Foreign Body Reaction to Biomaterials: On Mechanisms for Buildup and Breakdown of Osseointegration

骨整合 骨免疫学 异物 植入 异物巨细胞 免疫系统 细胞生物学 化学 免疫学 生物医学工程 牙科 医学 病理 生物 外科 兰克尔 激活剂(遗传学) 基因 生物化学
作者
Ricardo Trindade,Tomas Albrektsson,Pentti Tengvall,Ann Wennerberg
出处
期刊:Clinical Implant Dentistry and Related Research [Wiley]
卷期号:18 (1): 192-203 被引量:379
标识
DOI:10.1111/cid.12274
摘要

Abstract Background 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. Purpose 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. Materials and Methods A narrative review approach was taken in the development of this article. Results 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 FBGC s, 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. Conclusions 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.
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