实验性牙周炎动物模型研究

目的：建立一种近似人类临床牙周炎动物模型。方法：将大鼠随机分成对照组及实验组，并分别给予生理盐水肌肉注射、左上颌第2磨牙钢丝结扎和醋酸泼尼松龙肌肉注射。于实验第6周及第8周分2批处死大鼠。结果：实验组动物激素注射第4天后便出现了进食减少、倦怠少动等表现，符合中医肾虚的症状，并且出现了牙槽骨疏松、牙槽嵴吸收、牙周袋形成及破骨细胞活跃等病理性改变。对照组大鼠则无上述表现。结论：牙间结扎加糖皮质激素注射的方法可成功地建立近似于人类临床牙周炎的动物模型，为研究牙周炎提供了很好的方法。     

人骨保护素质粒转染抑制大鼠实验性牙周炎骨吸收的研究

目的:将自行构建的质粒载体pcDNA3.1-h OPG,通过体内转染,评价OPG直接基因转染疗法对大鼠实验性牙周炎牙槽骨吸收的影响,为牙周炎以及种植体周炎的生物治疗提供实验依据.方法:将30只SD大鼠随机分为3组,即I组生理盐水组(n=10,100μg/只)、Ⅱ组pcDNA3.1(-)组(n=10,100μg/只)、Ⅲ组pcDNA3.1-hOPG组(n=10,100μg/只).通过丝线结扎、接种牙周炎可疑致病菌、喂高糖软食诱发实验性牙周炎.结扎28d后处死,通过大体标本、组织学等观察牙槽骨吸收、OPG及破骨细胞变化.结果:Ⅲ组结扎侧OPG表达强度增加,牙槽骨吸收量减少(P＜0.05),活化破骨细胞数降低(P＜0.05).结论:OPG重组质粒转染,减少破骨细胞数量,有效减缓实验性牙周炎引起的牙槽骨吸收破坏.     

不同结扎方法对失神经支配大鼠牙周炎的影响

目的：比较牙颈部丝线结扎＋高糖饮食、正畸结扎丝结扎＋高糖饮食对失下牙槽神经支配下大鼠牙周炎进展的影响。方法：将80只2月龄SPF级Wistar雄性大鼠随机分为5组：离断下牙槽神经＋丝线结扎下颌第一磨牙＋高糖饮食组（P1组）;离断下牙槽神经＋正畸结扎丝结扎下颌第一磨牙＋高糖饮食组（P2组）;单纯诱导牙周炎组（P3组）;单纯离断下牙槽神经组（P4组）;假手术组（N组）。分别在1周、2周、4周、6周取标本,进行临床指标观察和组织学观察。结果： P4组和N组未见牙周炎表现, P1、 P2、 P3组均出现牙周炎, P1组较P2、 P3组牙周损害出现早且严重。结论：丝线结扎下颌第一磨牙＋高糖饮食更容易诱导失神经支配的大鼠形成牙周炎。     

实验性糖尿病牙周炎骨丧失动物模型研究

目的:建立实验性糖尿病牙周炎骨丧失动物模型,以进一步揭示糖尿病加重牙周炎骨丧失的细胞学机制.方法:选用6周龄雄性SD大鼠62只,随机分为糖尿病牙周炎组(DP)、牙周炎组(P)以及正常对照组(N).采用一次性腹腔注射链脲佐菌素(streptozotocin,STZ)的方法诱导大鼠糖尿病模型,采用丝线结扎联合口内接种细菌的方法建立牙周炎模型.动物分别于丝线结扎后3周和6周分批处死,进行HE染色、TRAP染色.观测指标包括:牙槽骨丧失,组织病理学比较,炎症区破骨细胞计数等.资料采用单因素方差分析统计学处理.结果:丝线结扎后3周和6周,大鼠牙槽骨丧失在N组与P组、N组与DP组、P组与DP组不同,组间两两比较均有统计学差异(P＜0.05),牙槽骨丧失DP组＞P组＞N组.炎症区单位长度破骨细胞数在N组、P组、DP组不同,N组与P组比较,N组与DP组比较、P组与DP组比较均有统计学差异(P＜0.05),其炎症区单位长度破骨细胞数DP组＞P组＞N组.结论:糖尿病可加重牙周炎牙周组织破坏,糖尿病条件下牙周炎骨丧失明显增加.糖尿病可能通过促进炎症部位破骨细胞生成,增强骨吸收,促进牙周炎骨丧失.     

