中华口腔医学杂志
中華口腔醫學雜誌
중화구강의학잡지
Chinese Journal of Stomatology
2015年
10期
619-623
,共5页
陈莉%李小彤%范晓川%魏晓清%王红梅
陳莉%李小彤%範曉川%魏曉清%王紅梅
진리%리소동%범효천%위효청%왕홍매
白细胞介素17%牙正畸牵引%牙周炎%牙周组织
白細胞介素17%牙正畸牽引%牙週炎%牙週組織
백세포개소17%아정기견인%아주염%아주조직
Interleukin-17%Orthodontic extrusion%Periodontitis%Periodontium
目的 研究正畸力作用下白介素17 (interleukin-17,IL-17)在不同状态牙周组织中的表达变化,探讨牙周炎正畸治疗机制.方法 77只6周龄SD大鼠按随机数字表法分为3个移动组(正常、牙周炎活动期和牙周炎恢复期移动组,每组21只)和2个对照组(牙周炎和空白对照组,每组7只).各牙周炎组大鼠采用结扎+涂易感菌+糖水喂养建立牙周炎活动期模型,牙周炎恢复期移动组建模后去除上述刺激因素并行牙周治疗,进入牙周炎恢复期.处死2个对照组大鼠,并用镍钛拉簧以0.49 N力近中移动各移动组大鼠上颌第一磨牙,并分别于移动后第3、7和14天处死(每组每个时间点7只).免疫组化检测牙周组织IL-17表达.实时定量PCR检测IL-17 mRNA表达.结果 免疫组化显示,与空白对照组相比,牙周炎对照组及3个移动组各检测时间点牙周组织IL-17均呈强阳性表达.实时定量PCR显示,除正常移动组和牙周炎恢复期移动组第14天IL-17 mRNA表达量(1.00±0.07和1.19±0.15)与空白对照组(1.00±0.00)差异无统计学意义外(P>0.05),其余各组各时间点IL-17mRNA表达量均显著高于空白对照组(P<0.05).牙周炎恢复期移动组第3和7天IL-17 mRNA表达较同时间点正常移动组显著增高、较同时间点牙周炎活动期移动组显著减小(P<0.05).结论 IL-17参与调节正常及牙周炎正畸牙齿移动.相对于正常牙周,牙周炎恢复期正畸力在初期更易增加IL-17的表达,IL-17于加力后期可恢复正常.而牙周炎活动期施加正畸力可使IL-17始终维持较高水平.
目的 研究正畸力作用下白介素17 (interleukin-17,IL-17)在不同狀態牙週組織中的錶達變化,探討牙週炎正畸治療機製.方法 77隻6週齡SD大鼠按隨機數字錶法分為3箇移動組(正常、牙週炎活動期和牙週炎恢複期移動組,每組21隻)和2箇對照組(牙週炎和空白對照組,每組7隻).各牙週炎組大鼠採用結扎+塗易感菌+糖水餵養建立牙週炎活動期模型,牙週炎恢複期移動組建模後去除上述刺激因素併行牙週治療,進入牙週炎恢複期.處死2箇對照組大鼠,併用鎳鈦拉簧以0.49 N力近中移動各移動組大鼠上頜第一磨牙,併分彆于移動後第3、7和14天處死(每組每箇時間點7隻).免疫組化檢測牙週組織IL-17錶達.實時定量PCR檢測IL-17 mRNA錶達.結果 免疫組化顯示,與空白對照組相比,牙週炎對照組及3箇移動組各檢測時間點牙週組織IL-17均呈彊暘性錶達.實時定量PCR顯示,除正常移動組和牙週炎恢複期移動組第14天IL-17 mRNA錶達量(1.00±0.07和1.19±0.15)與空白對照組(1.00±0.00)差異無統計學意義外(P>0.05),其餘各組各時間點IL-17mRNA錶達量均顯著高于空白對照組(P<0.05).牙週炎恢複期移動組第3和7天IL-17 mRNA錶達較同時間點正常移動組顯著增高、較同時間點牙週炎活動期移動組顯著減小(P<0.05).結論 IL-17參與調節正常及牙週炎正畸牙齒移動.相對于正常牙週,牙週炎恢複期正畸力在初期更易增加IL-17的錶達,IL-17于加力後期可恢複正常.而牙週炎活動期施加正畸力可使IL-17始終維持較高水平.
목적 연구정기력작용하백개소17 (interleukin-17,IL-17)재불동상태아주조직중적표체변화,탐토아주염정기치료궤제.방법 77지6주령SD대서안수궤수자표법분위3개이동조(정상、아주염활동기화아주염회복기이동조,매조21지)화2개대조조(아주염화공백대조조,매조7지).각아주염조대서채용결찰+도역감균+당수위양건립아주염활동기모형,아주염회복기이동조건모후거제상술자격인소병행아주치료,진입아주염회복기.처사2개대조조대서,병용얼태랍황이0.49 N력근중이동각이동조대서상합제일마아,병분별우이동후제3、7화14천처사(매조매개시간점7지).면역조화검측아주조직IL-17표체.실시정량PCR검측IL-17 mRNA표체.결과 면역조화현시,여공백대조조상비,아주염대조조급3개이동조각검측시간점아주조직IL-17균정강양성표체.실시정량PCR현시,제정상이동조화아주염회복기이동조제14천IL-17 mRNA표체량(1.00±0.07화1.19±0.15)여공백대조조(1.00±0.00)차이무통계학의의외(P>0.05),기여각조각시간점IL-17mRNA표체량균현저고우공백대조조(P<0.05).아주염회복기이동조제3화7천IL-17 mRNA표체교동시간점정상이동조현저증고、교동시간점아주염활동기이동조현저감소(P<0.05).결론 IL-17삼여조절정상급아주염정기아치이동.상대우정상아주,아주염회복기정기력재초기경역증가IL-17적표체,IL-17우가력후기가회복정상.이아주염활동기시가정기력가사IL-17시종유지교고수평.
Objective To investigate interleukin (IL)-17 expression induced by orthodontic force in periodontal ligament under different periodontal conditions.Methods Seventy-seven male SD rats were divided randomly into 5 groups:healthy movement group (HM),active periodontitis movement group (PM) recovery periodontitis movement group (RM),positive control group (PC) and normal control group (NC).Active periodontitis was set up by means of ligature+susceptible bacteria+suger water in PM,PC and RM groups.This stimulating factor was removed in RM group.NiTi spring was used to apply 0.49 N mesial force to move upper first molar of the rats in HM,PM and RM groups.HM,PM and RM group rats were sacrificed on day 3 (d3),day 7 (d7) and day 14 (d14).Expression changes of IL-17 in periodontal tissue in each group were measured using immunohistochemical stain and real time fluorescence quantitative PCR.Results IL-17 expression in periodontal ligament showed more positively in PM and RM groups compared with NC,PC and HM groups.No difference was found in the expression of IL-17 mRNA in NC (1.00±0.00) (P>0.05),except in HM d14 (1.00±0.07) and RM d14 (1.19±0.15).Higher expression of IL-17 mRNA (P<0.05) was found in other groups.The expression of IL-17 mRNA in RM d3 and d7 increased more than that in HM group in the same period (P<0.05) and it decreased significantly (P<0.05) compared with that in PM groups in the same period.Conclusions IL-17 was involved in the regulation of orthodontic tooth movement in different periodontal conditions.Orthodontic force caused limited increase of IL-17 mRNA expression in recovery phase of periodontitis at early stage,then back to normal.However,in active inflammatory periodontal tissue,orthodontic force kept IL-17 mRNA at high level.