Prostaglandin E2 receptor type 2-selective agonist prevents the degeneration of articular cartilage in rabbit knees with traumatic instability

[Introduction]Osteoarthritis (OA) is a common cause of disability in older adults. We have previously reported that an agonist for subtypes EP2 of the prostaglandin E2 receptor (an EP2 agonist) promotes the regeneration of chondral and osteochondral defects. The purpose of the current study is to analyze the effect of this agonist on articular cartilage in a model of traumatic degeneration. [Methods]The model of traumatic degeneration was established through transection of the anterior cruciate ligament and partial resection of the medial meniscus of the rabbits. Rabbits were divided into 5 groups; G-S (sham operation), G-C (no further treatment), G-0, G-80, and G-400 (single intra-articular administration of gelatin hydrogel containing 0, 80, and 400 μg of the specific EP2 agonist, ONO-8815Ly, respectively). Degeneration of the articular cartilage was evaluated at 2 or 12 weeks after the operation. [Results]ONO-8815Ly prevented cartilage degeneration at 2 weeks, which was associated with the inhibition of matrix metalloproteinase-13 (MMP-13) expression. The effect of ONO-8815Ly failed to last, and no effects were observed at 12 weeks after the operation. [Conclusions]Stimulation of prostaglandin E2 (PGE2) via EP2 prevents degeneration of the articular cartilage during the early stages. With a system to deliver it long term, the EP2 agonist could be a new therapeutic tool for OA

Numerical analysis of Al2O3 and TiO2 growth and oxygen dissolution in a metal substrate during the isothermal oxidation of an α-Ti alloy at 973 K

Oxide growth of Al2O3 and TiO2 as well as O dissolution during the oxidation of an α-Ti alloy at 973 K were simulated using the finite volume method coupled with the calculation of phase diagrams (CALPHAD) method. The results indicated that the addition of 11.02 at.% Al to a Ti–O system resulted in the formation of an 18-nm-thick Al2O3 layer, which decelerated TiO2 growth and O dissolution in the substrate. An increase in the O concentration at the oxide–metal interface was also inhibited by Al2O3 formation. A thin Al-depletion zone was formed at the oxide–metal interface. Furthermore, Al2O3 formation was restricted by the low concentration and diffusivity of Al in the substrate