SELENIUM DEFICIENCY AND FULVIC-ACID SUPPLEMENTATION INDUCES FIBROSIS OF CARTILAGE AND DISTURBS SUBCHONDRAL OSSIFICATION IN KNEE JOINTS OF MICE - AN ANIMAL-MODEL STUDY OF KASHIN-BECK DISEASE

Kashin-Beck disease is an acquired, chronic and degenerative osteoarti cular disorder. Selenium deficiency and fulvic acid in drinking water have been implicated in the cause of this disease. Pathologically, cho ndronecrosis of the growth plate and articular cartilage and subconseq uent disturbance of ossification were observed in the joints. In this animal model study, mice were fed with a selenium deficient diet and f ulvic acid supplemented drinking water for two generations. In undecal cified histological preparations of bone we carried out histological s taining to detect mineralized and unmineralized bone and cartilage. Th e results revealed that selenium deficiency and fulvic acid supplement ation induced degeneration of the articular cartilage in the knee join ts of mice. Dynamic fluorescent labelling of ossification, enzyme hist ochemical detection of alkaline phosphatase activity in osteoblasts an d a typical immunohistochemical localization of collagens type I and I I indicated the development of fibrocartilage at the articular surface of knee joints, resembling the early stages of osteoarthrosis. This b ecame obvious by disturbed development of the articular space and meni scus, markedly impaired formation of subchondral bone and early differ entiation failure during enchondral ossification. This animal model pr ovides an approach to study the molecular pathogenesis of Kashin-Beck disease.