骨质疏松是一种常见的骨骼疾病,临床分为原发性、继发性和特发性三种.原发性骨质疏松主要表现为绝经后骨质疏松和老年性骨质疏松;继发性骨质疏松是由某些代谢性疾病或者长期服用某些药物等因素所诱发[1].在中国,60岁以上人群骨质疏松总体患病率为36％,其中男23％,女49％ [2].人体和极大多数动物的胃肠道内定植着种类和数量繁多的肠道菌群,在肠道菌群中,有一类对机体代谢极其重要的微生物就是益生菌.益生菌主要具备营养作用、提高防御能力、延缓衰老、抑肿瘤、调节骨代谢等作用.因此,益生菌对于机体健康具有重要作用,目前国内外较多研究表明益生菌能够影响骨代谢,从而导致或改善骨质疏松,但是具体作用机制尚未得到完全阐明,现对其与骨质疏松相互关系的相关机制研究进展进行综述,本次研究经过本院医学伦理委员会同意.

An osteochondral defect is a common and frequent disease in orthopedics and treatment effects are not good, which can be harmful to patients. Hydrogels have been applied in the repair of cartilage defects. Many studies have reported that hydrogels can effectively repair osteochondral defects through loaded cells or non-loaded cells. As a new type of hydrogel, photo-crosslinked hydrogel has been widely applied in more and more fields. Meanwhile, 3D bioprinting serves as an attractive platform to fabricate customized tissue-engineered substitutes from biomaterials and cells for the repair or replacement of injured tissues and organs. Although photo-crosslinkable hydrogel-based 3D bioprinting has some advantages for repairing bone cartilage defects, it also has some disadvantages. Our aim of this paper is to review the current status and prospect of photo-crosslinkable hydrogel-based 3D bioprinting for repairing osteochondral defects.

[目的]分析开放性手部骨折Ⅰ期内固定术后感染细菌学特点及伤口修复方法.[方法] 2016年12月-2018年8月,对18例开放性手部骨折Ⅰ期内固定术后感染患者,取出内固定装置并清创,行带蒂旋髂浅动脉腹股沟皮瓣修复缺损区.[结果] 18例伤口,11例为革兰氏阳性菌,7例为革兰氏阴性菌.经取出内固定装置后感染得到控制,6例缺损面积较大未能直接缝合,使用带蒂皮瓣修复创面愈合良好,随访1年感染无复发,骨折愈合.[结论]内固定材料细菌生物膜形成,建议早期取出内固定装置,如伤口软组织缺损面积较大,可考虑使用带蒂旋髂浅动脉腹股沟皮瓣修复.

目的 探讨关节镜清理术联合关节腔注射消炎镇痛类药对疼痛症状严重的中期膝骨关节炎的治疗效果.方法 选择我院自2017年6月至2017年12月诊断为膝骨关节炎(Kellgren-Lawrence分级Ⅲ级)并接受关节镜清理术和关节腔注射消炎镇痛类药(酮咯酸氨丁三醇注射液、甲磺酸罗哌卡因、复方倍他米松注射液)治疗的50例疼痛症状严重的中期膝骨关节炎患者.记录患者入院时HSS评分、VAS评分、膝关节活动度和手术并发症发生例数,对所有患者进行定期连续性随访并记录患者术后的HSS评分、VAS评分、膝关节活动度.结果 末次随访时,45例膝关节疼痛基本消失,其余关节偶有疼痛,但是疼痛程度明显减轻.膝关节屈曲活动度由术前的70-100°改善为110～135°;3例膝关节伸直受限,其余伸直均达0°.HSS评分由术前平均79.92分改善为术后87.78分,VAS评分平均由术前5.74改善为术后2.12,连续行走距离由术前平均1154米即需要休息改善为2301米才需要休息,均与术前比较差异有统计学意义(P<0.05),49例患者感觉手术效果非常满意,仅1例患者感手术效果不甚满意.结论 关节镜清理术联合关节腔内注射消炎镇痛类药对于疼痛症状严重的中期膝骨关节炎患者具有较好的短期疗效.

