骨肉瘤患者同种异体骨移植后的组织学与扫描电镜观察

目的分析骨肉瘤患者同种异体骨植骨愈合与吸收的形态学特征及影响因素。方法收集2例骨肉瘤患者临床移植的大段异体骨标本,通过大体、组织学和扫描电镜观察,探讨移植骨愈合和吸收的形态学特点。结果例1观察到新骨的形成,植入骨与宿主骨发生骨性结合,在结合部位观察到骨爬行替代的演变过程。扫描电镜下看到愈合处多为松质骨,有形成面和吸收面及不同阶段的成骨细胞和各种形态的破骨细胞。例2植入骨和宿主骨发生自然离断,两端均吸收破溃,无愈合。宿主骨端有较多的破骨细胞和吸收窝,看不到形成面和成骨细胞。结论植骨方法、对接情况、固定方式、年龄及不同部位的供体骨均影响植骨愈合。     

骨移植并发感染时骨吸收的细胞学成分和植入骨辐照灭菌的作用

目的探讨骨移植后并发炎症感染时引起骨吸收的细胞成分。方法利用光镜、扫描电镜和光镜扫描电镜对比(LM/SEM)的方法,对10例感染骨标本进行观察,同时利用染菌和掺入内毒素的骨标本植入大鼠肌内进行验证。结果利用LM/SEM方法能在那些看似只有炎症细胞的骨吸收区发现破骨细胞,只是因其形态模糊而被光镜忽略。结论植入骨的吸收来自破骨细胞而不是炎症细胞。由于辐照灭菌不能消除染菌样品引起的炎症反应,辐照不能使内毒素灭活,因此控制骨产品的初始菌量是保证骨产品质量和降低植骨后出现炎症反应的重要措施。     

棕色瘤误诊为骨巨细胞瘤一例报告

棕色瘤,又称破骨细胞瘤,是继发于甲状旁腺功能亢进症的一种极其罕见的局灶性骨病.该病多由于甲状旁腺功能亢进持续分泌甲状旁腺激素,促使破骨细胞数量增加、活性增强,导致局部骨组织溶解吸收,代之以纤维组织增生.严重时,可有骨囊性改变,常伴出血,当含铁血黄素聚集于变性的纤维组织时,可表现为红棕色,故称为棕色瘤.实验室检查通常表现...     

大段同种骨移植5年后骨标本的病理表现

目的通过对1例骨肿瘤保肢术5年后因骨折取出的同种骨标本的病理学分析，探讨大段同种骨移植后在体内的修复过程。方法6岁女孩股骨骨肉瘤切除，行深冻辐照同种股骨干移植，长度20cm，术后骨愈合良好，5年后因意外致植入骨中下段斜劈形骨折，手术取出部分骨折片，进行光镜和扫描电镜观察，取未植入的同种骨材料作为对照。结果植入骨外观与对照相似；植入骨内的部分管腔扩大、形态不规则，骨表面及扩大的哈氏管表面见薄层新骨，黏合线清晰，哈氏管附近骨陷窝内见骨细胞；骨折面大量吸收窝，可见破骨细胞和成骨细胞。结论植入骨内已出现再血管化和一定程度的骨吸收及新骨形成。     

骨疏康对1型糖尿病大鼠体外培养的破骨细胞影响的初步探讨

目的 探讨骨疏康对1型糖尿病大鼠体外培养的破骨细胞影响。方法 用RANKL和M-CSF诱导1型糖尿病大鼠的股骨骨髓进行体外培养生成类破骨细胞样细胞(OLC)。实验分为正常对照组,1型糖尿病组,正常对照+骨疏康组,1型糖尿病+骨疏康组。骨疏康的浓度为20μg/ml。细胞培养7天后,贴壁细胞固定,抗酒石酸盐酸性磷酸酶染色,破骨细胞计数。结果 1型糖尿病大鼠与正常大鼠组的破骨细胞数比较无明显差别(P>0.05);经骨疏康干预后,1型糖尿病大鼠与正常大鼠的破骨细胞数都明显减少(P<0.01)。结论 1型糖尿病早期破骨细胞形成与正常对照组无明显差异。中药骨疏康明显抑制正常大鼠和1型糖尿病大鼠的破骨细胞形成。     

