vegf与种植体黏膜炎

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OBJECTIVES VEGF is prototypic marker of neovascularization, repeatedly proposed as intrinsic characteristic of peri-implantitis. This study aimed to assess pattern of VEGF in peri-implantitis, its correlation with titanium particles (TPs) and capacity as respective biomarker. MATERIAL AND METHODS Pathological specificity of VEGF was assessed in peri-implant granulations using immunohistochemistry, periodontal granulations represented Ti-free positive controls. VEGF was correlated to TPs, identified using scanning electron microscopy coupled with dispersive x-ray spectrometry. Diagnostic accuracy, sensitivity and specificity of VEGF were estimated in PICF specimens from peri-implantitis, peri-implant mucositis (PIM) and healthy peri-implant tissues (HI) using machine learning algorithms. RESULTS Peri-implantitis exhibited rich neovascular network with expressed density in contact zones toward neutrophil infiltrates without specific pattern variations around TPs, identified in all peri-implantitis specimens (mean particle size 8.9 ± 24.8 µm2; Ti-mass (%) 0.380 ± 0.163). VEGF was significantly more expressed in peri-implantitis (47,065 ± 24.2) compared to periodontitis (31,14 ± 9.15), and positively correlated with its soluble concentrations in PICF (p = 0.01). VEGF was positively correlated to all clinical endpoints and significantly increased in peri-implantitis compared to both PIM and HI, but despite high specificity (96%), its overall diagnostic capacity was average. Two patient clusters were identified in peri-implantitis, one with 8-fold higher VEGF values compared to HI, and second with lower values comparable to PIM. SIGNIFICANCE VEGF accurately reflects neovascularization in peri-implantitis that was expressed in contact zones toward implant surface without specific histopathological patter variation around TPs. VEGF answered requests for biomarker of peri-implantitis but further research is necessary to decrypt its exact underlying cause.

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To compare the 3-year clinical and radiographic outcomes of two different reconstructive surgical management of peri-implantitis using a bone substitute in combination with either concentrated growth factor (CGF) or collagen membrane (CM). Fifty-one patients who had at least one implant presenting peri-implantitis with an intrabony defect were filled with a xenogenic bone grafting material and covered either CGF or CM. Clinical and radiographic assessments were carried out at baseline and postoperative years 1 and 3. Three different composite outcomes were defined to evaluate treatment success at a 3-year follow-up. The effects of possible prognostic indicators on treatment success were identified by using multilevel regression analysis. The changes in probing depth (PD) and radiographic vertical defect depth (VDD) between baseline and year 1 and baseline and year 3 presented significantly greater decreases for the CM group in comparison with the CGF group (p < 0.05). No significant differences between the two treatment modalities were demonstrated regarding treatment success outcomes. History of periodontitis, VDD at baseline, and the number of intrabony defect walls revealed significant impacts on treatment success (p = 0.033; OR = 3.50, p = 0.039; OR = 0.975, and p = 0.024; OR = 7.0 and p = 0.019;OR = 6.0, respectively). CM in combination with a bone substitute seems to have slightly better outcomes compared to the CGF membranes in reconstructive surgical therapy of peri-implantitis. The history of periodontitis, baseline VDD, and peri-implant bone defect configuration could be possible predictors influencing treatment success. ClinicalTrials.gov NCT04769609. For the reconstruction of peri-implant bone defects, using a bone substitute in combination with a collagen membrane may show more favorable outcomes.