牙周炎动物模型初步研究

将Ｗｉｓｔａｒ大白鼠３８只分成四组：①对照组：每只每日肌注生理盐水０．４ｍｌ；②激素组：每只每日肌注醋酸强的松龙１．２５ｍｇ，溶于０．４ｍｌ生理盐水中；③结扎组：上颌第一磨牙牙颈部用正畸钢丝结扎；④激素＋结扎组。结果表明：肌注醋酸强的松龙组第６天大白鼠出现了中医辨证的肾虚临床症状；结扎组造成了牙周组织局部菌斑蓄积，导致局部机械性和炎症性刺激变化；两者共同作用下，激素＋结扎组大白鼠出现类似人类牙周炎     

实验性糖尿病牙周炎诱导骨细胞凋亡的初步研究

目的初步探讨糖尿病牙周炎条件下骨细胞的凋亡情况。方法选用6wk雄性SD大鼠62只,随机分为糖尿病牙周炎组（DP,n=22）、牙周炎（P,n=20）以及正常对照组（N,n=20）。采用一次性腹腔注射STZ（55mg/kg）的方法建立大鼠糖尿病模型,注射STZ后1wk检测血糖,血糖≥16.65mmol/L者定为糖尿病大鼠。采用丝线结扎大鼠上颌第二磨牙联合口内接种细菌的方法建立牙周炎模型。动物分别于丝线结扎后3wk和6wk分批处死,进行HE染色和原位细胞凋亡检测。观察指标包括：牙槽骨丧失（ABL）,骨细胞计数,骨细胞凋亡百分率。资料采用单因素方差分析统计学处理。结果丝线结扎后3周和6周,大鼠牙槽骨丧失在N组与P组、N组与DP组、P组与DP组不同,组间两两比较均有统计学意义（P〈0.05）,牙槽骨丧DP组〉P组〉N组。与N组比较,P组和DP组单位面积骨细胞数均减少,与P组比较,DP组单位面积骨细胞数亦显著减少（P〈0.05）。在丝线结扎后3周和6周,糖尿病牙周炎组（DP）骨细胞凋亡百分率均达到牙周炎组（P）的2倍左右。结论糖尿病条件下牙周炎骨丧失明显增加,糖尿病可加强牙周炎条件下牙周组织中骨细胞的凋亡,降低骨细胞的数量。     

Notch信号对骨免疫的调控及其在牙周炎发生中的可能作用

破骨细胞是进行性骨吸收的主要功能细胞,其与T细胞、B细胞间的相互影响在生理性骨改建中发挥重要作用。免疫细胞活性异常和破骨细胞过度活跃是引发病理性骨改建(如发生在牙周炎中的牙槽骨吸收)的病理基础。Notch信号是一类种系发生高度保守的跨膜蛋白,不仅参与调控T细胞和B细胞的分化和功能,而且对骨改建中的主要功能细胞-破骨细胞的分化有重要的调控作用。因此,深入探讨Notch信号在骨免疫中的作用机制,可为牙周炎的临床治疗提供新的思路和依据。本文就Notch信号对骨免疫的调控机制及其在牙周炎发生中的可能作用作一综述。     

牙周炎中M1型巨噬细胞与破骨细胞形成相关性研究

目的:探究牙周炎中M1型巨噬细胞与破骨细胞形成的相关性.方法:取2月龄C57BL/6J小鼠,丝线结扎建立右侧上颌牙周炎模型,左侧上颌作为自身对照.术后7 d收样,Micro-CT扫描分析牙槽骨吸收情况,苏木素-伊红(HE)、抗酒石酸酸性磷酸酶(TRAP)、CD80和诱导型一氧化氮合酶(iNOS)免疫荧光染色观察破骨细胞...     

