本文選題：牙周炎 + 骨吸收��； 參考：《鄭州大學(xué)》2017年碩士論文

【摘要】：背景在牙周炎病變過程中,炎性細(xì)胞因子和化學(xué)因子的存在上調(diào)了核因子κB受體活化因子配體(Receptor activator of nuclear factor-kappa B ligand,RANKL)的表達(dá),RANKL活化破骨細(xì)胞(Osteoclast,OC)前體細(xì)胞,隨后成熟的多核OC吸附到礦化的骨基質(zhì)表面進(jìn)行骨吸收。牙槽骨吸收是導(dǎo)致牙齒松動(dòng)和脫落的主要原因。預(yù)防牙槽骨的吸收,促進(jìn)牙槽骨的修復(fù)和再生是治愈牙周炎的關(guān)鍵。β-隱黃素是一種發(fā)現(xiàn)于水果和蔬菜中的類胡蘿卜素。β-隱黃素可以通過刺激成骨細(xì)胞(Osteoblast,OB)形成骨,抑制OC吸收骨來預(yù)防骨組織的喪失。以往的研究發(fā)現(xiàn)血清中低水平的β-隱黃素和牙周炎患病率增加有關(guān),牙周炎患者血清中β-隱黃素水平明顯較低;β-隱黃素可以抑制內(nèi)毒素(Lipopolysaccharide,LPS)誘導(dǎo)的炎癥反應(yīng),上調(diào)骨保護(hù)素(Osteoprotegerin,OPG)/RANKL的比值;注射β-隱黃素可以抑制LPS-誘導(dǎo)的小鼠牙槽骨骨密度(Bone mineral density,BMD)的降低。這些研究表明,β-隱黃素影響牙周炎的發(fā)生發(fā)展。然而,關(guān)于β-隱黃素對(duì)牙周炎牙槽骨吸收的影響研究較少,且其作用機(jī)理尚不十分明確。目的本研究的目的是通過檢測牙槽骨喪失量(Alveolar bone loss,ABL)、OC數(shù)目、RANKL及OPG的表達(dá)來評(píng)估β-隱黃素對(duì)大鼠實(shí)驗(yàn)性牙周炎牙周組織的作用,檢測其對(duì)牙周炎牙槽骨吸收的影響并分析其作用機(jī)制。方法30只雄性SD大鼠隨機(jī)分為三組:1)正常對(duì)照組(N);2)牙周炎模型組(P);3)β-隱黃素干預(yù)組(E)。P組、E組進(jìn)行實(shí)驗(yàn)性牙周炎造模,E組在造模的同時(shí)用β-隱黃素進(jìn)行干預(yù)。實(shí)驗(yàn)性牙周炎模型的誘導(dǎo):直徑0.2mm的正畸結(jié)扎絲環(huán)繞在雙側(cè)上頜第二磨牙牙頸部,同時(shí)在頰側(cè)牙齦齦溝內(nèi)注射大腸桿菌LPS(30μl/鼠),每48h注射1次,共3次。作為對(duì)照,N組注射等量的生理鹽水。β-隱黃素干預(yù):E組在注射LPS后在相同位點(diǎn)注射β-隱黃素(12μl/鼠),每48h 1次,共3次。P組注射等量的玉米油代替。實(shí)驗(yàn)第8天大鼠腹腔注射過量的10%水合氯醛處死,取雙側(cè)上頜組織(含牙齒、牙齦、牙周膜、牙槽骨)。右側(cè)上頜組織進(jìn)行形態(tài)學(xué)分析,測量釉牙骨質(zhì)界(Cemento-enamel junction,CEJ)到牙槽嵴頂(Alveolar bone crest,ABC)的距離。左側(cè)上頜組織進(jìn)行組織學(xué)和免疫組織化學(xué)分析,檢測牙槽嵴頂附近RANKL及OPG的表達(dá)。用抗酒石酸酸性磷酸酶(Tartrate-resistant acid phosphatasem,TRAP)檢測OC的數(shù)目。結(jié)果P組與N組相比,ABL增加、結(jié)合上皮(junctional epithelium,JE)根方遷移、牙槽骨吸收明顯,表明P組牙周炎建模成功。E組與P組相比,ABL減少,炎癥細(xì)胞浸潤減少,RANKL免疫標(biāo)記細(xì)胞及TRAP陽性多核細(xì)胞減少,OPG基因表達(dá)上調(diào)(P0.05)。而E組與N組相比,ABL和OC數(shù)目差異無統(tǒng)計(jì)學(xué)意義(P0.05)。結(jié)論β-隱黃素影響牙周炎的發(fā)生發(fā)展,抑制了牙周炎牙槽骨喪失。其可能的作用機(jī)制是通過下調(diào)RANKL/OPG的比值,減少OC的數(shù)目而發(fā)揮作用。
[Abstract]:Background in the process of periodontitis, the presence of inflammatory cytokines and chemical factors up-regulates the expression of nuclear factor 魏 B receptor activating factor ligand Receptor activator of nuclear factor-kappa B ligand RANKL and RANKL activated osteoclast (Osteoclastus) precursor cells. Then the matured polynuclear OC adsorbed on the surface of the mineralized bone matrix for bone resorption. Alveolar bone resorption is the main cause of tooth loosening and abscission. Preventing alveolar bone resorption and promoting alveolar bone repair and regeneration are the key to cure periodontitis. 尾 -Cryptoflavin, a carotenoid found in fruits and vegetables, can form bone by stimulating osteoblasts. Inhibition of OC absorption of bone to prevent loss of bone tissue. Previous studies have found that the low level of serum 尾 -cryptoflavin is associated with an increase in the prevalence of periodontitis, and that the serum level of 尾 -cryptoflavin is significantly lower in patients with periodontitis, and that 尾 -cryptoflavin can inhibit the inflammatory response induced by endotoxin lipopolysaccharide (LPSs). The ratio of osteoprotegerin / RANKL was up-regulated, and 尾 -cryptoflavin could inhibit the decrease of