Human fetal synovium-derived stem cells (SDSCs) were transduced with lentiviral vectors to overexpress LKB1 (liver kinase B1) or CRISPR associated protein 9 (Cas9)-single-guide RNA (sgRNA) vectors to knock it out. Following expansion, transduced human fetal SDSCs were induced for chondrogenic, adipogenic, and osteogenic differentiation. Overexpression of LKB1 led to decreases in chondrogenic and adipogenic potentials, which were enhanced by knockout of LKB1. LKB1 did not obviously affect osteogenic differentiation.

The objective of this study was to define in vitro the effects of osteoarthritic (OA) milieu and hypoxia on good manufactured practice-adipose-derived mesenchymal stromal cells (GMP-ASC) that are commonly utilized in cell therapies. Hypoxia increased GMP-ASC proliferation. OA milieu-treated GMP-ASC showed an increase in cellular migration, as well as in CXCR3, CCR3, and IL6R and a decrease in CCR1 and CCR2 receptors in hypoxia. CXCL10/IP10 was the only chemokine of the OA milieu down-modulated after treatment with GMP-ASC.

Non-invasive anterior cruciate ligament (ACL) rupture is an emerging small animal model of post-traumatic osteoarthritis (PTOA). The non-invasive nature of this model may make it uniquely suited to study important OA phenomena. Here, PTOA following ACL rupture by a non-invasive knee injury (NIKI) device was characterized to establish the fundamental pathology and time course of this model in rats. NIKI-injured knees exhibited changes to the bone, cartilage, synovium, and synovial fluid biomarker profile, hallmark indicators of PTOA-like pathology.

This study has successfully established an in vitro test protocol to characterize the cell-accelerated corrosion behavior of CoCrMo alloy in conditioned cell culture media of different periprosthetic cell types. Macrophages activated with wear particles had a significant effect on the increased corrosion rate and the overall corrosion kinetics. Thus, macrophages can alter the electrochemical environment that drives the passivation and preferential dissolution processes at the microstructure level of the alloy, thus accelerating damage caused by corrosion.