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Peri‐implantitis is not periodontitis: Scientific discoveries shed light on microbiome‐biomaterial interactions that may determine disease phenotype
Periodontology 2000 ( IF 17.5 ) Pub Date : 2021-03-10 , DOI: 10.1111/prd.12372
Georgios A. Kotsakis 1 , Daniel G. Olmedo 2
Affiliation  

Peri‐implantitis is an immune‐mediated biological complication that is attributed to bacterial biofilms on the implant surface. As both periodontitis and peri‐implantitis have similar inflammatory phenotypes when assessed cross‐sectionally, treatment protocols for peri‐implantitis were modeled according to those used for periodontitis. However, lack of efficacy of antimicrobial treatments targeting periodontal pathogens coupled with recent discoveries from open‐ended microbial investigation studies create a heightened need to revisit the pathogenesis of peri‐implantitis compared with that of periodontitis. The tale of biofilm formation on intraoral solid surfaces begins with pellicle formation, which supports initial bacterial adhesion. The differences between implant‐ and tooth‐bound biofilms appear as early as bacterial adhesion commences. The electrostatic forces and ionic bonding that drive initial bacterial adhesion are fundamentally different in the presence of titanium dioxide or other implant alloys vs mineralized organic hydroxyapatite, respectively. Moreover, the interaction between metal surfaces and the oral environment leads to the release of implant degradation products into the peri‐implant sulcus, which exposes the microbiota to increased environmental stress and may alter immune responses to bacteria. Clinically, biofilms found in peri‐implantitis are resistant to beta‐lactam antibiotics, which are effective against periodontal communities even as monotherapies and demonstrate a composition different from that of biofilms found in periodontitis; these facts strongly suggest that a new model of peri‐implant infection is required.

中文翻译:

种植体周围炎不是牙周炎:科学发现揭示了可能决定疾病表型的微生物与生物材料的相互作用

种植体周围炎是一种免疫介导的生物并发症,可归因于植入物表面的细菌生物膜。由于当进行横断面评估时,牙周炎和牙周炎的炎症表型相似,因此,根据牙周炎的使用方法对牙周炎的治疗方案进行了建模。然而,针对牙周病原体的抗微生物治疗缺乏疗效,加上开放式微生物研究的最新发现,与牙周炎相比,迫切需要重新审视种植体周炎的发病机理。在口腔内固体表面形成生物膜的故事始于防护膜形成,这支持了最初的细菌粘附。细菌粘附开始时,就会出现植入物和牙齿结合的生物膜之间的差异。在存在二氧化钛或其他植入合金的情况下,驱动初始细菌粘附的静电力和离子键分别与矿化的有机羟基磷灰石有根本的不同。此外,金属表面和口腔环境之间的相互作用导致植入物降解产物释放到植入物周围沟中,这使微生物群暴露于增加的环境压力下,并可能改变对细菌的免疫反应。临床上,在种植体周围炎中发现的生物膜对β-内酰胺类抗生素具有抗性,即使以单一疗法也可有效对抗牙周病,并且其成分不同于在牙周炎中发现的生物膜。这些事实强烈表明,需要一种新的种植体周围感染模型。
更新日期:2021-04-22
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