State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Division of Plastic and Reconstructive Surgery, Department of Surgery, School of Medicine, Stanford University, Palo Alto, CA, USA.
Clin Oral Implants Res. 2020 Dec;31(12):1159-1172. doi: 10.1111/clr.13662. Epub 2020 Sep 15.
Oral implants transmit biting forces to peri-implant bone. In turn, those forces subject peri-implant bone to mechanical stresses and strains. Here, our objective was to understand how peri-implant bone responded to conditions of normal versus hyper-loading in a mouse model.
Sixty-six mice were randomly assigned to 2 groups; both groups underwent bilateral maxillary first molar extraction followed by complete healing. Titanium alloy implants were placed in healed sites and positioned below the occlusal plane. After osseointegration, a composite crown was affixed to the implant so masticatory loading would ensue. In controls, the remaining dentition was left intact but in the hyper-loaded (test) group, the remaining molars were extracted. 3D finite element analysis (FEA) calculated peri-implant strains resulting from normal and hyper-loading. Peri-implant tissues were analyzed at multiple time points using micro-computed tomography (µCT) imaging, histology, enzymatic assays of bone remodeling, and vital dye labeling to evaluate bone accrual.
Compared to controls, hyper-loaded implants experienced a 3.6-fold increase in occlusal force, producing higher peri-implant strains. Bone formation and resorption were both significantly elevated around hyper-loaded implants, eventually culminating in a significant increase in peri-implant bone volume/total volume (BV/TV). In our mouse model, masticatory hyper-loading of an osseointegrated implant was associated with increased peri-implant strain, increased peri-implant bone remodeling, and a net gain in bone deposition.
Hyper-loading results in bone strain with catabolic and anabolic bone responses, leading to a net gain in bone deposition.
口腔种植体将咬合力传递到种植体周围的骨组织。反过来,这些力使种植体周围的骨组织承受机械应力和应变。在这里,我们的目的是了解在小鼠模型中,种植体周围的骨组织如何对正常和超负载条件做出反应。
66 只小鼠被随机分为 2 组;两组均行双侧上颌第一磨牙拔除,然后完全愈合。钛合金种植体被放置在愈合部位,并位于咬合平面以下。在骨整合后,将复合冠固定在种植体上,以进行咀嚼负荷。在对照组中,保留其余的牙齿完整,但在超负载(试验)组中,其余的磨牙被拔除。三维有限元分析(FEA)计算了正常和超负载下种植体周围的应变。使用微计算机断层扫描(µCT)成像、组织学、骨重塑的酶学检测和活染料标记,在多个时间点分析种植体周围组织,以评估骨沉积。
与对照组相比,超负载的种植体承受的咬合力增加了 3.6 倍,产生了更高的种植体周围应变。超负载种植体周围的骨形成和骨吸收均显著增加,最终导致种植体周围骨体积/总体积(BV/TV)显著增加。在我们的小鼠模型中,骨整合种植体的咀嚼超负载与种植体周围应变增加、种植体周围骨重塑增加以及骨沉积净增加有关。
超负载导致骨应变,伴有分解代谢和合成代谢的骨反应,导致骨沉积净增加。