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Can Peri-Implant Crevicular Fluid Assist in the Diagnosis of Peri-Implantitis? A Systematic Review and Meta-Analysis

  • Autores: Fernanda Faot, Gustavo G. Nascimento, Amália M. Bielemann, Thiago D. Campão, Fábio Renato Manzolli Leite, Marc Quirynen
  • Localización: Journal of periodontology, ISSN 0022-3492, Vol. 86, Nº. 5, 2015, págs. 631-645
  • Idioma: inglés
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  • Resumen
    • Background: A broader understanding of the immune inflammatory profile of peri-implant diseases could be helpful in the development of host-targeted preventive and therapeutic strategies. The aim of this study is to answer two clinical questions: 1) whether patients with peri-implantitis (PP) present higher prevalence of any specific inflammatory cytokine in peri-implant crevicular fluid (PICF) compared with healthy patients; and 2) whether local inflammation measured in PICF can be used as a predictor for incipient PP.

      Methods: A systematic review of the literature on the most common cytokines released in PICF in healthy and PP-affected sites was conducted from 1996 up to and including October 2013 using predefined search strategies. Cross-sectional and prospective longitudinal studies were considered. Meta-analyses were done separately for healthy, mucositis (MU), and PP outcomes.

      Results: Interleukin (IL)-1β was the most studied cytokine (n = 12), followed by tumor necrosis factor (TNF)-α (n = 10). Other cytokines were also linked to PP, such as IL-4, IL-6, IL-8, IL-10, IL-12, and IL-17. Statistical differences were revealed when IL-1β release was compared between healthy implant sites and PP (P = 0.001) or MU sites (P = 0.002), respectively; when PP and MU were compared, no statistical differences could be detected (P = 0.80). For TNF-α release, significant differences were found between healthy and PP implants (P = 0.02).

      Conclusions: PICF containing inflammatory mediators, such as IL-1β and TNF-α, can be used as additional criteria for a more robust diagnosis of peri-implant infection. Additionally, once the inflammatory process is installed, no differences were found between peri-implant MU and PP.

      Peri-implantitis (PP) is the result of an interplay between a bacterial challenge to the implant-bearing tissues and the host immune response. It is speculated that the onset, severity, and extent of the disease depends on a variety of individual characteristics.1 In addition to oral hygiene and smoking, systemic conditions, such as immune-mediated diseases, diabetes, and obesity, are key factors for progressive peri-implant tissue breakdown.

      The expression of proinflammatory mediators, such as cytokines, chemokines, and matrix metalloproteinases, has been studied, but the intracellular signaling pathways associated with each of them is complex.2 Proinflammatory cytokines, i.e., interleukin (IL)-1β and tumor necrosis factor (TNF)-α, have been explored as biochemical markers of peri-implant disease in clinical studies because of their noticeably elevated concentration in crevicular fluid from diseased sites.3,4 Periodontal tissue inflammation via the biofilm starts with a cellular activation through an interaction between bacterial endotoxins (e.g., lipopolysaccharides) and cell receptors (e.g., toll-like receptor-4) and nucleotide-binding oligomerization domain receptors (NOD-like receptors).5,6 A complex activation of multiple intracellular signaling pathways is initiated with subsequent phosphorylation culminating in nuclear transcription of proinflammatory messengers.7 The cytokine network, activated in diseased peri-implant tissue, is complex because of the overlapping role of many cytokines and is subject to shifts depending on disease activity.7 Considering this complexity, it is important to comprehend the signaling pathways involved in cytokine expression in peri-implant diseases to design new approaches to modulate the host response affecting the whole cytokine profile.

      Different research groups have explored the cytokines expressed in peri-implant pockets.3,4,8,9 Attempts were made to categorize these cytokines into T-helper (Th) 1-type and Th2-type profiles.10 Presently, it is known that the cytokine profile in PP includes Th1- and Th2-type responses.4 The cytokine profile in inflamed periodontal tissue might be similar for peri-implant tissue.11,12 Up to now, a profound analysis of the studies performed to evaluate the main cytokines in crevicular fluid of individuals with peri-implant diseases has not been performed. A broader understanding of the immune inflammatory profile of peri-implant diseases could be helpful in the development of host-targeted preventive and therapeutic strategies. Two critical reviews exploring this topic were conducted previously and suggested the potential role of peri-implant crevicular fluid (PICF) as an additional PP diagnostic.12,13 However, both reviews did not follow any protocol for a systematic review, nor did they even present meta-analyses. Their work is expanded here by providing, to the best of the authors’ knowledge, the first systematic review that compares the inflammatory profile of PICF in individuals with peri-implant diseases with healthy individuals.

      Hence, considering the absence of strong evidence exploring the relation between levels of inflammatory cytokines in PICF and peri-implant diseases, this study aims to review systematically the current evidence on the topic and summarize the studies that directly assessed the levels of the cytokines in PICF of individuals with peri-implant diseases.


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