Floating shoulder is no osseoligamentous connection between the humeral shoulder joint with the axial skeleton. The osseoligamentous of shoulder joint connection compose a ring, including clavicle,acromion, coracoid, glenoid fossa, surgical or anatomical scapula neck, acromioclavicular ligament and coracolclavicular ligament. This ring is known as superior shoulder suspensory complex (SSSC). The double disruptions of this ring are recognized to create a potentially unstable anatomical situation. Thus, floating shoulder is also characterized as double or more disruptions of SSSC. Surgical reduction and fixation for the displacement of those fractures at one or more sites is recommended in previous reports. We present 2 cases of patients with acromial and coracoid displaced fractures which belong to a type of the double disruptions of SSSC, there were still osseoligamentous connection between the humeral shoulder joint with the axial skeleton. The patient’s shoulder function after nonoperative management was satisfactory.

高能量跟骨损伤带来的后续创伤感染发生率逐年升高,原因在于跟骨大部分为松质骨,受伤后血液在松质骨内部淤积,导致细菌滋生,而跟骨皮肤软组织较薄,受创后易出现软组织损伤现象.跟骨创伤性骨髓炎非手术治疗主要根据药敏长疗程抗感染治疗.手术治疗原则为清除病灶、空腔内填充局部药物释放系统、软组织重建以及骨缺损修复;局部药物(抗生素)释放载体包括骨水泥、硫酸钙等,骨缺损可采用膜诱导成骨、植入带抗生素人工骨、开放植骨等.本文就跟骨创伤性骨髓炎的手术及非手术治疗方式进行阐述,为临床治疗提供参考.

Background:This study aimed to investigate the clinical features, current management strategies, and outcomes of open pelvic fracture patients.Methods:We performed a retrospective review of data on patients with blunt trauma and open pelvic fractures admitted to our trauma center over a 5-year period (January 2013 to December 2017). Demographic as well as clinical data including injury mechanism, injury severity score (ISS), fracture classifications, transfusion requirements, interventions, length of hospital and intensive care unit (ICU) stay, and prognosis were investigated. Univariate analysis and binary logistic regression were used to identify the risk variables of death. Finally, a brief literature review was performed to understand the current capacity of treatment and prognosis of this type of injury.Results:Forty-six patients (36 male and 10 female) were included in this study, mean age 43.2 ± 14.2 years. The overall mortality rate was 17.4%; 43.5% of the patients were hypotensive (systolic blood pressure (SBP) <90 mmHg) on arrival. The average ISS was 31.7 ± 6.7, and the average packed red blood cell (PRBC) transfusion during the first 24 h was 9.6 ± 7.4 units. Five patients (10.9%) underwent transcatheter arterial embolization in the early stage of management. The average hospital and ICU length of stay were 53.0 ± 37.6 days and 14.3 ± 15.3 days, respectively. Statistically significant differences were found in ISS, PRBC units received with the first 24 h, SBP, lactate and base excess on admission, and mechanism of injury when comparing between the death and the survival groups ( p < 0.05). ISS and lactate on admission were found to be the independent risk factors for mortality.Conclusion:The mortality rate of open pelvic fractures remains high. ISS and lactate on admission were the independent risk factors for mortality. Optimization of the trauma care algorithms for early identification and treatment of this injury could be the key to decreasing mortality.

INTRODUCTION:Isolated metacarpal tuberculosis is rare in orthopedic surgery. In the case of poor efficacy of traditional treatment methods, such as debridement surgery and anti-tuberculosis treatment, it is necessary to consider whether there is a special type of infection. We describe a case of metacarpal tuberculosis with Nocardia infection in a patient.PATIENT CONCERNS:A 65-year-old male patient who suffered from pain and dysfunction lasted for 6 years.DIAGNOSES:Confirmation of the diagnosis was finally achieved by isolation of M tuberculosis and Nocardia actinomycetes from bone specimens.INTERVENTIONS:The patient underwent debridement surgery, Masquelet technique was used during the operation, and oral antibiotics were combined after surgery.OUTCOMES:Bone graft surgery was performed 6 weeks after the first surgery. We followed up on bone healing at 1 and 3 months postoperatively.CONCLUSION:Tissue-specific necrosis usually occurs in particular types of infections such as tuberculosis, which limits the spread of antibiotics. Masquelet technique seems to bring new options to solve this problem. The performance of Nocardia infection is similar to that of tuberculosis infection, so it is difficult to identify clinically. Therefore, for cases where tuberculosis is suspected, and anti-tuberculosis treatment is ineffective, the possibility of Nocardia infection needs to be considered.

