An etiogeno-pathological study on Kashin-Beck disease / 西安交通大学学报(医学版)

ABSTRACT

【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.