Objective The biological seal (BS) at the implant-tissue interface is essential for the success of dental implants (DIs), and the absence of a proper BS can lead to peri-implantitis. The basement membrane (BM) and junctional epithelium are critical for sealing the peri-implant mucosa, and laminin 332 is an important protein in binding the epithelium to the implant surface. The aim of this study was to evaluate the response of oral keratinocytes to titanium dental implant surfaces biofunctionalized with laminin 332. Design The dental implant surface was treated with a piranha solution to create hydroxyl (OH) groups, facilitating biofunctionalization with laminin 332. The modified surface underwent scanning electron microscopy, surface roughness evaluation, and chemical composition analysis. Human keratinocytes from the Cal-27 line were then cultured on the modified implants for 24 and 48 h to assess viability, morphology, cytokine secretion, and mRNA expression of tissue repair-associated genes. Results The results showed that laminin 332 biofunctionalization of the implant surface resulted in lower values of Ra, Rq and positive surface roughness parameters Rsk, Rku and Rv. The elemental composition showed an increase in nitrogen and carbon content corresponding to protein binding. The biofunctionalized surfaces did not affect cell viability and promoted cytokine secretion (IL-1a and IL-8) and a significant increase (p < 0.05) in MCP-1, EGF, FGF, TGF and VEGF gene expression compared to the control. Conclusion In conclusion, laminin 332 coating Ti implants was shown to be effective in promoting keratinocyte adhesion, spreading, and viability. This approach could be an alternative way to improve biocompatibility.

This study evaluated the clinical and tomographic outcomes of socket healing. Immediate implants were placed in the molar area, and the gap was filled with either deproteinized bovine bone mineral (B) or collagen matrix (BM), n = 14/group. Scores of epithelization healing, immunoassay for VEGF, IL-1β, and FGF from wound exudate, keratinized mucosa variation (ΔKM), and bone levels were evaluated. The B group had slower tissue maturation than BM (p < 0.05), but gingival epithelialization was similar (p > 0.05). At the restorative phase, the B group exhibited greater ΔKM at prosthesis installation—1 to 2 months of postoperative (increase of 0.29 mm) compared to the BM group (reduction of −1.5 mm) (p < 0.05). Inflammatory tissue responses as well as vertical and horizontal bone remodeling were similar (p > 0.05). Crestal bone remodeling was limited to less than 0.8 mm for both groups. Taken together, the B and BM groups behaved similarly and promoted stable conditions for biomaterial incorporation in the socket healing after immediate implant placement in molar areas.

Little is known about the in-vivo dynamics of biofilms associated with medical-device infections and their interplay with systemic inflammation, local immune responses, and tissue healing processes. There may be an opportunity to tailor therapeutic strategies to target these dynamics to improve treatment outcomes. We investigated immune responses to a methicillin-susceptible (ATCC 12600) and a multi-drug resistant (L1101) S. aureus strain using a rat subcutaneous implant model, analyzing local and systemic inflammation through 19 gene expressions over 21 days. Our goals were to identify differences in the immune response due to infection and also with respect to the two strains. We observed that systemic inflammation, indicated by α-2-macroglobulin, was elevated in the initial stages (up to day 7). Local inflammatory cytokine levels (IL-6, TNF-α, IL-6, TNF-α, IL-1β, IL10, IL-17, IL12a, IL12b,IFNG) varied by strain, typically higher against the clinical strain. Infections generally hindered early macrophage (MCSF1) and T-cell (CD4, CD5, CD6, CD8A) recruitment, particularly in cases involving the clinical strain. Conversely, a better healing response was observed in the infection of the more susceptible ATCC 12600 strain (VEGF, CXCR1, CXCR2, MMP-1, MMP-3, MMP-13). These results are crucial for understanding immune responses to such infections, guiding therapeutic strategies.

