补肾坚骨汤对牙周炎大鼠血清白细胞介素-6和骨钙素影响的实验研究

目的：通过检测牙周炎大鼠血清中白细胞介素-6（interleukin-6/IL-6）和骨钙素（O steocalcin/OC）水平的变化,观察光学显微镜下牙周组织的形态改变,探讨补肾坚骨汤对牙周炎大鼠的治疗作用及可能机制。方法：雄性12月龄SD大鼠24只,8只为正常对照组（N）,其余成功建立大鼠牙周炎模型之后,分为牙周炎模型对照组（D）、补肾坚骨汤治疗组16g/（kg·d）（H）,给予补肾坚骨汤灌胃4周,每日一次,每次5m L,各组大鼠末次给药后24 h处死,摘取上颌骨制作牙体牙周组织联合切片,H E染色,在光学显微镜下观察牙周的组织学改变;采用ELISA法检测外周血IL-6和OC的水平。结果：牙周炎模型对照组牙周组织表现为明显的炎症破坏,牙槽骨吸收明显,而补肾坚骨汤治疗组牙周组织炎症明显减轻,牙槽骨吸收减少且骨修复反应明显;牙周炎模型对照组血清IL-6水平显著高于正常对照组和补肾坚骨汤治疗组（P〈0.05）;牙周炎模型对照组血清OC水平显著低于正常对照组和补肾坚骨汤治疗组（P〈0.05）。结论：补肾坚骨汤可能通过降低牙周炎大鼠血清中IL-6水平,升高OC水平,减轻牙周组织炎症,促进牙周组织再生,其作用机制还需进一步深入研究。     

连翘苷对牙周炎大鼠p38 MAPK/c-Fos 信号通路及破骨细胞活化的影响

目的:探讨连翘苷对牙周炎大鼠p38丝裂原活化蛋白激酶(p38 MAPK)/c-Fos信号通路及破骨细胞活化的影响.方法:建立牙周炎大鼠模型,随机分为模型组、连翘苷低剂量组、连翘苷中剂量组、连翘苷高剂量组、维生素C组,每组12只,另取12只设为对照组,分组处理后,亚甲蓝染色检测大鼠牙槽骨吸收(釉牙骨质界到牙槽嵴顶距离)情况;HE染色检测各组大鼠牙周组织病理形态;TRAP染色检测各组大鼠牙周组织中破骨细胞数目;酶联免疫吸附试验(ELISA)检测大鼠血清肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)水平;蛋白免疫印迹实验检测大鼠牙周组织p38 MAPK/c-Fos通路相关蛋白表达情况.结果:与对照组相比,模型组大鼠牙周组织呈现上皮残缺、破裂,形态异常,牙周膜纤维排列紊乱,可见炎性细胞浸润等病理损伤,釉牙骨质界到牙槽嵴顶距离、破骨细胞数目、TNF-α、IL-6水平、牙周组织p38 MAPK/c-Fos通路相关蛋白c-Fos表达、p-p38 MAPK/p38 MAPK明显升高(P<0.05).与模型组相比,连翘苷低、中、高剂量组及维生素C组大鼠牙周组织病理损伤减轻,釉牙骨质界到牙槽嵴顶距离、破骨细胞数目、TNF-α、IL-6水平、牙周组织c-Fos蛋白表达、p-p38 MAPK/p38 MAPK降低,且连翘苷各组呈剂量依赖性(P<0.05),连翘苷高剂量组与维生素C组相比,差异无统计学意义(P>0.05).结论:连翘苷可下调p38 MAPK/c-Fos信号通路,抑制牙周炎症及破骨细胞活化,减轻牙周组织损伤,改善牙周炎大鼠症状.     

