interleukin-8 and Peri-Implantitis

A study is made of the usefulness of cytokines (such as interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-10 (IL-10) and interleukin-12 (IL-12)) as markers of periimplant disease (mucositis and periimplantitis). An increase in the levels of these cytokines in dental implant crevicular fluid may give rise to a lack of osteointegration, bone loss or implant failure.. To review the literature relating IL-6, IL-8, IL-10 and IL-12 levels to dental implant surgery and periimplantitis.. A PubMed literature search was made of articles in English and Spanish, using the key words "cytokine and dental implants", cytokine and periimplantitis", "IL-6, IL-8, IL-10, IL-12 and dental implants", "IL-6, IL-8, IL-10, IL-12 and periimplantitis". Fourteen articles were found and classified into two groups relating interleukin levels to: a) periimplant disease; and b) their influence upon dental implant osteointegration without periimplant disease.. An increase in interleukin levels is observed in patients with periimplant disease, though there is controversy over the effect of interleukins in crevicular fluid and periimplantitis in relation to implant failure or the development of periimplant disease.

Topics: Biomarkers; Humans; Interleukin-10; Interleukin-12; Interleukin-6; Interleukin-8; Peri-Implantitis

To investigate expression of gene markers for the plasminogen system, inflammation, and bone resorption/remodelling in peri-implant crevicular fluid samples from healthy subjects, subjects with mucositis and subjects with peri-implantitis. A possible inhibitory effect of suppuration on the analysis of gene expression in samples from subjects with peri-implantitis was also analysed.. Peri-implant crevicular fluid (PICF) was sampled from 25 healthy subjects (H), 25 subjects with mucositis (M) and 25 subjects with peri-implantitis (P) using paper points and suction tips. The samples were analysed by quantitative polymerase chain reaction (qPCR). The following biomarkers associated with the plasminogen system, inflammation and bone resorption/ remodelling were investigated: interleukin-1 beta (IL-1β), interleukin 8 (IL-8), tissue plasminogen activator (tPA), plasminogen activator inhibitor 2 (PAI-2), tartrate-resistant acid phosphatase (TRAP) and cathepsin K (CatK).. IL-1β and IL-8 were significantly upregulated in the P group, and tPA and PAI-2 were significantly upregulated in the M group. These four genetic markers were oppositely regulated in samples from the subjects in the mucositis compared with the peri-implantitis group. TRAP and CatK showed no differences between the groups. The presence of suppuration did not have a detectable effect on gene analysis in samples from subjects with peri-implantitis.. Markers for the plasminogen system and inflammation could be used to distinguish between mucositis and peri-implantitis. The results suggested that the plasminogen system was sufficiently upregulated allowing for resolution of inflammation and healing at the inflamed implant site in subjects with mucositis, whereas such upregulation was insufficient resulting in impaired healing and prolonged inflammation in subjects with peri-implantitis. The combination of tissue inflammation and low levels of tPA was a strong predictor of marginal bone loss in this study. It may be an interesting candidate for the unambiguous diagnosis of mucositis and peri-implantitis independent of radiographs and could possibly constitute a powerful future tool for rapid assessment of the periimplant tissue condition and the effect of subject treatment.

Topics: Acid Phosphatase; Adult; Aged; Aged, 80 and over; Biomarkers; Bone Remodeling; Bone Resorption; Cathepsin K; Cross-Sectional Studies; Dental Implants; Female; Gingival Crevicular Fluid; Humans; Interleukin-1beta; Interleukin-8; Isoenzymes; Male; Middle Aged; Peri-Implantitis; Plasminogen; Plasminogen Activator Inhibitor 2; Serine Proteinase Inhibitors; Stomatitis; Suppuration; Tartrate-Resistant Acid Phosphatase; Tissue Plasminogen Activator

Our aim was to examine the effect of titanium particles and lipopolysaccharide (LPS) from P. gingivalis on the inflammatory profile expression of human gingival fibroblasts (hGFs), cultured on rough titanium discs, in an in vitro peri-implantitis simulation.. Human gingival fibroblasts cultured on SLA and TCP surfaces were challenged with LPS, titanium particles or both. At 24, 48 and 72 h after treatment, MTT assay was performed to assess cell proliferation. FDA/PI staining was performed for the same time periods, in order to evaluate cell viability/apoptosis. At 5 and 7 days after the treatment, qPCR was performed to assess gene expressions of IL-6, IL-8 and COL1A1, as well as SEM on titanium discs.. All groups presented a significant increase of their population between the time periods of examination. Regarding the interleukin gene expression, the combination of LPS and particles significantly increased the levels of Interleukin-8. Treatment with LPS and particles also induced a significant increase of Interleukin-6 and collagen. FDA/PI microscopy has revealed several apoptotic cells in the treatment groups. SEM micrographs have shown the difficulty of hGFs to adhere on rough surfaces.. The combination of titanium particles and LPS significantly upregulated the expression of IL-6, IL-8 and Col-1a. It appears that particles may arouse similar reactions to the endotoxin, while synergistically intensifying it.

