颈前路减压后自体髂骨与钛网植骨重建颈椎稳定性对比研究

目的：比较颈前路减压自体髂骨植骨与钛网植骨重建颈椎稳定性。方法：脊髓型颈椎病患者41例，男23例，女18例；年龄39～63岁；病程9个月～3．9年。随机分为两组，采用颈前路减压自体髂骨植骨22例；钛网植骨加Orion钢板内固定19例。观察椎间隙高度变化，生理曲度变化，植骨融合率及融合时间。结果：所有患者均获随访，随访时间10～40个月，平均23．2个月。植骨均获骨性愈合，植骨融合时间，椎间高度丢失，Cobb角丢失，两组比较均有统计学差异，自体髂骨植骨组优于钛网植骨组。术前后椎间高度比较两组均有显著变化（P〈0．01）。结论：两种融合方式近期均能有效重建和维持颈椎稳定性，但在融合时间，椎间高度丢失，生理曲度丢失方面髂骨植骨优于钛网植骨。钛网植骨并不具有独特优点，应严格掌握适应证。     

Mechanical and hypoxia stress can cause chondrocytes apoptosis through over-activation of endoplasmic reticulum stress

ObjectiveTo examine the role of mechanical force and hypoxia on chondrocytes apoptosis and osteoarthritis (OA)-liked pathological change on mandibular cartilage through over-activation of endoplasmic reticulum stress (ERS).MethodsWe used two in vitro models to examine the effect of mechanical force and hypoxia on chondrocytes apoptosis separately. The mandibular condylar chondrocytes were obtained from three-week-old male Sprague–Dawley rats. Flexcell 5000T apparatus was used to produce mechanical forces (12%, 0.5 Hz, 24 h vs 20%, 0.5 Hz, 24 h) on chondrocytes. For hypoxia experiment, the concentration of O₂ was down regulated to 5% or 1%. Cell apoptosis rates were quantified by annexin V and propidium iodide (PI) double staining and FACS analysis. Quantitative real-time PCR and western blot were performed to evaluate the activation of ERS and cellular hypoxia. Then we used a mechanical stress loading rat model to verify the involvement of ERS in OA-liked mandibular cartilage pathological change. Histological changes in mandibular condylar cartilage were assessed via hematoxylin & eosin (HE) staining. Immunohistochemistry of GRP78, GRP94, HIF-1α, and HIF-2α were performed to evaluate activation of the ERS and existence of hypoxia. Apoptotic cells were detected by the TUNEL method.ResultsTunicamycin, 20% mechanical forces and hypoxia (1% O₂) all significantly increased chondrocytes apoptosis rates and expression of ERS markers (GRP78, GRP94 and Caspase 12). However, 12% mechanical forces can only increase the apoptotic sensitivity of chondrocytes. Mechanical stress resulted in OA-liked pathological change on rat mandibular condylar cartilage which included thinning cartilage and bone erosion. The number of apoptotic cells increased. ERS and hypoxia markers expressions were also enhanced. Salubrinal, an ERS inhibitor, can reverse these effects in vitro and in vivo through the down-regulation of ERS markers and hypoxia markers.ConclusionWe confirmed that mechanical stress and local hypoxia both contributed to the chondrocytes apoptosis. Mechanical stress can cause OA-like pathological change in rat mandibular condylar cartilage via ERS activation and hypoxia existed in the meantime. Both mechanical forces and hypoxia can induce ERS and cause chondrocytes apoptosis only if the stimulate was in higher level. Salubrinal can protect chondrocytes from apoptosis, and relieve OA-liked pathological change on mandibular condylar cartilage under mechanical stress stimulation.     

掺锶硫酸钙骨修复材料体外细胞相容性研究

目的验证掺锶硫酸钙复合骨修复材料的细胞毒性和细胞相容性。方法用a-半水硫酸钙（a—CSH）和氯化锶（SrClz）采用混合共结晶法制备6组不同掺锶量的掺锶硫酸钙骨修复材料,用MTT法来检测细胞增殖情况,对各组材料进行细胞碱性磷酸酶活性测定。结果MTT实验显示,细胞在各组掺锶硫酸钙材料浸提液中均正常增殖,培养7d时掺锶材料各组OD值均高于a—CSH组（P〈0．01）;碱性磷酸酶活性测定结果显示,成骨细胞碱性磷酸酶活性在掺锶材料浸提液中增加（P〈O．05）,且当掺锶量为0．5％时最明显。共培养结果显示,细胞能在各组掺锶硫酸钙材料上紧密贴附生长,共培养4d后,掺锶0．3％和0．5％材料上的细胞多于a—CSH组,但差异无统计学意义（P-0．061,P-0．057）。结论掺锶硫酸钙骨修复材料无细胞毒性且有较好的细胞相容性,成骨样细胞能在其上正常地贴附生长。     

掺锶硫酸钙复合骨修复材料修复松质骨骨缺损研究

目的初步验证掺锶硫酸钙复合骨修复材料修复松质骨骨缺损的能力。方法建立直径5mm、深度12mm的新西兰兔股骨髁包容性骨缺损模型,取含锶量为0．5％的掺锶硫酸钙骨缺损进行修复。术后4、8、12w连续X线摄片,观察骨缺损修复情况。术后12w处死动物,取动物双股骨下段,进行股骨远端缺损区压凹实验。术后8、12w取标本行HE染色,光镜观察材料及周围组织的变化和植入材料内新骨的形成情况。采用ImageplusCCD系统对植骨区的成骨情况进行定量分析。结果x线显示掺锶硫酸钙组术后12w时原骨缺损区域已完全被新骨填充,其密度与正常骨组织密度接近;a-半水硫酸钙组术后12w时骨缺损区内部仍可见少量植入材料的碎片。术后12w掺锶硫酸钙组和a一半水硫酸钙组股骨髁骨缺损区压缩强度均高于空白对照组（P=0．000,P0．000）;两组间比较掺锶硫酸钙组压缩强度高于a-半水硫酸钙组（p=0．007）;掺锶硫酸钙组压缩强度与正常对照组相比差异无统计学意义（P=1．000）。术后8、12w掺锶硫酸钙组和“半水硫酸钙组新骨形成率均明显高于空白对照组（P=0．000）,且掺锶硫酸钙组新骨形成率均明显高于a半水硫酸钙组（P=0．030,P=0．043）。结论现阶段制备的0．5％掺锶硫酸钙材料在松质骨包容性骨缺损区内有明显的促成骨作用,在12w内比基质材料a-半水硫酸钙能更好的修复骨缺损。