【Objective】 To find and identify the cause of Kashin-Beck disease (KBD). 【Methods】 We reviewed the bone slices of the KBD autopsy cases preserved in our institute, and observed the leukocyte lesions in peripheral blood smears of KBD children under a light microscope and ultrastructural lesions of leukocytes in KBD children under an electron microscope. We also observed the damages in cultured chondrocytes induced by plasma of children with KBD in an experiment. 【Results】 From the chondrocytes, bone marrow blood cells in KBD autopsy cases and leukocytes of KBD children, the entire pathological process in all the three type cells showed the same specific coagulation necrosis: the nucleus was enlarged; eosinophilic red inclusion bodies in varying sizes appeared in the nucleus, which were accompanied by dissolution and decrease of nuclear chromatin. If the lesion continued to deteriorate and progress, the entire nucleus would transform into a large red mass, and then subsequent series of changes of the inclusion bodies occurred; the cell body shrank and the cytoplasm was stained red. The cultured chondrocytes had replicated a cytopathic model equivalent to specific chondrocyte necrosis in the autopsy cases of KBD, and the viral nucleocapsids were detected in the nuclei of the cultured chondrocytes, with outcomes induced by plasma of the KBD children in the experiment. The same viral nucleocapsids as previously mentioned were also found in the nuclei of the white blood cells of the children with KBD. In the bone marrows of the autopsy cases, hyperemia, edema, fibrin exudation, focal necrosis of hematopoietic matrix and trabecular bone, and fibrosis all appeared. 【Conclusion】 The inclusion body formations were showed in the nuclei of necrotic chondrocytes, bone marrow blood cells of KBD autopsy cases, and in the nuclei of leukocytes in peripheral blood smears of KBD children. The inclusion body formation is the most well-known pathomorphological result of the viral cytocidal infection. Especially important is the positive results of cultured chondrocytes induced by plasma of KBD children in the experiment. What caused the necrosis of the three types of cells in KBD seems to be the twice-detected virus nucleocapsids, suggesting that this virus may have been the cause of KBD. There was an acute osteomyelitis with infectious delayed hypersensitivity in the bone marrows of the autopsy cases of KBD. KBD is a systemic infectious disease caused by the virus. All lesions in the cartilage, bone marrow, and blood are only parts of the systemic lesions.

The relationship of cause-result between low selenium (Se) and Kashin-Beck disease (KBD) was probed by the prospective study of epidemiological method with regarding low-Se as an exposure factor in this paper. 597 healthy children lived in KBD areas with low, middle and high prevalence were divided into the low-Se exposed group and the non-low-Se exposed group according to their Se content in hair. The low-Se exposed group was divided into three subgroups, such as Se content in hair≤110 ng/g, 110 ng/g＜Se content in hair≤150 ng/g and 150 ng/g＜Se content in hair≤200 ng/g, respectively. Six new cases of the total with KBD (incidence was 0.574% person-year) were found in the low-Se exposed group during three years period of the investigation. No new case was found in the non low-Se exposed group . KBD incidence was not significantly different between those two groups. Two new cases were found in children with Se content in hair kept below 110 ng/g during three years (incidence: 1.21% person-year). SMR in each group indicated that the new cases observed in the low-Se exposed group was remarkable lower than the new cases expected. It was not observed that the dose-response relationship between low-Se and KBD, and was not supported that the low-Se was a predominant factor to cause KBD.