目的 分析骨转换标志物血清1型胶原羧基端肽(β-CTX)和血清1型前胶原氨基端前肽(PINP)在亚临床型甲状腺功能减退(简称亚甲减)合并骨质疏松症患者中的表达,并探讨其能否作为判断该类患者骨质疏松程度及脆性骨折发生风险的预测指标.方法 选取2016年7月至2019年6月收治的骨质疏松症合并亚甲减患者62例(骨松甲减组),以及同期收治的单纯骨质疏松症伴骨痛患者65例(骨松骨痛组),并纳入同年龄段健康体检者68例(正常对照组).比较3组间骨代谢标志物,如血钙、血磷、血镁、碱性磷酸酶、25羟维生素D、骨密度、T值、甲状腺激素、甲状旁腺素以及骨转换标志物血清PINP及β-CTX浓度水平.结果 骨松甲减组、骨松骨痛组及正常对照组骨代谢及骨转换标志物中血钙、血磷、血镁、碱性磷酸酶、甲状旁腺素水平差异无统计学意义(P均>0.05),而25羟维生素D、骨密度、T值、β-CTX及PINP水平差异有统计学意义(P均<0.05).结论 骨松甲减组PINP、β-CTX水平降低,为低转换型骨质疏松,不能依靠骨转换标志物作为骨松甲减组骨质疏松程度的判断指标及预测骨折发生风险.

BACKGROUND:This study aimed to determine whether erythropoietin could repair glucocorticoid-induced osteonecrosis of the femoral head after the systemic or local administration of recombinant human erythropoietin. MATERIALS AND METHODS:Gelatin microspheres were used to load recombinant human erythropoietin for local delivery. Forty-eight Wistar rats were included in the glucocorticoid-induced osteonecrosis of the femoral head model and randomly divided into the placebo, systemic erythropoietin and local erythropoietin groups. Eight weeks later, all rats were killed and their tissues were subjected to radiographic, histological, histometric, quantitative polymerase chain reaction and western blot analyses. RESULTS:Our results show that the use of recombinant human erythropoietin increased bone volume, trabecular number, trabecular thickness and trabecular separation compared with the placebo. Erythropoietin administration significantly improved the expression of runt-related transcription factor 2, alkaline phosphates, hypoxia-inducible factor-1α and vascular endothelial growth factor in the femoral head. We also found that the local injection of erythropoietin could better mediate hypoxia-inducible factor-1α-controlled osteogenic and angiogenic factor expression and better repair the glucocorticoid-induced osteonecrosis of the femoral head. CONCLUSIONS:The use of recombinant human erythropoietin exerted effects on improving the bone structures in glucocorticoid-induced osteonecrosis of the femoral head and up-regulated the expression of runt-related transcription factor 2, alkaline phosphates, hypoxia-inducible factor-1α and vascular endothelial growth factor. It provided a novel idea that erythropoietin administration could repair glucocorticoid-induced osteonecrosis of the femoral head by improving bone formation and angiogenesis and may be associated with the hypoxia-inducible factor-1α pathway. The sequential delivery of erythropoietin from gelatin microspheres seems worth recommending.

Objective To explore the role of the steroids induced adipogenesis in pathogenesis ot glucocorticoid-induced osteonecrosis of the femoral head (ONFH).Methods Femoral heads respectively diagnosed glucocortcoid-induced ONFH and osteoarthritis (OA),which were obtained during total hip arthroplasty,were made histopathological and immunohistochemistry study.Osteoblasts cultured in DMEM (H) medium with 10％ FBS supplemented with dexamethasone in different concentrations (0,1×10-8,1×10-7,1×10-6 mol/L) were divided into 3 groups.Three groups were received alizarin red staining and oil red O staining at different time.The expression of PPAR-γand Runx2 were performed by immunohistochemistry study.SD rats were injected high-dose of methylprednisolone to establish a steroid-induced ONFH model.At 12th weeks after intervention,histopathological and immunohistochemistry were performed for the presence of osteonecrosis and adipogeneisis,Runx2 and PPAR-γ expression in the femoral head.Results The number and the size of adipocytes significantly increased in ONFH group by comparison with OA group.The expression of PPAR-γ was increased while Runx2 expression was decreased in ONFH group,compared to the OA group.Compared with control group,dexamethasone (1 ×10-6,10-7 mol/L) significantly induced the mRNA expression of PPAR-γ,while the expression of Runx2 was significantly decreased.Osteoblasts treated with 10-6 mol/L dexamethasone can promote osteoblast transdifferentiated into adipocytes.Evidence of osteonecrosis and adipogenesis were observed in steroid treated rats.The number and the size of adipocytes were increased significantly compared with control group.At the same time,the expression of PPAR-γ was increased and the Runx2 was decreased.Conclusion The steroids stimulating the PPAR-γ expression and inhibiting the Runx2 expression,which resulted in BMSCs differentiating into adipocytes and inhibited osteoblasts differentiation activity,may be one of important pathogenesis mechanism of steroid-induced ONFH.

