动物模型,牙龈增生 z-bo 2020-08-08 518

　　(1) Reproduction method Take clean-grade ICR male mice with a body weight of 18-22 g for 6 to 8 weeks, and feed them with cyclosporin A (Cyclosporin A, CsA) at a dose of 30 mg/kg body weight every day for 4 consecutive weeks. High-quality olive oil was administered for 4 weeks and sacrificed by cervical dislocation. The entire anterior mandibular specimen was immediately taken and fixed in 10% neutral formaldehyde buffer for about 48 hours. Measure the gingival vertical height, mesiodistal width and the thickness between the lips and tongue of the model animal's mandibular anterior teeth under a stereo microscope, and calculate the product of the three, which is approximately the gingival volume. The above specimens were decalcified with 100g/L EDTA for 20-24 days, routinely dehydrated and embedded, and longitudinally sliced the mandibular anterior gingiva according to the long-axis sagittal plane of the tooth, stained with HE, and observed the gingival epithelium and gingival connective tissue under a light microscope. Pathological changes. At the same time, under a light microscope, an image analysis system was used to measure the epithelial thickness of the lingual gingival margin of the mouse mandibular anterior teeth.

　　(2) Model characteristics At 4 weeks, the lingual gingiva of the model animal's mandibular anterior teeth showed spherical hypertrophy, and the gingival margin was hypertrophic. The posterior mandibular gingiva also showed different degrees of hypertrophy, but not as significant as the anterior teeth. Microscopic histopathological observations showed that at 4 weeks, the model animal’s gingiva had the typical histopathological changes of CsA-induced gingival hyperplasia: gingival marginal epithelium, sulcus epithelium and combined epithelium all proliferated and thickened, and the cell volume of each layer of epithelium increased. And the number of layers has also increased, the spine hyperplasia is more obvious, and the cell body is hypertrophy; the amorphous material (stratum corneum) of the epithelium from the epithelium in the sulcus to the gingival margin is also thickened; there are obvious epithelial spikes or spikes widening at the gingival margin And stretched deep into the connective tissue, bifurcation formed or connected to each other in the lamina propria into a mesh; a large amount of extracellular matrix components in the connective tissue were accumulated and blood vessels expanded.

　　(3) Comparative medicine Cyclosporine A, as a highly effective immunosuppressant, has been widely used to prevent and treat rejection after tissue and organ transplantation. However, when the drug is used clinically, it can cause certain side effects such as hepatotoxicity, nephrotoxicity and neurotoxicity to the body. Since the 1980s, foreign scholars have generally observed that the important side effect of the drug in the oral cavity is drug-induced gingival hyperplasia, but the scope of the clinical incidence of CsA-induced gingival hyperplasia is not consistent. CsA can act on the target receptors of the gingival tissue through saliva, blood, and gingival crevicular fluid, causing gingival epithelial hyperplasia, increased number of epithelial layers, spine hyperplasia and epithelial spike prolongation, bifurcation formation, or in the lamina propria. Spikes are interconnected into a network, a large amount of extracellular matrix components in connective tissue are accumulated, and blood vessels are dilated. It is speculated that the increase in androgen synthesis in fibroblasts caused by CsA may be an important factor in the pathogenesis of gum hyperplasia. At present, the pathogenesis of human drug-induced gingival hyperplasia induced by CsA has not been clarified, and a good animal model is an effective means to study its pathogenesis. The pathological changes of this model are similar to the clinical manifestations of human drug-induced gingival hyperplasia, and it is an ideal animal model for studying the pathogenesis of human gingival hyperplasia induced by CsA.