RESUMEN
【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.
RESUMEN
Kashin-Beck disease(KBD) is an endemic and deforming osteochondropathy and its etiology remains unclear up to now.The prevalence of the disease is the severest in the western China and the effective methods for prevention and cure still need further study.This article summarized the progression and problems to be investigated for three main hypotheses of KBD by reviewing literature published at home and abroad.Integrating with his own research work and his team members,the author suggested that excessive apoptosis and dedifferentiation of chondrocytes besides classic chondrocytic necrosis in KBD growth plate and articular cartilage,differences of gene expression profiles in cartilage and peripheral blood mononuclear cells,proteomic markers and short tandem repeat polymorphism in KBD patients were significantly different from those of the healthy subjects from both KBD-areas and non KBD-areas,and those of osteoarthritis patients.The important objectives in the future are to understand ① the gene and proteomic markers for chondrocytic necrosis in KBD,② environmental factors that cause the damage to KBD chondrocytes,③ the way it selectively impairs chondrocytes in the deep zone of growth and joint cartilage by interacting with susceptible gene related to KBD,and ④ effective intervention methods.