微波灭活松质骨的动物实验研究

目的探讨置入式微波对猪活体状态下,正常松质骨组织的灭活作用及其灭活范围、形态、短期内病理变化.方法采用12头清洁级成年猪,根据数字随机法分为术后2、4周2个时间组,每组6只猪.术后2、4周分别处死参加实验的6只猪,每组取猪的胫骨、股骨干骺端松质骨部位共24个实验对象,再次根据数字随机法分为灭活时间120 s,240 s,360 s 3个小组,每组8个样本,采用微波治疗仪进行灭活,灭活功率为60 W,微波频率为2450 MHz.每个标本行大体形态和组织学观察.结果标本大体观察见置入式微波在相同功率下不同工作时间的灭活形态基本恒定,纵截面上看类似一个椭圆形,微波灭活的范围随着时间的增加明显增大,且微波灭活形态随着灭活时间的增加逐渐趋于近似圆形.组织学观察微波灭活2周后凝固区内骨小梁结构基本正常,骨细胞完全坏死,可见大量凝固性坏死灶,其外围形成了由肉芽组织构成的交界区;微波灭活后4周凝固区内凝固性坏死灶已被吸收,边缘坏死骨小梁周围见大量破骨细胞及类骨质沉积,交界区肉芽组织大量侵入坏死骨区域,与破骨细胞一起吸收死骨,并可见新生骨小梁的形成.结论置入式微波对活体松质骨有明确的灭活作用,灭活形态基本恒定,灭活范围内细胞坏死彻底.松质骨微波灭活后,骨坏死区域修复进程快于皮质骨.     

破骨细胞体外分离培养及其骨吸收活动的观察

目的 建立大鼠破骨细胞体外分离培养方法，为体外研究破骨细胞骨吸收机理奠定基础。方法 采用出生24h内的Wistar大鼠，从其四肢长骨中分离出破骨细胞，与盖玻片、骨磨片共同培养，观察破骨细胞的形态结构及体外骨吸收活性。结果 相差显微镜及光镜观察到分离的细胞含多个核，能够移动，胞浆有伪足样突起，这些细胞用目前公认的鉴定破骨细胞的标志—抗酒石酸酸性磷酸酶染色呈阳性反应，扫描电镜观察到这些细胞能在骨片上形成典型的骨吸收陷窝。结论 用此方法分离培养的细胞为具有骨吸收活性的破骨细胞。     

破骨细胞及其分化调节机制的研究进展

正人体骨骼是一个动态的、不断更新的组织,据调查,成年人每年大约有10%的骨骼会发生骨重建~([1]),骨重建主要涉及骨吸收和骨形成两个方面,二者保持动态平衡维系着骨的正常代谢,如果二者失去平衡将会引起相应的骨骼疾病~([2-5])。骨质疏松症和关节假体周围骨溶解均是常见的骨代谢性疾病,主要原因就是由骨吸收功能强于骨形成,二者失去平衡引起。破骨细胞是人体惟一的具有骨吸收功能的细胞,因此研究破骨细胞的分化机制具有重要意义。     

RANKL,M-CSF和破骨细胞体外培养

骨是一不断更新的组织，骨重建贯穿生命过程的始终。骨重建包括骨吸收和随后进行的骨形成。骨形成和骨吸收的动态平衡维持着正常的骨代谢。当骨吸收大于骨形成时，导致骨量减少。骨吸收的主要细胞是多核的破骨细胞(0steoclast，0C)。近年来，随着分子生物学和细胞生物学的发展，人们     

17β-雌二醇对破骨细胞骨架和骨吸收功能影响的实验研究

目的　研究17β-雌二醇对体外培养破骨细胞细胞骨架的影响,以及这种影响与骨吸收功能之间的关系。方法　在破骨细胞培养液中加入不同浓度的17β-雌二醇,用F-actin特异性抗体进行免疫荧光染色,激光共聚焦显微镜观察破骨细胞细胞骨架的变化情况,同时用扫描电镜观察破骨细胞在骨片形成骨吸收陷窝数目及面积的变化。结果　随着17β-雌二醇浓度的升高,实验组破骨细胞F-actin相对荧光强度从(89 6±7 5)%下降至(34 7±5 4)% (与对照组荧光强度相比),细胞内微丝收缩变短,排列紊乱,细胞波状缘消失,破骨细胞伸展面积从(1289±53)μm2 /细胞核下降至(406±42)μm2 /细胞核,同时,骨吸收陷窝的数目和面积从(131 5 ±11 7)个/片和(2157±51)μm2 减少到(16 8±4 0 )个/片和(965±75)μm2。生理浓度(10-7mol/l)及其以上17β-雌二醇处理组与对照组比较,差异有显著性(P<0 01 )。结论　17β-雌二醇影响破骨细胞内细胞骨架的结构,下调F-actin的表达,降低破骨细胞的活动能力,从而抑制破骨细胞的骨吸收功能。     

