Trindade Ricardo, Albrektsson Tomas, Tengvall Pentti, Wennerberg Ann
Department of Prosthodontics, Faculty of Odontology, Malmö University, Malmö, Sweden.
Department of Biomaterials, Institute of Clinical Sciences, Göteborg University, Göteborg, Sweden.
Clin Implant Dent Relat Res. 2016 Feb;18(1):192-203. doi: 10.1111/cid.12274. Epub 2014 Sep 25.
The last few decades have seen a progressive shift in paradigm, replacing the notion of body implants as inert biomaterials for that of immune-modulating interactions with the host.
This text represents an attempt at understanding the current knowledge on the healing mechanisms controlling implant-host interactions, thus interpreting osseointegration and the peri-implant bone loss phenomena also from an immunological point of view.
A narrative review approach was taken in the development of this article.
Osseointegration, actually representing a foreign body reaction (FBR) to biomaterials, is an immune-modulated, multifactorial, and complex healing process where a number of cells and mediators are involved. The buildup of osseointegration seems to be an immunologically and inflammatory-driven process, with the ultimate end to shield off the foreign material placed in the body, triggered by surface protein adsorption, complement activation, and buildup of a fibrin matrix, followed by recruitment of granulocytes, mesenchymal stem cells, and monocytes/macrophages, with the latter largely controlling the longer term response, further fusing into foreign body giant cells (FBGC), while bone cells make and remodel hydroxyl apatite. The above sequence results in the FBR that we call osseointegration and use for clinical purposes. However, the long-term clinical function is dependent on a foreign body equilibrium, that if disturbed may lead to impaired clinical function of the implant, through a breakdown process where macrophages are again activated and may further fuse into FBGCs, now seen in much greater numbers, resulting in the start of bone resorption - due to cells such as osteoclasts with different origins and possibly even macrophages degrading more bone than what is formed via osteoblastic activity - and rupture of mucosal seals, through complex mechanisms in need of further understanding. Infection may follow as a secondary event, further complicating the clinical scenario. Implant failure may ensue.
Dentistry is still to embrace the concept of the biomaterials' healing- and immune-modulating effect when in contact with body tissues. The presented knowledge has the potential to open the door for a different interpretation of past, current, and future observations in dental implant science. From a clinical standpoint, it seems recommendable to react as rapidly as possible when facing peri-implant bone loss, trying to reestablish a foreign body equilibrium if with some bone resorption.
在过去几十年中,范式发生了渐进性转变,将身体植入物作为惰性生物材料的概念,替换为与宿主进行免疫调节相互作用的概念。
本文旨在尝试理解目前关于控制植入物与宿主相互作用的愈合机制的知识,从而也从免疫学角度解释骨结合以及种植体周围骨丢失现象。
本文采用叙述性综述方法撰写。
骨结合实际上代表了对生物材料的异物反应(FBR),是一个免疫调节、多因素且复杂的愈合过程,涉及多种细胞和介质。骨结合的形成似乎是一个由免疫和炎症驱动的过程,其最终目的是屏蔽体内放置的异物,该过程由表面蛋白吸附、补体激活以及纤维蛋白基质的形成引发,随后募集粒细胞、间充质干细胞和单核细胞/巨噬细胞,其中后者在很大程度上控制长期反应,并进一步融合形成异物巨细胞(FBGC),而骨细胞形成并重塑羟基磷灰石。上述过程导致了我们称为骨结合并用于临床目的的异物反应。然而,长期临床功能取决于异物平衡,如果这种平衡受到干扰,可能会导致植入物临床功能受损,这一破坏过程中巨噬细胞会再次被激活并可能进一步融合形成数量更多的FBGC,导致骨吸收开始——这是由于不同来源的破骨细胞等细胞,甚至可能是巨噬细胞降解的骨量超过成骨细胞形成的骨量——以及黏膜封闭破裂,其机制复杂,有待进一步了解。感染可能作为继发事件发生,使临床情况更加复杂。植入物可能会失败。
牙科在接触身体组织时,仍需接受生物材料具有愈合和免疫调节作用这一概念。本文所呈现的知识有可能为牙科种植科学中过去、当前和未来的观察结果提供不同的解释。从临床角度来看,面对种植体周围骨丢失时,似乎建议尽快做出反应,若存在一定骨吸收,尝试重新建立异物平衡。