【摘要】：目的： 牙根吸收是正畸治療中的常見并發(fā)癥，是牙根吸收與修復之間失衡所致。牙骨質是覆蓋在牙根表面的一層礦化結締組織，是牙周膜附著的重要結構。炎癥或異常機械力刺激會激活破牙骨質前體細胞的分化、成熟，從而引起牙骨質的破壞，甚至波及牙本質而導致不可逆性牙根吸收，在這一過程中起中心作用的是成牙骨質細胞。成牙骨質細胞是牙周組織中牙骨質形成的重要功能細胞，在牙根形成、牙骨質修復過程中起著關鍵性作用，其主要功能是分泌新生的牙骨質樣組織，形成牙骨質基質，對已經(jīng)吸收的牙根表面進行修復。地塞米松是一種類固醇類激素，能增強組織的礦化能力，刺激成骨細胞表達礦化相關基因，在成骨過程中有著重要的地位，但國內(nèi)外對于地塞米松作用于成牙骨質細胞后的分子生物學研究很少。因此，本研究的目的是探討地塞米松對小鼠成牙骨質細胞株OCCM-30增殖活性、細胞粘附和礦化功能的影響，以初步了解地塞米松在成牙骨質細胞修復過程中所起的作用，從而為牙骨質再生提供理論依據(jù)。 方法： 本研究將地塞米松作用于成牙骨質細胞株OCCM-30，利用CCK-8法、細胞內(nèi)ALP活性檢測、茜素紅染色鑒定礦化結節(jié)以及Q-PCR檢測等方法，對不同濃度地塞米松作用下的，成牙骨質細胞的增殖能力、粘附及礦化能力進行初步研究。 結果： 1．地塞米松能夠抑制成牙骨質細胞的增殖，且高濃度者（1×10-4mol/L）效果強度高于低濃度者。 2．成牙骨質細胞具有ALP活性，和對照組相比，實驗組ALP活性明顯增高。 3．茜素紅染色結果顯示，實驗組與對照組相比，礦化結節(jié)的數(shù)量呈明顯增多趨勢，，其中以1×10-7mol/L濃度組增加最為明顯。 4．Q-PCR結果顯示，細胞粘附功能相關基因Cadherin-11和N-CadherinmRNA的表達隨地塞米松濃度的增大而增加。 5．Q-PCR結果顯示，礦化相關基因ALP、BSP、OCN、Rumx-2mRNA的表達與對照組相比明顯增高。 結論： 地塞米松可以增加成牙骨質細胞的粘附及礦化功能，并可能由此影響牙根吸收和修復的過程。
[Abstract]:Objective: root resorption is a common complication in orthodontic treatment. Cementum is a layer of mineralized connective tissue covering the root surface and an important structure of periodontal ligament attachment. Inflammation or abnormal mechanical stimulation can activate the differentiation and maturation of osteoclastic precursor cells, which can lead to the destruction of cementum, and even to dentin, leading to irreversible root resorption. Cementoblasts play a central role in this process. Cementoblasts are important functional cells in the formation of cementum in periodontal tissue. They play a key role in root formation and cementum repair. Their main function is to secrete new cementoid tissue to form cemental matrix. Repair the absorbed root surface. Dexamethasone is a steroid hormone that enhances tissue mineralization and stimulates osteoblasts to express mineralization-related genes, which plays an important role in osteogenesis. However, there are few studies on molecular biology of dexamethasone acting on cementoblasts at home and abroad. Therefore, the purpose of this study was to investigate the effects of dexamethasone on OCCM-30 proliferation, cell adhesion and mineralization in mouse cementoblast cell lines, and to explore the role of dexamethasone in the process of cementoblasts repair. So as to provide theoretical basis for cementum regeneration. Methods: in this study, dexamethasone was applied to cementoblast cell line OCCM-30, by CCK-8 assay, intracellular ALP activity detection, alizarin red staining for the identification of mineralized nodules and Q-PCR detection. The effects of dexamethasone on the proliferation, adhesion and mineralization of cementoblasts were studied. Results: 1. Dexamethasone could inhibit the proliferation of cementoblasts, and the effect of dexamethasone at high concentration (1 脳 10-4mol/L) was higher than that of low concentration. 2. The activity of ALP was found in cementoblasts, and the activity of ALP in experimental group was significantly higher than that in control group. 3.The results of alizarin red staining showed that the number of mineralized nodules in the experimental group was obviously increased compared with that in the control group, especially in the 1 脳 10-7mol/L group. 4.Q-PCR results showed that the expression of Cadherin-11 and N-CadherinmRNA increased with the increase of dexamethasone concentration. 5.Q-PCR results showed that the expression of mineralization-related gene ALP,BSP,OCN,Rumx-2mRNA was significantly higher than that of the control group. Conclusion: dexamethasone can increase the adhesion and mineralization of cementoblasts and may affect the process of root resorption and repair.
【學位授予單位】：廣州醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2014
【分類號】：R783.5

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