Kaschin-beck disease (KBD) is a kind of endemic deformable osteoarthropathy that mainly changes the deep layer necrosis of articular epiphyseal cartilage. This disease often presents multiple and symmetrical invasion of intrachondral osteogenesis bone; leading to endochondral osteogenesis disorder, tubular bone shortening and secondary deformity arthropathy. Mainly occurs in children and adolescents.
1 Kaschin-Beck disease model
(1) Reproduction method The conventional full-price nutrient feed, the T-2 toxin is added to the intended intake of quantitative feed at a dose of 100μg/kg body weight per day. The feed is prepared by body weight once a week. The purity of T-2 toxin is 99%, the mother liquor is prepared with anhydrous ethanol, diluted with distilled water, and the quantitative solution is added to the quantitative feed and mixed carefully. The experiment period is 30 days.
(2) Model characteristics During the experiment, the animal's mobility, standing and walking posture, joint shape, feather color, etc. were no different from the control. The weight and length of the left tibia, the frontal transverse diameter of the epiphyseal cartilage on the tibia, and the frontal transverse diameter of the middle tibia. No significant changes. Under a light microscope, the thickness of the right tibial epiphyseal cartilage proliferation layer (measure the average value at 6-8 positions) and the thickness of the proliferation layer to the top of the metaphysis (the latter is marked by the sight of the bone formation) (every 0.5 The thickness of the epiphyseal cartilage proliferation layer in the experimental group was greater than that in the control group.
(3) The previous research reports of comparative medicine have confirmed that when chicks are infected with T-2 toxin (each dose of T-2 toxin 100μg/kg body weight per day), the distance between the legs will increase after the first week, and the knee joint Pathological changes such as mild thickening, difficulty in standing up, and staggering gait; when the chicks were raised for 30 days, no focal chondrocyte necrosis similar to KBD-like lesions was observed in the epiphyseal cartilage of the upper tibia. It shows that the 4-week experiment is sufficient to show the toxic effect of T-2 toxin on cartilage tissue, but the growth and development of the model animal's osteochondral tissue is basically normal, which may be related to the selected animal species, the nutritional composition of the basic feed and the experimental time. As for whether there are significant differences in the responsiveness of different strains of chicks to the model-building factor T-2 toxin, the experimental results have not yet been confirmed.
2 Miniature pig model of Kashin-Beck disease
(1) Reproduction method Experimental miniature pigs are fed low-selenium feed (prepared with low-selenium corn produced in low-selenium areas) for 1 month, and T-2 toxin is added to each per day (prepared with absolute ethanol to make mother liquor every week) When used, it is diluted with water and mixed into the feed) 1.5mg/kg body weight is fed for 67 days, and then for 36 days, 3, 6, and 9 mg of T-2 toxin are added to the feed. The other experimental group added sodium selenite to the feed.
(2) Characteristics of the model Pathological observations showed that the articular cartilage of mini-pigs had deep band necrosis or flaky necrosis. The necrosis could spread to the middle and superficial layers. Red-stained chondrocyte remnants were seen in the necrotic foci, and cell cluster reactions were seen near the necrotic foci. The content of 3 components of proteoglycan in the experimental group of minipigs decreased, suggesting that the effect of T-2 toxin on the metabolism of articular cartilage matrix is mainly manifested as low proteoglycan synthesis and metabolism.
(3) Comparative medicine T-2 toxin is the most toxic of the trichothecenes produced by Fusarium. Recent studies have shown that it is toxic to cartilage. Feeding miniature pigs with T-2 toxin feed for more than 100 days, both the pure toxin group and the toxin plus selenium group of miniature pigs suffered from deep banded necrosis or lamellar necrosis of articular cartilage, and its characteristics are very similar to the pathological changes of human KBD .