School of Dentistry, The University of Queensland, Herston, Queensland, Australia.
School of Dentistry, University of Adelaide, Adelaide, South Australia, Australia.
Periodontol 2000. 2022 Oct;90(1):176-185. doi: 10.1111/prd.12456. Epub 2022 Aug 2.
Historically, there has been broad consensus that osseointegration represents a homeostasis between a titanium dental implant and the surrounding bone, and that the crestal bone loss characteristic of peri-implantitis is a plaque-induced inflammatory process. However, this notion has been challenged over the past decade by proponents of a theory that considers osseointegration an inflammatory process characterized by a foreign body reaction and peri-implant bone loss as an exacerbation of this inflammatory response. A key difference in these two schools of thought is the perception of the relative importance of dental plaque in the pathogenesis of crestal bone loss around implants, with obvious implications for treatment. This review investigates the evidence for a persistent foreign body reaction at osseointegrated dental implants and its possible role in crestal bone loss characteristic of peri-implantitis. Further, the role of implant-related material release within the surrounding tissue, particularly titanium particles and corrosion by-products, in the establishment and progression in peri-implantitis is explored. While it is acknowledged that these issues require further investigation, the available evidence suggests that osseointegration is a state of homeostasis between the titanium implant and surrounding tissues, with little evidence that a persistent foreign body reaction is responsible for peri-implant bone loss after osseointegration is established. Further, there is a lack of evidence for a unidirectional causative role of corrosion by-products and titanium particles as possible non-plaque related factors in the etiology of peri-implantitis.
从历史上看,人们广泛认为骨整合代表了钛牙科种植体与周围骨骼之间的一种动态平衡,而种植体周围炎特征性的牙槽骨丧失是一种由菌斑引起的炎症过程。然而,在过去的十年中,一种理论的支持者对这一观点提出了挑战,该理论认为骨整合是一种炎症过程,其特征是异物反应,种植体周围骨丧失是这种炎症反应的加剧。这两种观点的一个关键区别在于对牙菌斑在种植体周围牙槽骨丧失发病机制中的相对重要性的看法,这对治疗有明显的影响。本综述调查了在骨整合的牙科种植体上持续存在异物反应的证据及其在种植体周围炎特征性的牙槽骨丧失中的可能作用。此外,还探讨了植入物相关材料在周围组织中的释放,特别是钛颗粒和腐蚀产物,在种植体周围炎的建立和进展中的作用。虽然人们承认这些问题需要进一步研究,但现有证据表明,骨整合是钛植入物与周围组织之间的一种动态平衡状态,几乎没有证据表明在骨整合建立后,持续的异物反应是导致种植体周围骨丧失的原因。此外,缺乏证据表明腐蚀产物和钛颗粒作为可能与菌斑无关的因素在种植体周围炎发病机制中的单向因果作用。