膝半月板损伤临床自然转归的研究

目的: 探讨损伤半月板无治疗情况下临床及创缘的变化,为临床治疗提供理论依据. 方法: 自2001年1月至2011年12月选择膝关节外伤而未诊治过的初诊68例患者,经临床表现(疼痛、交锁、不稳等)及膝关节MRI检查诊断为半月板损伤的患者行关节镜检查,其中32例半月板无法修复行全切术,男21例,女11例,年龄15～49岁,平均25岁,损伤至关节镜检查平均时间46周. 观测指标:①膝关节术前术后Lysholm评分. ②关节镜下半月板的损伤部位、类型和状态. ③组织学观察:切取半月板损伤创缘不同部位的组织,一部分甲醛固定、石蜡包埋切片、HE染色、光镜观察;另一部分3%戊二醛固定、环氧树脂包埋、柠檬酸铅染色、电镜观察. 结果: 32例均获随访,时间1年以上. 术后3个月与术前Lysholm评分比较差异有统计学意义(t=15.6,P<0.01).关节镜下可见典型表现28例:创缘中部与两端有新旧之别;非典型表现4例. 光镜下可见典型表现26例:创缘中部少量类上皮细胞,两端交界部有较为明显的组织愈合细胞(成纤维细胞等);非典型表现2例. 电镜下可见典型表现25例:伤缘中部偶见细胞(同源及类上皮)胞核胞浆呈萎缩状态,伤缘两端交界部成纤维细胞体积增大、突起较多、胞核较大,胞浆内含较多粗面内质网、游离核糖体和高尔基复合体,软骨细胞呈圆形或卵圆形,核大而圆,胞浆内较多的粗面内质网和游离核糖体,软骨细胞周围有软骨陷窝;非典型表现3例. 结论: 半月板损伤后未治疗或愈合之前负重活动,将导致创面长度增大,临床症状加重,提示半月板损伤后早期诊断治疗,及时有效制动是半月板痊愈、避免后期手术切除的关键. 无法修复的半月板全切后近期临床效果满意.     

一氧化氮对骨关节病软骨退变影响的研究进展

骨关节病（ｏｓｔｅｏａｒｔｈｒｉｔｉｓ,ＯＡ）是一种严重危害老年人健康的慢性进行性骨关节疾病,随着社会人口的老龄化,该病的发生越来越多。关节软骨的退变是ＯＡ的最直接原因,而ＮＯ（ｎｉｔｒｉｃｏｘｉｄｅ,ＮＯ）又与软骨的退变有极为密切的关系。ＮＯ是生物体内一种结构简单的多功能生物信息分子,在人体正常功能和许多疾病的发生中起着十分重要的作用。有关生物体内ＮＯ合成及作用的综述已有许多,本文就ＮＯ和ＯＡ软骨退变的相关研究进展进行综述。１　ＯＡ患者及动物体内ＮＯ的产生临床研究表明,ＯＡ患者血清及关节液中Ｎ…     

骨关节病关节软骨细胞凋亡的研究进展

骨关节病(ｏｓｔｅｏａｒｔｈｒｉｔｉｓ,ＯＡ)是一种严重危害老年人健康的慢性进行性骨关节疾病,随着社会人口的老龄化,该病的发生会越来越多。弄清ＯＡ的病因,一直是骨科医生面临的重大课题。现已证明,关节软骨的退变是ＯＡ最直接原因。软骨细胞是成熟软骨中唯一的与修复破坏软骨组织有关的细胞类型,ＯＡ关节软骨和非ＯＡ正常关节软骨相比,软骨细胞明显减少。软骨细胞的减少与ＯＡ发生发展关系密切。细胞死亡可以使细胞减少,细胞死亡分为细胞坏死和细胞凋亡,近期观察到ＯＡ软骨有软骨细胞凋亡存在[1]。本文综述了骨关节病关节软骨细胞凋亡…     

