Could cytokine levels in the peri‐implant crevicular fluid be used to distinguish between healthy implants and implants with peri‐implantitis? A systematic review

Duarte, Poliana Mendes; Serrão, Caroline Ribeiro; Miranda, Tamires Szeremeske; Zanatta, Luiz Carlos Silveira; Bastos, Marta Ferreira; Faveri, Marcelo; Figueiredo, Luciene Cristina; Feres, Magda

doi:10.1111/jre.12354

Cited by 107 publications

(128 citation statements)

References 31 publications

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“…20,21 Increased expression of these proinflammatory cytokines have also been detected in the PISF of patients with peri-implantitis. 22,23 Furthermore, findings from a recent meta-analysis showed that tobacco smoking impairs new bone formation around dental implants and jeopardizes bone-to-implant contact. 24 Nicotine in tobacco smoke has been reported to reduce the cellular healing response and increase the levels of the oral bacterial count (a potential risk factor that may lead to peri-implantitis) in CS.…”

Section: Discussionmentioning

confidence: 99%

Clinical and radiographic peri‐implant parameters and proinflammatory cytokine levels among cigarette smokers, smokeless tobacco users, and nontobacco users

Akram

Vohra

Bukhari

et al. 2017

Clin Implant Dent Rel Res

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Section: Discussionmentioning

confidence: 99%

Clinical and radiographic peri‐implant parameters and proinflammatory cytokine levels among cigarette smokers, smokeless tobacco users, and nontobacco users

Akram

Vohra

Bukhari

et al. 2017

Clin Implant Dent Rel Res

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“…In their systematic review, Duarte et al (2016) [47] investigated whether the levels of crevicular fluid cytokines could be used to distinguish between healthy implants and peri-implantitis. The authors noted that most studies found no significant differences in the levels of anti-inflammatory cytokines (such as IL-10) and RANKL between healthy implants and implants with peri-implantitis.…”

Section: Discussionmentioning

confidence: 99%

Polymorphisms of Il-10 (-1082) and RANKL (-438) Genes and the Failure of Dental Implants

Ribeiro

Melo

Neto

et al. 2017

International Journal of Dentistry

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Background. Genetic polymorphisms in certain cytokines and chemokines have been investigated to understand why some individuals display implant flaws despite having few risk factors at the time of implant. Purpose. To investigate the association of genetic polymorphisms in interleukin- (IL-) 10 [-1082 region (A/G)] and RANKL [-438 region (A/G)] with the failure of dental implants. Materials and Methods. This study included 90 partially edentulous male and female patients who were rehabilitated with a total of 245 Straumann dental implants. An implant was considered a failure if any of the following occurred: mobility, persistent subjective complaint, recurrent peri-implant infection with suppuration, continuous radiolucency around the implant, probing depth ≥ 5 mm, and bleeding on probing. Buccal mucosal cells were collected for analysis of RANKL438 and IL-10. Results. The implant success rate in this population was 34.4%. The mutant allele (G) in RANKL had an incidence of 52.3% and mutant allele (A) in IL-10 was observed in 37.8%. No statistically significant difference was detected between the failure of the implant and the genotypes and allelic frequencies. Conclusion. No association was detected between the genetic polymorphisms of RANKL (-438) and IL-10 (-1082) and the failure of dental implants in the population studied.

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“…Analysis of the peri-implant crevicular fluid (PICF) composition from diseased and healthy implants concerning pro- and anti-inflammatory cytokines, matrix metalloproteinases, matrix proteins and bone turnover markers have been providing relevant information on the activity of local bone cells in an attempt to understand the mechanisms leading to the induced alveolar bone loss in peri-implantitis [43,51]. Although a number of methodological limitations arises, a variety of studies shows increased levels of the pro-inflammatory cytokines IL-1β, IL-6, IL-17, TNF-α, IL-12, but especially IL-1β, in the PICF of implants with peri-implantitis, when compared with healthy implants [52-62].…”

Section: Bone Cells Activity During Peri-implantitismentioning

confidence: 99%

“…However, as stressed on a recent systematic review [51] that compared the PICF levels of these markers in healthy and diseased implants, the available information is mostly concerned with few classical pro-inflammatory markers and, more recently, with factors relevant on the osteoblast/osteoclast interaction. The comparison of several important cytokines involved in innate, T-helper and T-regulatory responses, such as IFN-γ, IL-23, IL-2, IL-11, TGF-β, macrophage inflammatory proteins, G-CSF, GM-CSF has never been properly performed [51]. Also, not much data is available regarding the bone cell crosstalk and also the interplay between immune and bone cells in the context of the peri-implantitis.…”

Section: Bone Cells Activity During Peri-implantitismentioning

confidence: 99%

Bone Cells Dynamics during Peri-Implantitis: a Theoretical Analysis

Fernandes¹,

Gomes

2016

JOMR

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ObjectivesThe present manuscript aims a detailed characterization of the bone cells dynamics during physiological bone remodelling and, subsequently, to address the cellular and molecular mechanisms that play a fundamental role in the immune-inflammatory-induced uncoupled bone remodelling observed in peri-implantitis.ResultsAn intimate relationship between the immune system and bone is acknowledged to be determinant for bone tissue remodelling and integrity. Due to the close interaction of immune and bone cells, the two systems share a number of surface receptors, cytokines, signalling pathways and transcription factors that are involved in mutual regulatory mechanisms. This physiological equilibrium is disturbed in pathological conditions, as verified in peri-implantitis establishment and development. Activation of the innate and adaptive immune response, challenged by the local bacterial infection, induces the synthesis of high levels of a variety of pro- and anti-inflammatory cytokines that disturb the normal functioning of the bone cells, by uncoupling bone resorption and formation, ending up with a net alveolar bone loss and subsequent implant failure. Most data points to an immune-inflammatory induced osteoclast differentiation and function, as the major underlying mechanism to the uncoupled bone resorption to bone formation. Further, the disturbed functioning of osteoblasts, reflected by the possible expression of a fibro-osteoblastic phenotype, may also play a role.ConclusionsAlveolar bone loss is a hallmark of peri-implantitis. A great deal of data is still needed on the cellular and humoral crosstalk in the context of an integrated view of the osteoimmunologic interplay occurring in the peri-implantitis environment subjacent to the bone loss outcome.

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Could cytokine levels in the peri‐implant crevicular fluid be used to distinguish between healthy implants and implants with peri‐implantitis? A systematic review

Cited by 107 publications

References 31 publications

Clinical and radiographic peri‐implant parameters and proinflammatory cytokine levels among cigarette smokers, smokeless tobacco users, and nontobacco users

Clinical and radiographic peri‐implant parameters and proinflammatory cytokine levels among cigarette smokers, smokeless tobacco users, and nontobacco users

Polymorphisms of Il-10 (-1082) and RANKL (-438) Genes and the Failure of Dental Implants

Bone Cells Dynamics during Peri-Implantitis: a Theoretical Analysis

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