微小RNAs在破骨细胞分化调控中的研究进展

微小RNAs（miRNAs）是一组由22~25个核苷酸构成的非编码单链RNA,具有基因转录后调控功能,广泛参与细胞增殖、分化、凋亡、组织炎症及肿瘤发生等过程。破骨细胞是体内唯一具有骨吸收功能的细胞,受成骨细胞及炎症因子的调控,在牙周炎骨吸收过程中具有重要作用。miRNAs对破骨细胞的分化、成熟及功能具有多重调控作用。本文就miRNAs调控破骨细胞分化和功能的可能机制,及其在牙周炎骨吸收过程中的作用进行综述。     

牙髓干细胞对牙周炎中破骨细胞的作用

目的研究牙髓干细胞（DPSC）对牙周炎中破骨细胞形成及牙槽骨再生的影响,并初步探索DPSC对小鼠破骨细胞的作用机制。 方法体外诱导小鼠骨髓单核细胞破骨分化,观察破骨细胞组（OC组）及其与DPSC共培养组（OC+DPSC组）的抗酒石酸酸性磷酸酶（TRAP）染色情况,实时荧光定量聚合酶链反应（PCR）检测破骨分化相关基因包括活化T细胞核因子（NFATc1）、基质金属蛋白酶9（MMP-9）及TRAP的表达差异。体内构建小鼠慢性牙周炎模型,通过微计算机体层摄影（micro-CT）扫描后三维重建,比较慢性牙周炎+0.9%氯化钠溶液注射组（NS组）和慢性牙周炎+DPSC注射组（DPSC组）釉牙骨质界至牙槽嵴顶（CEJ-ABC）距离,并对标本进行苏木精-伊红和TRAP染色,观察DPSC对小鼠破骨细胞及牙槽骨再生的影响。采用SPSS 20.0软件进行数据统计分析,采用独立样本t检验及校正t检验分析组间差异。 结果体外TRAP染色发现,与DPSC共培养明显抑制成熟破骨细胞形成,OC+DPSC组成熟破骨细胞均数（4.2 ± 0.2）少于OC组均数（6.8 ± 0.2）,差异有统计学意义（t= 15.922,P<0.001）;破骨细胞表面积均数（0.046 ± 0.007）mm²也明显小于OC组（0.763 ± 0.015）mm²,差异有统计学意义（t = 83.174,P<0.001）。相对OC组,OC+DPSC共培养组的MMP-9、NFATc1及TRAP的mRNA相对表达量明显降低,均值分别为0.38 ± 0.17（t = 6.217,P = 0.003）、0.24 ± 0.12（t = 10.569,P = 0.003）和0.55 ± 0.13（t = 6.077,P = 0.026）。micro-CT扫描结果显示,DPSC注射组CEJ-ABC的平均距离为（0.215 ± 0.017）mm,明显小于0.9%氯化钠溶液组（0.311 ± 0.022）mm,差异有统计学意义（t= 10.921,P<0.001）,组织学观察下DPSC组炎症反应较0.9%氯化钠溶液组轻,且破骨细胞更少。 结论DPSC可通过抑制牙周炎破骨细胞的形成从而促进牙槽骨再生,有望作为一种可局部注射的骨代谢双向调节生物制剂,治疗临床上包括牙周炎等因骨代谢失衡引起的炎症性骨吸收疾病。     

环肌酸抑制大鼠牙周炎周围牙槽骨吸收的实验研究

目的:通过体外和体内实验探讨环肌酸对牙周炎造成的牙槽骨吸收的抑制作用.方法:体外实验通过细胞活力测定、碱性磷酸酶染色和茜素红染色、抗酒石酸酸性磷酸酶染色和实时反转录聚合酶链反应(RT-PCR)等检测,评价环肌酸对成骨细胞和破骨细胞增殖和分化的影响.动物实验将20只大鼠分为4组,A组为对照组,B组采用牙周结扎+生理盐水注...     

细胞凋亡在糖尿病大鼠牙周炎中参与牙槽骨吸收的实验研究

目的研究糖尿病伴牙周炎牙槽骨破坏机制,初步探讨牙周组织细胞凋亡在该类疾病中所起的作用。方法采用腹腔注射链脲佐菌素（Streptozocin,STZ）制备SD大鼠糖尿病模型,并利用0.2mm不锈钢丝环扎大鼠磨牙颈部制备牙周炎动物模型。观察牙周组织细胞在高血糖状态及正常血糖状态下的组织形态并检测细胞凋亡情况。结果高血糖状态下大鼠牙周炎发病程度明显高于血糖正常大鼠。牙周组织中成骨细胞及牙周膜成纤维细胞凋亡数量高血糖组高于血糖正常组,而破骨细胞数量则相反。结论高血糖状态下牙周炎病损程度较正常血糖状态下严重,牙周组织细胞凋亡参与和加重病程。     