Fractional laser photothermolysis, long established in dermatology, enables controlled microthermal injury that stimulates repair without scarring, but its potential in oral tissue regeneration has not been systematically explored. In this study, we conducted the first controlled experimental evaluation of a 1550 nm erbium fiber laser for oral mucosa regeneration. Thirty-two rabbits underwent fractional photothermolysis at energy levels of 70, 100 and 130 kJ, with gingival biopsies collected at 1, 14, 28 and 42 days for histological and immunohistochemical assessment of epithelial repair, stromal remodeling, inflammation and angiogenesis. All energy modes produced microcoagulation columns followed by progressive epithelial thickening, fibroblast proliferation and neoangiogenesis. The 70 kJ mode occasionally led to residual fibrosis, whereas higher energies (100–130 kJ) promoted effective connective tissue remodeling and de novo tissue formation without scarring. Complete epithelial recovery occurred within two weeks, indicating a safe and optimal interval for repeated exposure. Overall, the results demonstrate that 1550 nm fractional photothermolysis is a safe and effective method to induce regenerative responses in oral tissues, establishing a foundation for its translational application in periodontal and peri-implant regeneration.

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OBJECTIVES The aim of the present study was to explore the feasibility of ultrasonography (US) for clinical imaging of peri-implant tissues. MATERIAL AND METHODS Patients with ≥ 1 implant, a CBCT scan, an US scan, and clinical photographs taken during the surgery were included. The crestal bone thickness (CBT) and facial bone level (FBL) were measured on both US and CBCT modalities, and direct FBL measurements were also made on clinical images. US measurements were compared with CBCT and direct readings. RESULTS A total of 8 implants from 4 patients were included. For FBL measurements, US and direct (r2=0.95) as well as US and CBCT (r2=0.85) were highly correlated, whereas CBCT correlated satisfactorily with the direct reading (r2=0.75). In one implant without facial bone, CBCT was not able to measure CBT and FBL accurately. The estimated bias for CBT readings was 0.17 ± 0.23 mm (p=0.10) between US and CBCT. US blood flow imaging was successfully recorded and showed a wide dynamic range among patients with different degrees of clinical inflammation. CONCLUSION US is a feasible method to evaluate peri-implant facial crestal bone dimensions. Additional US features, e.g., functional blood flow imaging, may be useful to estimate the extent and severity of inflammation.

Abstract Objective: Aim of present study was to evaluate gingival tissue samples obtained from healthy and diseased sites of teeth and dental implants in terms of hypoxia and collagenase activity. Methods: Four study groups were created as Group-1; healthy individuals (H), Group-2; periodontitis patients with stage 3 grade B (P), Group-3; patients with peri-implant mucositis. Group-4; patients with peri-implantitis (P-IMP). Plaque index (PI), gingival index (GI) and probing pocket depth (PPD) were recorded. Gingival and peri-implant mucosal biopsies were obtained. Fibroblast and inflammatory cells were counted. Hypoxia-inducible factor (HIF)-1α, prolyl hydroxylase (PH), matrix metalloproteinase (MMP)-8, tissue inhibitor of MMPs (TIMP)-1, cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) levels were determined via immunohistochemistry. Results: Healthy controls had highest fibroblast cell counts and lowest inflammatory cell counts compared to other groups. Peri-implantitis and periodontitis samples had similar fibroblast and inflammatory cell counts, while peri-implant mucositis had higher fibroblast cells and lowered inflammatory cells compared to periodontitis and peri-implantitis samples. HIF-1α, COX-2 and iNOS levels were lowest in healthy controls and increased in other groups. Peri-implant mucositis samples had significantly lower expressions of HIF-1α, COX-2 and iNOS compared to peri-implantitis and periodontitis groups. PH expressions were lower in periodontitis and peri-implantitis groups compared to healthy controls and peri-implant mucositis groups. MMP-8 levels were lower in healthy group compared to other groups while levels were similar in periodontitis, peri-implant mucositis and peri-implantitis groups. TIMP levels were similar in groups. Conclusion: Periodontitis, peri-implantitis, and peri-implant mucositis samples exhibited higher inflammation and lower fibroblast cell counts and tend to have increased tissue collagenase activity, hypoxia and inflammation compared to healthy samples.

