(1) Replication method Rats weighing 180~220g are anesthetized by intraperitoneal injection of sodium pentobarbital at a dose of 30mg/kg body weight. After anesthesia, the attachment of the gingival epithelium is destroyed, and then the neck of the tooth (taken in the tooth Two stitches on the upper neck of the neck), prednisolone acetate was injected into the quadriceps femoris muscle of the hind limbs of the rat, 1.25 mg/mouse, for 3 days, and the Keyes 2000 formula feed (fructose 56%, degraded milk powder 28%) , Flour 6%, yeast 4%, clover meal 3%, animal liver meal 1%, salt 2%) and a small amount of vegetables plus the rat’s own fecal water. At the 7th week and the 11th week after the operation, the animals were taken to record the gingival index (GI) value, and then sacrificed for routine pathological tissue sectioning and observation under a light microscope.
(2) Model features: The histopathological observation of the model animal microscope showed that the gingival epithelium proliferated and connected into a network at 1 week, the blood vessels were dilated and congested, and there was a large number of inflammatory cell infiltration; the gingival epithelium was proliferated, and there was some vasodilation and congestion in the connective tissue. A small amount of acute inflammatory cells and a large number of chronic inflammatory cell infiltration can be seen, the periodontal main fiber bundles are broken, most of the alveolar bone is obviously absorbed horizontally (more Haxipu’s lacuna and osteoclasts are visible), and a few are accompanied by vertical absorption. Combined with the epithelium, it can be seen that the nail process is formed, which proliferates toward the root and peels off the tooth to form a periodontal pocket, with many chronic inflammatory cells in the pocket. This model uses the endocrine disorders in rats, supplemented by periodontal disease diet (high-sugar food plus rat’s own feces) as a local factor, resulting in a powerful infectious agent that can accelerate or aggravate the periodontal inflammation and tooth Pathological changes such as trough bone resorption shorten the time for animal model establishment. This model uses silk thread to ligate the teeth and sew 2 stitches on the gums to fix them. The silk thread on the gum margin provides a place for high sugar to attach. The high sugar diet also provides conditions for the growth of plaque bacteria. In addition, the stool contains bacteria. As an infectious substance, it can directly act on periodontal tissues. Long-term continuous stimulation can cause disease. The model making method is simple and easy to implement, the modeling time is short, and the lesion features are typical.
(3) Comparative Medicine Periodontitis, as an infectious and destructive disease, is the main cause of tooth loss in adults. The establishment of an ideal experimental periodontitis animal model can provide experimental basis for the investigation of the etiology and clinical process of periodontal inflammation damage, and can be used for the screening of therapeutic drugs. This model production method confirms that simple systemic factors acting on animals cannot cause periodontitis, while local stimulating factors are the key to inducing animal periodontitis. Systemic factors can be aggravated in the presence of local irritating factors or inflammatory damage. The development of periodontitis. Systemic factors combined with local factors are more obvious than periodontitis symptoms caused by local factors or systemic factors alone. It can be seen that during the onset of periodontitis, local factors are the initiating factors that directly cause inflammation, and systemic factors are the basis of the disease. Under the action of local factors, they promote the aggravation of the disease and accelerate the destruction of periodontal tissue. The pathogenesis of this model is closer to that of human periodontitis, and its application value is higher than that of periodontitis animal models replicated by other methods.