大骨节病儿童及成人关节软骨中甲状旁腺激素相关肽的表达

目的 探索甲状旁腺激素相关肽(PTHrP)在大骨节病儿童及成人关节软骨中的表达及分布。方法 应用免疫组化方法比较正常儿童和成人与大骨节病儿童和成人关节软骨中PTHrP的表达。结果 ①大骨节病儿童关节软骨表层、中层、深层PTHrP阳性细胞表达率分别为30％、24％和31％，中层、深层表达率比正常儿童明显增高(P＜0．01)；②大骨节病成人关节软骨表、中、深层PTHrP阳性细胞表达率分别为54％、46％和16％，各层细胞阳性表达率均明显高于正常组(P＜0．01)。②大骨节病儿童与成人比较各层软骨细胞PTHrP的阳性表达差异均有显著意义(P＜0．01)，表现为表、中层成人高于儿童，深层儿童高于成人。结论 大骨节病患者关节软骨中PTHrP阳性表达率高于正常对照。     

过量氟对大鼠部分组织中钙、镁、磷水平的影响

目的：研究慢性氟中毒大鼠在不同染氟剂量及时间内，体内不同组织中钙（Ca)、镁（Mg)、磷（P）水平的变化，探讨过量氟对不同组织中各元素水平的影响。方法：SD大鼠70只分为对照组和低，中，高剂量染氟组，观察实验后3个月（42只）和5个月（28只）的变化。低钙喂养，3个月及5个月后，取氟中毒大鼠心、肝、肾、脾、肌肉、四肢骨及血清，分析，分析F,Ca,P,Mg含量，结果：大鼠氟后各组织氟含量均有不同程度升高，随时间不同，组织中的氟含量呈现动态过程，经多元逐回归分析，大鼠染氟3个月后肌肉中F与Ca,P，肝脏中F与Mg，四肢骨中F与Mg，心脏中F与Ca呈显著性相关（P＜0．05），染氟5个月后肝脏中F与Ca，四肢骨中F与Mg，心脏中F与Ca，肾脏中F与P，Mg呈显著性相关（P＜0．05）。结论：氟中毒大鼠不同组织中相关元素含量随染氟剂量，时间不同而不同。     

大骨节病关节软骨真菌毒素环境反应基因表达谱研究

目的 比较分析真菌毒素环境反应基因在大骨节病(Kashin-Beck disease,KBD)和正常关节软骨中的表达谱差异,探讨真菌毒素环境反应基因与KBD软骨损伤的关系.方法 采集9例KBD患者和9例正常对照关节软骨样本,提取总RNA.采用Agilent基因表达芯片评估真菌毒素环境反应基因在软骨样品中的表达量,并计算每个基因在KBD和正常对照软骨中表达量的比率(简称表达率).采用GSEA软件计算每个基因功能分类表达量的NES指数及P值.结果 ①T-2毒素、脱氧镰刀菌烯醇、玉米赤霉烯酮、黄曲霉毒素B1、伏马菌素B1和赫曲霉毒素A相关的15个环境反应基因在KBD和正常对照关节软骨中的表达水平存在差异(表达率＞2.0或＜0.5),其中13个基因在KBD软骨中上调,包括BAX、BCL2、COL5A2、FER1L3、GSTT2、IGFBP2、IGFBP4、PDE8B、SOCS3、THBS1、TMSL8、VGLL3和TUBB2A(表达率＞2.0);2个基因在KBD软骨中下调,包括POSTN和FABP4(表达率＜0.5).上述15个基因功能主要涉及胶原、细胞凋亡、代谢和生长发育等.②真菌毒素相关的4个凋亡基因功能分类和5个生长发育基因功能分类在KBD关节软骨中上调(NES＞0),包括ANTI_APOPTOSIS、REGULATION OF PROGRAMMED_CELL_DEATH、APOPTOSIS_GO、EGULATION_OF_APOPTOSIS、ORGAN MORPHOGENES IS、ANATOMICAL_STRUCTURE_ DEVELOPMENT、ORGAN_DEVELOPMENT、SYSTEM DEVELOPMENT和REGULATION—OF_DEVELOPMENTAL_PROCESS (NES＞0且P＜ 0.05).结论 KBD软骨中存在多种真菌毒素的环境反应基因表达且显著不同于正常对照,提示真菌毒素可能通过影响相关环境反应基因在关节软骨中的表达,诱发软骨细胞功能障碍和关节软骨损伤.     

