Chinese Journal of Tissue Engineering Research ›› 2021, Vol. 25 ›› Issue (10): 1604-1608.doi: 10.3969/j.issn.2095-4344.3071
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Deng Xiongwei1, Han Jie2
Received:
2020-02-17
Revised:
2020-02-25
Accepted:
2020-05-09
Online:
2021-04-08
Published:
2020-12-18
Contact:
Han Jie, Associate chief physician, Master’s supervisor, Department of Joint and Sports Medicine, Ruikang Hospital, Guangxi University of Chinese Medicine, Nanning 530011, Guangxi Zhuang Autonomous Region, China
About author:
Deng Xiongwei, Master candidate, Guangxi University of Traditional Chinese Medicine, Nanning 530001, Guangxi Zhuang Autonomous Region, China
Supported by:
CLC Number:
Deng Xiongwei, Han Jie. Advantages and problems of induced membrane technology in the treatment of infectious nonunion[J]. Chinese Journal of Tissue Engineering Research, 2021, 25(10): 1604-1608.
治疗感染性骨不连是以消除感染、促进骨折愈合、尽可能地恢复关节功能为目的,因此治疗感染性骨不连的首要任务是控制感染。Masquelet 技术分为2期,一期在解决感染的基础上形成诱导膜,为骨组织生长提供了适宜的生长空间;二期在诱导膜形成的基础上植入填塞物,可保持骨组织的连续性,有利于维持肢体的形态,事实证明这是一种有效的治疗方法[3-5]。 法国学者MASQUELET等于20世纪70年代治疗骨不连时发现了该技术[4],其对感染性骨不连的治疗也有着显著疗效。该手术分2个阶段:①第一阶段,术前做好充分准备,包括对患肢功能评估并标记好手术部位;围术期应抗感染治疗,保持伤口清洁干燥。麻醉成功后消毒铺单,术中清除坏死组织,包括瘢痕、肉芽组织和细菌形成的生物膜,因为坏死组织可能会再次导致感染,还会阻碍骨组织生长甚至形成血管栓塞。一期彻底清除病灶是完成骨重建的首要保障。创口需用含有抗生素的生理盐水反复冲洗,防止感染蔓延至邻近关节,须根据病灶细菌培养结果使用抗生素,清创时直至断端出现点状样血液组织。彻底清创后断端骨质缺损,肢体失去稳定性,要求维持肢体原有形态,固定方式有单边外固定、环形外固定、髓内钉或石膏。依据骨缺损位置选择稳定肢体的方式,骨中段缺损时一般选择直径较小的髓内钉再填塞富含抗生素的聚甲基丙烯酸甲酯骨水泥,有利于早期肢体功能锻炼;邻近关节缺损时首先选择胯膝关节外固定。肢体稳定后,测量肢体两断端缺损长度,根据缺损长度植入聚甲基丙烯酸甲酯骨水泥,然后闭合创面。为发挥骨水泥的优点,在彻底清除坏死的组织后常常植入骨水泥塑形,骨水泥植入范围包括整个髓腔及周围正常骨组织,这样能抑制细菌的生长并维持肢体形态。②在第一次手术后的6-8周进入第二阶段治疗,沿着骨水泥块表面锐性切开并剥离诱导膜,操作过程中保护软组织,更不能破坏诱导膜的完整性;在骨缺损处植入颗粒状自体松质骨,随即关闭诱导膜。自体骨具有良好的重塑骨组织结构作用,无排斥反应,常将髂骨、胫骨近端、腓骨作为供骨来源。此外,术者需要对缺损处有动态的把握,移植骨量既要覆盖整个缺损处又要考虑诱导膜能完整闭合。 2.1 诱导膜的形成 在实施Masquelet技术过程中产生诱导膜。首先填补缺损,周围软组织受到填塞物的刺激会在填塞物表面生长出一层伪膜,随着组织的生长,伪膜可达2 mm厚,最终形成诱导膜[6]。