Osteoclasts and the resorption of bone by transplanted mammary carcinoma in rats

Rat mammary tumour cells were grafted to parietal bones as an experimental model to study the nature of bone resorption around metastatic carcinomas in the skeleton. After periods of growth of from 6 to 56 days bones and tumours were removed and embedded in epoxy resin. The appearances were compared with those found when whole parathyroid glands were grafted in similar positions. Tumours were evident in all animals at the time of death and some were palpable five days after grafting. In 15 of the 21 animals with tumour, osteoclasts and resorption were found, and in only two of these were the tumour cells not separated from the bone surfaces. In 6 animals killed between 6 and 12 days after grafting there was new bone formation without resorption. There were osteoclasts and resorption under the grafted parathyroid glands which were always separated from the resorbing cells by fibrous tissue. The appearances of the bone surfaces under the tumours and the parathyroid glands suggested that the resorption in both situations was similar, was brought about by the secretion of a locally active agent and mediated by osteoclasts. This is further support for the role of osteoclasts in bone resorption around metastatic carcinomas.     

Bone resorption by macrophage polykaryons of giant cell tumour of tendon sheath.

The antigenic phenotype, ultrastructure and bone resorbing ability of mononuclear and multinucleated giant cells of four giant cell tumour of tendon sheath (GCTTS) lesions was assessed. Both the giant cells and the mononuclear cells exhibited the antigenic phenotype of cells of the monocyte/macrophage lineage. The giant cells, unlike osteoclasts, did not respond morphologically to calcitonin and showed ultrastructural and immunophenotypic features of macrophage polykaryons. However, like osteoclasts, the giant cells showed direct evidence of resorption pit formation on bone slices. This indicates that the GCTTS is composed of cells of histiocytic differentiation with the giant and mononuclear cell components expressing a similar antigenic phenotype. Bone resorption by macrophage polykaryons shows that this is not a unique defining characteristic of osteoclasts. Qualitative differences in the degree and pattern of bone resorption by macrophage polykaryons distinguish it from that of osteoclasts and may underlie the clinical behaviour of osteolytic lesions.     

Suppression by incadronate of invasion and growth of A-375 human melanoma in mandible in nude mice

Frequent invasion of oral cancers into the neighboring jaw bones is a major cause of increased mortality. Moreover, majority of patients with these oral cancers suffer from functional inconveniences and esthetic disadvantages during clinical course and after surgical treatments. Understanding of the mechanisms underlying oral cancer invasion into jaw bones is, therefore, critical to the better management of oral cancer patients. To study the pathophysiology of mandibular invasion of oral cancers, we established an animal model by inoculating the A-375 human melanoma cells onto mandible through masseter muscle in nude mice. Histological study showed that A-375 tumor cells aggressively destroyed the mandibular cortical bones and invaded into the bone marrow cavities. Histochemical examination revealed that there were numerous tartrate-resistant acid phosphatase-positive osteoclasts on the residual bone surfaces facing A-375 tumors. To examine the role of osteoclasts in mandibular bone invasion of A-375 tumors, we next studied the effects of the bisphosphonate incadronate (INC), a potent inhibitor of osteoclastic bone resorption, using this model. Daily subcutaneous injections of INC (1 mg/kg) markedly decreased A-375-increased osteoclasts, increased numbers of apoptotic osteoclasts and inhibited mandibular cortical bone destruction. Furthermore, INC significantly suppressed the growth of A-375 tumors, increased numbers of apoptotic A-375 cells and decreased the tumor-associated blood vessel density. These results suggest that invasion and growth of oral cancers in mandibular bone is dependent on osteoclastic bone resorption and that INC can inhibit the aggressive behavior of oral cancer through inhibiting osteoclastic bone resorption.     