Objective To study the effects of alendronate in preventing early glucocorticoidsinduced osteonecrosis of femoral head( ONFH) in rats by micro-CT.Methods 200 SD rats were divided into two groups randomly:140 rats were in the experimental group,and 60 rats were in the control group.The experimental group were injected alendronate solution intraperitoneally and the control group were injected physiological saline intraperitoneally for two weeks.Then all the rats were injected high-dose of methylprednisolone for four weeks continuously.At the 2nd week,the 4th week,the 8th week and the 12th week after intervention,the rats in each group were sacrificed.The samples were stained by hematoxylin and eosin( HE) to calculate the success rates of glucocorticoid-induced osteonecrosis of the femoral head and the trabeculae of the femoral head were scanned by Micro-CT.Results The success rate of glucocorticoid-induced osteonecrosis of the femoral head in the experiment group was 30%,but it was about50 % in the control group.At the 2nd week,the 4th week,the 8th week,and the 12th week after alendronate intervention beginning,accroding to Micro-CT examination,the average trabecular space of the femoral head in the experimental group was 0.766,0.761,0.753,and 0.501 um respectively; the average trabecular number was 6.146,6.159,6.194,and 6.723 respectively; the average trabecular thickness was 0.097,0.101,0.109,and 0.138 um respectively.The results among the 2nd week,the4th week,and the 8th week had no significant、statistical meaning( P > 0.05),but comparing to the 12th week,the results had significant difference( P < 0.05).Comparing to the control group,at the 12th week,the micro-CT results of the average trabecular space,average trabecular number and average trabecular thickness were 0.765 um,6.141 and 0.093um respectively.These micro-CT results of the two groups had obviously statistical significance( P < 0.05).Conclusions Alendronate plays a certain role in the prevention of osteonecrosis of the femoral head caused by glucocorticoids in the early stage in rats according to the micro-CT results,but whether alendronate has the same effects on osteonecrosis of femoral head in human still needs more multi-center clinical trials.

OBJECTIVE:To review the recent developments in the mechanisms of glucocorticoids induced osteonecrosis of femoral head (ONFH) and introduce a new theory of ONFH.DATA SOURCES:Both Chinese- and English-language literatures were searched using MEDLINE (1997 - 2011), Pubmed (1997 - 2011) and the Index of Chinese-language Literature (1997 - 2011).STUDY SELECTION:Data from published articles about mechanisms of glucocorticoids induced ONFH in recent domestic and foreign literature were selected. Data extraction Data were mainly extracted from 61 articles which are listed in the reference section of this review.RESULTS:Glucocorticoids are steroid hormones secreted by the adrenal cortex that play a pivotal role in the regulation of a variety of developmental, metabolic and immune functions. However, high dose of exogenous glucocorticoids usage is the most common non-traumatic cause of ONFH. Glucocorticoids can affect the metabolisms of osteoblasts, osteoclasts, bone marrow stromal cells and adipocytes which decrease osteoblasts formation but increase adipocytes formation and cause ONFH finally.CONCLUSIONS:Glucocorticoids affect the differentiation of mesenchymal stem cells, through activating or inhibiting the related transcript regulators of osteogenesis and adipogenesis. At last, the size and volume of mesenchymal stem cells derived adipocytes will increase amazingly, but the osteoblasts will be decreased obviously. In the meantime, the activity of the osteoclasts will be activated. So, these mechanisms work together and lead to ONFH.

Objective To study the mechanism of glucocorticoid-induced osteonecrosis of femoral head(ONFH) by comparing the histopathological changes and expression levels of PPARγ,Runx2,DKK-1 of ONFH and hip osteoarthritis.Methods 40 patients who were diagnosed as ONFH or hip osteoarthritis were enrolled in the study.ONFH group and osteoarthritis group contained 20 patients each.Histopathological and immunohistochemistry studies were performed for expression of PPARγ、Runx2、and DKK-1.Results Percentage of empty lacunae in ONFH group was over 50%.The positive expression of PPARγ and DKK-1 was abundant while expression of Runx2 was poor in glucocorticoid-induced ONFH.Comparing with ONFH group,in the hip osteoarthritis group,the number and diameter of empty lacunae were more small and the columnar trabeculae showed lower expression level of PPARγ,and DKK-1,yet expression of Runx2 was much higher.Conclusions PPARγ,DKK-1,Runx2 are key factors in regulation of bone marrow stromal cells(MSC) differentiation.Exogenous glucocorticoids could up regulate the level of PPARγ and DKK-1 while reduce the level of Runx2,which would cause obvious decrease of osteoblasts but significant increase of MSC derived adipocytes.Meanwhile,the activation of osteoclasts is enhanced and the bone remodeling is impaired,so that ONFH will be induced.