Ameliorative effect of quercetin on the destruction caused by experimental periodontitis in rats

Cheng W‐C, Huang R‐Y, Chiang C‐Y, Chen J‐K, Liu C‐H, Chu C‐L, Fu E. Ameliorative effect of quercetin on the destruction caused by experimental periodontitis in rats. J Periodont Res 2010; 45: 788–795. © 2010 John Wiley & Sons A/S Background and Objective: The purpose of this study was to evaluate the effect of quercetin, a flavonol that exhibits anti‐inflammatory properties, on experimental periodontal destruction in rats. Material and Methods: Osteoclast formation on maxillary palatal alveolus was induced with daily lipopolysaccharide (LPS) injections (0, 1 or 5 mg/mL) for 3 d. Five days later, the osteoclasts on bony surfaces were counted after histochemical staining for tartrate‐resistant acid phosphatase. The effect of intragastric quercetin on the osteoclast formation was evaluated in the following three groups: quercetin (75 mg/kg/d by oral feeding); LPS (5 mg/mL); and quercetin plus LPS. Moreover, the effect of quercetin on the ligature‐induced periodontitis around maxillary second and mandibular first molars was further evaluated by microcomputerized tomography (on days 0, 4, 8 and 12) and by histometry (on day 8). Results: A dose‐dependent increase in osteoclasts occurred after LPS injections. However, quercetin (75 mg/kg) reduced the 5 mg/mL LPS‐induced osteoclasts. Using microcomputerized tomography, the bone crest levels at ligation sites were found to be significantly more apical than at the control sites on days 8 and 12; however, the apically located bone crests rebounded in rats from the quercetin‐plus‐ligation group. Histometry demonstrated significantly more coronal alveolar crest bone levels, less inflammatory cell‐infiltrated connective tissue areas and less connective tissue attachments in the ligation‐plus‐quercetin group compared with those in the ligation group. Conclusion: As the quercetin could reduce the LPS‐induced osteoclast formation and the ligature‐enhanced periodontal inflammation and bone loss, we suggest that it may have an ameliorative effect on periodontal destruction.     

Postoperative Weight Loss Masks Metabolic Impacts of Periodontitis in Obese Rodents

Background: Postoperative weight loss (POWL) is expected to occur in combined models of obesity and periodontitis. This study explores the confounding effects of POWL on the impact of ligation‐induced periodontitis on glucose and lipid metabolism in obese animals. Methods: Combined mouse models of diet‐induced obesity (DIO) and ligation‐induced periodontitis (5‐ or 10‐day ligation) were studied. Fasting serum glucose (FSG), fasting insulin (Fins), and lipids including triglyceride (TG), total cholesterol (TC), and low‐ and high‐density lipoprotein cholesterol (HDLC), were detected via biochemistry and enzyme‐linked immunosorbent assay. POWL and homeostasis model assessment of insulin resistance (HOMA‐IR) were calculated. Analysis of covariance was performed to identify confounding effects of POWL. Results: The obesity, periodontitis, and 10‐day groups exhibited greater POWL than corresponding controls (P <0.01). Without considering POWL, conflicting results were found, including: 1) contradictory changes in HDLC caused by obesity or periodontitis; and 2) unequal levels of FSG, TC, and HDLC between days 5 and 10 in the sham‐ligation controls. Moreover, upregulating effects of periodontitis were found only on TG in the DIO mice, whereas those on Fins, HOMA‐IR, and HDLC were statistically veiled. After the confounding effects of POWL were filtered, periodontitis promoted increased levels of not only TG but also Fins, HOMA‐IR, and HDLC in the DIO mice (P <0.05). Conclusions: When analyzing the interrelationship between obesity and periodontitis, the confounding effects of an imbalanced POWL should be considered. Otherwise, impact of periodontitis on metabolic dysregulation in obese animals may be underestimated.     