Topics: Cells, Cultured; Fibroblasts; Gingiva; Humans; Interleukin-6; Interleukin-8; Lipopolysaccharides; Peri-Implantitis; Porphyromonas gingivalis; Titanium

To investigate the pro-inflammatory cytokine profiles in patients with or without cardiovascular disease (CVD) and with or without peri-implantitis.. Serum, peri-implant crevicular fluid (PICF), and gingival crevicular fluid (GCF) were collected from patients with (n = 82) or without CVD (n = 46) at the most severe peri-implantitis site including sites with periodontitis. A panel of proinflammatory molecules including high-sensitivity C-reactive protein (hsCRP), fibrinogen, interleukin-1 beta (IL-1β), IL-6, plasma tumor necrosis factor-alpha (TNF-α), matrix metallo-proteinase-8 (MMP-8), osteoprotegerin (OPG), vascular endothelial growth factor (VEGF), IL-17, IL-8, tissue inhibitor of metalloproteinase-2 (TIMP-2), myeloperoxidase (MPO), and prostaglandin E. Serum IL-1β, TNF-α and fibrinogen were significantly higher in CVD patients than those without. Serum fibrinogen displayed a trend of higher concentration in patients with radiographic bone loss (RBL) ≥2 mm (P = 0.08). PICF TNF-α exhibited a significantly higher detection level in the CVD patients that is coincided with the local peri-implant inflammation. In addition, PICF MMP-8 was significantly higher in the RBL ≥2 mm sites than the healthy implants; whereas IL-1β, IL-8, MMP-8, and TIMP-2 proved to be the significant predictors for peri-implant disease. GCF TNF-α collected from patients with periodontitis was significantly associated with CVD cases.. The augmented expression of local and systemic pro-inflammatory cytokines found in the current study supports the weak association between the chronic peri-implantitis with increasing severity and CVD.

Topics: Cardiovascular Diseases; Dental Implants; Fibrinogen; Gingival Crevicular Fluid; Humans; Interleukin-8; Matrix Metalloproteinase 8; Peri-Implantitis; Periodontitis; Tissue Inhibitor of Metalloproteinase-2; Tumor Necrosis Factor-alpha; Vascular Endothelial Growth Factor A

Peri-implant mucositis and peri-implantitis cases increase in number with the increase of implant applications. Peri-implant mucositis and peri-implantitis are defined as inflammatory diseases with inflammation and loss in soft and hard tissue, similar to the other periodontal diseases. As observed in many diseases, genetic predisposition factors also affect the progress of periodontitis and peri-implantitis.. This study examines if there is any solid genetic predisposition causing periodontitis and peri-implantitis formation in Turkish patients.. In order to evaluate single nucleotide polymorphism (SNP), Interleukin-8 (IL-8) and N-formyl-L-methionyl-L-leucyl-phenylalanine (fMLP), playing a role in the chemotaxis of neutrophils, and Fc Gamma Receptor IIA (FcγRIIA) and Fc Gamma Receptor IIIA (FcγRIIIA), playing a role in the antigen-antibody complexes and phagocytosis, were selected. Thirty-two Turkish non-smoking subjects, having periodontitis, thirty-three Turkish non-smoking subjects, having peri-implantitis and thirty-three Turkish non-smoking healthy subjects were selected. In total 98 adults participated in our study. Collected saliva samples from the participants were used for DNA isolation. SNPs were determined in these subgroups of the study by means of genotype-specific polymerase chain reactions.. When IL-8 A-251T, FcγRIIa -H131 and FcγRIIIa -V158 polymorphism were evaluated, no significant difference was found between periodontitis, peri-implantitis and healthy groups. However, this study observed that fMLP Receptor (FPR1) gene polymorphism creates a significant difference in individuals at higher risk of periodontitis or peri-implantitis.. Results show that individuals with the G genotype have a higher risk of periodontitis, while individuals with G / C genotype have higher risk of peri-implantitis.

