中西药干预后肠源性5-羟色胺和骨密度的变化

目的观察补肾壮骨冲剂和阿仑膦酸钠对骨质疏松症(osteoporosis,OP)患者的肠源性5-羟色胺(5-hydroxytryptamine,5-HT)浓度和骨密度的影响,探讨其作用机制。方法将120例原发性骨质疏松症患者分为补肾壮骨冲剂组和阿仑膦酸钠组,分析在药物治疗前后肠源性5-HT浓度和骨密度的差异。(1)本研究所有样本为2011年5月-2012年12月到广州军区广州总医院住院部及门诊部就诊的确诊为原发性骨质疏松症的患者。(2)肠源性5-HT测定:上午8:00～9:00抽取禁食12 h后空腹肘静脉血3 ml,3000 r/min即时离心5 min后,将血清置于-80℃冰箱保存,采用酶联免疫分析法检测5-HT的含量。(3)骨密度测定:采用美国GE公司生产的Lunar Prodigy双能X线(DEXA)骨密度仪,检测各部位BMD。(4)骨生化指标测定:采用酶联免疫分析法检测血清中肠源性5-HT的含量、电化学发光免疫分析法分析血清P1NP、β-Crosslaps、PTH的含量。结果补肾壮骨冲剂组治疗后左侧股骨颈、Ward’s三角和左侧股骨近端处骨密度上升,血清中的5-HT、PINP、β-Crosslaps及PTH浓度全面下降。阿仑膦酸钠组治疗后除腰椎外,其余各部位的骨密度都明显上升,血清中的5-HT、PINP、β-Crosslaps及PTH浓度全面下降。补肾壮骨冲剂组与阿仑膦酸钠组治疗后相关指标比较,两组骨密度改善情况未见明显差别,两组在治疗后的各项骨代谢指标改善情况未见明显差别。结论补肾壮骨冲剂和阿仑膦酸钠均可在提高骨密度同时减低肠源性5-HT浓度,与Ulrike提出的"肠源性5-HT与骨密度成负相关"这个结论相符。     

骨肽注射液配合阿仑膦酸钠对老年男性2型糖尿病性骨质疏松症患者骨代谢及骨密度的影响

目的探讨在老年男性2型糖尿病性骨质疏松症患者中采用骨肽注射液配合阿仑膦酸钠治疗对骨代谢及骨密度(BMD)的影响。方法将我院就治的96例老年男性2型糖尿病性骨质疏松症患者随机分为对照组(48例)和试验组(48例),对照组采用钙尔奇联合阿仑膦酸钠治疗,试验组在对照组的基础上加用骨肽注射液,观察对比两组临床疗效、骨代谢指标醋酸纤维素(Ca)、碱性磷酸酶(ALP)、骨特异性碱性磷酸酶(BAP)、骨钙素(OC)、BMD及不良反应发生率。结果试验组总有效率为93.75%,明显高于对照组72.92%(P0.05);治疗后,两组ALP、BAP、OC及BMD较治疗前显著改善(P0.05),且试验组上述指标改善程度明显优于对照组(P0.05)。结论采用骨肽注射液配合阿仑膦酸钠治疗老年男性2型糖尿病性骨质疏松症疗效确切,不良反应较少。     

金天格胶囊在预防绝经后女性骨质疏松性骨折中的作用

目的 观察金天格胶囊在治疗绝经后女性骨质疏松的疗效,判断其预防骨折发生的概率。方法 选取绝经后骨质疏松女性238名,随机分为4组,第1组：金天格59例,第2组：钙尔奇D +金天格58例,第3组：钙尔奇D +金天格+阿仑膦酸钠 63例,第4组：钙尔奇D +阿仑膦酸钠58例;服药剂量：金天格1. 2mg,tid;钙尔奇D 600mg qd;福善美70mg qw。分别在服药前、服药后3、6个月检测骨密度（bone mineral densities, BMD)、血清1型原胶原N -端前肽（PINP)和1型胶原交联C -末端肽 (CTX)。结果 各组骨密度无明显变化（P >0.05);服药3个月,4组的PINP分别下降了 18.2% ,22. 3% ,62. 3% ,55. 8%,CTX 分别下降了 24. 3% ,29. 7% ,68. 7% ,57. 8% ;服药 6 个月,4 组的 PINP 分别下降了 19. 4% ,23.6% ,63. 5% ,62% ,CTX 分别下降了28. 1%、28.3%、69.9%、64.5%。结论 金天格胶囊可以明显降低骨转化指标,能有效辅助治疗骨质疏松和预防骨折的发生。     