目的 研究在不同浓度地塞米松作用下,体外培养的大鼠颅骨成骨细胞能否转分化为脂肪细胞,以进一步探讨糖皮质激素性骨质疏松症发病的具体机制.方法 将原代培养的大鼠颅骨成骨细胞分为四组,分别用含不同浓度的地塞米松(0 mol/L、10-8 mol/L、10-7 mol/L、10-6mol/L)的DMEM(H)培养基培养.于作用后第7天、21 d,采用倒置相差显微镜观察细胞形态的变化,进行细胞化学染色(茜素红钙结节染色、油红O染色),并采用实时荧光定量RT-PCR检测PPARγ-2、LPL及ALP基因mRNA的表达.结果 在10-6、10-7mol/L的地塞米松作用下,大鼠成骨细胞矿化能力减弱,胞浆中出现脂滴,RT-PCR结果显示脂肪细胞标志基因PPAR(γ)-2、LPL mRNA表达增高,成骨细胞标志基因ALP mRNA表达减少.而10-8mol/L地塞米松对成骨细胞的分化有促进作用.结论 长期、大剂量应用糖皮质激素可促进大鼠颅骨成骨细胞转分化为成熟的脂肪细胞,这可能是糖皮质激素性骨质疏松症的发病机制之一.

激素性股骨头坏死(osteonecrosis of femoral head,ONFH)是由于长期使用激素类药物,以股骨头血供受损,骨细胞及骨髓成份死亡及随后修复,继而导致股骨头结构改变、股骨头塌陷、关节功能障碍为特征的代谢性疾病[1].目前,对ONFH发病机制的研究较多,包括骨内高压学说、凝血机制改变学说、脂肪栓塞学说、骨质疏松学说、骨细胞凋亡学说等[2-3].

<正>股骨头坏死(osteonecrosis of femoral head,ONFH)是一种破坏性退行性疾病,病情进展可以发生软骨下骨和关节面软骨的塌陷。该病多发生于青壮年,平均发病年龄38岁。如果不采取积极的治疗,绝大多数患者最终都需要行全髋关节置换。目前提及的病因有如下理论:激素性、酒精性、创伤性及一些特

<正>Wnt是一种分泌型糖蛋白,参与调节细胞的增殖、分化、凋亡及细胞功能[1]。近年来,研究发现Wnt信号转导通路是骨形成的重要调节途径,而糖皮质激素可通过多个环节影响该途径从而影响骨形成。因此,上调或下调这条通路中相关因子的表达或改变它们的功能将导致成骨细胞功能的改变及

[Objective] To analyze the causes of the patients who underwent total hip arthroplsty(THA) in West China Hospital from 1998 to 2007.[Method]In order to analysis the causes of the patients who underwent THA in West China Hospital from 1998 to 2007,we collected and reviewed the history of these patients and classified the annual data according to total number of patients,gender,age and the diagnosis. [Result] The total number of the patients underwent THA and the artio of gender(male/female) was increasing year by year in the last ten years.The most common cause of the patients who undergone THA was osteonecrosis of the femoral head(ONFH),there were 1 211 cases.The other causes including 984 patients were diagnosed as osteoarthritis of the hip,947 were ONFH caused by femoral neck fracture,180 traumatic osteoarthirtis of the hip,100 osteoarthritis of the hip secondary from the old infection,including bacteria and tuberculosis infection,while rheumatoid arthritis and ankylosing spondylitis of the hip were listed the final two causes.[Conclusion]In our study,the main diseases which lead to THA in Chinese people are ONFH,osteoarthritis of the hip,traumatic ONFH.The total number of patients undergoing THA was increasing in the last ten years.

The Wnt signaling pathway plays a vital role in the process of osteoblast proliferation and differentiation. In recent years,a number of studies have found that this pathway can be impeded by an inhibitor,DKK-1. Over-expression of DKK-1 could affect bone formation and even lead to osteopenia. Blocking the DKK-1 as indicated by some researchers,could help to restore the function of osteoblast,and therefore increase bone mass. These findings suggest that using DKK-1 as a novel target could provide a new way for treating osteoporosis. Here,we reviewed the growing literature on the mechanism of DKK-1 inhibiting Wnt signaling transduction as well as its role in osteoporosis.

1 概述 股骨头坏死的发病机制中以骨内压增高理论受到众多学者的青睐,而该理论的核心是由于骨髓基质细胞向成骨细胞和脂肪细胞分化失衡.成人正常骨髓中骨髓基质细胞向脂肪细胞和成骨细胞都有分化,此消彼长,并且保持平衡,维持正常生理状态.