中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2012年
52期
9792-9796
,共5页
发育性髋关节脱位%愈合%胶原纤维%基质金属蛋白酶2%几丁糖%医学植入体
髮育性髖關節脫位%愈閤%膠原纖維%基質金屬蛋白酶2%幾丁糖%醫學植入體
발육성관관절탈위%유합%효원섬유%기질금속단백매2%궤정당%의학식입체
背景:发育性髋关节脱位是小儿骨科常见畸形之一,预防手术后关节粘连主要手段是功能练习,但锻炼的时机选择则受限于关节囊愈合情况.
目的:观察兔关节囊切开后愈合过程的形态学以及几丁糖干预后基质金属蛋白酶2的表达,探讨关节囊愈合机制.
方法:新西兰大白兔制作关节囊切开-愈合模型,左侧(实验侧)在关闭前注入医用几丁糖1 mL,右侧(对照侧)则仅行切开后关闭,不予几丁糖干预.各组在处死兔的第一时间取髋关节囊,所得标本采用 Masson 染色法行胶原染色分析和ABC免疫组织化学法检测基质金属蛋白酶2表达.
结果与结论:胶原染色显示术后3-28 d,对照侧和实验侧的胶原分布和排列均呈逐渐变好趋势,但早期水肿和断裂明显.对照侧的胶原纤维形态完整性、断裂间隙和排列致密与规律程度均差于实验侧.基质金属蛋白酶2表达检测结果则显示对照侧和实验侧基质金属蛋白酶2表达均为阳性,其强度规律表现为随时间增加呈逐渐加强趋势,但是并不完全同步,其中对照侧在术后7 d有明显下降随后则开始增强,但最终仍弱于实验侧,实验侧则呈增强趋势,除术后3 d弱于对照侧外,其余各时间点表达明显强于对照侧.结果可见关节囊愈合过程中基质金属蛋白酶2通过降解变性胶原明胶的特异能力参与重建,而且重建塑形过程要大于28 d,几丁糖可以延缓早期胶原组织变性、抑制炎性反应并促进愈合.
揹景:髮育性髖關節脫位是小兒骨科常見畸形之一,預防手術後關節粘連主要手段是功能練習,但鍛煉的時機選擇則受限于關節囊愈閤情況.
目的:觀察兔關節囊切開後愈閤過程的形態學以及幾丁糖榦預後基質金屬蛋白酶2的錶達,探討關節囊愈閤機製.
方法:新西蘭大白兔製作關節囊切開-愈閤模型,左側(實驗側)在關閉前註入醫用幾丁糖1 mL,右側(對照側)則僅行切開後關閉,不予幾丁糖榦預.各組在處死兔的第一時間取髖關節囊,所得標本採用 Masson 染色法行膠原染色分析和ABC免疫組織化學法檢測基質金屬蛋白酶2錶達.
結果與結論:膠原染色顯示術後3-28 d,對照側和實驗側的膠原分佈和排列均呈逐漸變好趨勢,但早期水腫和斷裂明顯.對照側的膠原纖維形態完整性、斷裂間隙和排列緻密與規律程度均差于實驗側.基質金屬蛋白酶2錶達檢測結果則顯示對照側和實驗側基質金屬蛋白酶2錶達均為暘性,其彊度規律錶現為隨時間增加呈逐漸加彊趨勢,但是併不完全同步,其中對照側在術後7 d有明顯下降隨後則開始增彊,但最終仍弱于實驗側,實驗側則呈增彊趨勢,除術後3 d弱于對照側外,其餘各時間點錶達明顯彊于對照側.結果可見關節囊愈閤過程中基質金屬蛋白酶2通過降解變性膠原明膠的特異能力參與重建,而且重建塑形過程要大于28 d,幾丁糖可以延緩早期膠原組織變性、抑製炎性反應併促進愈閤.
배경:발육성관관절탈위시소인골과상견기형지일,예방수술후관절점련주요수단시공능연습,단단련적시궤선택칙수한우관절낭유합정황.
목적:관찰토관절낭절개후유합과정적형태학이급궤정당간예후기질금속단백매2적표체,탐토관절낭유합궤제.
방법:신서란대백토제작관절낭절개-유합모형,좌측(실험측)재관폐전주입의용궤정당1 mL,우측(대조측)칙부행절개후관폐,불여궤정당간예.각조재처사토적제일시간취관관절낭,소득표본채용 Masson 염색법행효원염색분석화ABC면역조직화학법검측기질금속단백매2표체.
결과여결론:효원염색현시술후3-28 d,대조측화실험측적효원분포화배렬균정축점변호추세,단조기수종화단렬명현.대조측적효원섬유형태완정성、단렬간극화배렬치밀여규률정도균차우실험측.기질금속단백매2표체검측결과칙현시대조측화실험측기질금속단백매2표체균위양성,기강도규률표현위수시간증가정축점가강추세,단시병불완전동보,기중대조측재술후7 d유명현하강수후칙개시증강,단최종잉약우실험측,실험측칙정증강추세,제술후3 d약우대조측외,기여각시간점표체명현강우대조측.결과가견관절낭유합과정중기질금속단백매2통과강해변성효원명효적특이능력삼여중건,이차중건소형과정요대우28 d,궤정당가이연완조기효원조직변성、억제염성반응병촉진유합.
BACKGROUND:The developmental dislocation of the hip is a kind of common orthopaedics deformity. Function practice is the main measure to prevent articular adhesion after operation. But the right time choice depends on the healing degree of the capsule of hip joint. @@@@OBJECTIVE:To observe the morphology of hip joint capsule cut-healing model of the rabbits and the expression of matrix metal oproteinase 2 after chitosan induction, so as to explore the healing mechanism of hip capsule. @@@@METHODS:New Zealand white rabbit was used to establish the hip joint capsule cut-healing model, the left hip joint capsule (experimental group) was injected with 1 mL chitosan before closure, and the right hip joint capsule (control group) was closed after cutting without chitosan induction. The capsules were immediately obtained after executed the rabbit, then the col agen analysis was performed by Masson staining, and the expression of matrix metal oproteinase 2 was detected by ABC immunohistochemical method. @@@@RESULTS AND CONCLUSION:The col agen staining showed that col agen distribution and arrangement in these two groups were gradual y changed to the better trend from 3 days to 28 days, but the early edema and fracture were obvious. The integrity of the col agen fiber morphology, the fracture gap and arrangement dense and regularity level in the control group were worse than those in the experimental group. Detection of the matrix metal oproteinase 2 showed that the expression of matrix metal oproteinase 2 was positive in both groups and grown stronger with the time increasing, but not ful y synchronized. The expression of matrix metal oproteinase 2 in the control group was decreased at 7 days after operation and final y weaker than that in the experimental group, while the expression in the experimental group was continued increasing and stronger than that in the control group, excepted for the 3rd day after operation. Matrix metal oproteinase 2 participates in the reconstruction process through digesting degenerated col agen, and the reconstruction process should be longer than 28 days. Chitosan can promote healing process through delaying tissue necrosis degeneration and depressing inflammatory reaction.