阿仑膦酸钠治疗绝经后妇女骨质疏松症临床分析

目的评价阿仑膦酸钠片治疗绝经后妇女骨质疏松症的临床疗效、安全性、依从性。方法对50例患骨质疏松症的绝经后妇女随机分为治疗组30例,服用阿仑膦酸钠,1次/周;对照组20例,服用钙尔奇D片,1次/天,两组疗程均为6个月。结果阿仑膦酸钠治疗组骨密度定量测定较治疗前有明显提高（P〈0.01）,疼痛症状改善;总有效率93.5%,与钙尔奇D组比较有统计学意义（P〈0.05）。结论阿仑膦酸钠治疗绝经后妇女骨质疏松症疗效好。     

补肾壮骨颗粒剂对老年男性骨转换指标的影响

目的 观察补肾健脾活血中药对老年男性骨密度(BMD)、骨特异性碱性磷酸酶(BAP)、抗洒石酸酸性磷酸酶5b(TRAP5b)、氨基端和中段骨钙素(BGP)的影响.方法 采用自身前后对照的方法,临床选取符合骨量减少及骨质疏松患者的老年男性病例35例,平均年龄(75.56±5.8)岁,给予口服补肾壮骨颗粒剂,钙尔奇D片和法能胶丸做为基础用药.分别测定服药前及服药半年后患者BMD、BAP、TRAP5b、BGP4项骨转换指标,并将服药前后测定值做比较.结果 服药半年后患者的BMD及BAP较服药前升高明显(P＜0.05),有统计学意义;TRAP5b较服药前降低(P＜0.05),有统计学意义;而BGP服药前后改善不明显,(P＞0.05),无统计学意义.结论 补肾健脾活血中药与钙剂、维生素D联合应用,能抑制骨吸收,降低血清TRAP5b;促进骨形成,提高血清BAP及BGP含量,减缓骨量丢失,提高骨密度,有效防治老年男性骨质疏松症.     

阿仑膦酸钠预防非骨水泥型假体周围早期骨丢失的临床研究

目的 探讨阿仑膦酸盐对非骨水泥型人工假体周围早期骨量的影响.方法 50例患者随机分为对照组和治疗组,术后1周对照组予以口服钙尔奇D1片,治疗组予以固邦10mg＋钙尔奇D片.连续服用3周.休息2周.5周为1疗程,连续5个疗程.分别于术后7天、3个月、6个月行假体周围骨密度（DEXA）检测.结果 50例病例中,45例获得完整随访.术后3个月、6个月假体周围骨量（ROI1区和ROI7区）对照组与治疗组相比有显著性差异（P＜0.01）.结论 阿仑膦酸钠能有效预防假体周围早期骨量减少.     

唑来膦酸与阿仑膦酸钠治疗骨质疏松性髋部骨折的临床疗效对比

目的回顾性分析唑来膦酸与阿仑膦酸钠对骨质疏松性髋部骨折患者的临床疗效和安全性比较。方法从2016年1月至2017年10月就诊的骨质疏松性髋部骨折患者中筛选出分别接受唑来膦酸和阿仑膦酸钠治疗至少1年的老年患者作为研究对象,分为观察组(唑来膦酸治疗)和对照组(阿仑膦酸钠治疗)。收集所有患者治疗前及治疗1年后视觉模拟评分(VAS)、股骨骨密度和骨代谢标志物变化情况,进行组间比较,观察药物不良反应和再发骨折情况。结果治疗1年后两组患者术后骨密度明显升高,VAS评分、Ⅰ型胶原氨基端前肽(PINP)、Ⅰ型胶原羧基端肽(CTX)水平较治疗前均显著下降(P均0. 05)。治疗后观察组VAS评分、CTX水平显著低于同期对照组(P0. 05),两组骨密度、PINP、药物不良反应发生率以及再发骨折差异均无统计学意义(P0. 05)。结论唑来膦酸和阿仑膦酸钠用于骨质疏松性髋部骨折均安全有效。但在缓解骨折术后骨痛症状,改善骨代谢,提高患者依从性方面,唑来膦酸优于阿仑膦酸钠。     

