兰州地区正常人群骨密度及骨质疏松检出率结果分析

目的调查兰州地区正常人群骨密度值及骨质疏松患病率,分析其变化规律。为骨质疏松防治提供依据。方法采用美国GE-Lunar公司生产的Prodigy型双能X线骨密度仪分别测试1212例20～85岁受试者的L1-4及股骨上段（包括股骨颈,Wards区,及粗隆部位）的骨密度（BMD）值。按年龄、性别进行分组,以10岁为1个年龄段。结果男女性骨密度峰值均出现于30～39岁组,且骨密度值随年龄增加而渐降低,进入50～69岁组,女性的骨量丢失速度明显加快,尤以Wards区明显,50岁后骨质疏松发病率,男性为12.1%,女性为46.7%。结论骨密度随年龄增长而下降,骨质疏松发病率也随之增加,同年龄组女性发病率明显高于男性。     

资阳地区定量超声跟骨骨量测定的流调分析

目的调查四川资阳地区健康人群骨密度值及骨质疏松患病率,为骨质疏松的诊断和防治提供科学依据。方法对资阳地区人群亚群抽样1976例,应用日本FURUNO公司生产的超声骨量测定仪CM100测试受试者的右跟骨的超声速度(SOS)值。结果男女骨量峰值(PBM)均出现在20～39岁组,随年龄增加骨量逐渐下降。女性50岁以后骨量丢失明显加快,60～69岁年龄组骨量丢失最快;男性70岁以后骨量丢失明显加快。80岁以前各年龄组女性骨量丢失明显高于男性,80岁以后男性骨量丢失高于女性,但累计骨量丢失女性仍明显高于男性。结论骨量随年龄增长而下降,骨质疏松发病率也随之增加。女性骨量丢失明显高于男性,女性骨质疏松发病率也明显高于男性。     

大庆地区1096例汉族人群骨密度调查及骨质疏松发生率分析

目的 调查大庆市1096例健康汉族人群骨密度,了解该地区健康人群骨量峰值、骨密度变化的规律及骨质疏松发生率。方法 采用美国GE公司生产的Luner Prodigy Advance型骨密度仪,检测受试者腰椎和股骨颈骨密度（BMD）。将1096例检测结果按不同性别每5岁为1年龄组,应用SPSS19.0软件统计分析骨密度测量指标及骨质疏松（OP）发生率。结果 大庆市汉族男、女性人群腰椎骨密度峰值分别为1.197±0.203、1.192±0.145,股骨颈骨密度峰值分别为0.977±0.157、0.918±0.128。其峰值骨量年龄男性为45～49岁,50岁以后开始缓慢下降。其峰值骨量年龄女性为40～49岁,50岁以后开始缓慢下降。50～54岁年龄段男性骨质疏松症发生率为5.56%,女性为5.67%;55～59岁年龄段男性骨质疏松症发生率为7.32%,女性为11.51%;60～64岁年龄段男性骨质疏松症发生率为15.15%,女性为28.28%;65～69岁年龄段男性骨质疏松发生率为26.67%,女性为29.41%;70～74岁年龄段男性骨质疏松发生率为25.00%,女性为44.44%;75～79岁年龄段男性骨质疏松发生率为36.36%,女性为77.78%;80岁以上男性骨质疏松发生率为66.67%,女性为83.33%。结论 大庆市汉族人群不同年龄及同年龄组两性之间比较骨密度测定值差异显著（P<0.01）。55岁以后各年龄段女性骨质疏松发生率明显高于男性（P<0.01）。本研究报告的骨密度峰值大于沈阳地区,与合肥地区相近,略低于贵阳地区。OP发生率与合肥地区比较相近,略低于沈阳地区。     

北京昌平地区老年人骨质疏松情况及相关因素调查

目的 调查北京昌平地区60岁以上老年人的骨质疏松情况.方法 采用随机整群抽样调查,抽取昌平地区992名60岁以上老年人测量前臂骨骨密度并问卷调查一般情况.结果 昌平地区60岁以上人群总体骨质疏松率为49.19%,男性为9.68%,女性为39.92%.总体骨密度平均T值为-1.8998,男性为-1.1416,女性为-2.2812,随年龄的增加,整体骨质疏松发病率也在增高,女性骨量减少和骨质疏松发生率均高于男性,而且女性在60～69岁之间骨量减少高于其他年龄段.骨折与骨密度呈负相关关系,而骨密度与性别、体重、身高、年龄、饮酒均有关.结论 北京昌平地区60岁以上的老年人骨质疏松发生率较高,提醒广大医务工作者应广泛开展骨质疏松健康教育.     