等位基因HLA-A*02∶09与4种HLA单倍体的关系及应用

目的 观察等位基因HLA-A＊02∶09与4种单倍体的关系,以通过筛检相关单倍体缩小模棱两可确认实验的检测范围.方法 采用PCR-SSO-Luminex方法检测的HLA-A＊02∶01和A＊02∶09的模棱两可样本通过EXON4-7补充实验确认HLA-A＊02∶09阳性样本,并观察是否携带特定单倍体.结果对205例A＊02∶01/02∶09的模棱两可样本进行了确认实验,包含携带4种单倍体的样本58例,3例检出A＊02∶09;未携带4种单倍体的147例未检出A＊02∶09.结论 HLA-A＊02∶01/02∶09模棱两可的比例较高,筛检高危单倍体可有效缩小骨髓库入库样本发生A＊02∶01/02∶09这一组模棱两可时的确认实验的检测范围.     

T-2毒素对软骨细胞P53、Bcl—xL和Caspase-3表达的影响

目的 观察T-2毒素对软骨细胞P53、Bcl-xL和caspase-3表达的影响.方法 采用胎儿软骨细胞体外培养,培养基中加入不同浓度的T-2毒素(1～20μ/L)连续培养5 d.采用Western blot检测软骨细胞P53、Bcl-xL和Caspase-3蛋白表达水平;用RT-PCR法检测软骨细胞P53、Bcl-xL和Caspase-3 mRNA的表达.结果 与对照组比较,不同浓度(1～20μL)的T-2毒素均能引起Caspase-3蛋白表达水平升高而Bcl-xL蛋白表达水平下降(P＜0.05);当T-2毒素浓度达到10～20μg/L时,P53蛋白和Caspase-3 mRNA表达水平明显升高(P＜0.05)而Bcl-xLmRNA的表达水平无显著性下调(P＞0.05);T-2毒素浓度达到20μ/L可以引起P53 mRNA表达水平明显升高(P＜0.05).结论 T-2毒素诱导软骨细胞发生的凋亡可能与T-2毒素上调软骨细胞P53、caspase-3表达,同时下调Bcl-xL表达有关.     

松质骨骨基质明胶负载软骨细胞移植修复兔膝关节软骨缺损

目的 应用松质骨骨基质明胶(bone matrix gelatin，BMG)负载兔软骨细胞移植修复同种异体关节软骨缺损。方法 BMG载软骨细胞，体外培养12d后植入同种异体新西兰兔膝关节软骨缺损。对照组植入BMG或不作任何植入。移植前用胰蛋白酶处理关节软骨缺损。术后2、4、8、12、24周行解剖显微镜、组织学、电镜观察和免疫组织化学染色。结果 BMG术后8周降解。实验组术后24周关节软骨缺损以软骨组织修复，与周围软骨及软骨下骨愈合良好。Safranin-O、免疫组织化学染色证实其基质有蛋白多糖和Ⅱ型胶原，电镜观察表明修复组织软骨细胞及基质与正常关节软骨一致。BMG对照组以部分软骨组织修复，空白对照组以纤维组织修复。结论 松质骨BMG可作为软骨组织工程的天然细胞支架，其负载软骨细胞移植能修复同种异体兔关节软骨缺损。     