bone mineral density induced by LPS-induced bone density. These studies suggest that 尾-Cryptoflavin affects the occurrence and development of periodontitis. However, the effect of 尾 -Cryptoflavin on alveolar bone resorption in periodontitis is less studied, and its mechanism is not very clear. Objective to evaluate the effect of 尾 -cryptoflavin on periodontal tissue in rats with experimental periodontitis by detecting the number of alveolar bone loss and the expression of RANKL and OPG in alveolar bone. To detect the effect on alveolar bone resorption in periodontitis and analyze its mechanism. Methods Thirty male Sprague-Dawley rats were randomly divided into three groups: control group (n = 1) and control group (n = 2). Induction of experimental periodontitis model: orthodontic ligation of diameter 0.2mm was performed around the neck of bilateral maxillary second molar, and Escherichia coli LPS(30 渭 l / rat was injected into the gingival sulcus of buccal side, once every 48 hours, for 3 times. 尾 -Cryptoflavin injected 12 渭 l of 尾 -Cryptoflavin at the same site after injection of LPS, once every 48 hours, and the same amount of corn oil was injected into the group of 尾 -Cryptoflavin at the same site after the intervention of 尾 -Cryptoflavin once every 48 hours. Rats were killed with 10% chloral hydrate injected intraperitoneally on the 8th day of the experiment, and bilateral maxillary tissues (including teeth, gingiva, periodontal membrane and alveolar bone) were taken. The distance between Cemento-enamel junction (CEJ) and Alveolar bone crestus (ABC) was measured. The expression of RANKL and OPG near alveolar crest was detected by histological and immunohistochemical analysis in left maxillary tissue. The number of OC was detected by tartrate-resistant acid phosphatasemem TRAPs resistant to tartaric acid phosphatase. Results compared with group N, the ABL in group P was increased, the root side migration and alveolar bone resorption were obvious, which indicated that the ABL of periodontitis in group P was less than that in group P. Inflammatory cell infiltration decreased RANKL immunolabeled cells and TRAP positive multinucleated cells decreased the expression of OPG gene upregulated (P0.05). There was no significant difference in the number of ABL and OC between group E and group N (P 0.05). Conclusion 尾 -cryptoflavin affects the occurrence and development of periodontitis and inhibits the loss of alveolar bone in periodontitis. Its possible mechanism is to reduce the number of OC by down-regulating the ratio of RANKL/OPG.
【學(xué)位授予單位】：鄭州大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R781.42

【參考文獻(xiàn)】

相關(guān)期刊論文 前5條

1 唐琪;王仁飛;陳莉麗;;實(shí)驗(yàn)性牙槽骨吸收動(dòng)物模型的建立[J];浙江實(shí)用醫(yī)學(xué);2008年01期

2 蘇軍;劉魯川;毛永利;李楠;潘利峰;溫秀杰;;SD大鼠牙周炎動(dòng)物模型的建立[J];牙體牙髓牙周病學(xué)雜志;2006年11期

3 王麗珍,李德懿;牙周病常用實(shí)驗(yàn)動(dòng)物牙體解剖、牙周組織學(xué)研究與評(píng)價(jià)[J];上海口腔醫(yī)學(xué);2004年02期

4 羅云綱,楊濤,許力強(qiáng),黃洋;牙周炎動(dòng)物模型的建立[J];吉林大學(xué)學(xué)報(bào)(醫(yī)學(xué)版);2004年02期

5 楊明華,張東生,陳湘華,呂英,武影;大黃素抑制脂多糖誘導(dǎo)性動(dòng)物牙周炎的組織學(xué)研究[J];江蘇醫(yī)藥;2002年09期

，

本文編號(hào)：1856653