6月1日起,公安部交管局在全国开展“一盔一带”安全守护行动,依法查纠摩托车、电动自行车骑乘人员不佩戴安全头盔以及汽车驾乘人员不使用安全带行为. 如何佩戴安全头盔?为什么要强调佩戴头盔?头盔有哪些结构,是如何实现防护的?如何选购合适的头盔?我们一起来听听专家的建议.

目的 比较通道辅助跟腱微创吻合术与传统开放手术对急性跟腱断裂患者的临床效果.方法 采用回顾性临床队列研究分析2017年1月—2018年12月陆军军医大学大坪医院战创伤医学中心收治的急性跟腱断裂患者,根据接受手术方式将患者分为传统开放手术组和微创手术组.分析比较两组患者性别、年龄、伤侧、跟腱断裂部位至跟腱止点距离、受伤至手术时间、手术耗时、手术切口长度、术中出血量、术后6个月和12个月AOFAS评分及患肢小腿最大周径和相关并发症发生率.结果 根据纳入及排除标准,最终纳入47例,其中男性45例,女性2例;年龄20～71岁,平均38.3岁;微创手术组17例和传统手术组30例.微创手术组与传统开放手术组相比,年龄、性别、伤侧、跟腱断裂部位至跟腱止点距离和受伤至手术时间比较差异无统计学意义(P>0.05).微创手术组与传统开放手术组手术耗时[(40.0±19.5)min vs.(67.7±18.8)min]、切口长度[(2.4±0.6)cm vs.(9.6±3.2)cm]和术中出血量[(13.2±6.1)mL vs.(21.8±14.2)mL]比较差异有统计学意义(P<0.05).功能方面,术后6个月微创手术组AOFAS评分显著高于传统手术组[(91.1±8.5)分vs.(82.6±13.1)分],差异有统计学意义(P<0.05),但术后12个月两组患者AOFAS评分(93.9±6.1 vs.90.9±5.8)比较差异无统计学意义(P>0.05).微创手术组与传统手术组相比,小腿周径术后6个月[(30.1±3.7)cm vs.(29.1±3.6)cm]、术后12个月[(32.8±3.9)cm vs.(31.1±3.8)cm],差异无统计学意义(P>0.05).并发症方面,传统手术组出现2例再断裂、1例切口感染,微创手术组无并发症发生,但两组比较差异无统计学意义(P=0.292).结论 通道辅助跟腱微创吻合术相较于传统开放手术,术后远期功能无显著性差异,但可缩短手术时间、减小手术切口、减少术中出血并且早期功能更佳.

骶骨是人体负重线上的轴心,与周围腰椎髂骨构成复杂韧带骨结构复合体.高能量损伤多见,应力骨折及骨质疏松性骨折等也有报道,骶骨骨折的分型从最早的Denis分型,侧重神经损害的Roy-Ca-mille分型,侧重腰椎骶骨稳定性的ISSLE分型,侧重骨盆环稳定性的AO分型以及较新的引入韧带评价的LSICS评分,反映了临床医生对骶骨及其周围损伤的认识不断深化.骶骨骨折治疗重点是重建骨盆环稳定、重建脊柱骨盆稳定以及神经损伤治疗,微创化及坚强固定是主要的发展方向.同时本文也介绍了笔者单位对骶骨骨折的治疗情况.

