An interventional study of Nonsurgical Mechanical Debridement With 1% Chlorhexidine Gel in One-Piece Dental Implant, Bone-Level Implant and Two-Piece Dental Implant, sponsored by Cuneyt Asim Aral. Completed at 1 site in Turkey (Türkiye). Open to participants aged 18 Years and older, including healthy volunteers. Per ClinicalTrials.gov, last updated 2026-10-23.
Sponsored by Cuneyt Asim Aral · Not applicable, Interventional, and Treatment
The goal of this clinical study was to learn whether the design of a dental implant affects how the gums around it respond to treatment of peri-implant mucositis, an early and reversible inflammation of the soft tissue around a dental implant. The study included systemically healthy, non-smoking adults with one-piece implants (made as a single unit) or two-piece bone-level implants (with a separate connecting part above the implant). The main questions were whether inflammation-related proteins in the fluid around the implant (interleukin-1 beta, interleukin-10, matrix metalloproteinase-8, and tissue inhibitor of metalloproteinases-1), clinical signs of inflammation, and selected bacteria changed differently after treatment around one-piece and two-piece implants.
Researchers compared implants with healthy gums and implants with peri-implant mucositis for each implant design, and compared the treatment response of the two designs over 3 months. All participants had a gum and implant examination, including plaque, bleeding, and pocket depth measurements and an assessment of gum thickness around the implant, and gave small samples of fluid and plaque from around the implant using paper strips and paper points. Participants with peri-implant mucositis received professional cleaning of the implant with an ultrasonic device with plastic-capped tips, a single application of chlorhexidine gel, and personal oral hygiene instructions, and returned 1 and 3 months later for repeat examinations and sampling.
BACKGROUND Peri-implant mucositis is a plaque-associated inflammatory lesion of the soft tissues around dental implants and is considered the precursor of peri-implantitis. In two-piece bone-level implants, the implant-abutment interface and the internal cavity may act as reservoirs for bacterial penetration and retention, whereas one-piece implants have no such junction and a continuous transmucosal component. Whether this structural difference affects the host response to nonsurgical mucositis therapy had not been investigated together with clinical and microbiological changes. The primary aim of this study was to compare the changes in peri-implant sulcus fluid (PISF) levels of interleukin-1 beta (IL-1β), interleukin-10 (IL-10), matrix metalloproteinase-8 (MMP-8), and tissue inhibitor of metalloproteinases-1 (TIMP-1) over 3 months after nonsurgical therapy around one-piece and two-piece bone-level implants.
STUDY DESIGN The study was conducted at the Department of Periodontology, Faculty of Dentistry, İnönü University, Malatya, Türkiye, and consisted of two phases. In the cross-sectional phase, implants with peri-implant health and implants with peri-implant mucositis were compared for each implant design at baseline. In the prospective phase, implants with peri-implant mucositis received nonsurgical therapy and were re-examined and re-sampled 1 and 3 months after treatment. The one-piece implants were monoblock implants in which the endosseous and transmucosal portions are manufactured as a single unit (Monoimplant Rough B, Novodent SA, Switzerland), and the two-piece implants were bone-level implants from the same manufacturer (Implantswiss, Novodent SA, Switzerland). All implants had been placed by the same periodontist. Diagnoses were based on the 2017 World Workshop classification of periodontal and peri-implant diseases and conditions.
CLINICAL EXAMINATION All clinical measurements were performed by a single calibrated examiner. Plaque index, gingival index, probing depth, and bleeding on probing were recorded at six sites around each implant with a plastic periodontal probe. Keratinized mucosal width was measured at the mid-buccal aspect. Peri-implant soft-tissue phenotype was assessed with a color-coded probe, and mucosal thickness was measured by transgingival probing under topical anesthesia at 1, 2, and 3 mm apical to the buccal mucosal margin using an endodontic spreader and a caliper. Intra-examiner reliability was assessed by repeated measurements 10 days apart.
SAMPLING Samples were collected between 09:00 and 11:00 on the day after the clinical examination to avoid interference from probing-induced bleeding. After isolation and removal of supragingival deposits, subgingival plaque was collected with sterile paper points inserted at the mesial and distal aspects of each implant for 30 s. PISF was then collected with two paper strips inserted into the sulcus for 30 s each. Samples contaminated with blood or saliva were discarded, and all samples were stored at -80°C until analysis.
NONSURGICAL THERAPY Implants with peri-implant mucositis received mechanical debridement with an ultrasonic device fitted with polyetheretherketone-capped tips to avoid alteration of the implant surface. After isolation, 1% chlorhexidine gel was delivered into the peri-implant sulcus in a single session with a syringe and a 22-gauge needle. Participants were asked to avoid food and fluid intake for at least 2 hours and received individualized oral hygiene instructions, including the use of interdental brushes of appropriate size.