Topics: Adult; Genetic Predisposition to Disease; Humans; Interleukin-8; Mucositis; Peri-Implantitis; Periodontitis; Polymorphism, Single Nucleotide

The impact of oral commensal and pathogenic bacteria on peri-implant mucosa is not well understood, despite the high prevalence of peri-implant infections. Hence, we investigated responses of the peri-implant mucosa to Streptococcus oralis or Aggregatibacter actinomycetemcomitans biofilms using a novel in vitro peri-implant mucosa-biofilm model. Our 3D model combined three components, organotypic oral mucosa, implant material, and oral biofilm, with structural assembly close to native situation. S. oralis induced a protective stress response in the peri-implant mucosa through upregulation of heat shock protein (HSP70) genes. Attenuated inflammatory response was indicated by reduced cytokine levels of interleukin-6 (IL-6), interleukin-8 (CXCL8), and monocyte chemoattractant protein-1 (CCL2). The inflammatory balance was preserved through increased levels of tumor necrosis factor-alpha (TNF-α). A. actinomycetemcomitans induced downregulation of genes important for cell survival and host inflammatory response. The reduced cytokine levels of chemokine ligand 1 (CXCL1), CXCL8, and CCL2 also indicated a diminished inflammatory response. The induced immune balance by S. oralis may support oral health, whereas the reduced inflammatory response to A. actinomycetemcomitans may provide colonisation advantage and facilitate later tissue invasion. The comprehensive characterisation of peri-implant mucosa-biofilm interactions using our 3D model can provide new knowledge to improve strategies for prevention and therapy of peri-implant disease.

Topics: Aggregatibacter actinomycetemcomitans; Biofilms; Cells, Cultured; Chemokine CCL2; Dental Implants; HSP70 Heat-Shock Proteins; Humans; Interleukin-6; Interleukin-8; Models, Immunological; Mouth Mucosa; Peri-Implantitis; Prosthesis-Related Infections; Streptococcus oralis; Titanium; Tumor Necrosis Factor-alpha

Porphyromonas gingivalis and Tannerella forsythia secrete proteases, gingipains and KLIKK-proteases. In addition, T. forsythia produces a serpin (miropin) with broad inhibitory spectrum. The aim of this pilot study was to determine the level of expression of miropin and individual proteases in vivo in periodontal and peri-implant health and disease conditions. Biofilm and gingival crevicular fluid (GCF)/ peri-implant sulcular fluid (PISF) samples were taken from healthy tooth and implant sites (n = 10), gingivitis and mucositis sites (n = 12), and periodontitis and peri-implantitis sites (n = 10). Concentration of interleukin-8 (IL-8), IL-1β and IL-10 in GCF was determined by enzyme-linked immunosorbent assay. Loads of P. gingivalis and T. forsythia and the presence of proteases and miropin genes were assessed in biofilm by quantitative PCR, whereas gene expression was estimated by quantitative RT-PCR. The presence of P. gingivalis and T. forsythia, as well as the level of IL-8 and IL-1β, were associated with disease severity in the periodontal and peri-implant tissues. In biofilm samples harboring T. forsythia, genes encoding proteases were found to be present at 72.4% for karilysin and 100% for other KLIKK-protease genes and miropin. At the same time, detectable mRNA expression of individual genes ranged from 20.7% to 58.6% of samples (for forsylisin and miropsin-1, respectively). In comparison with the T. forsythia proteases, miropin and the gingipains were highly expressed. The level of expression of gingipains was associated with those of miropin and certain T. forsythia proteases around teeth but not implants. Cumulatively, KLIKK-proteases and especially miropin, might play a role in pathogenesis of both periodontal and peri-implant diseases.

Topics: Bacterial Proteins; Biofilms; Biomarkers; Dental Implants; Gene Expression Regulation, Bacterial; Genes, Bacterial; Gingival Crevicular Fluid; Gingivitis; Humans; Interleukin-10; Interleukin-1beta; Interleukin-8; Mucositis; Peptide Hydrolases; Peri-Implantitis; Periodontitis; Pilot Projects; Porphyromonas gingivalis; Protease Inhibitors; RNA, Messenger; Serpins; Sweden; Tannerella forsythia

This study evaluated the presence of cytokines (IL-1

Topics: Adult; Case-Control Studies; Cytokines; Cytomegalovirus; Female; Healthy Volunteers; Herpesvirus 1, Human; Herpesvirus 2, Human; Herpesvirus 3, Human; Herpesvirus 4, Human; Herpesvirus 6, Human; Herpesvirus 8, Human; Humans; Interleukin-1beta; Interleukin-8; Male; Middle Aged; Peri-Implantitis; Saliva; Tumor Necrosis Factor-alpha; Viral Envelope Proteins

