Department of Restorative Sciences, School of Dentistry, University of Minnesota, Minneapolis, MN, USA.
Department of Periodontics, School of Dentistry, UTHealth, San Antonio, TX, USA.
BMC Oral Health. 2019 Jul 15;19(1):150. doi: 10.1186/s12903-019-0837-y.
Animal studies are pivotal in allowing experimentation to identify efficacious treatment protocols for resolution of peri-implantitis. The purpose of this investigation was to characterize an expedited dog peri-implantitis model clinically, radiographically, and microbiologically.
Eight hound dogs underwent extractions (week 0) and implant (3.3 × 8.5 mm) placement with simultaneous surgical defect creation and ligature placement for induction of peri-implantitis (week 10). Ligatures were replaced at 6 weeks (week 16) and removed after 9 weeks (week 19) when supporting bone loss involved approximately 50% of the peri-implant bone. Microbial samples from the defects and healthy control implant sites collected at week 19 were analyzed utilizing a microarray. Clinical measures of inflammation were obtained and radiographic bone loss was measured from periapical radiographs. Radiographic depth and width measurements of bony defect were repeated at weeks 10 (baseline), 16, and 19. Canonical analysis of principal coordinates was used to visualize overall differences in microbial abundance between peri-implantitis and healthy implants.
This accelerated disease protocol led to intrabony defect creation with a mean depth and width of 4.3 mm and 3.5 mm, respectively after 9 weeks of ligature placement. Microbial identification revealed 59 total bacteria in peri-implant sites, 21 of which were only present in peri-implant sites as compared to healthy controls. Overall microbial beta diversity (microbial between-sample compositional diversity) differed between peri-implantitis and healthy implants (p = 0.009).
Within the limitations of this study, this protocol led to expedited generation of peri-implant defects with a microbial profile indicative of a shift to disease and defect patterns conducive to regenerative treatment. However, the possibility of potential spontaneous resolution of lesions due to the lack of a chronicity interval as compared to chronic disease models need to be further clarified and considered during preclinical peri-implantitis model selection.
动物研究在允许实验以确定治疗方案以解决种植体周围炎的疗效方面起着至关重要的作用。本研究的目的是从临床、放射学和微生物学角度描述加速犬种植体周围炎模型。
八只猎犬接受拔牙（第 0 周）和种植体（3.3×8.5mm）植入，同时进行手术缺损形成和结扎放置以诱导种植体周围炎（第 10 周）。结扎物在 6 周（第 16 周）更换，并在 9 周（第 19 周）去除，此时支持骨的损失约占种植体周围骨的 50%。第 19 周从缺陷和健康对照种植体部位采集的微生物样本利用微阵列进行分析。获得炎症的临床指标，并从根尖片测量放射学骨损失。在第 10 周（基线）、16 周和 19 周重复测量骨缺损的放射学深度和宽度。主坐标典范分析用于可视化种植体周围炎和健康种植体之间微生物丰度的整体差异。
这种加速疾病方案导致骨内缺损形成，在结扎放置 9 周后，平均深度和宽度分别为 4.3mm 和 3.5mm。微生物鉴定显示种植体部位有 59 种总细菌，其中 21 种仅存在于种植体部位，而不存在于健康对照部位。种植体周围炎和健康种植体之间的总体微生物β多样性（微生物样本间组成多样性）不同（p=0.009）。
在本研究的限制范围内，该方案导致加速生成种植体周围缺损，微生物谱表明向疾病转变，缺损模式有利于再生治疗。然而，与慢性疾病模型相比，由于缺乏慢性期，病变可能会自发缓解，因此在选择临床前种植体周围炎模型时需要进一步阐明和考虑这一点。
