Department of Morphology and Pathology, Jundiai Medical School, Jundiai, 13202-550, Brazil.
Sao Carlos Institute of Chemistry, University of Sao Paulo (USP), Sao Carlos, 13566-590, Brazil.
Sci Rep. 2023 Jan 2;13(1):28. doi: 10.1038/s41598-022-24424-x.
Lesions with bone loss may require autologous grafts, which are considered the gold standard; however, natural or synthetic biomaterials are alternatives that can be used in clinical situations that require support for bone neoformation. Collagen and hydroxyapatite have been used for bone repair based on the concept of biomimetics, which can be combined with chitosan, forming a scaffold for cell adhesion and growth. However, osteoporosis caused by gonadal hormone deficiency can thus compromise the expected results of the osseointegration of scaffolds. The aim of this study was to investigate the osteoregenerative capacity of collagen (Co)/chitosan (Ch)/hydroxyapatite (Ha) scaffolds in rats with hormone deficiency caused by experimental bilateral ovariectomy. Forty-two rats were divided into non-ovariectomized (NO) and ovariectomized (O) groups, divided into three subgroups: control (empty defect) and two subgroups receiving collagen/chitosan/hydroxyapatite scaffolds prepared using different methods of hydroxyapatite incorporation, in situ (CoChHa1) and ex situ (CoChHa2). The defect areas were submitted to macroscopic, radiological, and histomorphometric analysis. No inflammatory processes were found in the tibial defect area that would indicate immune rejection of the scaffolds, thus confirming the biocompatibility of the biomaterials. Bone formation starting from the margins of the bone defect were observed in all rats, with a greater volume in the NO groups, particularly the group receiving CoChHa2. Less bone formation was found in the O subgroups when compared to the NO. In conclusion, collagen/chitosan/hydroxyapatite scaffolds stimulate bone growth in vivo but abnormal conditions of bone fragility caused by gonadal hormone deficiency may have delayed the bone repair process.
骨量丢失的病变可能需要自体移植物,这被认为是金标准;然而,天然或合成生物材料是可以在需要支持新骨形成的临床情况下使用的替代物。胶原蛋白和羟基磷灰石已基于仿生学的概念用于骨修复,可以与壳聚糖结合,形成细胞黏附和生长的支架。然而,性腺激素缺乏引起的骨质疏松症可能会影响支架骨整合的预期结果。本研究旨在研究胶原蛋白(Co)/壳聚糖(Ch)/羟基磷灰石(Ha)支架在实验性双侧卵巢切除引起的激素缺乏大鼠中的骨再生能力。42 只大鼠分为未卵巢切除(NO)和卵巢切除(O)组,分为三组:对照组(空缺陷)和两组接受胶原蛋白/壳聚糖/羟基磷灰石支架,使用不同的羟基磷灰石掺入方法制备,原位(CoChHa1)和异位(CoChHa2)。对缺损区域进行宏观、放射学和组织形态计量学分析。胫骨缺损区域未发现表明支架免疫排斥的炎症过程,从而证实了生物材料的生物相容性。所有大鼠均观察到从骨缺损边缘开始的骨形成,NO 组,特别是接受 CoChHa2 的大鼠的骨形成体积更大。与 NO 组相比,O 组的骨形成较少。总之,胶原蛋白/壳聚糖/羟基磷灰石支架在体内刺激骨生长,但性腺激素缺乏引起的骨脆弱的异常情况可能会延迟骨修复过程。