连翘苷对牙周炎大鼠p38 MAPK/c-Fos 信号通路及破骨细胞活化的影响

目的:探讨连翘苷对牙周炎大鼠p38丝裂原活化蛋白激酶(p38 MAPK)/c-Fos信号通路及破骨细胞活化的影响.方法:建立牙周炎大鼠模型,随机分为模型组、连翘苷低剂量组、连翘苷中剂量组、连翘苷高剂量组、维生素C组,每组12只,另取12只设为对照组,分组处理后,亚甲蓝染色检测大鼠牙槽骨吸收(釉牙骨质界到牙槽嵴顶距离)情况;HE染色检测各组大鼠牙周组织病理形态;TRAP染色检测各组大鼠牙周组织中破骨细胞数目;酶联免疫吸附试验(ELISA)检测大鼠血清肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)水平;蛋白免疫印迹实验检测大鼠牙周组织p38 MAPK/c-Fos通路相关蛋白表达情况.结果:与对照组相比,模型组大鼠牙周组织呈现上皮残缺、破裂,形态异常,牙周膜纤维排列紊乱,可见炎性细胞浸润等病理损伤,釉牙骨质界到牙槽嵴顶距离、破骨细胞数目、TNF-α、IL-6水平、牙周组织p38 MAPK/c-Fos通路相关蛋白c-Fos表达、p-p38 MAPK/p38 MAPK明显升高(P<0.05).与模型组相比,连翘苷低、中、高剂量组及维生素C组大鼠牙周组织病理损伤减轻,釉牙骨质界到牙槽嵴顶距离、破骨细胞数目、TNF-α、IL-6水平、牙周组织c-Fos蛋白表达、p-p38 MAPK/p38 MAPK降低,且连翘苷各组呈剂量依赖性(P<0.05),连翘苷高剂量组与维生素C组相比,差异无统计学意义(P>0.05).结论:连翘苷可下调p38 MAPK/c-Fos信号通路,抑制牙周炎症及破骨细胞活化,减轻牙周组织损伤,改善牙周炎大鼠症状.     

补肾合剂对牙周炎大鼠外周血中肿瘤坏死因子α含量的影响

目的通过观测牙周炎大鼠外周血中肿瘤坏死因子α(tumor necrosis factor alpha, TNF-α)水平的变化,来探讨中药补肾合剂治疗牙周炎的机理.方法选用60只10月龄SD大鼠,随机分成6组,每组10只.A组为正常对照组,B～F组建立大鼠牙周炎模型.B组为牙周炎模型对照组,C和E组为补肾合剂治疗组,C组治疗4周处死,E组治疗12周处死.D和F组为阳性对照组,分别与C、E组同时处死.血清中TNF-α水平采用酶联免疫吸附试验测定,同时观测各阶段大鼠的生活情况及牙周炎模型处牙周组织形态学改变情况.结果治疗组大鼠外周血中TNF-α的含量在实验的各阶段均明显低于对照组并有统计学意义,同时治疗组大鼠的全身及牙周组织情况均好于相应的对照组.结论补肾合剂可降低牙周炎大鼠外周血中TNF-α的含量,改善全身及牙周局部状况.     

2型糖尿病对大鼠牙周组织及TNF-α、IL-6和PAI-1水平影响的研究

目的观察2型糖尿病伴牙周炎大鼠牙周组织及血清肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)及纤溶酶原活化物抑制因子-1(PAI-1)水平的变化,探讨TNF-α、IL-6及PAI-1的表达对2型糖尿病牙周炎大鼠牙周组织改建过程中组织变化的影响。方法清洁级8~9周龄Wistar大鼠60只,分为4组:(1)伴牙周炎糖尿病组(n=15);(2)不伴牙周炎糖尿病组(n=15);(3)伴牙周炎非糖尿病组(n=15);(4)不伴牙周炎非糖尿病组(正常对照组,n=15)。采用腹腔内注射链脲佐菌素(streptozotocin,STZ)法建立大鼠糖尿病模型。给药后每周1次,连续4周测定大鼠尾静脉血糖水平,以判断大鼠糖尿病建模情况。用浸有牙龈卟啉单胞菌株的丝线结扎左侧上颌第二磨牙牙颈部,复制实验性牙周炎模型。实验性牙周炎建模20周后,采用腹腔注射水合氯醛法在全麻状态下处死大鼠。从腹主动脉采集血液,ELISA法检测血清TNF-α、IL-6及PAI-1水平。处死前测量术区的牙周附着情况。制作牙体牙周联合切片,观察牙周组织学改变。结果糖尿病组大鼠表现为血糖和体质量水平显著升高(P<0.05);糖尿病组大鼠血清胰岛素水平和胰岛素抵抗指数得分均显著升高(P<0.05);用浸有牙龈卟啉单胞菌株的丝线结扎后,牙周炎组表现为典型的牙周炎临床特征;与不伴牙周炎糖尿病组相比,伴牙周炎糖尿病组大鼠血清TNF-α、IL-6及PAI-1水平显著升高(P<0.05)。结论糖尿病通过促进血清炎性因子的表达,降低牙周组织对局部致病因子的抵抗力,从而加重、加速牙周炎的进展。     