The roles of toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-κB) in peri-implantitis are unclear. Here, we used a canine model of peri-implantitis to explore the effects of inhibiting NF-κB with pyrrolidine dithiocarbamate (PDTC) on the inflammatory response in ligature-induced peri-implantitis.. After successfully establishing the peri-implantitis model, beagles were randomly assigned to normal, model or PDTC groups. ELISA tests were used to determine the levels of interleukin (IL)-1, IL-6, IL-8 and tumor necrosis factor alpha (TNF-α). Immunohistochemistry was employed to assess the expression of NF-κB p65. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to determine the mRNA levels of TLR4 and NF-κB p65, and western blot analysis was used to measure the protein levels of TLR4 in periodontal tissues from each group. Periodontal ligament fibroblasts (PDLFs) were cultured and subsequently classified into PDLF normal, PDLF model, PDLF LPS, PDLF PDTC, and PDLF LPS + PDTC groups. An immunofluorescence assay was used to measure the expression level of NF-κB p65. The CCK-8 assay and flow cytometry were performed to evaluate cell proliferation and apoptosis.. The in vitro results indicated that NF-κB p65 and TLR4 were upregulated in canine periodontal tissues, and PDTC could suppress the expression levels of NF-κB p65 and TLR4. Inflammation could increase TLR4 protein expression in canine periodontal tissue, and PDTC could inhibit the inflammation-induced increase in TLR4 protein expression. These results revealed that PDTC could reverse the LPS-induced increases in the levels of IL-1, IL-6, IL-8 and TNF-α. In vivo, the results demonstrated that PDTC inhibited the LPS-induced NF-κB p65 upregulation, and PDTC could reverse the inhibitory effect of the PDLF model + LPS on the proliferation of periodontal fibroblasts. The results also showed that in the PDLF model, LPS promoted PDLF apoptosis by inducing implant periodontitis in canines, but PDTC inhibited the PDLF apoptosis and relieved implant periodontitis in canines.. Based on our results, we concluded that PDTC can inhibit the expression of NF-κB and alleviate the inflammatory response induced by LPS, thereby preventing periodontal inflammation and reducing the development of peri-implantitis.

Topics: Animals; Cell Cycle Checkpoints; Cell Proliferation; Cells, Cultured; Dogs; Fibroblasts; Interleukin-1beta; Interleukin-6; Interleukin-8; Lipopolysaccharides; NF-kappa B; Peri-Implantitis; Periodontium; Pyrrolidines; Thiocarbamates; Toll-Like Receptor 4; Transcription Factor RelA; Tumor Necrosis Factor-alpha; Up-Regulation

The aim of the present study was to investigate how heavy smoking influences the clinical, microbiological, and host-response characteristics in peri-implant sulcus fluid of patients with healthy dental implants.. A total of 29 individuals with 74 dental implants were included in the present study; 20 implants were in heavy smokers and 54 were in non-smokers. The modified gingival index, modified plaque index, and probing pocket depth were evaluated. Periodontopathogenic bacteria Tannerella forsythia, Treponema denticola, and Porphyromonas gingivalis were evaluated, together with the total bacterial load. Peri-implant sulcus fluid samples were analyzed for the quantification of interleukin-8, interleukin-1β, interleukin-6, interleukin-10, and tumor necrosis factor-α.. No significant differences in the clinical parameters evaluated were found between the groups, although smokers had poorer peri-implant parameters. Among the smokers, subgingival microbiota was composed of a greater number of periodontal pathogens; these differences were not statistically significant. Smokers showed a greater expression of interleukin-1β, interleukin-6, interleukin-10, and tumor necrosis factor-α, but interleukin-8 was slightly higher among non-smokers, but not significantly.. Although smokers presented deeper probing depths, bleeding on probing, and peri-implant microbiota composed of a greater number of periodontal pathogens than in non-smoking patients, these data did not show significant differences. In the present study, and in relation to the samples analyzed, smoking alone did not influence the immunological and microbiological parameters in dental implants with healthy peri-implant tissues. Further studies with larger samples are required to better evaluate the influence of smoking on dental implants.