低硒、低碘及联合对亲代和子代大鼠骨、软骨生长的影响

Objective To study the effects of selenium deficiency,iodine deficiency and combined selenium and iodine deficiency on bone and cartilage growth in the parental and the first filial generation rats. Methods Forty-eight weanling healthy SD rats were randomly divided into selenium deficieney, iodine deficiency, combined selenium and iodine deficiency and control groups according to their body mass. These rats were fed with selenium deficiency, iodine deficiency, combined selenium and iodine deficiency, and normal fodder, respectively. The parental rats (about 3 months old) were mated in each group 8 weeks after the beginning of the experiment. Right tibias and left knee joints were collected when the parental generation rats were about 6 months and the first filial generation rats were about 3 months old. Tibial length, mid-shaft tibial diameter, and articular cartilage diameters of the right tibias were measured by vernier caliper. Left knee joints were embedded and cut into sections and the thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes in growth plate cartilage were observed under the light microscope. Results The selenium deficiency had significant effect on serum selenium level of the parental and the first filial generation rats(F value were 239.56,232.68, P< 0.01), and also on serum T4 level of the first filial generation rats(F value were 6.95, P < 0.05). The iodine deficiency had significant effect on serum T3 and T4 level in the two generations rats(F value were 14.11,14.05,30.29,34.53, P < 0.01 ). There were interactions between selenium deficiency and iodine deficiency on serum T4 level in the first filial generation rats (F= 5.99, P< 0.05). The serum selenium of selenium deficiency group[ (30.28 ± 6.34), (43.95 ± 9.75)μg/L],combined selenium and iodine deficiency group[ (30.33 ± 5.18), (35.40 ± 3.16)μg/L] were significantly lower than iodine deficiency group[(345.83 ± 29.55), (245.24 ± 9.95)μg/L] and the controls[ (358.64 ± 30.50), (236.50 ±9.75) μg/L] in the two generations. The serum T3 of combined selenium and iodine deficiency group [(0.55 ± 0.05 ),(0.88 ± 0.14)nmol/L] were significantly lower than the controls[(0.75 ± 0.08), (1.26 ± 0.26)nmol/L] in the two generations. The serum T4 of iodine deficiency [ (24.11 ± 2.29), (42.10 ± 8.92) nmol/L ] and combined selenium and iodine deficiency group[ (20.66 ± 1.93), (26.55 ± 5.98)nmol/L] were significantly lower than the controls[ (36.15 ±2.74), (52.79 ± 8.84)nmol/L] and selenium deficiency group[ (28.12 ± 3.33), (52.02 ± ll.99)nmol/L] in the two generations. The selenium deficiency and iodine deficiency had significant effect on tibial length, thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes in first filial generation rats(F values were 24.31,6.98,40.76,56.15,25.24,82.82, 10.07,5.57, P <0.05 or <0.01). There were interactions between selenium deficiency and iodine deficiency on tibial length, thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes (F values were 5.68,24.86,41.82,9.12, P <0.05 or <0.01 ). The tibial length of the selenium deficiency group[ (33.17 ± 0.34)mm] and combined selenium and iodine deficiency group[ (31.30 ± 0.87)mm] were significantly lower than the controls[ (34.12 ± 0.32)mm, P< 0.05]. Thickness of the growth plate cartilage [ (1.60 ± 0.18)mm ], layers of proliferative chondrocyte (8.54 ± 0.81), and hypertrophic chondrocyte (4.95 ± 0.37)of the combined selenium and iodine deficiency group were significantly decreased when compared to the selenium deficiency group[ (3.03 ± 0.10)mm, 14.68 ± 0.84,6.60 ± 0.31], iodine deficiency group[ (2.90 ± 0.09)mm, 13.75 ±0.33,6.61 ± 0.84 ] and the controls [ (3.19 ± 0.09) mm, 14.94 ± 0.36, 6.64 ± 0.26, P <0.05]. Thickness of the growth plate cartilage, layers of proliferative chondrocyte of the iodine deficiency group were lower than the controls(P<0.05). Conclusions Selenium deficiency impair tibial growth in first filial generation rats, iodine deficiency retarded the chondroncyte proliferation and decreases the thickness of growth plate cartilage in first filial generation rats, and combined selenium and iodine deficiency significantly impair the growth of bone and cartilage in first filial generation rats.