壳寡糖对牙周炎大鼠牙槽骨吸收及Th17/Treg平衡和OPG/RANKL/RANK通路的影响

目的: 探讨壳寡糖对牙周炎大鼠牙槽骨吸收及Th17/Treg平衡和OPG/RANKL/RANK通路的影响。方法: 建立牙周炎大鼠模型,随机分为模型组、壳寡糖低剂量组、壳寡糖中剂量组、壳寡糖高剂量组和甲硝唑组,每组12只,另取12只作为对照组。分组处理后,评估牙龈指数、牙槽骨吸收值;H-E染色观察牙周组织病理形态学变化;流式细胞术检测外周血中Th17/Treg细胞比值;酶联免疫吸附试验（ELISA）检测各组大鼠血清中IL-17、TGF-β、RANKL、OPG水平,实时荧光定量PCR（qRT-PCR）检测各组大鼠牙周组织OPG、RANKL mRNA表达水平。采用SPSS 24.0软件包对数据进行统计学分析。结果: 与对照组相比,模型组大鼠牙周组织呈现牙周膜纤维束断裂、排列紊乱,毛细血管扩张、增生,炎症细胞浸润等病理损伤;牙龈指数、牙槽骨吸收值、Th17/Treg比值、血清RANKL及IL-17水平、牙周组织RANKL mRNA水平显著升高（P<0.05）,血清OPG及TGF-β水平、牙周组织OPG mRNA水平显著降低（P<0.05）。与模型组相比,壳寡糖低、中、高剂量组和甲硝唑组大鼠牙周组织病理损伤减轻;牙龈指数、牙槽骨吸收值、Th17/Treg比值、血清RANKL及IL-17水平、牙周组织RANKL mRNA水平显著降低（P<0.05）,血清OPG及TGF-β水平、牙周组织OPG mRNA水平显著升高（P<0.05）,且壳寡糖各组呈剂量依赖性,壳寡糖高剂量组与甲硝唑组相比,差异无统计学意义（P>0.05）。结论: 壳寡糖可促使Th17/Treg平衡恢复正常,上调OPG表达,下调RANKL表达,抑制牙周炎大鼠牙槽骨吸收,改善其临床症状。     