LABORATORY ANALYSES PISF IL-1β, IL-10, MMP-8, and TIMP-1 were quantified with sandwich enzyme-linked immunosorbent assay (ELISA) kits and expressed as total amounts per implant (two pooled strips, each collected for 30 s). The IL-1β/IL-10 and MMP-8/TIMP-1 ratios were calculated from the total amounts. Total DNA was extracted from the plaque samples, and Porphyromonas gingivalis, Fusobacterium nucleatum, Treponema denticola, and Filifactor alocis were analyzed by quantitative polymerase chain reaction (qPCR) with species-specific primers and universal 16S rRNA gene primers as the reference for total bacterial load. Relative abundance was expressed as ΔCt (Ct of the target species minus Ct of the 16S rRNA gene), and a species was considered not detected when no amplification occurred within 40 cycles.
SAMPLE SIZE The sample size was calculated with G*Power 3.1.9.7 from previously reported PISF IL-1β total amounts in healthy and inflamed implants (effect size d=0.87). With a two-sided alpha of 0.05 and 80% power, 22 implants per group (88 implants in total) were required.
STATISTICAL ANALYSIS Nonparametric methods were used. The four groups were compared at baseline with the Kruskal-Wallis test followed by Dunn's post hoc test with Bonferroni adjustment. Within-group changes over time were analyzed with the Friedman test followed by Bonferroni-adjusted Wilcoxon signed-rank tests. The two mucositis groups were compared at each time point and for reductions from baseline with the Mann-Whitney U test, with Hodges-Lehmann estimates and 95% confidence intervals for biomarker reductions. Categorical variables were compared with the chi-square test, and detection frequencies with Fisher's exact test between groups and Cochran's Q test followed by exact McNemar tests within groups. A two-sided p\<0.05 was considered statistically significant.
265 studies on the registry are indexed under Mucositis; 34 are open to participants now.
This study's enrollment of 88 is above the median of 45 across 215 interventional studies indexed under Mucositis.
Browse Mucositis studies →Cuneyt Asim Aral is the lead sponsor of 2 studies on the registry; none are open to participants now.
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Before you join, the study team explains what taking part involves — its purpose, what happens, the risks and possible benefits — and answers your questions, so you can decide freely. Consent is usually recorded on a form (the informed consent form, ICF) signed by you or, where the law allows, by someone legally authorised to decide for you.
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Immunosuppression
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Two-piece bone-level implants diagnosed with peri-implant mucositis received nonsurgical therapy and were re-examined and re-sampled 1 and 3 months after treatment.
Procedure: Nonsurgical Mechanical Debridement With 1% Chlorhexidine Gel
One-piece implants diagnosed with peri-implant mucositis received nonsurgical therapy and were re-examined and re-sampled 1 and 3 months after treatment.
Procedure: Nonsurgical Mechanical Debridement With 1% Chlorhexidine Gel
Two-piece bone-level implants with peri-implant health. No treatment was given, and clinical, biochemical, and microbiological data were collected at baseline only for cross-sectional comparison.
One-piece implants with peri-implant health. No treatment was given, and clinical, biochemical, and microbiological data were collected at baseline only for cross-sectional comparison.
Ultrasonic mechanical debridement of the implant with polyetheretherketone-capped tips, followed by a single submucosal application of 1% chlorhexidine gel delivered into the peri-implant sulcus with a syringe and a 22-gauge needle, and individualized oral hygiene instructions including the use of interdental brushes.
Also known as: Nonsurgical peri-implant mucositis therapy
Change in Peri-Implant Sulcus Fluid Interleukin-1 Beta (IL-1β) Total Amount
Total amount of IL-1β in peri-implant sulcus fluid (pg per implant, two pooled paper strips each collected for 30 s), measured by enzyme-linked immunosorbent assay (ELISA). Changes from baseline were compared between one-piece and two-piece bone-level implants with peri-implant mucositis. Baseline values were also compared between implants with peri-implant health and peri-implant mucositis of both designs.
Time frame: Baseline, 1 month, and 3 months after treatment
Change in Peri-Implant Sulcus Fluid Interleukin-10 (IL-10) Total Amount
Total amount of IL-10 in peri-implant sulcus fluid (pg per implant, two pooled paper strips each collected for 30 s), measured by ELISA.
Time frame: Baseline, 1 month, and 3 months after treatment
Change in Peri-Implant Sulcus Fluid Matrix Metalloproteinase-8 (MMP-8) Total Amount
Total amount of MMP-8 in peri-implant sulcus fluid (ng per implant, two pooled paper strips each collected for 30 s), measured by ELISA.
Time frame: Baseline, 1 month, and 3 months after treatment
Change in Peri-Implant Sulcus Fluid Tissue Inhibitor of Metalloproteinases-1 (TIMP-1) Total Amount
Total amount of TIMP-1 in peri-implant sulcus fluid (pg per implant, two pooled paper strips each collected for 30 s), measured by ELISA.