Abstract Hypertensive individuals present alterations in their calcium metabolism that consequently decrease the concentration of this mineral in the bone tissue. Objectives to evaluate the morphological and functional characteristics of the peri-implant bone tissue that was formed during the healing process by the placement implants using two different surface treatments: hydrophilic Acqua™ (ACQ) and rough NeoPoros™ (NEO), in spontaneously hypertensive (SHR) and normotensive rats (Wistar) whether or not treated with losartan. Methodology In total, 96 male rats (48 Wistar and 48 SHR) were divided into eight subgroups: absolute control rough (COA NEO), absolute control hydrophilic (COA ACQ), losartan control rough (COL NEO), losartan control hydrophilic (COL ACQ), SHR absolute rough (SHR NEO), SHR absolute hydrophilic (SHR ACQ), SHR losartan rough (SHRL NEO), and SHR losartan hydrophilic (SHRL ACQ). The rats medicated with losartan received daily doses of the medication. NeoPoros™ and Acqua™ implants were installed in the tibiae of the rats. After 14 and 42 days of the surgery, the fluorochromes calcein and alizarin were injected in the rats. The animals were euthanized 67 days after treatment. The collected samples were analyzed by immunohistochemistry, biomechanics, microcomputerized tomography, and laser confocal scanning microscopy analysis. Results The osteocalcin (OC) and vascular endothelium growth factor (VEGF) proteins had moderate expression in the SHRL ACQ subgroup. The same subgroup also had the highest implant removal torque. Regarding microarchitectural characteristics, a greater number of trabeculae was noted in the control animals that were treated with losartan. In the bone mineralization activity, it was observed that the Acqua™ surface triggered higher values of MAR (mineral apposition rate) in the COA, COL, and SHRL groups (p<0.05). Conclusion the two implant surface types showed similar responses regarding the characteristics of the peri-implant bone tissue, even though the ACQ surface seems to improve the early stages of osseointegration.

The objective of the present study was to validate key mole­cular markers of bone tissue repair as indicators of osseointegration on systemic and local levels, and evaluate their trans­lational parallelism. This was achieved by comparing the configurational consistency of expression profiles between an experimental rat model and a pilot clinical investigation in human patients to synchronize systemic and local molecular responses. The hypothesis was that alumina-coated titanium implants would exhibit faster dynamics of angiogenic and osteogenic biomarkers, indicating accelerated osteoinduction, osteoconduction, and osseointegration compared with uncoated titanium. The pilot clinical study comprised the patients after total hip arthroplasty (n=6): three with uncoated titanium implants and three with alumina ceramics. Serum samples were collected from these patients in one and six months post-surgery. The experimental rat model comprised 160 Wistar females implanted with modified intrafemoral implants (seven surface types, including uncoated and alumina-coated titanium), with serum and peri-implant tissue samples collected in one, two, four, and eight weeks. Serum levels of vascular endothelial growth factor, bone morphogenetic protein 2, and osteoprotegerin were determined by enzyme-linked immunosorbent assay, while the corresponding local expression of vascular endothelial growth factor receptor, bone morphogenetic protein 2, and receptor activator of nuclear factor kappa-B was assessed by immunohistochemistry. The results demonstrated that alumina-coated implants induced an accelerated and synchronized molecular cascade in the rat model, which was qualitatively replicated in the clinical cohort. The systemic vascular endothelial growth factor peak manifested early, at one week in rats and one month in humans, and exhibited a strong parallelism with local microvessel density in the animal model, confirming rapid angiogenic activation. In both species, the expression of bone morphogenetic protein 2 increased earlier and to a greater extent in the alumina-coated groups, indicating more rapid osteoinduction. Local receptor activator of nuclear factor kappa-B activity demonstrated an early rise and a four-week peak in the groups with coated implants, consistent with controlled and timely bone remodelling. The study indicates that alumina coatings promote accelerated osseointegration by advancing the time course of healing, a conclusion supported by the observed translational parallelism of the investigated markers.