阿仑膦酸钠在甲状腺功能亢进症继发骨质疏松症中的临床应用

目的:评价阿仑膦酸钠在甲状腺功能亢进继发性骨质疏松症治疗中的有效性及安全性。方法:2008年4月至2009年11月门诊收治经双能X线骨吸收仪(DXA)证实有骨质疏松或骨量减少的27例甲状腺功能亢进患者,男7例,女20例;年龄30～61岁,平均(41.52±10.7)岁。根据随机数字表将患者随机分成A、B两组。A组14例,抗甲状腺药物加钙尔奇D口服治疗,抗甲状腺药物随着甲状腺功能的变化调整剂量,钙尔奇D每天600mg;B组13例,抗甲状腺药物加钙尔奇D加阿仑膦酸钠口服治疗,抗甲状腺药物、钙尔奇D治疗方法与A组一致,阿仑膦酸钠每周1次,每次70mg。同时选取21例健康自愿者作为对照组,不予任何干预。治疗1年后复查A、B两组患者腰椎、股骨颈、桡骨远端一般资料,比较A、B两组治疗前后骨密度(T值、Z值、BMD)及一般资料的变化,并与对照组比较,观察是否可达到完全恢复。结果:A组仅股骨颈、桡骨远端1/3处的BMD较治疗前明显上升(P值均为0.000),而B组腰椎、股骨颈、桡骨远端1/3处的T值、Z值、BMD均较治疗前明显上升(P<0.05),但均不能恢复至正常人群水平。A组腰椎、股骨颈、桡骨远端1/3处的BMD较治疗前分别升高(4.34±10.5)%、(3.21±1.38)%、(1.95±0.44)%;B组腰椎、股骨颈、桡骨远端1/3处的BMD较治疗前分别升高(6.10±8.12)%、(4.10±5.64)%、(3.10±3.23)%,各部位BMD上升的幅度,两组之间有统计学差异(P<0.05)。两组一般资料治疗后较治疗前相比,AKP均下降,体重、BMI均上升,甲状腺功能均下降至正常(P均<0.05)。结论:阿仑膦酸钠联合抗甲状腺药物治疗甲状腺功能亢进引起的骨量丢失,对骨密度的改善,较单用抗甲状腺药物更有效,而且较安全。     

阿仑膦酸钠联合钙尔奇D与钙尔奇D单药治疗对老年女性糖尿病骨质疏松疗效的观察

目的观察阿仑膦酸钠(ALN)联合钙尔奇D与钙尔奇D单药治疗老年女性糖尿病骨质疏松症的骨密度变化以及ALN的安全性。方法老年女性2型糖尿病(T2DM)骨质疏松患者72例,随机分为:ALN联合钙尔奇D组37例,给予ALN(70mg/w)和钙尔奇D(600mg/d);钙尔奇D组35例(600mg/d)总疗程6个月。采用双能X线骨密度测量仪(DXA)测定治疗前后腰椎及髋部骨密度。结果钙尔奇D组治疗前后腰椎及髋部骨密度各部位均有增加,但仅在L1及L4部位T值治疗前后有统计学差异(P0.05);ALN联合钙尔奇D治疗组,腰椎和髋部骨密度均有增加,尤其在腰椎的L1、L3、L4及L总部位均有统计学意义(P0.05)。ALN主要不良反应为上腹部不适,钙尔奇D则以便秘为主。结论ALN联合钙尔奇D治疗可以明显提高老年女性糖尿病骨质疏松患者的骨密度,并具有良好的耐受性和安全性。     

