Abstract
Osteoarthritis (OA) is a progressive degenerative disease characterized by cartilage degradation, synovial inflammation, subchondral sclerosis and osteophyte formation. It has a multifactorial etiology with potential contributions from heredity, endocrine function, abnormal mechanical load and nutrition. Of particular considerations are trace element status. Several trace elements, such as boron and magnesium are essential for normal development of the bone and joint in human. While cadmium correlates with the severity of OA. The present review focuses on the roles of trace elements (boron, cadmium, copper, iron, magnesium, manganese, selenium, zinc) in OA and explores the mechanisms by which they act.
Highlights
Osteoarthritis (OA) is a prevalent age-related degenerative disease, which is characterized by degeneration of articular cartilage and damage to the other joint tissues [1]
Selenium can improve the antioxidant activity of chondrocytes under oxidative stress, scavenging reactive oxygen species, reducing the adverse effect of reactive oxygen species on cartilage homeostasis, relieving the cartilage damage induced by oxidative stress, thereby protecting cartilage
Many trace elements affect the onset and progression of OA. Some trace elements such as boron and magnesium are conducive to the prevention and treatment of OA
Summary
Osteoarthritis (OA) is a prevalent age-related degenerative disease, which is characterized by degeneration of articular cartilage and damage to the other joint tissues [1]. Relieving OA symptom; Promoting cartilage injury healing; Enhancing cartilage formation; Promoting articular cartilage and subchondral bone regeneration; Activating cartilage immune response; Enhancing anti-inflammatory cytokine secretion, inhibiting inflammatory response, reducing cartilage tissue lesion; Restraining NO release, enhancing anti-catabolism; Improving collagen cross-linking, enhancing COL II synthesis; Increasing chondrocyte viability; Promoting chondrocyte proliferation and maturation; Raising chondrogenic gene expression, enhancing chondrogenesis differentiation of MSCs
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