INTRODUCTION Solid abdominal organ hemorrhage remains one of the leading causes of death both on the battlefield of modern warfare and in the civilian setting. A novel, temporary hemostatic device combining CELOX and direct intra-abdominal physical compression was invented to control closed SAOH during transport to a medical treatment facility. MATERIALS AND METHODS A swine model of closed, lethal liver injury was established to determine hemostasis. The animals were randomly divided into group A (extra-abdominal compression), group B (gauze packing), group C (intra-abdominal compression), group D (CELOX coverage), and group E (intra-abdominal compression and CELOX coverage) with six swines per group. Survival time (ST), blood loss (BL), vital signs, pathologic examination, and CT-scan were monitored to further observe the effectiveness of the device. RESULTS Group E had an average 30-minute extension in ST (74.3 ± 15.4 minutes versus 44.0 ± 13.8 minutes, p = 0.026) with less BL (46.0 ± 13.0 versus 70.8 ± 8.2 g/kg, p = 0.018), and maintained mean arterial pressure≥70 mmHg and cardiac output ≥ 3.5 L/minute for a longer time. No significant differences were observed in ST and BL of groups B and E, and there were no marked differences in ST and BL of groups A, C, and D. No CELOX clots were noted in the spleen, pancreas, lungs, heart, kidneys, or the adjacent large vessels in groups D and E. Compared to group A, the CT-scan showed better hepatic hemorrhage control in group E. CONCLUSIONS The device, which combined 20 g of CELOX particles and 20 pieces of CELOX (8 g) sponge tablets with 50-mmHg intra-abdominal compression for 10 minutes, prolonged the ST by an average of 30 minutes with less BL. It was not markedly different from the full four quadrants gauze packing of liver in hemostatic effect, with no CELOX clot formation in other organs.

Type 1 diabetes mellitus (T1DM) is a pathological condition associated with osteopenia. WNT/β-catenin signaling is implicated in this process. Trabecular and cortical bone respond differently to WNT/β-catenin signaling in healthy mice. We investigated whether this signaling has different effects on trabecular and cortical bone in T1DM. We first established a streptozotocin-induced T1DM mouse model and then constitutively activated β-catenin in osteoblasts in the setting of T1DM (T1-CA). The extent of bone loss was greater in trabecular bone than that in cortical bone in T1DM mice, and this difference was consistent with the reduction in the expression of β-catenin signaling in the two bone compartments. Further experiments demonstrated that in T1DM mice, trabecular bone showed lower levels of insulin-like growth factor-1 receptor (IGF-1R) than the levels in cortical bone, leading to lower WNT/β-catenin signaling activity through the inhibition of the IGF-1R/Akt/glycogen synthase kinase 3β (GSK3β) pathway. After β-catenin was activated in T1-CA mice, the bone mass and bone strength increased to substantially greater extents in trabecular bone than those in cortical bone. In addition, the cortical bone of the T1-CA mice displayed an unexpected increase in bone porosity, with increased bone resorption. The downregulated expression of WNT16 might be responsible for these cortical bone changes. In conclusion, we found that although the activation of WNT/β-catenin signaling increased the trabecular bone mass and bone strength in T1DM mice, it also increased the cortical bone porosity, impairing the bone strength. These findings should be considered in the future treatment of T1DM-related osteopenia.