骨关节结核发病机制的相关实验研究

目的研究骨关节结核的发病机制。方法采用不同浓度结核分枝杆菌超声裂解产物体外诱导破骨细胞的生长;通过体外颅骨吸收实验,观察不同浓度结核分枝杆菌超声裂解产物诱导破骨细胞生成和钙离子释放的关系;体内注射结核分枝杆菌超声裂解产物,从血钙浓度和组织学方面观察骨质变化。结果结核分枝杆菌超声裂解产物能够在体外诱导破骨细胞生长,且破骨细胞数量的增加依赖细菌浓度的提高。钙离子释放与细菌诱导破骨细胞的数量相关,体内注射细菌能够引起破骨细胞数量增加、钙离子释放和骨质吸收。结论骨、关节结核的发病很可能与结核菌诱导破骨细胞增生有关。     

The origin and nature of stromal osteoclast-like multinucleated giant cells in breast carcinoma: implications for tumour osteolysis and macrophage biology

The origin and nature of osteoclast-like multinucleated giant cells (OMGCs), in extraskeletal neoplasms, is uncertain. The ultrastructure, antigenic phenotype and function of OMGCsm in a breast carcinoma were studied in order to clarify the relationship between OMGCs, osteoclasts and other cells of the mononuclear phagocyte system (MPS). OMGCs resorbed cortical bone in a manner similar to osteoclasts. However, unlike osteoclasts, OMGCs did not possess a ruffled border or clear zone, and expressed HLA-DR and Fc receptors and CD14, CD16, CD18 and CD11 (p150,95) antigens. In addition, OMGCs failed to respond morphologically to calcitonin and were directly stimulated by parathyroid hormone (PTH) to increase bone resorption. These findings suggest that OMGCs are a specific type of macrophage polykaryon distinct from both osteoclasts and other types of inflammatory polykaryon. Occasional smaller (20-25 microns) macrophage-like cells were also associated with resorption pits. Bone resorption by OMGCs isolated from the breast indicates that a cell of the MPS can be transplanted to a new tissue location and perform a highly specialised function appropriate to an MPS cell of that tissue (i.e. the osteoclast). PTH stimulation of bone resorption by OMGCs suggests that PTH or a PTH-like protein, may be involved in the bone resorption and consequent hypercalcaemia associated with metastatic breast cancer.     

Bisphosphonates and osteomyelitis of the jaw: a pathogenic puzzle

The maxillary and mandibular bones undergo high-turnover remodeling to maintain mechanical competence. Common dental or periodontal diseases can increase local bone turnover. Bisphosphonates (BPs) accumulate almost exclusively in skeletal sites that have active bone remodeling. The maxillary and mandibular bones are preferential sites for accumulation of BPs, which become buried under new layers of bone and remain biologically inactive for a long time. Surgical odontostomatological procedures create open bony wounds that heal quickly and without infection, as a result of activation of osteoclasts and subsequently osteoblasts. Once BPs are removed from the bone via activation of osteoclasts after a tooth extraction or a periodontal procedure, they induce osteoclast apoptosis. This inhibition of osteoclast bone resorption impairs bone wound healing because of decreased production of cytokines derived from the bone matrix, and the bone is exposed to the risk of osteomyelitis and necrosis. The pathogenic relationship between BPs and osteonecrosis of the jaw is unclear, but there is evidence to indicate an association between high-dose BP treatment and exposure to dental infections or oral surgical procedures. A better knowledge of the interactions between BPs and jaw and maxillary bone biology will improve clinical and therapeutic approaches.     

骨转移生化指标研究进展

肿瘤骨转移发生时,破骨细胞和成骨细胞释放至血和尿中的骨生化指标明显升高,有望用于骨转移的早期诊断,但其准确性和有效性尚待大样本的前瞻性研究评价.大多数骨生化指标高水平与骨转移患者不良预后显著相关,对疾病进展和疗效监测则具有重要临床意义.     

节段性切除一期骨重建治疗长骨纤维结构不良

目的 探索治疗长骨纤维结构不良(FD)降低复发率的新途径。方法 从1988年7月至2001年8月采用节段性切除，一期骨重建治疗四肢FD27例29个骨。术式包括：(1)瘤段骨切除，离体切刮灭活再植，行自家骨或同种异体骨移植(ATBG，ALBG)。(2)全桡骨切除，自家腓骨置换(ATFR)1例。(3)同种异体腓骨置换(ALFR)3例4骨。除1例采用普通钢板外，28个骨均以L一梯形钢板(L—TCP)固定，其中1例合并克氏针固定。另一侧单一克氏针固定。平均骨缺损12．3cm(7．8～23．5cm)。结果 22例23个骨随访1年至13年8个月，2例切口感染，均于术后1～2年治愈。全部截骨处均愈合，仅1例股骨上端FD并发髋内翻。2例复发，为酒精灭活再植病例。17例18个肢体的关节功能优，良好、尚可各2例，1例差。结论 瘤体骨节段性切除，一期骨重建的术式不仅可以有效地降低复发率，而且有利于骨愈合和恢复功能，减少并发症。