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Can Peri‐Implant Crevicular Fluid Assist in the Diagnosis of Peri‐Implantitis? A Systematic Review and Meta‐Analysis
Author(s) -
Faot Fernanda,
Nascimento Gustavo G.,
Bielemann Amália M.,
Campão Thiago D.,
Leite Fábio R. M.,
Quirynen Marc
Publication year - 2015
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2015.140603
Subject(s) - peri implantitis , medicine , implant , peri , tumor necrosis factor alpha , cytokine , meta analysis , mucositis , immune system , systematic review , gastroenterology , dentistry , immunology , surgery , medline , biology , chemotherapy , biochemistry
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.