目的 观察重组人甲状旁腺素(parathyroid hormone,PTH 1-34)对1型糖尿病(type 1 diabetes mellitus,T1DM)小鼠手术诱导的关节炎模型早期骨关节炎(osteoarthritis,OA)的影响.方法 分别取12周龄的C57BL/6J雄性小鼠,采用完全随机分组法分为野生小鼠组(WT组)、T1DM小鼠组(T1DM组)和T1 DM小鼠PTH1-34干预组(T1DM+PTH组),利用链脲佐菌素(streptozotocin,STZ;45 mg/kg)腹腔注射建立T1DM小鼠模型,3组右下肢内侧半月板切除手术诱导OA小鼠模型;以野生小鼠未建模的左下肢作为对照组.标本获得后分别采用CT扫描重建、HE染色、番红O-固绿染色、OA软骨组织病理学评分观察小鼠膝关节软骨下骨骨量的变化及OA样改变,并进行统计学分析.结果 CT扫描分析显示WT组OA关节软骨下骨骨体积占组织总体积百分比(BV/TV)较对照组关节下降(0.329vs 0.351,P＜0.05),软骨下骨骨小梁数量(Tb.N)及厚度(Tb.Th)分别下降9.9％和8.2％(P＜0.05);T1 DM组OA关节软骨下骨BV/TV较WT组OA关节下降明显(0.241 vs 0.329,P＜0.05),软骨下骨Tb.N及Tb.Th分别下降20.2％和11.2％ (P ＜0.05);T1DM +PTH组OA关节较T1 DM组OA关节软骨下骨BV/TV改善明显(0.301 vs0.241,P＜0.05),软骨下骨Tb.N及Tb.Th分别上升14.9％和9.9％(P＜0.05).组织病理学评分显示建模组均形成OA样改变,评分结果提示:T1DM组OA关节关节炎评分明显高于WT组OA关节(P＜0.05);应用PTH 1-34干预,T1 DM+ PTH组小鼠OA关节关节炎评分低于T1DM组OA关节(P＜0.05).结论 OA早期伴有软骨下骨骨量降低,T1DM可加速骨量的丢失并促进OA早期进展,使用PTH1-34后可逆转T1DM小鼠OA早期软骨下骨骨量丢失,在T1DMOA发生早期起到保护作用.

目的:研发以"Celox"和"自膨海绵"联合控制闭合性腹腔出血的一种临时止血装置,并在猪闭合性致死性肝损伤模型上评价其止血效果.方法:建立猪闭合性致死性肝损伤模型,并于肝损伤5 min后进行实验干预,将动物随机分为空白对照组(A)、纱布填塞组(B)、止血装置组(C),每组均为4只;监测各组存活时间、失血量、生命指标、血液指标,并对其行CT检查及死亡后组织学检查.结果:C组存活时间明显长于A组(81±12 min vs 44±14 min,P<0.05),平均出血量与A、B组比较差异无统计学意义(P>0.05),且B组和C组在损伤30 min后凝血系统功能更亢进,C组死亡后组织学检查未见明显其它脏器继发损伤.结论:该临时止血装置可延长动物猪闭合性肝损伤大出血的死亡时间,保持一定程度的生命体征平稳,且未见明显其它继发损伤.

In recent years, several studies have found that the disruption of type IA receptor of bone morphogenetic proteins (BMPR1A) could increase bone mass. However, whether disruption of BMPR1A could have an effect on bone quality and bone strength is currently unknown. Osteoblast-targeted conditional knockout (cKO) of BMPRIA by crossing 3.2-kb Col1-CreER™ mice with BMPR1A fx +/+ mice was conducted. Then, in vitro and in vivo studies were employed to examine the effect of BMPR1A knockout on bone quality and bone strength. It was found that the ultimate force and stiffness of the femora decreased significantly in cKO mice when compared to control mice. The content of collagen and mineralization level decreased as the structure of the collagen became disorganized. The morphology of osteocytes in cKO mice was abnormal as well. The expression level of osteocalcin, a marker for the terminal differentiation of osteoblasts, decreased in cKO mice. This data indicated that the differentiation of osteoblasts in cKO mice was impaired. Immunohistochemistry examination revealed deregulated expression of dickkopf 1(DKK1) in osteocytes in cKO mice. Adding DKK1 to the culture medium reversed these effects. In conclusion, even though disruption of BMPR1A could increase bone mass, it also impairs bone quality and bone strength.

