title: Histopathology of chondronecrosis development in knee articular cartilage in a rat model of Kashin-Beck disease using T-2 toxin and selenium deficiency conditions.
abstract: The objective of this study is to observe pathogenic lesions of joint cartilages in rats fed with T-2 toxin under a selenium deficiency nutrition status in order to determine possible etiological factors causing Kashin-Beck disease (KBD). Sprague-Dawley rats were fed selenium-deficient or control diets for 4 weeks prior to their being exposed to T-2 toxin. Six dietary groups were formed and studied 4 weeks later, i.e., controls, selenium-deficient, low T-2 toxin, high T-2 toxin, selenium-deficient diet plus low T-2 toxin, and selenium-deficient diet plus high T-2 toxin. Selenium deficiencies were confirmed by the determination of glutathione peroxidase activity and selenium levels in serum. The morphology and pathology (chondronecrosis) of knee joint cartilage of experimental rats were observed using light microscopy and the expression of proteoglycans was determined by histochemical staining. Chondronecrosis in deep zone of articular cartilage of knee joints was seen in both the low and high T-2 toxin plus selenium-deficient diet groups, these chondronecrotic lesions being very similar to chondronecrosis observed in human KBD. However, the chondronecrosis observed in the rat epiphyseal growth plates of animals treated with T-2 toxin alone or T-2 toxin plus selenium-deficient diets were not similar to that found in human KBD. Our results indicate that the rat can be used as a suitable animal model for studying etiological factors contributing to the pathogenesis (chondronecrosis) observed in human KBD. However, those changes seen in epiphyseal growth plate differ from those seen in human KBD probably because of the absence of growth plate closure in the rat.
authors.affiliation: Institute of Endemic Diseases, Xi'an Jiaotong University College of Medicine, Xi'an 710061, Shaanxi, People's Republic of China.
authors.forename: Fang
authors.initials: F
authors.lastname: Guan
authors.forename: Siyuan
authors.initials: S
authors.lastname: Li
authors.forename: Zhi-Lun
authors.initials: ZL
authors.lastname: Wang
authors.forename: Haojie
authors.initials: H
authors.lastname: Yang
authors.forename: Senghai
authors.initials: S
authors.lastname: Xue
authors.forename: Wei
authors.initials: W
authors.lastname: Wang
authors.forename: Daiqing
authors.initials: D
authors.lastname: Song
authors.forename: Xiaorong
authors.initials: X
authors.lastname: Zhou
authors.forename: Wang
authors.initials: W
authors.lastname: Zhou
authors.forename: Jing-Hong
authors.initials: JH
authors.lastname: Chen
authors.forename: Bruce
authors.initials: B
authors.lastname: Caterson
authors.forename: Clare
authors.initials: C
authors.lastname: Hughes
mesh_terms: D000821:Animal Feed / Q000009:adverse effects / Q000032:analysis; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D002357:Cartilage Diseases / Q000139:chemically induced / Q000473:pathology*; D002358:Cartilage, Articular / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D019902:Chondrocytes / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005979:Glutathione Peroxidase / Q000097:blood; D006132:Growth Plate / Q000187:drug effects / Q000473:pathology; D057767:Kashin-Beck Disease / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D009336:Necrosis / Q000139:chemically induced / Q000473:pathology; D011509:Proteoglycans / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012643:Selenium / Q000097:blood / Q000172:deficiency* / Q000493:pharmacokinetics; D013264:Stifle / Q000378:metabolism / Q000473:pathology*; D013605:T-2 Toxin / Q000633:toxicity*
chemical_list: D011509:Proteoglycans; D005979:Glutathione Peroxidase; D012643:Selenium; D013605:T-2 Toxin