胰岛素、阿仑膦酸钠治疗新诊断老年糖尿病骨质疏松症患者骨密度及骨转换指标的研究

目的通过观察胰岛素、阿仑膦酸钠干预,观察在糖尿病骨质疏松症治疗12个月后股骨颈(Femur Neck)骨密度(BMD)及骨特异性碱性磷酸酶(BAP)、骨钙素(BGP)、抗酒石酸酸性磷酸酶-5b(TRAP-5b)等血清骨转换指标的变化。方法选取在我院治疗的糖尿病骨质疏松症患者128例,随机分成4组,即对照组(METF)、胰岛素组(INSU)、二甲双胍+阿仑膦酸钠组(METF+ALEN)、胰岛素+阿仑膦酸钠组(INSU+ALEN),每组同时服用钙尔奇D片作为基础用药,分别于服药前及服药12月后,测定4组患者股骨颈BMD及血BAP、BGP、TRAP-5b,分析治疗前后以及治疗组与对照组间的差异。结果 INSU+ALEN组治疗12月可见患者骨密度较前增加,治疗前后有统计学意义(P0.05),METF、INSU组较前无明显改变,治疗前后无统计学意义(P0.05),METF+ALEN组治疗12月可见患者BMD较前略有增加,治疗前后无统计学意义(P0.05),INSU+ALEN组治疗后BMD的增加明显高于其它组(P均0.05)。INSU+ALEN治疗组患者治疗12月后血清BAP、BGP显著升高(P0.05),TRAP-5b显著降低(P0.05);将上述指标与对照组、其它治疗组比较,BAP、BGP、TRAP-5b差异显著(P均0.01);METF、INSU、METF+ALEN组治疗12月可见患者血清BAP、BGP较前略有增加,TRAP-5b略有降低,治疗前后无统计学意义(P0.05)。结论胰岛素是糖尿病骨质疏松症首选治疗,可增加骨量,预防骨丢失。阿仑膦酸钠能抑制骨吸收,促进骨形成,减缓骨量丢失,提高骨密度,二者联用可有效防治糖尿病骨质疏松症。     

跖骨感染骨外露的显微外科治疗

[目的]回顾总结跖骨骨感染骨外露的显微外科治疗方法。[方法]自1995年～2005年采用显微外科技术治疗214例跖骨骨外露骨感染患者。[结果]全部病例获得随访1～10年，平均随访3年，14例游离植皮术后皮肤成活良好，199例术后皮瓣全部成活，1例腓肠神经营养血管皮瓣移位修复术出现远端部分皮肤坏死，后经换药处理后，伤口自然愈合。皮瓣移植术后质地良好，无溃疡复发。患足均可负重走路。[结论]应用显微外科技术治疗跖骨骨感染骨外露可获得较好的疗效。     

Assessment of bone density and bone loss

Osteoporosis International - Dual-energy X-ray absorptiometry has become the standard for the evaluation of osteoporosis. It is useful both for identifying those people who are going to be at risk...     

Aneurysmal bone cyst of the occipital bone

A 13 years boy presented with a painless hard and fixed swelling in occipital region for the last three months. Plain X-ray, CT scan and MRI showed an expansile multi loculated cystic lesion in occipital bone. Histopathological examination revealed it to be an aneurysmal bone cyst. Treatment of choice is surgery. However, radiotherapy may be helpful in incompletely excised lesions.     

Genetic regulation of bone mass: from bone density to bone strength

Osteoporosis is a common disease characterized in adults by diminished bone density. Bone is an organ that evolves and grows throughout life, and establishing optimal bone density in childhood and adolescence serves to buffer bone loss later in life. Bone density, a measurable entity, is the clinical substitute for bone strength, or the ability to defend against fracture. Chronic diseases may adversely affect optimal peak bone density. Bone density is under genetic control, as revealed by three lines of investigations. These include (1) the finding of quantitative trait loci for bone density, (2) the finding that specific mutations in genes that are important in the development of osteoblast or osteoclast lineages alter bone density, and (3) the linkeage of known polymorphisms for genes involved in mineral homeostasis to bone density and/or fracture. Future therapeutics for improving peak bone density or delaying bone loss later in life may take advantage of the genetic nature of bone density development.This work was presented in part at the IPNA Seventh Symposium on Growth and Development in Children with Chronic Kidney Disease: The Molecular Basis of Skeletal Growth, 1–3 April 2004, Heidelberg, Germany     

