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
Cl. Yang et al., 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, Virchows Archiv. A. Pathological anatomy and histology, 423(6), 1993, pp. 483-491
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.