槲皮素脂质体对糖尿病牙周炎大鼠牙周组织的作用及血清AGEs的影响

目的:通过对Ⅱ型糖尿病牙周炎大鼠进行槲皮素干预,观察大鼠牙周组织的组织学变化、牙槽骨吸收量、血糖值变化以及血清晚期糖基化终末产物(advanced glycation end products,AGEs)的变化,探讨槲皮素对糖尿病牙周炎大鼠牙周组织的保护作用.方法:40只雄性SD大鼠,随机分成4组:空白对照组(N组)、牙周炎对照组(P组)、糖尿病牙周炎非治疗组(DP组)和糖尿病牙周炎槲皮素治疗组(DP+Q组).N组正常喂养,P组建立牙周炎模型,DP组和DP+Q组建立糖尿病牙周炎模型,每组10只.建模成功后DP+Q组灌喂槲皮素脂质体,DP组灌喂空白脂质体,给药6周后测量各组血糖值,ELISA法测量血清AGEs含量,取上颌骨做牙周组织切片观察牙周组织病理变化,测量牙槽骨吸收量.结果:P组牙槽骨吸收量、牙周组织炎症水平高于N组(P<0.05);DP组血糖值、血清AGEs含量、牙周组织炎症程度、牙槽骨吸收量均高于N组和P组(P<0.05);DP+Q组大鼠血糖值、血清AGEs含量、牙周组织炎症水平、牙槽骨吸收量均低于DP组(P<0.05).结论:槲皮素对糖尿病牙周炎大鼠的牙周组织有保护效果,其作用机制与降低血糖值与血清AGEs含量有关.     

探讨葛根素基于p38丝裂原活化蛋白激酶通路对慢性牙周炎小鼠症状的改善作用及对牙周组织生长的影响

目的:建立慢性牙周炎小鼠模型,探讨葛根素对慢性牙周炎小鼠的治疗作用及其对牙周组织生长情况的影响,并探讨其作用机制.方法:将实验小鼠随机分为对照组、模型组、葛根素低剂量组、葛根素中剂量组和葛根素高剂量组.除对照组外,其余各组均采用正畸钢丝结扎法建立慢性牙周炎模型,并分别在建模后的第3、5、7和9天将2μL牙龈卟啉菌液和15μL 1 mg/mL的脂多糖(lipopolysaccharide,LPS)0.9％氯化钠溶液均匀注射到全部牙周组织.建模4周后,对葛根素低、中、高剂量组小鼠进行灌胃给药,剂量分别为200、400、800 mg/kg,对照组和模型组小鼠给予等量的羧甲基纤维素钠(sodium carboxyl methyl cellulose,CMC-Na)溶液,给药溶液现用现配,每天1次,共治疗2周.观察各组实验小鼠的活动状态及表现,通过酶联免疫吸附试验检测各组小鼠外周血清中肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-1β(interleukin-1β,IL-1β)和白细胞介素-6(interleukin-6,IL-6)的浓度,通过Western Blot(蛋白质印迹法)实验检测小鼠牙周组织中p38丝裂原活化蛋白激酶(p38MAPK)和磷酸化的p38丝裂原活化蛋白激酶(P-p38MAPK)的表达水平.结果:建立小鼠慢性牙周炎模型4周后,实验小鼠食欲减退,活动状态低迷,表现出慢性牙周炎症状:牙龈明显红肿、肥大,牙龈组织松软,部分出现溃疡现象,探诊出血明显,并有自发出血倾向.酶联免疫吸附试验检测结果显示:与对照组比较,模型组小鼠外周血清中的TNF-α、IL-1β和IL-6的水平显著升高(P<0.01);与模型组比较,葛根素低、中、高剂量组小鼠外周血清中TNF-α、IL-1β和IL-6的水平降低(P<0.05).Western Blot检测结果显示:与对照组比较,模型组小鼠牙龈组织中p38MAPK和P-p38MAPK的蛋白表达水平显著升高;与模型组比较,葛根素低、中、高剂量组小鼠牙龈组织中p38MAPK和P-p38MAPK的蛋白表达水平显著降低(P<0.01).结论:葛根素能够缓解小鼠慢性牙周炎的症状,减轻牙周炎症反应,对于小鼠慢性牙周炎有显著的改善和治疗作用,且可能是通过p38MAPK信号通路发挥治疗作用.     

