More and more evidences showed that cartilage harbored local progenitor cells that could differentiate toward osteoblast, chondrocyte, and adipocyte. However, our previous results showed that osteoarthritis derived chondroprogenitor cells (OA-CPC) exhibited strong osteogenic potential even in chondrogenic condition. How to promote their chondrogenic potential is the key for cartilage repair and regeneration in osteoarthritis. Recently, lipid availability was proved to determine skeletal progenitor fate. Therefore, we aim to determine whether lipid inhibition under 3D culture condition could enhance OA-CPC chondrogenesis. Moreover, glucose concentration was also evaluated for chondrogenic capacity. Although there are many researches showed that lower glucose promotes chondrogenesis, in our results, we found that OA-CPC in high concentration of glucose (4.5g/L) with lipid inhibitor (GW1100) showed strongest chondrogenic potential, which could form largest cell pellet with strong proteoglycan staining, COL II expression and no COL I expression. Besides, COL2A1 was increased and COL10A1 was decreased significantly by GW1100 under high glucose condition in 2D culture. Interestingly, although the expression level of MMP13 was not changed by GW1100 at RNA and protein level, less MMP13 protein secreted out of cell nuclear. In summary, we estimated that higher glucose and lower lipid supplies benefit OA-CPC chondrogenesis and cartilage repair.

Osteoarthritis is one of the major causes of immobility. Most commonly, osteoarthritis manifests at the knee joint. Prevalence of knee osteoarthritis (KNOA) increases with age. Another important risk factor for KNOA is obesity. Research has shown that obese subjects have almost four times the risk of developing KNOA, which may be explained by both an increased knee loading. In medial compartment KNOA, the knee adduction moment (KAM) during gait is considered a marker for disease severity. KAM is dependent of the magnitude of the ground reaction force and its moment arm relative to the knee joint centre. In addition, obesity has been reported to augment KAM during gait. However, after removal of the direct contributions of body weight, KAM parameters may be different due to obesity-related gait adaptations to limit knee loading. While KAM has been thoroughly investigated during gait, little is known about KAM during stair negotiation, during which knee loads are higher compared to gait. The aim of the current study is therefore to compare normalized KAM during the stance phase of stair negotiation between lean KNOA patients, obese KNOA patients, and healthy controls. This case control study included 20 lean controls, 14 lean KNOA patients, and 16 obese KNOA patients. All subjects ascended and descended a two-step staircase at a self-selected, comfortable speed. Radiographic imaging and MRI were used to evaluate knee cartilage and KNOA status. Motion analysis was performed with a three-dimensional motion capture system. Kinetic data were obtained by one force platform. The parameters of study included: stance phase duration, toe-out angle, KAM peaks and KAM impulse. During stair ascent obese KNOA patients showed a longer stance phase than healthy controls (P 0.050). Despite high between-subject variability, KAM impulse was found 45% higher in the obese KNOA group during stair descent, when compared to healthy controls (P =0.012). The absence of a significant effect of groups on the normalized KAM during stair negotiation may be explained by a lower ambulatory speed in the obese KNOA group, that effectively lowers GRFz. Decreasing ambulatory speed may be an effective strategy to lower KAM during stair negotiation.