近年来,磷酸钙和硫酸钙骨水泥作为新的可吸收填塞物具有可吸收性,减少了对组织的损害,缩短了诱导膜技术治疗周期,同时还有良好的骨结构[7-9]。此外,运用聚甲基丙烯酸甲酯骨水泥诱导形成的膜具有营养周围组织和促进骨组织形成的作用。但是许多可吸收填塞物的抗冲击力差,导致形成的诱导膜功能较弱,还存在无法动态掌握吸收速度、吸收过快不利于缺损处骨组织生长等缺点,因此治疗部位不能承受太大的压力,特别是关节处和受重部位。总之,可吸收填塞物具有巨大的研究价值,抗冲击力更强和促进骨组织形成能力更强的可吸收填塞物可以缩短骨折愈合时间和减少取骨带来的损害[10-11]。 2.2 诱导膜的功能 诱导膜的生物结构及功能与骨膜相 仿[12-19],可以诱导骨干细胞形成成骨细胞,进而促进骨组织生长。通过对诱导膜细胞与骨干细胞的RNA序列观察,发现它们存在相似的片段。同样,诱导膜的成纤维细胞中的转录因子——核心结合因子,它也具有使骨干细胞形成成骨细胞的能力。镜下可以看到诱导膜表现出成骨钙化的功能,说明其本身就具有成骨的能力。诱导膜凭借自身的机械强度在填塞物的表面形成一个密闭的生长空间,有利于缺损处植骨,促进骨折愈合,防止周围组织长入。此外,完整的诱导膜可显著减少术后感染,由于诱导膜血运丰富,可以在骨膜表面形成一道屏障,因此能避免感染的发生。ZHAO等[20]在动物模型中发现填塞物与诱导膜之间存在一定空间,有利于填塞物的取出,不会使诱导膜的功能遭到破坏,可以保证植骨后诱导膜的完整性。GUDA等[21]治疗动物骨缺损时发现,诱导膜和植骨联合运用取得的效果往往比单独运用一种好。诱导膜具有独特的功能并富含促成骨因子,如血管内皮生长因子、骨形态发生蛋白2、转化生长因子β1[12,22-23]。有研究表明,血管内皮生长因子可以有效地促进血管生成,骨形态发生蛋白2和血管内皮生长因子的表达随着填塞物放置时间的延长而逐渐升高,两者相互作用促进骨生长细胞形成,有利于骨组织生长,且骨组织间隙含有许多骨生长细胞,他们也具有成骨功能,为骨的形成提供原料[16-17,24]。血管内皮生长因子能使骨缺损周围受损血管组织再生,使成骨细胞得到充足的营养,加速骨组织的生长,显著缩短成骨时间。此外,转化生长因子β1可控制血管内皮生长因子的表达,而诱导膜的功能及骨组织的生长又受两者的调节。 2.3 诱导膜治疗感染性骨不连相关因子的表达 无论从解剖学还是功能角度去重建各种原因导致的感染性骨不连,均是一个很大的挑战。骨搬运被认为是有效的方法,它能解决传统植骨术存在不可控制的骨吸收缺陷,但仍然存在治疗周期长、需多次手术、皮肤切割及对接端骨不连等问题。而诱导膜技术的出现有望克服前面那些方法的缺点,这一技术取得良好的效果归咎于诱导膜可分泌丰富的血管内皮生长因子、骨形态发生蛋白2、转化生长因子β1等多种生长因子。 2.3.1 转化生长因子β1的表达 转化生长因子β1作为一种蛋白多肽对细胞的生长具有调节功能,影响着骨组织的生 长[25]。此外,转化生长因子β作为一种细胞因子主要集中在骨组织和血液中,转化生长因子在各组织中具有不同的形态功能。当骨组织的连续性受到破坏后,转化生长因子β甚至是外源的转化生长因子β可以对成骨细胞产生刺激而促进骨组织生长。由于成骨细胞主要产生转化生长因子β1,能在其表面形成相应的受体,当两者相互作用会形成诱导骨组织生长的信号通路,进而促进骨折愈合。通过观察转化生长因子β1 mRNA在人体不同年龄阶段表达促骨组织生长的差异,发现机体气血旺盛时转化生长因子β1 mRNA表达促骨组织生长量明显增多,进一步说明老年时期转化生长因子β1分泌量少,容易发生骨折。同样,骨不连的愈合不仅与周围组织的血运及骨形态的固定有关[26-27],也与影响骨组织生长的因子及骨重塑刺激相关。因此,维持肢体原有的形态和保证丰富的血液供应是达到骨性愈合的首要保障。HARA等[28]的研究发现肢体骨折后,随着时间的演变,机体骨组织愈合的同时血清中转化生长因子β1浓度相应地逐渐升高;而骨不连患者由于调节成骨细胞的转化生长因子β1浓度下降,导致骨组织生长受阻,表明转化生长因子β1在骨组织生长中发挥了很重要的作用。因此,骨组织生长因子的活性受到破坏会导致骨不连的发生。 2.3.2 骨形态发生蛋白的表达 骨形态发生蛋白可分泌许多骨组织所需的蛋白进而促进骨的形成。同样,骨形态发生蛋白作为一种生长因子能促进相关细胞分化,有利于骨组织生长。通过观察比较骨形态发生蛋白与转化生长因子β中cDNAs的相应片段,发现骨形态发生蛋白从属于转化生长因子β超家族[29]。