Topics: Aged; Bacterial Load; Cross-Sectional Studies; Cytokines; Dental Implants; Dental Plaque Index; Dental Prosthesis, Implant-Supported; Female; Gingival Crevicular Fluid; Humans; Interleukin-10; Interleukin-1beta; Interleukin-6; Interleukin-8; Male; Middle Aged; Peri-Implantitis; Periodontal Index; Periodontal Pocket; Porphyromonas gingivalis; Prospective Studies; Smoking; Spain; Tannerella forsythia; Treponema denticola; Tumor Necrosis Factor-alpha

Dental implants are one of the most frequently used treatment options for tooth replacement. Approximately 30% of patients with dental implants develop peri-implantitis, which is an oral inflammatory disease that leads to loss of the supporting tissues, predominately the bone. For the development of future therapeutic strategies, it is essential to understand the molecular pathophysiology of human dental peri-implant infections. Here, we describe the gene and protein expression patterns of peri-implantitis bone tissue compared with healthy peri-implant bone tissue. Furthermore, cells from the osteoblastic lineage derived from peri-implantitis samples were immortalized and characterized. We applied microarray, quantitative reverse transcription polymerase chain reaction, fluorescence-activated cell sorting, and Western blot analyses. The levels of typical bone matrix molecules, including SPP1, BGLAP, and COL9A1, in patients with peri-implantitis were reduced, while the inflammation marker interleukin 8 (IL8) was highly expressed. RUNX2, one of the transcription factors of mature osteoblasts, was also decreased in peri-implantitis. Finally, the human telomerase reverse transcriptase immortalized cell line from peri-implantitis exhibited a more fibro-osteoblastic character than did the healthy control.

Topics: Adult; Aged; Alveolar Process; Bone Matrix; Cell Culture Techniques; Cell Line, Transformed; Cell Lineage; Cell Separation; Cell Transformation, Viral; Collagen Type IX; Core Binding Factor Alpha 1 Subunit; Female; Fibroblast Growth Factors; Fibroblasts; Gene Expression Profiling; Humans; Interleukin-8; Male; Middle Aged; Osteoblasts; Osteocalcin; Osteopontin; Peri-Implantitis; PPAR gamma; Telomerase

Due to the world-wide increase in treatments involving implant placement, the incidence of peri-implant disease is increasing. Late implant failure is the result of the inability to maintain osseointegration, whose most important cause is peri-implantitis. The aim of this study was to analyze the clinical, microbiological, and immunological aspects in the peri-implant sulcus fluid (PISF) of patients with healthy dental implants and patients with peri-implantitis.. PISF samples were obtained from 24 peri-implantitis sites and 54 healthy peri-implant sites in this prospective cross-sectional study. The clinical parameters recorded were: modified gingival index (mGI), modified plaque index (mPI) and probing pocket depth (PPD). The periodontopathogenic bacteria Tannerella forsythia, Treponema denticola and Porphyromonas gingivalis were evaluated, together with the total bacterial load (TBL). PISF samples were analyzed for the quantification of Interleukin (IL)-8, IL-1β, IL-6, IL-10 and Tumor Necrosis Factor (TNF)-α using flow cytometry (FACS).. The mGI and PPD scores in the peri-implantitis group were significantly higher than the healthy group (p < 0.001). A total of 61.5% of the patients with peri-implantitis had both arches rehabilitated, compared with 22.7% of patients with healthy peri-implant tissues; there was no implant with peri-implantitis in cases that received mandibular treatment exclusively (p < 0.05). Concentrations of Porphyromonas gingivalis (p < 0.01), association with bacteria Porphyromonas gingivalis and Treponema denticola (p < 0.05), as well as the TBL (p < 0.05) are significantly higher in the peri-implantitis group. IL-1β (p < 0.01), IL-6 (p < 0.01), IL-10 (p < 0.05) and TNF-α (p < 0.01) are significantly higher at the sites with peri-implantitis compared to healthy peri-implant tissue, while IL-8 did not increase significantly.. The results of the present study involving a limited patient sample suggest that the peri-implant microbiota and which dental arch was rehabilitated involved could contribute to bone loss in peri-implantitis. A significant relationship is observed between the concentration of cytokines (interleukins 1β, 6 and 10 and TNF-α) and the inflammatory response in peri-implantitis tissue.