This study aimed to investigate the clinical characteristics and early soft tissue response to zirconium oxide (Zr) and titanium (Ti) healing abutments in dogs. Eight implants (four at each hemi-mandible) were inserted after bilateral mandibular third and fourth premolars and first molar extraction in dogs. Then, two Zr and two Ti healing abutments were connected to each unilateral mandible eight weeks later. The ligation method was used to create a peri-implant mucositis model and the 24 abutments were divided into four groups: Zr or Ti healing abutments with ligation (ZrL, TiL) or non-ligation (ZrN, TiN). The clinical indices, peri-implant crevicular fluid (PICF), and inflammatory cytokines (TNF-α and IL-1β) were measured and analyzed on days 0 and 28. The dogs were then sacrificed on day 28, soft tissues around the implants were harvested, and inflammation infiltration was tested by immunohistochemistry. Normal distribution test and two-way analysis of variance was used to analyze the data. The results showed that the clinical indices were similar for Zr and Ti healing abutments. There was significantly more PICF in the ZrL and TiL groups compared to in the ZrN and TiN groups. The TNF-α levels in PICF were significantly different between ZrL and ZrN groups on day 28. And the TNF-α levels in PICF were significantly higher in TiL group on day 28 than that on day 0. However, the number of inflammatory cells was not significantly different between the groups as measured by immunohistochemistry. These data indicate that soft tissue responses to Zr healing abutments with peri-implant mucositis were comparable to those of Ti healing abutments in vivo, providing a theoretical foundation for the clinical application of Zr abutments.

The presence of foreign materials in the tissues, represented in the present study by the insertion of dental implants, creates artificial structures that can sometimes cause adverse consequences, which implies the obligation to perform a complex medical assessment before inserting dental implants. This assessment appreciates the quality of the tissue, depending on which the use of a certain type of biomaterial is indicated and focuses on a certain surgical technique. We assessed the clinical, histopathological (HP) and immunohistochemical (IHC) aspects of peri-implant soft tissue in patients who did not show mobility or imagistic signs of bone resorption, three months after implant insertion, some of them showing no inflammatory clinical signs. Immunohistochemically, on the sections of the peri-implant mucosa, we assessed the presence of mast cells, vascularization and the process of angiogenesis. Mast cells are key cells actively involved in the pathogenesis of peri-implant inflammation, having an immunomodulatory role. Vasodilation and angiogenesis, determined by the release of chemical mediators by degranulation of mast cells under the action of pathogens, induce tissue remodeling, ensuring the healing and formation of a tissue to form a barrier that effectively prevents the development of a bacterial biofilm. Thus, the control of the activity of these cells is important for the management of the local inflammatory process. The correlations between the clinical, HP and IHC behavior of the peri-implant soft tissue bring important information for the clinic, emphasizing the need to identify a therapeutic strategy to modulate mast cell activity, in order to prevent and treat peri-implant disease, to ensure osseointegration and longer survival of the dental implant.

