Microbiological Profile and Human Immune Response Associated with Peri‐Implantitis: A Systematic Review

Abstract

Purpose To evaluate and synthesize the existing evidence on the microbiological and human immune response associated with peri‐implantitis in comparison to healthy implants. Materials and methods Three electronic databases (MEDLINE, Embase, and Cochrane Library) were searched in October 2019 to identify clinical studies evaluating the microbiota and the immune response associated with peri‐implantitis. Two reviewers independently screened the studies and used the full text to extract the data. A qualitative synthesis was performed on the extracted data and summary tables were prepared. Due to clinical and methodological heterogeneity among included studies, no meta‐analysis was performed. Results Forty studies were included in this review. Of these, 20 studies compared the microbiological profile of peri‐implantitis with healthy implants. Nineteen studies focused on the immune response associated with peri‐implantitis in comparison to healthy implants. Three studies focus on gene polymorphism associated with peri‐implantitis. The most commonly reported bacteria associated with peri‐implantitis were obligate anaerobe Gram‐negative bacteria (OAGNB), asaccharolytic anaerobic Gram‐positive rods (AAGPRs), and other Gram‐positive species. In regard to immune response, the most frequently reported pro‐inflammatory mediators associated with peri‐implantitis were IL‐1β, IL‐6, IL‐17, TNF‐α. Osteolytic mediator, e.g., RANK, RANKL, Wnt5a and proteinase enzymes, MMP‐2, MMP‐9, and Cathepsin‐K were also expressed at higher level in peri‐implantitis sites compared to control. Conclusions Peri‐implantitis is associated with complex and different microbiota than healthy implants including bacteria, archaea, fungi, and virus. This difference in the microbiota could provoke higher inflammatory response and osteolytic activity. All of this could contribute to the physiopathology of peri‐implantitis.

The Impact of Peri-Implantitis on Systemic Diseases and Conditions: A Review of the Literature

“…e microbiological and inflammatory pattern of periimplantitis is the representation of a host immune response, which is characterized by the expression of proinflammatory mediators which are similar to those expressed by periodontitis, namely, IL-1β, IL-6, IL-17, and TNF-a, and mediators of osteolysis which are RANK, RANKL, Wnt5a and proteinase enzymes, MMP-2, MMP-9, and cathepsin K [19].…”

“…All the above-described features of peri-implantitis lesions could be the representation of a more intense inflammatory response around dental implants than around teeth, and inflamed tissue is less “anatomically confined.” [ 17 ] Another paper confirmed such outcomes, also reporting that peri-implantitis lesions showed more neutrophils, macrophages, and other inflammatory cells than periodontitis lesions [ 18 ]. The microbiological and inflammatory pattern of peri-implantitis is the representation of a host immune response, which is characterized by the expression of proinflammatory mediators which are similar to those expressed by periodontitis, namely, IL-1 β , IL-6, IL-17, and TNF-a, and mediators of osteolysis which are RANK, RANKL, Wnt5a and proteinase enzymes, MMP-2, MMP-9, and cathepsin K [ 19 ].…”

Oral Osteomicrobiology: The Role of Oral Microbiota in Alveolar Bone Homeostasis

“…Microbial diversity and richness vary during peri-implantitis. The microbes most associated with peri-implantitis are obligate anaerobe Gram-negative bacteria, asaccharolytic anaerobic Gram-positive rods, and other Gram-positive species ( Kensara et al., 2021 ). The peri-implantitis microbiome is commensal-depleted and pathogen-enriched, with an abundance of Porphyromonas and Treponema ( Sanz-Martin et al., 2017 ) sp.…”

“…The most frequently reported pro-inflammatory mediators associated with peri-implantitis are interleukin (IL)-1β, IL-6, IL-17, and tumor necrosis factor‐α (TNF-α). Osteolytic mediators such as receptor of NF-κB, RANKL, and Wnt5a, as well as proteinases such as matrix metalloproteinase-2, matrix metalloproteinase-9, and cathepsin-K are also reportedly upregulated in peri-implantitis sites compared to controls ( Kensara et al., 2021 ). It is worth noting that implants have an impact on remote periodontal sites, as elevated inflammation and accelerated bone loss have been detected in intact, distant teeth ( Heyman et al., 2020 ).…”

“…Patients with periodontitis have been shown to have an upregulated expression of RANKL in periodontal tissue, and the level of RANKL was highly correlated with the severity of periodontitis ( Nagasawa et al., 2007 ); moreover, periodontitis-induced alveolar bone loss and osteoclast differentiation were markedly suppressed in RANKL-deficient mice ( Tsukasaki et al., 2018 ). RANKL is also reportedly upregulated in periapical lesions and peri-implantitis sites ( Duka et al., 2019 ; Kensara et al., 2021 ). It is also worth noting that OPG-knockout mice spontaneously developed severe alveolar bone loss, suggesting that not only the upregulation of RANKL, but also the downregulation and/or degradation of OPG is involved in periodontal bone loss ( Koide et al., 2013 ).…”