Topics: Aged; Bacterial Load; Bacteroides; Cross-Sectional Studies; Dental Arch; Dental Implants; Dental Plaque Index; Dental Prosthesis, Implant-Supported; Female; Gingival Crevicular Fluid; Humans; Interleukin-10; Interleukin-1beta; Interleukin-6; Interleukin-8; Male; Middle Aged; Peri-Implantitis; Periodontal Index; Periodontal Pocket; Periodontium; Porphyromonas gingivalis; Prospective Studies; Treponema denticola; Tumor Necrosis Factor-alpha

The aim was to assess clinical inflammatory parameters, cytokine levels and bacterial counts in samples from implant crevicular fluid in cases with untreated peri-implantitis.. Several bacterial species known to up-regulate pro-inflammatory cytokines have been associated with peri-implantitis. The Luminex magnet bead technology was used to study cytokines in crevicular fluid. The checkerboard DNA-DNA hybridization method was used to study bacterial counts in samples from 41 implants (41 individuals).. Profuse bleeding and suppuration was found in 25/41 (61.0%) of the implants. The reliability of duplicate cytokine processing was high. In the presence of profuse bleeding, higher pg/ml levels of IL-1β (p = 0.02), IL-8 (p = 0.04), TNF-α (p = 0.03) and VEGF (p = 0.004) were found. Higher concentrations of IL-1β were found in the presence of suppuration, and if Escherichia coli (p = 0.001) or Staphylococcus epidermidis (p = 0.05) could be detected.. Profuse bleeding and/or suppuration in untreated peri-implantitis can be associated with higher concentrations of IL-1β, IL-8, TNF-α and VEGF in peri-implant crevicular fluid. A higher concentration of IL-1β in peri-implant crevicular fluid was found in samples that were positive for E. coli or S. epidermidis.

Topics: Adult; Alveolar Bone Loss; Bacteria; Bacterial Load; Cytokines; Dental Implants; DNA, Bacterial; Escherichia coli; Female; Gingival Crevicular Fluid; Gingival Hemorrhage; Humans; Interleukin-1beta; Interleukin-8; Male; Peri-Implantitis; Periodontal Pocket; Staphylococcus epidermidis; Suppuration; Tumor Necrosis Factor-alpha; Vascular Endothelial Growth Factor A

This study aimed to measure the levels of GM-CSF, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12, IFN-γ and TNF-α in peri-implant crevicular fluid (PICF) and saliva from patients with peri-implant disease.. Twenty two total edentulous patients were divided into two groups: Mucositis (MU) patients with bone loss around the implants until the first thread and pocket depth ≤3 mm, and Peri-implantitis (PI) patients with at least one implant with bone loss around two or more threads and pocket depth ≥4 mm. The clinical parameters evaluated were probing pocket depth, bleeding on probing, and percentage of plaque. PICF samples were collected from MU sites, and from shallow (SPI) and deep (DPI) sites in PI. Unstimulated whole and parotid duct saliva was collected from all patients. The cytokines were measured by a multiplexed immunoassay.. PI patients had a higher percentage of plaque compared with MU (P = 0.02). MU sites had lower pocket depth compared to SPI (P = 0.001) and to DPI (P ≤ 0.001). In PICF, the levels of IL-1β were significantly higher in SPI sites compared to MU (P = 0.03). In the saliva from parotid, IL-8 and IL-12 were significantly higher in patients with PI (P = 0.04).. Elevated levels of IL-1β in PICF seem to be a characteristic trait of patients with peri-implantitis. The parotid duct saliva showed a significant increase in expression of IL-8, which might be related to a systemic response.

Topics: Cytokines; Dental Plaque Index; Female; Gingival Crevicular Fluid; Humans; Interleukin-1beta; Interleukin-8; Male; Middle Aged; Mucositis; Peri-Implantitis; Periodontal Index; Saliva

To assess inflammatory reactions of fibroblasts in the pathophysiology of peri-implantitis, we compared the pro-inflammatory and matrix-degrading responses of gingival and granulation tissue fibroblasts from periodontally healthy controls, peri-implantitis, and periodontitis lesions to an in vitro challenge with Porphyromonas gingivalis.. Fibroblasts from periodontally healthy, peri-implantitis and periodontitis donors were challenged with viable P. gingivalis. The inflammatory reactions of fibroblasts were analyzed before and after 6 h P. gingivalis challenge, and 2.5 and 18 h after removal of the challenge. Gene expression and induction of pro-inflammatory mediators, and matrix metalloproteinases (MMPs) were assessed by real-time polymerase chain reaction. Protein expression was measured by enzyme-linked immunosorbent assay.. Non-challenged fibroblasts from peri-implantitis and periodontitis lesions expressed higher levels of interleukin (IL)-1β, IL-8, and monocyte chemotactic protein (MCP)-1 than fibroblasts from periodontally healthy individuals. The P. gingivalis challenge induced expression of IL-1β, IL-8, IL-6, MCP-1, and MMP-1 in periodontitis and peri-implantitis fibroblasts, but not in fibroblasts from periodontally healthy individuals. MMP-8 expression was higher in non-challenged peri-implantitis fibroblasts than in fibroblasts from periodontally healthy individuals. However, the P. gingivalis challenge downregulated MMP-8 gene expression in peri-implantitis fibroblasts. After removal of the P. gingivalis challenge, peri-implantitis fibroblasts sustained higher induction of IL-1β, MCP-1, and MMP-1 compared to periodontitis fibroblasts.. Fibroblasts from peri-implantitis and periodontitis lesions gave a more pronounced inflammatory response to the P. gingivalis challenge than fibroblasts from healthy donors. They may therefore be involved in the development of inflammation in peri-implantitis and periodontitis. Moreover, the sustained upregulation of inflammatory mediators and MMP-1 in peri-implantitis fibroblasts may play a role in the pathogenesis of peri-implantitis.