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Abstract Objective To study the effect of implanting the percutaneous bone‐anchored hearing system (BAHS) itself and inflammation of the peri‐abutment skin warrant clarification. In this study, we aimed to acquire further insight into the immune responses related to BAHS surgery and peri‐implant skin inflammation. Materials and Methods During surgery and 12 weeks post‐implantation, skin biopsies were obtained. If applicable, additional biopsies were taken during cases of inflammation. The mRNA expression of IL‐1β, IL‐6, IL‐8, TNFα, IL‐17, IL‐10, TGF‐ß, MIP‐1α, MMP‐9, TIMP‐1, COL1α1, VEGF‐A, FGF‐2 TLR‐2, and TLR‐4 was quantified using qRT‐PCR. Results Thirty‐five patients agreed to the surgery and 12‐week biopsy. Twenty‐two patients had mRNA of sufficient quality for analysis. Ten were fitted with a BAHS using the minimally invasive Ponto surgery technique. Twelve were fitted with a BAHS using the linear incision technique with soft‐tissue preservation. Five biopsies were obtained during episodes of inflammation. The post‐implantation mRNA expression of IL‐1β (P = .002), IL‐8 (P = .003), MMP9 (P = .005), TIMP‐1 (P = .002), and COL1α1 (P < .001) was significantly up‐regulated. IL‐6 (P = .009) and FGF‐2 (P = .004) mRNA expression was significantly down‐regulated after implantation. Within patients, no difference between post‐implantation mRNA expression (at 12 weeks) and when inflammation was observed. Between patients, the expression of IL‐1β (P = .015) and IL‐17 (P = .02) was higher during cases of inflammation compared with patients who had no inflammation at 12‐week follow‐up. Conclusions As part of a randomized, prospective, clinical trial, the present study reports the molecular profile of selected cytokines in the soft tissue around BAHS. Within the limit of this study, the results showed that 12 weeks after BAHS implantation the gene expression of some inflammatory cytokines (IL‐8 and IL‐1β) is still relatively high compared with the baseline, steady‐state, expression. The up‐regulation of anabolic (COL1α1) and tissue‐remodeling (MMP‐9 and TIMP1) genes indicates an ongoing remodeling process after 12 weeks of implantation. The results suggest that IL‐1β, IL‐17, and TNF‐α may be interesting markers associated with inflammation.

Objective Peri-implantitis (PI) is one of the main reasons for dental implant failure. Until now, the etiology and pathogenesis of PI remain unclear. Methods In this study, we used differentially expressed genes (DEGs) analysis and gene function enrichment analysis to assess the expression profile of peri-implant bone tissue and gingiva in PI public data from the Gene Expression Omnibus (GEO) database. Then, we used gingival tissues from patients with PI and healthy individual to construct gene coexpression networks to reveal the biological functions of the genes in PI using RNA sequencing data. Afterward, key gene modules were selected to reveal the critical biological process or signaling pathway using Hallmark's gene enrichment and expression analysis of the related pathway members in PI. Results DEGs were enriched in the formation of cellular responses to external stimuli in bone tissue. Cytokine production, lymphocyte activation, immune response-regulating signaling pathway, and blood vessel development were the top GO biology process or pathways of the DEGs in gingival tissue. Weighted gene coexpression network analysis (WGCNA) of RNA-seq data was used to assess the results of correlation analysis between modules and traits and correlation analysis between modules and functions. kMEpurple, kMEgreen, and kMEred modules were selected as the key gene modules. Signaling pathways and gene expression analysis were performed on selected modules, such as IL2/STAT5 signaling pathway, TNFα signaling pathway via NFκB, and angiogenesis were enriched in kMEpurple module. Hedgehog signaling pathway, Wnt β-catenin signaling pathway, and IL2/STAT5 signaling pathway were enriched in kMEgreen module. Peroxisome, IL2/STAT5 signaling pathway, and epithelial-mesenchymal transformation process were enriched in kMEred module. All the enrichment results of key modules contained IL2/STAT5 signaling pathway. Conclusion. Differential gene and enrichment analysis based on public data showed differences in gene expression patterns and biological process between bone and gingival tissues in PI. This spatial-temporal heterogeneity is reflected in the formation of cellular responses to external stimuli, which was enriched in bone tissue, but cytokine production, lymphocyte activation, immune response regulating signaling pathway, and blood vessel development were enriched in gingival tissue. WGCNA and Hallmark gene sets enrichment analysis of the gingival tissue expression profile and showed that IL2-mediated activation of immune cells could be a critical mechanism in PI. As a new clinical treatment alternative, we suggest that IL2/STAT5 pathway blockers could be helpful in the treatment of PI.