Accumulating evidence suggests that Wnt/β-catenin signaling plays a central role in controlling bone mass. We previously reported that constitutive activation of β-catenin (CA-β-catenin) in osteoblasts potentially has side effects on the bone growth and bone remodeling process, although it could increase bone mass. The present study aimed to observe the effects of osteoblastic CA-β-catenin on bone quality and to investigate possible mechanisms of these effects. It was found that CA-β-catenin mice exhibited lower mineralization levels and disorganized collagen in long bones as confirmed by von Kossa staining and sirius red staining, respectively. Also, bone strength decreased significantly in CA-β-catenin mice. Then the effect of CA-β-catenin on biological functions of osteoblasts were investigated and it was found that the expression levels of osteocalcin, a marker for the late differentiation of osteoblasts, decreased in CA-β-catenin mice, while the expression levels of osterix and alkaline phosphatase, two markers for the early differentiation of osteoblasts, increased in CA-β-catenin mice. Furthermore, higher proliferation rate were revealed in osteoblasts that were isolated from CA-β-catenin mice. The Real-time PCR and western blot examination found that the expression level of c-myc and cyclin D1, two G1 progression-related molecules, increased in osteoblasts that were isolated from the CA-β-catenin mice, and the expression levels of CDK14 and cyclin Y, two mitotic-related molecules that can accelerate cells entering into S and G2/M phases, increased in osteoblasts that were isolated from the CA-β-catenin mice. In summary, osteoblastic CA-β-catenin kept osteoblasts in high proliferative state and impaired the terminal osteoblast differentiation, and this led to changed bone structure and decreased bone strength.

ABSTRACTTrabecular bone and cortical bone have different bone remodeling levels, and the underlying mechanisms are not fully understood. In the present study, the expression of Wnt/β‐catenin signaling and its downstream molecules along with bone mass in trabecular and cortical bone were compared in wild‐type mice, constitutive activation of β‐catenin (CA‐β‐catenin) mice and β‐catenin deletion mice. It was found that the expression level of most of the examined genes such as Wnt3a, β‐catenin, osteocalcin and RANKL/OPG ratio were significantly higher in trabecular bone than in cortical bone in wild‐type mice. CA‐β‐catenin resulted in up‐regulated expression of the above‐mentioned genes except for RANKL/OPG ratio, which were down‐regulated. Also, CA‐β‐catenin led to increased number of osteoblasts, decreased number of osteoclasts and increased bone mass in both the trabecular bone and cortical bone compared with wild‐type mice; however, the extent of changes was much greater in the trabecular bone than in the cortical bone. By contrast, null β‐catenin led to down‐regulated expression of the above‐mentioned genes except for RANKL/OPG ratio. Furthermore, β‐catenin deletion led to decreased number of osteoblasts, increased number of osteoclasts and decreased bone mass when compared with wild‐type mice. Again, the extent of these changes was more significant in trabecular bone than cortical bone. Taken together, we found that the expression level of Wnt/β‐catenin signaling and bone remodeling‐related molecules were different in cortical bone and trabecular bone, and the trabecular bone was more readily affected by changes in the Wnt/β‐catenin signaling pathway. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:812–819, 2017.

Accumulating evidence demonstrates that the Wnt/β-catenin signaling pathway plays a dominant role in bone repair. However, the role of Wnt/β-catenin signaling in the remodeling phase during bone fracture healing is currently unknown. In the present study, β-catenin was activated at different levels or deleted in mice at the late stage of fracture healing, and the effects on healing quality were investigated. Deletion of β-catenin disturbed bone remodeling, as confirmed by increased bone resorption and decreased bone formation, and significantly decreased bone strength compared with wildtype mice. In addition, the constitutive activation of β-catenin significantly increased the bone mass and delayed the bone remodeling process, resulting in slightly impaired bone strength. In contrast, a slight activation of β-catenin significantly increased bone formation and slightly hindered bone resorption. These effects lead to improved bone fracture healing quality compared with wildtype mice. In summary, the present study provides the first demonstration showing that Wnt/β-catenin signaling should be maintained at a slightly activated level during the late stage of fracture healing to ensure better bone fracture repair.