目前发现存在许多种骨形态发生蛋白,除骨形态发生蛋白1外,其余全为转化生长因子β超家族的一份子。此外,骨形态发生蛋白具有诱导软组织和血供系统组织原始未灭活间充质细胞向骨组织细胞转化的功能。RIPAMONTI等[30]研究表明,在促进骨组织细胞转化的所有骨形态发生蛋白成员中,骨形态发生蛋白2,4,6,7和9表现出最强的成骨能力,且在骨组织生长初期的分化细胞中均有上升的趋势,在骨组织生长过程中持续表达。有学者研究骨形态发生蛋白促进小鼠大腿骨组织生长的功能,发现骨形态发生蛋白6和骨形态发生蛋白9能促进骨组织的形成,且骨形态发生蛋白9表现出最强的促进骨组织形成能力[31]。由于骨形态发生蛋白9很早与异位骨化联系在一起,最新研究发现骨形态发生蛋白9不仅能延续骨组织的活性,而且其他骨形态发生蛋白成员促进骨组织生长的能力远低于骨形态发生蛋白9,根据这些研究结果,治疗骨折、骨折后骨不连可以取得更好的疗效[32]。相关研究表明,一旦骨细胞中缺乏骨形态发生蛋白2,骨组织将停止生长,骨折愈合延迟,从而说明骨形态发生蛋白2对骨愈合有至关重要的影响。因此,骨形态发生蛋白2影响软骨生长,主要是因其阻碍骨细胞的分化,进而导致骨化中心形成时间显著延长[33]。另外,在体外骨形态发生蛋白2可以通过自身调节的方式影响其他骨形态发生蛋白活性的功能[34]。由于机体内骨形态发生蛋白2表达时间比其他骨形态发生蛋白早,这有助于诱导其他骨形态发生蛋白生成,促进肢体骨性愈合。然而,虽然骨形态发生蛋白2对成骨产生很大的影响,但集成骨干细胞的功能微 弱[35]。虽然无法确定骨形态发生蛋白2具体作用于哪个成骨细胞,但根据目前受认可的微型创伤自我调节方式,骨细胞受到创伤刺激产生应激反应,吸收失活的骨组织,而缺损部位又可以生长出新的骨组织[36]。通过观察小鼠体内的骨祖细胞,发现其向成骨细胞转化的功能缺失是由于缺乏骨形态发生蛋白2表达[37]。通过以上研究发现骨形态发生蛋白2会影响骨祖细胞向骨细胞增殖分化。除了成骨细胞的功能遭到破坏外,骨折一旦发生,由于缺少骨形态发生蛋白2 表达机体将不能产生自我修复的功能,MI等[38]最早证实了这一发现。从骨形态发生蛋白2分离出特有的调节序列能实现对骨形态发生蛋白2表达的调控。然而,调节序列中的增强子最可能被骨折愈合初期产生的炎症递质激活,一旦被激活后它们可以通过骨膜细胞产生新的骨形态发生蛋白2。 2.3.3 血管内皮生长因子表达 良好的血供能保证骨组织的正常修复。然而,血管生成需要依靠多种生长因子参与调节,这些生长因子包括血小板源性生长因子、成纤维细胞生长因子、骨形态发生蛋白2、血管内皮生长因子等。既往认为骨组织重建的过程是破骨细胞-成骨细胞功能偶联的结果,即所谓的“二元调控”。XIE等[39]报道了由破骨前体细胞分泌的血小板源生长因子BB可诱导H型血管生成,H 型血管所分泌出的大量成纤维生长因子、骨形态发生蛋白在分子水平偶联成骨[40]。GOURON等[41]研究证实诱导膜含有丰富的血供,在诱导膜组织中靠近聚甲基丙烯酸甲酯边缘聚集了大量破骨前体细胞,因此可以推测诱导膜中可能存在CD31hiEmcnh血管:故认为三元调控机制和其血管化特性与诱导成骨活性密切相关。多项动物实验证实,血管内皮生长因子的浓度和血管密度高度相关,血管内皮生长因子在新生血管形成中扮演着重要角色。HMGB1具有核因子和细胞外因子双重功能,FENG等[42]研究表明 HMGB1和它的受体相互结合后可诱导成血管细胞的迁移和增殖,在组织再生中发挥重要作用。此外,血小板源生长因子BB可诱发骨髓源性内皮祖细胞的迁移,骨髓源性内皮祖细胞可通过分泌血管内皮生长因子间接地促进骨内新血管形成。相关研究表明,被称为血小板内皮细胞黏附分子的CD31主要黏附在内皮细胞和造血细胞上。存在于内皮细胞细胞质中的CD31与内皮细胞的迁移及新血管形成密切相关,是用来检测新血管生成的常用标记物[43]。同样,Endomucin-1( Emcn)作为一种跨膜Ⅰ型O糖蛋白被认为在血管生长中具有重要作用。PARK-WINDHOL等[44]研究发现Emcn可调控血管内皮生长因子受体2活性,影响血管内皮生长因子诱导的内皮细胞的迁移、生长和管形态形成。最新研究表明,新生血管不仅建立了新的微循环,还向骨组织输入氧气和营养,可直接促进成骨[45]。 "
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