Topics: Cell Culture Techniques; Cells, Cultured; Chemokine CCL2; Chronic Periodontitis; Cytokines; Female; Fibroblasts; Gingiva; Granulation Tissue; Humans; Inflammation Mediators; Interleukin-1beta; Interleukin-6; Interleukin-8; Male; Matrix Metalloproteinase 1; Matrix Metalloproteinase 8; Matrix Metalloproteinases; Middle Aged; Peri-Implantitis; Porphyromonas gingivalis; Real-Time Polymerase Chain Reaction; Time Factors; Up-Regulation

Titanium wear particles have been found in peri-implant tissues, but their role in the pathogenesis of peri-implantitis remains unclear. We aimed to determine the in vitro inflammatory responses of peri-implant granulation tissue fibroblasts (PIGFs) to titanium particles alone and in the presence of viable Porphyromonas gingivalis.. Peri-implant granulation tissue fibroblasts were challenged either with TiO2 particles, P. gingivalis or a combination of TiO2 particles and P. gingivalis. Gene expression and protein production of pro-inflammatory mediators by PIGFs were measured with PCR and ELISA, respectively.. Higher doses of TiO2 were toxic to PIGFs and in sub-toxic doses, TiO2 caused an increase in gene expression of tumour necrosis factor (TNF)-A and increased protein production of TNF-α, interleukin (IL)-6 and IL-8. A challenge with P. gingivalis alone induced gene expression of TNF-A, IL-1β, IL-6 and IL-8. A combined challenge with TiO2 and P. gingivalis caused a stronger increase in gene expression of TNF-A and protein production of TNF-α and MCP-1 than P. gingivalis alone.. TiO2 particles and P. gingivalis, individually, can induce pro-inflammatory responses in PIGFs. Furthermore, TiO2 particles and viable P. gingivalis further enhance gene expression and production of TNF-α by PIGFs. Therefore, Ti wear particles in the peri-implant tissues in combination with P. gingivalis infection may contribute to the pathogenesis of peri-implantitis by enhancing the inflammation in peri-implant tissues.

Topics: Bacteriological Techniques; Cell Culture Techniques; Cell Survival; Cells, Cultured; Chemokine CCL2; Dental Materials; Female; Fibroblasts; Gene Expression Regulation; Gene Expression Regulation, Bacterial; Granulation Tissue; Humans; Inflammation Mediators; Interleukin-1beta; Interleukin-6; Interleukin-8; Male; Middle Aged; Peri-Implantitis; Porphyromonas gingivalis; Titanium; Tumor Necrosis Factor-alpha

Current therapies for peri-implantitis apply the same clinical protocols as those used for the treatment of periodontitis; however, outcomes remain unpredictable. We hypothesized that resident fibroblasts of the peri-implantitis stroma and periodontitis stroma differ in their phenotype and response to host immune factors. Fibroblasts are highly heterogeneous and comprise discrete subtypes with the potential of modulating inflammatory activities. The aim of the present study was to characterize the expression of receptors for complement C1q of innate immunity on human peri-implantitis fibroblasts and investigate effects of C1q on the proinflammatory properties of the cells.. Fibroblasts were cultured from gingival tissues exhibiting peri-implantitis and periodontitis, and from healthy gingivae as a control. Expression of C1q receptors for the collagen (cC1qR) and globular domains (gC1qR) of the protein was determined by flow cytofluorometric analysis (FITC) of specific antibodies bound to the surface of the cells. Secretion of C1q-inducible proinflammatory mediators was quantified after 24 h incubation using array-based ELISAs.. The percentage of fibroblasts FITC-positive for cC1qR was 67, 75 and 12% in peri-implantitis, healthy and periodontitis cultures, respectively, whereas the percentage of gC1qR FITC-positive fibroblasts was 5, 3 and 59%, respectively. The C1q interactions with peri-implantitis and healthy fibroblasts increased secretion of the chemokines interleukin-6 and interleukin-8 twofold, and monocyte chemoattractant protein-1 fourfold over baseline values, whereas periodontitis fibroblasts were unresponsive. Complement C1q increased levels of vascular endothelial growth factor sevenfold and transforming growth factor-β1 12-fold over baseline values in peri-implantitis cultures, only.. Peri-implantitis fibroblasts differ from periodontitis fibroblasts in phenotypic expression of cC1qR and function, and from healthy fibroblasts in proinflammatory, angiogenic and fibrogenic function. Peri-implantitis fibroblasts may represent a novel subtype.