染料木素对牙周炎小鼠牙周组织的影响

目的 本研究旨在评估染料木素（genistein,GEN）对丝线结扎诱导的牙周炎小鼠牙槽骨吸收以及牙龈组织中炎症因子表达情况的影响。方法 以雄性C57小鼠为研究对象,采用丝线结扎法建立小鼠牙周炎模型,实验组给予GEN。4周后使用显微镜和ImageJ软件分析GEN对小鼠牙槽骨吸收情况的影响。并采用实时荧光定量PCR法检测GEN治疗后,牙周炎小鼠牙龈组织中肿瘤坏死因子（tumor necrosis factor-α,TNF-α）、白细胞介素-1β(interleukin-1β,IL-1β)、白细胞介素-6(interleukin-6,IL-6)以及白细胞介素17a(interleukin-17a,IL-17a)的mRNA表达情况。结果 给予GEN(20mg/kg和40mg/kg)治疗后,牙周炎小鼠的牙槽骨吸收明显少于无GEN治疗组（P <0.05）。并且GEN治疗小鼠牙龈组织中TNF-α、IL-1β、IL-6和IL-17a的mRNA表达亦显著降低（P <0.05）。结论 染料木素可显著减轻牙周炎导致的牙周组织破坏,有望成为一种新型的牙周炎治疗药物。     

人参皂甙Rg-1对牙周炎大鼠牙周组织中TNF-α、IL-1β表达的影响

目的：检测牙周炎大鼠牙周组织中肿瘤坏死因子-α（tumor necrosis factor-α,TNF-α）、白介素-1β（in-terleukin-1β,IL-1β）水平的变化,探讨人参皂甙Rg-1对其表达的影响及治疗牙周炎的机理。方法：选用100只体重160-200g Wistar大白鼠,随机分成10组,每组10只。A组：正常对照组,与F组同时处死。B-J组建立牙周炎大鼠模型。B-E组：人参皂甙Rg-1治疗组,给药后第1、2、3、4周末处死。F-J组：牙周炎对照组,于造模成功后第0、1、2、3、4周末处死。取大鼠上颌磨牙牙周组织标本作切片,光镜观察,采用免疫组织化学法检测TNF-α、IL-1β水平变化,进行统计学分析。结果：F组牙周组织中TNF-α、IL-1β表达明显高于A组（P〈0.05）;各时间段牙周炎治疗组牙周组织中TNF-α、IL-1β表达明显低于相应的牙周炎组（P〈0.05）。结论：人参皂甙Rg-1可以抑制实验性牙周炎大鼠牙周组织中TNF-α、IL-1β的表达,具有治疗牙周炎的作用。     

Peripheral kappa opioid receptors activation reduces alveolar bone loss in rats by modulating interleukin-6 and -10

Objective

The beneficial effects of kappa opioid agonist U-50,488 in preventing periodontal disease (PD) progression in rats have already been described, but its mechanism of action is unknown. The present study evaluated the expression of TNF-α, IL-6, IL-8 and IL-10 in the gingival tissues of rats with ligature-induced PD, treated with U-50,488. It also correlated the effects of this agonist with myeloperoxidase (MPO) activity and the presence of osteoclasts.

Design

Male Holtzman rats weighing 250–300 g were divided into four groups: (1) control, (2) ligature, (3) ligature + saline and (4) ligature + kappa agonist. Experimental PD was induced by placing a sterile silk ligature around the 2nd left upper molar. Rats from groups 3 to 4 were locally administered with either saline or U-50,488, respectively, from day 3 to day 5 following ligation. After 5 or 11 days, the rats were euthanized and periodontal tissue samples were collected for histological and morphometric analysis and for determination of TNF-α, IL-6, IL-8, IL-10 and MPO.

Results

Ligature placement induced significant alveolar bone loss. The number of osteoclasts, degree of MPO activity, IL-6, IL-8 and TNF-α expression were also increased by PD. U-50,488 reduced both bone loss and the number of osteoclasts, but did not alter histological inflammatory infiltrate or MPO activity. U-50,488 significantly reduced IL-6 and increased IL-10 levels, but did not affect TNF-α and IL-8.

Conclusion

Lowering the levels of IL-6 and increasing IL-10 are important mechanisms by which U-50,488 reduces alveolar bone loss in ligature-induced periodontal disease.     

