[The Role of Platelet-Derived Growth Factor-AA in the Pathogenesis and Development of Osteoarthritis].

Osteoarthritis (OA) is a chronic degenerative disease involving the entire joint. The pathogenesis and progression of OA bear close connection to the destruction and the abnormal metabolism of cartilage, subchondral bones and synovium. Platelet derived growth factor-AA (PDGF-AA) is a critical mitogenic and chemotactic factor for a variety of cells, including chondrocytes, mesenchymal stem cells, osteoclasts and osteoblasts, and PDGF-AA promotes effective wound repair. This paper reviewed the pathological changes of cartilage, subchondral bones and synovium in the process of OA development, and summarized research progress regarding the effect of PDGF-AA on the tissues and related cells mentioned above. Current studies have basically clarified the pathological changes of cartilage, subchondral bones and synovium in OA patients, and have shown that PDGF-AA serves critical regulatory function in the tissues or cells involved in OA, the internal mechanism of which remains unclear, though. More studies should be done to find ways to apply PDGF-AA for clinic purpose and to diagnose and treat OA on the cellular basis.

[Research Progress of Fibroblast Growth Factor 8's Role in the Regulation of Bone Development and Homeostasis].

The proper development and the homeostasis maintenance of bones are important prerequisites for the normal functioning of the human body. Bone developmental deformities or homeostasis disorders, such as Kashin-Beck disease, craniosynostosis, cleft palate and osteoarthritis, severely affect the life of patients, causing significant stress to the family and the society. Fibroblast growth factor 8 (FGF8) plays multiple functions through the course of the life of organisms. Abnormal expression of FGF8 may cause disorders of bone homeostasis and developmental abnormalities of bones. More and more studies have found that FGF8 may play an important role in bone development and may become a potential therapeutic target. Herein, we reviewed the role of FGF8 in a variety of skeletal abnormalities, intending to provide new perspectives for the prevention and treatment of related diseases in the future.

[Research Progress in Glucose Metabolism of Chondrocytes].

Chondrocytes have a limited supply of glucose and oxygen for metabolism since articular cartilages are relatively avascular. We herein reviewed the characteristics of chondrocyte glucose metabolism and the new research progress in chondrocyte glucose metabolism in the osteoarthritis process. Current research has shown that chondrocytes obtain glucose from synovial fluids and subchondral bones, take in glucose via specific glucose transporters, and metabolize glucose mainly through glycolysis and mitochondrial respiration to produce adenosine triphosphate (ATP). Glucose metabolism in chondrocytes is distinctive because it relies much more on glycolysis rather than mitochondrial respiration for ATP production, and shows Warburg effect and Crabtree effect. In osteoarthritic chondrocytes, the glucose metabolism disorder is presented as further suppression of mitochondrial respiration, over-active or impaired glycolysis, and decreased total production of ATP. However, the significance of the glucose supply for chondrocytes from synovial fluids and subchondral bones remains undefined. There are still disputes in the understanding of the changes in glycolytic pathways in osteoarthritic chondrocytes. Therefore, future research is needed to explore the characteristics of glucose metabolism in normal and osteoarthritic chondrocytes in order to develop new diagnostic and therapeutic strategies for osteoarthritis.