Topics: Cells, Cultured; Chemokine CCL2; Complement C1q; Fibroblasts; Fluorescent Antibody Technique; Gingiva; Humans; Immunity, Innate; Immunophenotyping; Inflammation Mediators; Interleukin-6; Interleukin-8; Membrane Glycoproteins; Peri-Implantitis; Periodontitis; Protein Structure, Tertiary; Receptors, Complement; Transforming Growth Factor beta1; Vascular Endothelial Growth Factor A

The aim of this study was to compare the levels of cytokines IL-6, IL-10 and IL-17 and the chemokine IL-8 in the peri-implant crevicular fluid (PCF) between the group of patients with peri-implantitis (PP) and peri-implantar healthy patients (HP).. The PCF was collected from 40 implants regarding 25 patients, being 14 patients with PP and 11 HP totalizing 20 implants from each group. The PCF samples collected from each patient were quantified for IL-6, IL-17, IL-8 and IL-10 using the enzymatic immunosorbent assay (ELISA).. The expression of IL-17 was significantly higher in the PP group when compared to HP (p < 0.05). There was no significant difference when comparing the levels of IL-6, IL-8 and IL-10 between both groups HP and PP. Also, there was a significant positive correlation between levels of IL-6 and IL-8 in the PP group.. This study demonstrates that in patients with peri-implantitis there is an increase of IL-17 which may induce the production of other inflammatory cytokines, contributing to the pathogenesis of bone loss in peri-implantitis.

Topics: Alveolar Bone Loss; Dental Implants; Female; Gingival Crevicular Fluid; Gingival Hemorrhage; Humans; Inflammation Mediators; Interleukin-10; Interleukin-17; Interleukin-6; Interleukin-8; Interleukins; Male; Middle Aged; Peri-Implantitis; Periodontal Pocket

High mobility group chromosomal protein B1 (HMGB1) and N2 (HMGN2), two members of high mobility group (HMG) family, play important role in inflammation. The purpose of this study was to investigate the expression of HMGB1 and HMGN2 in periodontistis.. The expression of HMGB1 and HMGN2 mRNA in gingival tissues and gingival crevicular fluid (GCF) in chronic periodontitis (CP), generalised aggressive periodontitis (G-AgP) patients and healthy subjects was detected by real-time PCR. The protein level of HMGB1 and HMGN2 in peri-implant crevicular fluid (PICF), peri-implant crevicular fluid of peri-implantitis (PI-PICF) and normal patients was determined by Western blotting. Furthermore, IL-1β, IL-6, IL-8, TNF-α and HMGB1 levels in GCF, PI-PICF and healthy-PICF samples from different groups were determined by ELISA.. HMGN2 expression was increased in inflamed gingival tissues and GCF from CP and G-ApG groups compared to control group. HMGB1 expression was the highest in the gingival tissues and GCF from CP patients and was accompanied by increased concentrations of IL-1β, IL-6, IL-8 proinflammaory cytokines.. To our knowledge, this is the first study reporting that the expression of HMGB1 and HMGN2 was increased in the gingival tissues and GCF in CP and G-AgP and the PICF in PICF. Our data suggest that HMGB1 may be a potential target for the therapy of periodontitis and PI.

Topics: Adolescent; Adult; Aged; Aggressive Periodontitis; Alveolar Bone Loss; Chronic Periodontitis; Dental Calculus; Dental Implants; Dental Plaque Index; Female; Gingiva; Gingival Crevicular Fluid; Gingival Hemorrhage; Gingivitis; HMGB1 Protein; HMGN2 Protein; Humans; Inflammation Mediators; Interleukin-1beta; Interleukin-6; Interleukin-8; Male; Middle Aged; Peri-Implantitis; Periodontal Pocket; Periodontitis; Periodontium; Tumor Necrosis Factor-alpha; Young Adult