Time frame: Baseline, 1 month, and 3 months after treatment
Change in Peri-Implant Sulcus Fluid IL-1β/IL-10 Ratio
Ratio of the total amount of interleukin-1 beta (IL-1β) to the total amount of interleukin-10 (IL-10) in peri-implant sulcus fluid (pg/pg), calculated for each implant from enzyme-linked immunosorbent assay (ELISA) measurements.
Time frame: Baseline, 1 month, and 3 months after treatment
Change in Peri-Implant Sulcus Fluid MMP-8/TIMP-1 Ratio
Ratio of the total amount of matrix metalloproteinase-8 (MMP-8, ng) to the total amount of tissue inhibitor of metalloproteinases-1 (TIMP-1, pg) in peri-implant sulcus fluid (ng/pg), calculated for each implant from enzyme-linked immunosorbent assay (ELISA) measurements.
Time frame: Baseline, 1 month, and 3 months after treatment
Change in Plaque Index
Plaque index recorded at six sites around the implant and averaged per implant (score 0 to 3, higher scores indicate more plaque).
Time frame: Baseline, 1 month, and 3 months after treatment
Change in Gingival Index
Gingival index recorded at six sites around the implant and averaged per implant (score 0 to 3, higher scores indicate more inflammation).
Time frame: Baseline, 1 month, and 3 months after treatment
Change in Probing Depth
Probing depth measured at six sites around the implant with a plastic periodontal probe and averaged per implant (mm).
Time frame: Baseline, 1 month, and 3 months after treatment
Change in Bleeding on Probing
Percentage of the six sites around the implant showing bleeding within approximately 10 s after gentle probing.
Time frame: Baseline, 1 month, and 3 months after treatment
Peri-Implant Soft-Tissue Phenotype
Phenotype assessed with a color-coded probe and classified as thin, medium, thick, or very thick, compared between one-piece and two-piece bone-level implants.
Time frame: Baseline
Peri-Implant Mucosal Thickness
Mucosal thickness measured by transgingival probing at 1, 2, and 3 mm apical to the buccal mucosal margin (mm), compared between one-piece and two-piece bone-level implants.
Time frame: Baseline
Keratinized Mucosal Width
Distance from the free mucosal margin to the mucogingival junction at the mid-buccal aspect of the implant (mm).
Time frame: Baseline
Change in Relative Abundance of Porphyromonas gingivalis in Subgingival Plaque
Relative abundance of Porphyromonas gingivalis in subgingival plaque determined by quantitative polymerase chain reaction (qPCR) and expressed as ΔCt (cycle threshold of Porphyromonas gingivalis minus cycle threshold of the 16S rRNA gene). Lower values indicate higher relative abundance. Non-detected samples (no amplification within 40 cycles) were assigned a Ct of 40.
Time frame: Baseline, 1 month, and 3 months after treatment
Change in Relative Abundance of Fusobacterium nucleatum in Subgingival Plaque
Relative abundance of Fusobacterium nucleatum in subgingival plaque determined by quantitative polymerase chain reaction (qPCR) and expressed as ΔCt (cycle threshold of Fusobacterium nucleatum minus cycle threshold of the 16S rRNA gene). Lower values indicate higher relative abundance. Non-detected samples (no amplification within 40 cycles) were assigned a Ct of 40.
Time frame: Baseline, 1 month, and 3 months after treatment
Change in Relative Abundance of Treponema denticola in Subgingival Plaque
Relative abundance of Treponema denticola in subgingival plaque determined by quantitative polymerase chain reaction (qPCR) and expressed as ΔCt (cycle threshold of Treponema denticola minus cycle threshold of the 16S rRNA gene). Lower values indicate higher relative abundance. Non-detected samples (no amplification within 40 cycles) were assigned a Ct of 40.
Time frame: Baseline, 1 month, and 3 months after treatment
Change in Relative Abundance of Filifactor alocis in Subgingival Plaque
Relative abundance of Filifactor alocis in subgingival plaque determined by quantitative polymerase chain reaction (qPCR) and expressed as ΔCt (cycle threshold of Filifactor alocis minus cycle threshold of the 16S rRNA gene). Lower values indicate higher relative abundance. Non-detected samples (no amplification within 40 cycles) were assigned a Ct of 40.
Time frame: Baseline, 1 month, and 3 months after treatment
Plan to share: Yes — De-identified individual participant data underlying the results reported in the publication, including clinical periodontal and peri-implant parameters, peri-implant sulcus fluid biomarker levels, and quantitative PCR results, will be shared.
Supporting information: Study protocol
Time frame: Data will be available after publication of the main results and for 5 years thereafter.
Access criteria: Data will be shared with qualified researchers who submit a methodologically sound proposal to the principal investigator, upon reasonable request and with a data sharing agreement, subject to approval by the İnönü University Clinical Research Ethics Committee where required.
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Cuneyt Asim Aral