan synthesis and so on. The blockade of this interaction results in suppressing over-production of proinflammatory factors and cell death in in vivo or in vitro experiments, suggesting that TWEAK/Fn14 signaling may be therapeutically relevant in IVD degeneration, and the targeting of TWEAK or Fn14 has been proposed as a potential therapeutic approach for autoimmune diseases such as Rheumatoid arthritis (RA). In this article, we discuss the biological features of TWEAK/Fn14 signaling and summarize recent advances in our understanding of the role of TWEAK/Fn14 signaling in the pathogenesis and treatment of IVD degeneration. We think that the blockade of TWEAK/Fn14 signaling may be a promising therapeutic strategy for IVD degeneration in the near future.