Imbalance of oxidative/anti-oxidative status induced by periodontitis is involved in apoptosis of rat submandibular glands

Objective

Epidemiologic studies suggest a relationship between periodontitis and salivary gland dysfunction. A rat periodontitis model was used to investigate whether a causal relationship exists between periodontitis and pathological changes of submandibular glands.

Design

Fourteen male Wistar rats (8 weeks old) were divided into two groups (n = 7/group): a control group and periodontitis group. Periodontitis was induced by ligature placement around the mandibular first molars. Serum levels for reactive oxygen metabolites, anti-oxidant and tumour necrosis factor (TNF)-α were measured at baseline, 2 and 4 weeks. At 4 weeks, the levels of 8-hydroxydeoxyguanosine were determined to evaluate oxidative damage of submandibular glands. Expression of TNF-α mRNA and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL) as well as histological findings were also evaluated in the submandibular glands.

Results

The rats with experimental periodontitis showed increase in the levels of serum reactive oxygen metabolites and TNF-α, and a decrease of anti-oxidant power in a time-dependent manner. At 4 weeks, these rats also had significantly increased levels of 8-hydroxydeoxyguanosine and TNF-α, and increased number of TUNEL-positive cells and vacuolisation in the submandibular glands compared to the control rats.

Conclusions

Imbalance of circulating oxidative/anti-oxidative status may be involved in vacuolisation and apoptosis of submandibular glands in the rat periodontitis model.     

Local administration of Tiludronic Acid downregulates important mediators involved in periodontal tissue destruction in experimental periodontitis in rats

ObjectiveThe purpose of this study was to evaluate whether local administration of TIL could influence the expression of the inflammatory mediators IL-1β, TNF-α, MMP-8 and COX-2 in rats with experimental periodontitis (EP).MethodsTwenty-four adult male rats (Rattus norvegicus, albinus, Wistar) were assigned to groups C, EP, EP-TIL (CControl group, EP–Periodontitis groups). On EP groups, a ligature was placed around maxillary 2nd molars on day 1. On group EP-TIL, 20 μL of TIL solution (1 mg/kg body weight) was injected into the subperiosteal palatal area adjacent to the maxillary 2nd molar every other day until euthanasia (day 11). Alveolar bone loss was morphometrically analyzed. mRNA expressions of IL-1β, TNF-α, MMP-8 and COX-2 were assessed by qPCR. IL-1β, TNF-α, MMP-8 and COX-2 were immunohistochemically analyzed. Data were analyzed statistically.ResultsGroup EP-TIL presented reduced alveolar bone loss when compared with group EP (p < 0.05). Group EP-TIL presented decreased mRNA expressions of IL-1β, TNF-α, MMP-8 and COX-2 and reduced immunolabeling of IL-1β, TNF-α and MMP-8 when compared with group EP (p < 0.05). No differences regarding the immunolabeling of COX-2 were found when group EP-TIL was compared with the other groups (p > 0.05).ConclusionWithin the limits of this study, it can be concluded that local administration of TIL downregulates important mediators involved in periodontal tissue destruction in ligature-induced periodontitis in rats.     

Parathyroid hormone-related peptide (1–34) reduces alveolar bone loss in type 1 diabetic rats

ObjectiveTo investigate the role of parathyroid hormone related protein (PTHrP) in diabetic periodontitis.MethodsAfter injected with 55 mg/kg streptozotocin, diabetic rats were treated subcutaneously with low-dose (40 μg/kg, once daily for 5 days per week), middle-dose (80 μg/kg) or high-dose (160 μg/kg) PTHrP(1–34) peptide. Treatment continued for 12 weeks. Changes in periodontal tissues were confirmed by micro-computerized tomography assay and H&E analysis. We used tartrate resistant acid phosphatase (TRAP) staining to identify osteoclast cells. The expression of TNF-α, IL-1β and IL-6 was assessed by immunohistochemistry and Western blot.ResultsTooth-supporting structure loss was observed in periodontal tissues of diabetic rats. PTHrP (1–34) attenuated alveolar bone loss, especially in the middle-dose and high-dose group. Whereas TNF-α, IL-1β and IL-6 protein levels were increased in the diabetic gingival tissues, PTHrP (1–34) treatment inhibited the increase of IL-1β and IL-6, but had no effect on TNF-α.ConclusionType 1 diabetes increased the susceptibility to periodontal disease. Intermittent administration of PTHrP (1–34) exhibited an inhibitory effect on alveolar bone resorption and the gingival inflammation in periodontal tissues of diabetic rats.     