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OBJECTIVE To describe and compare cytokines levels in clinically healthy sites of dental implants and natural teeth. MATERIALS AND METHODS A total of 90 dental implants in 71 periodontal healthy patients with function time of less than 6 months after the completion of the implant prosthesis were included in this study. PICF (peri-implant crevicular fluid) and GCF (gingival crevicular fluid) samples were collected from implants and the contralateral natural teeth. In addition, we performed a dynamic collection of crevicular fluid from 18 dental implants and their contralateral natural teeth at four time nodes (first day, first week, first month, third month). The profiles of 45 common cytokines in PICF and GCF were analyzed by Luminex multiplex assays. RESULTS The total volume of PICF was significantly higher when compared to the volume of GCF (p < 0.01). In contrast, the concentrations of IL-18, IL-2, IL-23, IL-21, IL-1α, IL-12p70, VEGF-A, HGF, FGF-2, BDNF, PlGF-1, MIP-1β, TNF-α, and IFN-γ in PICF were significantly lower than those in GCF (p < 0.05). In the longitudinal component of the study, the cytokines found in PICF underwent a brief wave of expression in the 3-month period, with the smallest gap difference of cytokine expression between the PICF and the GCF being at first month. CONCLUSIONS This study observed that the levels of 14 cytokine profiles were lower in PICF than in GCF. Within the implants load for one month, the levels of above differential cytokines in PICF increased and gradually approached the cytokine profiles in GCF.

IntroductionAngiogenesis occurs under physiological and pathological conditions and is regulated by cytokines and growth factors. Vascular endothelial growth factor (VEGF) is a multifunctional angiogenic cytokine that plays a significant role in inflammation and immune responses implicated in the pathogenesis of inflammatory processes in the implant- surrounding tissues.ObjectiveThe study investigated the concentration of VEGF in gingival crevicular fluid (GCF) in healthy and diseased soft tissues surrounding implants.Material and methodsClinical examinations were focused on assessing the periodontal status of soft tissues around dental implants with the use of Florida Probe. Bone loss was examined radiologically. VEGF concentrations were assessed by enzyme-linked immunoabsorbent assay (ELISA).ResultsVEGF concentrations were found higher in crevicular fluid around implants than in clinically healthy sites. They were also strongly correlated with the pocket depth.ConclusionsThe presence of VEGF in gingival crevicular fluid in patients with peri-implants can be implicated in the progression of peri-implantitis, possibly by promoting the formation of new blood vessels during angiogenic processes.

To explore the effect of low-level laser therapy (LLLT) on the healing of soft tissue around the implant after flap implantation and explore the possible mechanism. A total of 58 patients who underwent implant surgery were enrolled, with a total of 70 implants. They were randomly divided into the LLLT group and the control group. The LLLT group underwent LLLT with Nd:YAG (Fotona, 1064 nm) immediately after surgery and on the 2nd and 3rd day in the surgical area, while the control group did not receive any intervention. Pain assessment was performed in the first 3 days after surgery. The weight of peri-implant crevicular fluid (PICF), modified sulcus bleeding index (mSBI), gingival index (GI), and the expression levels of tumor necrosis factor-α (TNF-α), and vascular endothelial growth factor (VEGF) on the 7th and 14th days after surgery were evaluated. On the first 3 days after surgery, the pain score of the LLLT group was significantly lower than that of the control group. On the 7th and 14th day after surgery, the PICF volume, mSBI, GI, and TNF-α levels of the LLLT group were lower than those of the control group. The VEGF levels in the LLLT group were significantly higher than that in the control group. LLLT can promote the healing of the soft tissue after implantation, effectively relieve postoperative pain, improve clinical indicators, reduce TNF-α, and increase the expression level of VEGF, which is worthy of clinical application. Retrospectively Registered Trials ChiCTR2400087562 (07/30/2024)