Objective To investigate the role of bone morphogenetic protein receptor 1A(BMPR1A)-mediated signaling in osteoblast terminal differentiation in vivo.Methods LoxP/Cre system was used to conditionally knock out BMPR1A in osteoblast by cross-breeding Cre mice (3.2 kb collagen Ⅰ as promoter) with BMPR1A LoxP +/ + mice.Their offsprings lacking active Cre was grouped into control.Von Kossa staining,Alizarin red staining and scanning electron microscopy were carried out to observe the mineralization of osteoblast.Masson staining and sirius red staining were used for evaluation of collagen synthesis ability in osteoblast.Immunohistochemistry staining and cell cycle analysis were employed to mechanistically study terminal differentiation of osteoblast.Results Compared with control group,we found that BMPR1A knockout mice had attenuated bone mineralization associated with decreased intercellular connection and enlarged intercellular gap.Masson staining showed reduced collagen synthesis with irregular collagenic arrangement.In addition,fibroblast growth factor 23 (FGF23) and osteopontin (OPN) were upregulated.Cell cycle analysis found that a large number of osteoblast arrested at G phrase of cell cycle,which partly impeded the terminal differentiation of osteoblast.Conclusion BMPR1A plays an important role in osteoblast terminal differentiation.Knocking out BMPR1A leads to decreased bone mineralization and collagen synthesis.

Objective To investigate the difference of Wnt/β-catenin pathway and associating factorsexpression in cortical and trabecularbone.Methods β-catenin and associating factors such as related transcription factor-2 (Runx2),Osterixin in cortical and trabecular bone were examined in vitro and in vivo.Results Immunohistochemical staining on micerevealed that the expression levels of β-catenin,Runx2 and Osterix in cortical bone were significantly lower than those in trabecular bone [(20.30 ±1.21)％ vs.(25.80±1.10)％,(10.20 ±3.05)％ vs.(19.51 ±2.03)％,(13.90 ±2.06)％ vs.(23.74 ± 3.33) ％;P ＜ 0.05].The results of cellular immune fluorescence and real-time quantitative polymerase chain reaction (Real-time PCR) were identical with the Immunohistochemical staining.Conclusion The activity of Wnt/β-catenin signaling pathway and associating factors expressionin cortical bone were significantly lower than those in trabecular bone.

Objective To observe the expression pattern of dentin matrix protein1 (DMP1) as a promoter of Cre/loxP systems spatially and temporally.Methods E18.5,1,3 weeks old C57BL/6J mice and 4 weeks DMP1-Cre;ROSA 26genotype mice were bred.Immumohistochemical staining and β-galactosidase (3-gal) staining were employed to observe the expression pattern of DMP1 and DMP1-Cre;ROSA 26 mice.Results DMP1 showed no observable expression in late embryo stage of C57BL/6J mice.However,.in early growth stage,DMP1 was mainly expressed in osteocytes of cortical bones (compared with other cells,immuohistochemical staining positive cells:osteocytes 35 ± 3,osteoblasts 10 ± 1,chondrocytes 5 ± 1,P ＜0.01;n =5/group),and small amounts were found in osteoblasts,chondrocytes,and the growth plate;DMP1-Cre was found assembled in osteocytes (immuohistochemical staining positive cells:osteocytes 18 ±2,osteoblasts 5 ± 1 、chondrocytes 6 ±2;P ＜0.01),and a few in osteoblasts,chondrocytes (P ＜ 0.01) in DMP1-Cre;ROSA 25 mice.Conclusion DMP1-Cre expressed in many kinds of cells of skeletal system.More attention should be paid when it was used in relative gene manipulations and this effect should be taken into consideration in the analysis to the outcomes.

The Publisher regrets that this article is an accidental duplication of an article that has already been published, http://dx.doi.org10.1016/j.cjtee.2015.12.012. The duplicate article has therefore been withdrawn. The full Elsevier Policy on Article Withdrawal can be found at http://www.elsevier.com/locate/withdrawalpolicy.