Development of bone canaliculi during bone repair

We recently found that silver impregnation staining with protargol (silver protein), that is, a modified Bodian method, is useful for histologically identifying the details of bone canaliculi structure, using thin sections of decalcified bone tissues. With this staining method, we conducted the present study to assess the development of bone canaliculi during the process of intramembranous ossification using a fracture-like stimulation model of the rat femur. After making a drill-hole in the cortex of the rat femur, decalcified thin sections were obtained after 3, 5, 7, and 14 days by the standard paraffin-embedding procedure. Silver staining for bone canaliculi was performed using our previously reported technique. The results showed that woven bone covered the fracture surface of the cortex after 5 days, then immature lamellar bone attached to the woven bone after 7 days, and finally the lamellar bone matured and became thick with appositional growth after 14 days. The osteocytes in the woven bone appeared at an early stage of bone repair and developed a few canaliculi that were short and irregularly distributed in the osteoid matrix, while the osteocytes in the lamellar bone at a late stage formed many bone canaliculi that were long and regularly distributed in mature bone matrix. Therefore, we concluded that woven bone osteocytes may be necessary for induction of the lamellar bone osteocytes followed by active appositional growth of the lamellar bone at the early stage of bone repair, and also that both bone tissues could be clearly distinguished from one another based on the pattern of development of bone canaliculi by the osteocytes, as seen with the use of our sensitive staining method.     

重组合异种骨植骨修复骨囊肿所致骨缺损

2001年10月～2003年9月,笔者共收治28例骨囊肿患者,均采用病灶刮除,瘤腔灭活和重组合异种骨植骨治疗,获得满意疗效,体会如下。     

Transmembrane bone matrix gelatin-induced differentiation of bone

In response to chemically-defined bone matrix gelatin (BMG) inside a diffusion chamber implanted in a muscle pouch, mesenchymal cells migrate directionally, aggregate and differentiate into new bone, on theoutside of the chamber. BMG diffuses through double membranes 275 to 300 μm in thickness. The inner membrane of pore size is 0.025 μm and the outer membrane of pore size is 0.45 μm. The inner membrane is 1/20 the pore size and the combination is twice the thickness of membranes previously reported to transfer osteoinductive activity of living cells. Autoradiographs show³⁵S-cysteine-labelled BMG produces very high transmembrane grain counts while³H-proline labelled BMG produces very low transmembrane grain counts. Electron micrographs demonstrate that gelatin-derived, uranyl-acetate-stained fine granules interspersed with ruthenium red-staining coarse granules, diffuse through the membrane of 0.025 μm pore size from the inside out. Solitary pale-staining collagen fibrils, possibly formed in interstitial fluid by renaturation of BMG are found in the interior of the chamber and in the interior of the outer 0.45 μm but not the inner 0.025 μm pore size membrane. Densely-stained new bone collagen fiber bundles cover the outer membrane, fill the 0.45 μm subsurface pores for a depth of 0.20 to 30 μm, and thereby attach the new cartilage and bone deposits to the outer surface of the chamber. BMG powders solubilize rapidly in diffusion chambers and produce high yields of new bone. The relationship between denatured collagen and renatured gelatin fibrils in the process of transfer of the bone morphogen from BMG to mesenchymal cell receptors is an intriguing subject for further investigation.     

Aneurysmal bone cyst of the frontal bone

Aneurysmal bone cyst rarely affects the skull. We report two cases of aneurysmal bone cyst of the frontal bone. One of the cases is associated with pregnancy. The association of pregnancy with aneurysmal bone cyst and enlargement of the aneurysmal bone cyst during the pregnancy have been discussed.