Gingival crevicular fluid osteopontin levels in periodontal health and disease

BACKGROUND: Osteopontin (OPN), a glycosylated phosphoprotein, is a bone matrix component produced by osteoblasts, osteoclasts, and macrophages as a multifunctional cytokine. OPN anchors osteoclasts to the bone surface, and its absence leads to impaired bone resorption. The aim of the present study was to assess the relation between clinical parameters and concentrations of OPN within gingival crevicular fluid (GCF) from inflamed gingiva and periodontitis sites and, subsequently, after the treatment of periodontitis sites. METHODS: A total of 45 subjects were divided into the following three groups based on modified gingival index (MGI) and Ramfjord periodontal disease index (PDI) scores: healthy (group I), gingivitis (group II), and chronic periodontitis (group III). A fourth group consisted of 15 subjects from group III, 6 to 8 weeks after treatment (i.e., scaling and root planing [SRP]). GCF samples collected from each patient were quantified for OPN using the enzymatic immunometric assay. Further, the correlation between OPN levels in situ with clinical parameters was analyzed in all groups and before and after treatment in periodontitis patients. RESULTS: The highest mean OPN concentration in GCF (14.347 microg/ml) was observed in group III, and the lowest mean OPN concentration in GCF (2.522 microg/ml) was observed in group I. Its levels in group III decreased to 8.419 microg/ml after treatment (group IV). Further, GCF OPN levels in all the groups showed a statistically significant positive correlation with clinical attachment loss (P <0.05). CONCLUSIONS: OPN levels increase in GCF from healthy to periodontitis states, and periodontal treatment results in the reduction of OPN levels. The data indicate that OPN may play a key role in, and could be considered a biomarker of, periodontal disease progression.     

Use of hyaluronic acid binding protein for detection of hyaluronan in ligature-induced periodontitis tissue

This study was designed to demonstrate, by use of biotin-labeled hyaluronic acid binding protein (HABP) and an avidin-enzyme system, the localization of hyaluronan (HA) in periodontal tissue of beagle dogs during experimentally induced periodontitis. Experimental periodontitis was induced in the dogs by ligation of the gingival sulcus. Experimental tissue was collected at 0, 3, 7 and 21 days after ligation. HA was revealed by strong staining in the intercellular space around epithelial cells and periodontal ligament, and by light staining in the gingival connective tissue. According to the progression of periodontal tissue breakdown, HA was detected in a small number of leukocytes and monocytes, on the surface of osteoclasts, the surface of alveolar bone, thickened endothelium and in epithelial cells related to rete peg formation. Streptomyces hyaluronidase-treated specimens gave negative staining. This study suggests that HA may be associated with the inflammatory reaction in experimental periodontitis tissue.     

Use of hyaluronic acid binding protein for detection of hyaluronan in ligature-induced periodontitis tissue

This study was designed to demonstrate, by use of biotin-labeled hyaluronic acid binding protein (HABP) and an avidin–enzyme system, the localization of hyaluronan (HA) in periodontal tissue of beagle dogs during experimentally induced periodontitis. Experimental periodontitis was induced in the dogs by ligation of the gingival sulcus. Experimental tissue was collected at 0, 3, 7 and 21 days after ligation. HA was revealed by strong staining in the intercellular space around epithelial cells and periodontal ligament, and by light staining in the gingival connective tissue. According to the progression of periodontal tissue breakdown, HA was detected in a small number of leukocytes and monocytes, on the surface of osteoclasts, the surface of alveolar bone, thickened endothelium and in epithelial cells related to rete peg formation. Streptomyces hyaluronidase-treated specimens gave negative staining. This study suggests that HA may be associated with the inflammatory reaction in experimental periodontitis tissue.     