合肥地区1162例正常人群骨密度的分析研究

目的 了解合肥地区正常人群骨密度的变化规律和骨质疏松的患病率.方法 采用美国Lunar公司的双能x线骨密度仪对合肥地区1162名20～91岁居民进行腰椎2～4、股骨近端和前臂的骨密度测量.结果 男性腰椎骨密度峰值在30～34岁,女性腰椎骨密度峰值在25～29岁;男性股骨近端骨密度峰值在20～24岁,女性股骨近端骨密度峰值在25～29岁;男性前臂骨密度峰值在30～34岁,女性前臂骨密度峰值在35～39岁.峰值后随年龄增长而骨密度下降,女性在50～59岁出现明显加速,男性没有出现加速下降现象.合肥地区50岁以上男性骨质疏松的患病率为25.8%,女性骨质疏松的患病率为54.1%.两者之间差异有非常显著性(P<0.01).结论 合肥地区正常人群骨密度随年龄增长而降低,骨质疏松的患病率也随之增加,骨质疏松的患病率女性高于男性.     

广州地区1 530例骨密度分析及骨质疏松发病率研究

目的为了解广州地区正常人群骨密度(BMD)的变化规律和骨质疏松(OP)的患病率.方法采用美国Lunar公司的双能X线骨密度仪对广州地区1 530名20～89岁居民进行腰椎2-4和髋部骨密度测量.结果男性腰椎骨密度峰值在20～29岁,女性腰椎骨密度峰值在30～39岁,男性与女性髋部骨密度峰值均在30～39岁,峰值后随年龄增加而骨密度下降,女性在50～59岁出现明显加速,男性没有加速下降现象.广州地区男性50～89岁骨质疏松患病率26.53%,女性50～89岁骨质疏松患病率42.64%,两者之间差异有非常显著性(P＜0.01).结论广州地区女性骨质疏松患病率高于男性,预防骨质疏松的重点在女性,但对男性骨质疏松患者也不容忽视.     

湖北十堰地区正常人群骨密度调查研究

目的调查十堰地区正常人群的骨密度变化规律及骨质疏松患病情况,为骨质疏松的诊断和防治提供科学依据。方法选取居住在湖北十堰地区的居民3026例(男性1468例,女性1558例),用DTX-200骨密度仪(美国OSTEOMETER MEDITECH公司生产)测量非优势手尺桡骨远端1/3的BMD。结果男女性BMD均在30～39岁达到骨峰值,各年龄段男性的BMD均高于女性。女性从40～49岁开始(男性组从50～59岁开始),BMD开始明显下降(P0.05),骨量减少和骨质疏松的检出率明显增加(P0.05)。同龄组女性骨质疏松患病率比男性高(P0.05)。结论十堰地区正常人群BMD随年龄增长而降低,OP患病率随年龄增加而增加,女性OP患病率高于男性。     

莆田地区1337例骨密度调查

目的 调查莆田地区部分人群骨密度,建立莆田地区正常人群各年龄组的骨密度正常值范围,为骨质疏松的诊断、治疗和预防提供科学依据.方法 1337例(男466,女871)莆田地区健康人群采用美国Osteometer MediTech公司的DTX-200骨密度仪测定受试者前臂尺挠骨远端的BMD值.按年龄、性别进行分组以10岁为一个年龄段进行统计.用SPSS17.0分析软件进行统计学处理.结果 莆田地区男性女性骨密度峰值(PBM)均出现在30-39岁,分别为0.62±0.06和0.52±0.07,随后成下降趋势,同年龄段和同一测量部位的男性BMD均高于女性,女性在50岁以后,男性在70岁以后骨密度值明显下降.结论 骨质疏松发生率与增龄呈明显正相关,女性在50岁以后,男性在70岁以后,骨质疏松发生率明显增高,应尽早预防和治疗.     

佛山地区中老年人骨密度测定及骨质疏松患病率分析

目的了解佛山地区中老年人群骨密度（BMD）变化规律及骨质疏松（OP）患病率,为本地区骨质疏松症的防治提供参考。方法使用美国Hologic公司双能X线骨密度仪对839例广东省佛山地区40～85岁中老年人正位腰椎和股骨近端进行骨密度测定。结果随着年龄的增加（40岁以上）,男女性各部位BMD逐渐下降,女性更为明显,男性腰椎BMD下降程度较轻。男性腰椎50～岁组与60～岁组比较和60～岁组与70～岁组比较、女性腰椎60～岁组与70～岁组比较,差异无统计学意义（P〉0.05）,其余各组比较差异有显著性意义。腰椎的OP患病率最高,40~59岁男女患病率差异无显著性,60岁以后女性明显高于男性（P〈0.001）。40～84岁人群腰椎和股骨骨质疏松症发病率男性为27.1%和2.2%,女性为46.4%和11.8%,男女比较差异有非常显著性（P〈0.001）。结论佛山地区中老年人群BMD逐年下降,腰椎骨质疏松的患病率最高,研究的重点在中老年妇女。中老年人应坚持适当的体育活动,并注意防止跌倒导致的骨折发生。     