牙周炎伴COPD患者血清25-（OH）D、TNF-α和IL-6水平检测的研究

目的：探讨慢性牙周炎与慢性阻塞性肺疾病（chronic obstructive pulmonary disease,COPD）患者的血清25-（OH）D、TNF-α和IL-6水平变化及相互关系。方法：收集符合条件的COPD伴牙周炎患者[（C＋P）组]20例,单纯慢性牙周炎患者（P组）20例,同期门诊随诊的健康对照组（H组）20例。采集临床指标并采用ELISA法检测3组受试者血清25-（OH）D、TNF-α和IL-6的含量。结果：各组间牙周病指数有显著性差异。（C＋P）组与P组、H组相比,TNF-α和IL-6水平明显升高,差别有统计学意义（P〈0.05）;25-（OH）D水平较低,但差别无统计学意义。等级相关性分析结果显示H组血清25-（OH）D与IL-6呈负性相关关系（P〈0.05）,C＋P组血清25-（OH）D与Tnf-α呈负性相关关系（P〈0.05）。结论：25-（OH）D、TNF-α和IL-6可能与牙周炎和COPD病理机制相关,牙周炎和COPD之间存在一定的关联。     

糖尿病牙周病大鼠牙周龈沟液中TNF-α,IL-1β和LPS水平的研究

目的：本文主要研究了糖尿病牙周病大鼠模型龈沟液中TNF-α,IL-1β和LPS水平的改变。方法：15只大鼠通过注射链脲佐菌素建成糖尿病模型并使用丝线诱导成牙周病模型（组1）,15只大鼠丝线诱导成牙周病模型（组2）,15只大鼠链脲佐菌素注射建成糖尿病模型（组3）,15只系统健康大鼠作为正常对照组（组4）。用ELISA方法检测龈沟液中TNF-α,IL-1β和LPS水平。结果：组1与组2、3、4相比TNF-α,IL-1β和LPS水平较高（P〈0.05）,组2中的水平比组3、4高（P〈0.05）,组3的比组4的水平高（P〈0.05）。组间数据有统计学意义。结论：数据表明糖尿病可以提高牙周龈沟液中TNF-α,IL-1β和LPS的水平。     

Changes of adiponectin and inflammatory cytokines after periodontal intervention in type 2 diabetes patients with periodontitis

ObjectiveTo determine serum adiponectin, C-reactive protein (CRP), TNF-α and IL-6 levels in impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM) patients with periodontitis before and after periodontal intervention, and to investigate the relationship between T2DM and periodontitis.MethodsA total of 50 IGT and 106 T2DM patients with periodontitis were enrolled. The T2DM patients were divided into two groups: T2DM without macrovascular disease (DM1) group and T2DM with macrovascular disease (DM2) group. Each group was randomly divided into two subgroups according to whether they performed periodontal intervention. The normal control group (NC group) consisted of 30 healthy adults. The serum adiponectin, CRP, TNF-α and IL-6 levels were measured at baseline and 3 months after periodontal intervention.ResultsThe serum adiponectin levels at baseline had decreased tendency with significant difference between each two groups, while CRP, TNF-α, and IL-6 levels had increased tendency with significant difference between each two groups among NC, IGT, DM1 and DM2 groups (all P < 0.01). At 3 months after periodontal intervention, the serum adiponectin levels were increased than those without periodontal intervention (all P < 0.01), while CRP, IL-6 and TNF-α significantly decreased (all P < 0.05) in both IGT and DM1 groups. In DM2 group, only CRP levels at 3 months after periodontal intervention were significantly decreased (P < 0.05). Moreover, the HbAlc levels in T2DM patients were improved at 3 months after periodontal invention (P < 0.01).ConclusionPeriodontal intervention is helpful for glucose control, which may be associated with increased serum adiponectin levels and decreased inflammatory cytokine levels.     