Toll样受体⁃4抑制剂TAK⁃242对大鼠重度牙周炎骨吸收的影响

目的探讨Toll样受体?4(Toll like receptor?4,TLR?4)抑制剂TAK?242对大鼠重度牙周炎骨质吸收的影响,为重度牙周炎寻找辅助治疗手段提供实验基础。方法18只3周龄雄性Wistar大鼠随机分为3组(n=6),其中1组为正常对照组,另外2组以含有牙龈卟啉单胞菌(P.gingivalis)ATCC33277的5?0丝线结扎大鼠双侧上颌磨牙行重度牙周炎建模,分为牙周炎组、TAK?242组;TAK?242组从丝线结扎第1天起,通过尾静脉隔天注射1次溶于DMSO的TAK?242(2 mg/kg),另外两组注射相同体质量比例的DMSO溶剂,连续8周;第8周末处死3组大鼠,获取大鼠上颌骨标本,采用micro?CT扫描后三维重建,测量特定位点釉牙骨质界?牙槽嵴顶的距离评估骨丧失量,并对牙槽骨骨质相关参数和骨质微结构进行分析;组织学切片苏木精?伊(HE)染色观察牙周组织病理改变;甲基绿染色观察牙槽骨吸收情况;抗酒石酸酸性磷酸酶(TRAP)染色观察破骨细胞分布情况。结果Micro?CT定量分析显示:牙周炎组与TAK?242组牙槽骨吸收显著高于对照组;与牙周炎组相比,TAK?242组大鼠上颌第一磨牙近、远中根吸收位点的骨丧失均显著减轻(P<0.001),骨密度(P<0.05)与骨体积/总体积分数(P<0.01)显著增高,骨小梁数目与骨小梁厚度(P<0.01)相对增多,骨小梁分离度(P<0.01)和骨小梁结构模式指数显著降低。牙周炎组骨质呈现疏松多孔的蜂窝状结构,骨小梁结构恶化,向杆状结构转变;TAK?242组骨质微结构改善,骨量改善,骨小梁分布相对更致密,骨小梁结构与对照组更相似。HE染色发现牙周炎组与TAK?242组牙周附着丧失与牙槽骨吸收较对照组显著;与牙周炎组相比,甲基绿染色表明TAK?242组骨吸收减轻,TRAP染色显示破骨细胞浸润减少(P<0.001)。结论TLR?4抑制剂TAK?242能缓解大鼠重度牙周炎骨吸收,改善其多孔、稀疏、排列紊乱的炎症性骨小梁结构。     

Parathyroid hormone administration may modulate periodontal tissue levels of interleukin-6, matrix metalloproteinase-2 and matrix metalloproteinase-9 in experimental periodontitis

Background and Objective: Intermittent administration of the parathyroid hormone (1–34) has an anabolic effect on bone and it has been shown to reduce alveolar bone loss in experimental periodontitis models. The aim of the present study was to investigate the effect of parathyroid hormone on tissue degradation‐related factors in an experimental periodontitis model in rats. Material and Methods: Periodontitis was induced in seventy‐six male Wistar rats using ligature around the lower right first molars. The animals were then treated with parathyroid hormone (1–34) (T‐group) or vehicle (C‐group), three times a week for 15 d (C15, T15) or 30 d (C30, T30). At each experimental time‐point, the 19 rats were killed in each group and the gingival tissue around the first lower molar was removed and prepared for the following analyses: mRNA expression of interleukin‐1beta, interleukin‐6, matrix metalloproteinase (MMP)‐2 and MMP‐9, and gelatinolytic activity of MMP‐2 and MMP‐9. Hemimandibles were decalcified, and serial sections were processed and analyzed for interleukin‐6 immohistochemistry. Samples were also histochemically stained by tartrate‐resistant acid phosphatase (TRAP) to evaluate the number of osteoclasts present. Results: Parathyroid hormone‐treated samples showed decreased of levels of mRNA for interleukin‐6 in the T30 group (p < 0.01) and of MMP‐2 in the T15 and T30 groups (p < 0.05). Zymography assays demonstrated that treatment with parathyroid hormone led to a decrease in MMP‐9 activity (p < 0.01). TRAP staining of alveolar bone revealed that osteoclasts were present in higher numbers (p < 0.05) in the groups not treated with parathyroid hormone. Conclusion: These data suggest that intermittent administration of parathyroid hormone can down‐regulate the expression of biomarkers responsible for connective tissue breakdown and bone resorption, and potentially affect alveolar bone resorption activity.     

模拟高原低氧兔牙周炎模型血清和牙龈组织中sICAM-1及sVCAM-1的含量

目的:探讨血清和牙龈组织中可溶性细胞间黏附分子-1(sICAM-1)、可溶性血管黏附分子-1(sVCAM-1)在高原牙周病炎症反应中的作用。方法:将40只雄兔随机分为常氧对照组、常氧实验组、低氧对照组、低氧实验组,每组10只,采用正畸丝结扎下颌中切牙与牙周炎食谱的方法建立牙周炎模型,常氧组和低氧组分别在平原和模拟海拔5 000 m条件下饲养8周,对牙周组织取材进行组织学观察,用ELISA法检测各组实验动物血清和牙龈组织中sICAM-1、sVCAM-1表达情况。结果:低氧实验组sICAM-1、sVCAM-1浓度显著高于其余各组(P<0.05),且牙龈组织中浓度高于血清。结论:模拟高原低氧环境下黏附分子的表达上调,使牙周组织破坏加重,同时促使炎症反应向外周血管扩散。