AIM To compare the clinical and radiographic conditions and the expression of pro-inflammatory cytokines in peri-implant crevicular fluid (PICF) at two-piece/bone level (TP/BL) versus one-piece/tissue level (OP/TL) single implants with a laser-microgrooved collar after at least 5 years of loading. MATERIALS AND METHODS In total, 20 single TP/BL implants and 20 contralateral OP/TL implants, both with a laser-microgrooved collar surface, in 20 systemically and periodontally healthy subjects (12 males and 8 females, between the age of 36 and 64 [mean age of 49.7 ± 12.3 years]), were examined. Levels of IL-1β, IL-1RA, IL-6, IL-8, IL-17, b-FGF, G-CSF, GM-CSF, IFN, MIP-1β, TNF-α, and VEGF were assessed in PICF using the Bio-Plex 200 Suspension Array System. Plaque index (PI), probing depth (PD), bleeding on probing (BOP), and gingival recession (REC) were recorded. Radiographic crestal bone levels (CBL) were assessed at the mesial and distal aspects of the implant sites. RESULTS The mean PI, PD, BOP, and REC values had no significant differences in either group. A higher mean value of CBL with statistical difference was detected for TP/BL compared with OP/TL implants. The levels of IL-1β, IL-6, IL-8, GM-CSF, and MIP-1β and TNF-α were higher at TP/BL implants than at OP/TL implants. However, only IL-1β, IL-6, and TNF-α values presented significant differences between the groups. CONCLUSIONS Although after 5 years of loading single TP/BL and OP/TL implants with a laser-microgrooved collar surface presented similar good clinical conditions, a higher proinflammatory state and higher crestal bone loss were detected for TP/BL implants.

The aim of this study was to compare the expression of host-derived markers in peri-implant/gingival crevicular fluid (PCF/GCF) and clinical conditions at ceramic implants and contralateral natural teeth. As a secondary objective, we compared zirconia implants with titanium implants. One zirconia implant (ZERAMEX® Implant System) and one contralateral natural tooth were examined in 36 systemically healthy subjects (21 males, 15 females, mean age 58). The levels of Il-1β, Il-1RA, Il-6, Il-8, Il-17, b-FGF, G-CSF, GM-CSF, IFNɣ, MIP-1β, TNF-α, and VEGF were assessed in PCF/GCF using the Bio-Plex 200 Suspension Array System. The plaque index (PI), gingival index (GI), probing depth (PD), and bleeding on probing (BOP) were assessed at six sites around each implant or tooth. Titanium implants were also assessed when present (n = 9). The zirconia implants were examined after a loading period of at least 1.2 years (average 2.2 years). The mean PI was significantly lower at zirconia implants compared to teeth (p = 0.003), while the mean GI, PD, and BOP were significantly higher (p < 0.001). A correlation was found in the expression of Il-1RA, Il-8, G-CSF, MIP-1β, and TNF-α at zirconia implants and teeth. The levels of IL-1β and TNF-α were significantly higher at zirconia implants than at teeth. No significant differences were found between zirconia and titanium implants. A correlation was found between the levels of IL-1RA, IL-8, GM-CSF, and MIP-1β at zirconia and titanium implants. The correlation in the expression of five biomarkers at zirconia implants and teeth, and of four biomarkers at zirconia and titanium implants, is compatible with the existence of a patient-specific inflammatory response pattern. Higher mean GI, PD, and BOP around implants suggests that the peri-implant mucosa may be mechanically more fragile than the gingiva. Similar expression of selected biomarkers at zirconia implants and teeth and at zirconia and titanium implants reflects existence of patient-specific inflammatory response patterns.

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Gingival crevicular fluid (GCF) is an important source for the assessment of periodontal and peri-implant disease activity and response to periodontal therapy. GCF contains cellular components such as epithelium, bacteria, leukocytes, erythrocytes, viruses and their by-products, electrolytes, bacterial metabolic products, host and bacterial enzymes, and enzyme inhibitors such as acid phosphatase, alkaline phosphatase, cytokines, and immunoglobulins. In addition, it is also found that drugs taken systemically pass into the GCF.

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