沈阳地区人群5254例骨密度调查研究

目的 调查沈阳地区部分人群骨密度，为骨密度正常参考值数据提供资料，为沈阳乃至全国骨质疏松预防、诊断、治疗提供科学依据。方法 应用双能X线骨密度检测仪对沈阳各区县部分人群5254例进行骨密度检测，以分析软件进行统计、比较。结果 统计出各年龄组骨密度，计算骨密度丢失率及患病率，比较城乡及不同职业间骨密度差异。结论 沈阳地区男女骨密度峰值均在26-30岁年龄组，女性50岁、男性60岁以后骨密度丢失率、患病率升高，女性66-70岁年龄骨密度均值城乡有显著差异。     

杭州健康女性定量骨超声测定原发性骨质疏松

目的 评价杭州健康女性骨超声速度(SOS)值随增龄减少和骨质疏松患病率，建立杭州地区女性骨超声速度值参考数据库。方法 定量超声法测定1208例杭州地区健康女性桡骨远端(RAD)，第3指骨近节(PLX)，第V跖骨(MTR)和胫骨中段(TIB)的超声速度值。结果 RAD、PLX、MTR和TIBSOS峰值(Peak of SOS)均出现在40-45岁，TJB的SOS峰值出现在35—40岁，此后随年龄增长而下降。绝经后妇女在绝经后早期和晚期各有1个SOS快速减少期，前见于桡骨近端，平均年减少率为2．4％，后见于胫骨中段，平均年减少率为1．8％。各部位骨SOS累积减少率随年龄增长而增加，到85岁4部位累积减少为13％-18％。60岁以后骨质疏松性症(OP)检出率为45％-70％，OP检出率以桡骨远端最高，60-70岁平均为67％，第3指骨近端次之约50％，胫骨中段最低为36％；75岁以后分别为70％，65％和45％。结论 全身各部位骨超声速度值到达峰值的年龄不同，峰值也各有差异。绝经后妇女骨超声速度值随年龄增加减少较快，应予激素和补钙治疗，桡骨远端为本地区SOS检测和OP检出的敏感部位。     

Importance of echocardiography in prognosis of surgical outcomes in cholecystitis in elderly patients

The authors propose to use more often echocardiography (EchoCG) in examination of elderly (over 60 years) of age patients with cholecystitis that permits to increase surgical activity to 92.4%. Left ventricular ejection fraction is the most informative. When this fraction is lower than 45% surgery must be recommended on vital indications only. EchoCG was used in 155 patients with cholecystitis, 131 of them were operated. 2 (1.52%) patients died due to acute cardio-vascular insufficiency and pulmonary artery thromboembolism.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

目的 评价脊髓胶质细胞在小鼠骨癌痛形成中的作用.方法 健康雄性C3H/He小鼠40只,周龄8～10周,体重18～22 g,随机分为4组(n=10):假手术组(S组)、骨癌痛组(B组)、PBS组(P组)和米诺环素组(M组).S组跟骨骨髓腔内注射PBS 10 μl;余3组跟骨骨髓腔内注射含2×105个骨纤维肉瘤细胞的PBS 10 μl制备骨癌痛模型,于造模前即刻开始PBS组鞘内注射PBS 5μl,M组鞘内注射米诺环素(用PBS溶解为0.2 mmol/L)5μl,1次/d,连续11 d.于造模前1 d、造模后即刻、3、5、7、9、11 d时测定机械痛阈;于造模后3、7、9、11 d机械痛阈测定结束后测定冷痛阈.痛阈测定结束后处死小鼠,取脊髓组织,测定神经胶质纤维酸性蛋白(GFAP)和CD11b的表达水平.结果 与S组比较,B组和P组造模后3-11 d时、M组造模后3、5 d时机械痛阈升高,B组、P组和M组造模后7～11 d时冷痛阈升高,脊髓CD11b和GFAP表达上调(P<0.05).与B组比较,M组造模后3-11 d时机械痛阈降低,造模后7-11 d时冷痛阈降低,脊髓CD11b和GFAP表达下调(P<0.05).结论 脊髓胶质细胞(星形胶质细胞和小胶质细胞)的激活参与了小鼠骨癌痛的形成.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.