The role of psychologic stress-induced hypoxia-inducible factor-1α in rat experimental periodontitis

Background: Studies have shown that psychologic stress plays a significant role in the outcome of many diseases. The present study is designed to investigate the effect of stress on experimental ligature‐induced periodontal disease in rats by means of a variable moderate chronic stress model. Methods: Sixty‐six age‐matched male Wistar rats of specific pathogen‐free grade were randomly divided into four groups: 1) normal control group, naive rats; 2) experimental periodontitis group, received only silk ligatures at the gingival margins of the second maxillary molar; 3) stress‐stimulation group, treated only with experimental stress conditions; and 4) experimental periodontitis plus stress‐stimulation group (e.g., experimental groups also exposed to stress). Stress was imposed by means of restraint stress, cold‐water immersion stress, and cat shock stress, which were all applied randomly. The rats were sacrificed at weeks 1, 4, 6, and 8 of the experiment. Attachment losses (AL) were measured by a specially made periodontal probe. The histopathologic changes of periodontia stained with hematoxylin and eosin were observed under a microscope. The expression of hypoxia‐inducible factor‐1α used to evaluate tissue hypoxic degree in periodontal tissues was tested by immunohistochemistry. Results: Our results show that there was no significant difference of AL among the normal control and the stress‐stimulation groups (P >0.05); AL of the periodontitis plus stress‐stimulation group was significantly higher than that of the experimental periodontitis group at weeks 4, 6, and 8 (P <0.01), and the hypoxia‐inducible factor‐1α expression scores of the periodontitis plus stress‐stimulation group were significantly higher than those of the experimental periodontitis group at weeks 4, 6, and 8 (P = 0.0477). Conclusions: Stress‐stimulation may aggravate periodontitis by decreased tissue oxygenation in rats. We conclude that there is a correlation of periodontitis severity with psychologic stress and periodontal tissue hypoxia.     

慢性不可预知性应激对大鼠实验性牙周炎预后的影响

目的:探讨慢性不可预知性复合心理应激对大鼠实验性牙周炎模型牙周组织愈合的影响。方法:雄性SD大鼠128只,随机抽取32只作为正常对照组。其余96只大鼠用丝线结扎右上颌第二磨牙颈部,4周后,采用龈沟出血指数和牙周探诊深度验证牙周炎模型。同时将大鼠结扎丝线去除,随机分为牙周炎对照组、牙周炎+应激组、牙周炎+应激+应激对抗药物组,每组32只。实验第5周起,应激组和药物组大鼠每日给予慢性不可预知性应激,同时药物组每日按5 mg/kg腹腔注射氟西汀。于实验第4、5、6、8周进行大鼠体质量测量、行为学测试、血清学检测;采用组织学观察牙周组织炎症反应、牙槽骨丧失、附着丧失以及破骨细胞计数。结果:心理应激大鼠出现体质量增长减慢、行为异常、血清皮质酮与促肾上腺皮质激素浓度升高(P<0.05),心理应激影响下大鼠牙周炎的愈合进程减慢,炎细胞浸润面积、牙槽骨吸收量与破骨细胞计数在实验第6周和8周、附着丧失在第8周高于对照组(P<0.05)。抗应激药物可逆转心理应激对牙周炎愈合过程的影响,该组炎细胞浸润面积与牙槽骨吸收在第6周和8周、破骨细胞计数在第8周明显低于应激组(P<0.05)。结论:慢性不可预知性心理应激能影响牙周组织的愈合,影响牙周炎的预后。而药物对抗应激能够减轻这种影响。