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

C Yang; E Wolf; K Röser; G Delling; P K Müller

Selenium deficiency and fulvic acid supplementation induces fibrosis of cartilage and disturbs subchondral ossification in knee joints of mice

Standard

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. / Yang, C; Wolf, E; Röser, K; Delling, G; Müller, P K.

in: Virchows Arch A Pathol Anat Histopathol, Jahrgang 423, Nr. 6, 1993, S. 483-91.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Yang, C, Wolf, E, Röser, K, Delling, G & Müller, PK 1993, '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 Arch A Pathol Anat Histopathol, Jg. 423, Nr. 6, S. 483-91.

APA

Yang, C., Wolf, E., Röser, K., Delling, G., & Müller, P. K. (1993). 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 Arch A Pathol Anat Histopathol, 423(6), 483-91.

Vancouver

Yang C, Wolf E, Röser K, Delling G, Müller PK. 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 Arch A Pathol Anat Histopathol. 1993;423(6):483-91.

Bibtex

@article{7749a6a12a2341cb8d89fc9e1da7df96,

title = "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",

abstract = "Kashin-Beck disease is an acquired, chronic and degenerative osteoarticular disorder. Selenium deficiency and fulvic acid in drinking water have been implicated in the cause of this disease. Pathologically, chondronecrosis of the growth plate and articular cartilage and subconsequent disturbance of ossification were observed in the joints. In this animal model study, mice were fed with a selenium deficient diet and fulvic acid supplemented drinking water for two generations. In undecalcified histological preparations of bone we carried out histological staining to detect mineralized and unmineralized bone and cartilage. The results revealed that selenium deficiency and fulvic acid supplementation induced degeneration of the articular cartilage in the knee joints of mice. Dynamic fluorescent labelling of ossification, enzyme histochemical detection of alkaline phosphatase activity in osteoblasts and a typical immunohistochemical localization of collagens type I and II indicated the development of fibrocartilage at the articular surface of knee joints, resembling the early stages of osteoarthrosis. This became obvious by disturbed development of the articular space and meniscus, markedly impaired formation of subchondral bone and early differentiation failure during enchondral ossification. This animal model provides an approach to study the molecular pathogenesis of Kashin-Beck disease.",

keywords = "Animals, Benzopyrans, Cartilage, Articular, Collagen, Disease Models, Animal, Female, Fibrosis, Knee Joint, Male, Mice, Microscopy, Fluorescence, Osteoarthritis, Selenium, Journal Article, Research Support, Non-U.S. Gov't",

author = "C Yang and E Wolf and K R{\"o}ser and G Delling and M{\"u}ller, {P K}",

year = "1993",

language = "English",

volume = "423",

pages = "483--91",

journal = "VIRCHOWS ARCH",

issn = "0945-6317",

publisher = "Springer",

number = "6",

}

RIS

TY - JOUR

T1 - Selenium deficiency and fulvic acid supplementation induces fibrosis of cartilage and disturbs subchondral ossification in knee joints of mice

T2 - an animal model study of Kashin-Beck disease

AU - Yang, C

AU - Wolf, E

AU - Röser, K

AU - Delling, G

AU - Müller, P K

PY - 1993

Y1 - 1993

N2 - Kashin-Beck disease is an acquired, chronic and degenerative osteoarticular disorder. Selenium deficiency and fulvic acid in drinking water have been implicated in the cause of this disease. Pathologically, chondronecrosis of the growth plate and articular cartilage and subconsequent disturbance of ossification were observed in the joints. In this animal model study, mice were fed with a selenium deficient diet and fulvic acid supplemented drinking water for two generations. In undecalcified histological preparations of bone we carried out histological staining to detect mineralized and unmineralized bone and cartilage. The results revealed that selenium deficiency and fulvic acid supplementation induced degeneration of the articular cartilage in the knee joints of mice. Dynamic fluorescent labelling of ossification, enzyme histochemical detection of alkaline phosphatase activity in osteoblasts and a typical immunohistochemical localization of collagens type I and II indicated the development of fibrocartilage at the articular surface of knee joints, resembling the early stages of osteoarthrosis. This became obvious by disturbed development of the articular space and meniscus, markedly impaired formation of subchondral bone and early differentiation failure during enchondral ossification. This animal model provides an approach to study the molecular pathogenesis of Kashin-Beck disease.

AB - Kashin-Beck disease is an acquired, chronic and degenerative osteoarticular disorder. Selenium deficiency and fulvic acid in drinking water have been implicated in the cause of this disease. Pathologically, chondronecrosis of the growth plate and articular cartilage and subconsequent disturbance of ossification were observed in the joints. In this animal model study, mice were fed with a selenium deficient diet and fulvic acid supplemented drinking water for two generations. In undecalcified histological preparations of bone we carried out histological staining to detect mineralized and unmineralized bone and cartilage. The results revealed that selenium deficiency and fulvic acid supplementation induced degeneration of the articular cartilage in the knee joints of mice. Dynamic fluorescent labelling of ossification, enzyme histochemical detection of alkaline phosphatase activity in osteoblasts and a typical immunohistochemical localization of collagens type I and II indicated the development of fibrocartilage at the articular surface of knee joints, resembling the early stages of osteoarthrosis. This became obvious by disturbed development of the articular space and meniscus, markedly impaired formation of subchondral bone and early differentiation failure during enchondral ossification. This animal model provides an approach to study the molecular pathogenesis of Kashin-Beck disease.

KW - Animals

KW - Benzopyrans

KW - Cartilage, Articular

KW - Collagen

KW - Disease Models, Animal

KW - Female

KW - Fibrosis

KW - Knee Joint

KW - Male

KW - Mice

KW - Microscopy, Fluorescence

KW - Osteoarthritis

KW - Selenium

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

M3 - SCORING: Journal article

C2 - 8291220

VL - 423

SP - 483

EP - 491

JO - VIRCHOWS ARCH

JF - VIRCHOWS ARCH

SN - 0945-6317

IS - 6

ER -