PeriodontitisNCT05281848
Effect of Smoking and Periodontal Therapy on Salivary and Gingival Crevicular IL-17 and IL-35
A study testing Non-surgical periodontal treatment in people with Periodontitis and Periodontal Diseases, run by Gazi University at 2 sites in Turkey (Türkiye).
Trial summary
Periodontal diseases are among the major causes of tooth loss. Smoking may play a role as a contributing factor in the development of periodontitis by reducing the immune response. Read more about this study
- Who is it for?
- Ages 18 to 70 yearsHealthy volunteers can take part
- Conditions the study is for
- Periodontitis, Periodontal Diseases, Smoking
- What is being tested?
- Non-surgical periodontal treatment
- Type of treatment
- Surgery or procedure
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 55 participants
- Where
- 2 sitesTurkey (Türkiye)
- Study dates
- 1 Jan 2018to 7 Mar 2022
- Phase
- Interventional
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 70 years
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Who may be able to join
- To be volunteer to participate in the study
- To be over 18
- Being systemically healthy
- Having greater than or equal to 15 teeth out of 3rd molar teeth
- To have localized or generalized periodontitis for the experimental group (clinical attachment loss in at least 6 surrounding areas and presence of greater than or equal to 5 mm periodontal pocket)
- For Smoking group; more than 10 cigarettes a day for more than 5 years
- For non-smokers; have not smoked for at least 3 years.
Who cannot join
- Have any systemic disease affecting periodontal condition
- To receive periodontal treatment in the last 6 months
- Use any medication that may affect the inflammatory process in the last 3 months
- Use local or systemic antibiotics in the last 3 months
- Pregnancy or lactation for female patients
- Regular use of mouthwash
Trial locations and contacts
2 sites in 1 country.
Turkey (Türkiye)2 sites
Gazi University Faculty of Dentistry
Ankara, 06500
Gazi University Faculty of Medicine Immunology Department
Ankara, 06560
About this study
Official title: Evaluation of the Effect of Non-surgical Periodontal Treatment on Salivary and Gingival Crevicular Fluid Levels of IL-17 and IL-35 in Periodontitis Patients as Smoker and Non-smoker
Periodontal diseases are among the major causes of tooth loss. Smoking may play a role as a contributing factor in the development of periodontitis by reducing the immune response. The role of cytokines in the pathogenesis of periodontal disease is clearly indicated in the literature; it has been shown that microorganisms that cause periodontal disease cause cytokine increase in saliva, gingival tissue and gingival crevicular fluid. Among these cytokines, interleukin (IL) -17 is proinflammatory and IL-35 is antiinflammatory and has been associated with periodontal disease.
Read the detailed description
Periodontal diseases are among the complex inflammatory diseases that are considered among the leading causes of tooth loss, mostly observed with multiple etiological factors. The complexity of periodontal disease is due to the presence of the biofilm and the accompanying host response together.
Smoking, which is considered as one of the risk factors in terms of periodontitis, is one of the most preventable risk factors that affect the periodonium with many different mechanisms. Smoking plays a role in the etiopathogenesis of periodontitis, with its physiological changes in gingival tissue and its effects on host response and is considered to be an established risk factor. Although the effects of smoking on host response and its role in increasing the risk of periodontal disease are still being investigated, its effects on natural and acquired immune response cells have been studied separately. Consequently, components of cigarette suppress the immune system's defense responses; however, it has been reported to exacerbate pathological reactions.
The process of progression from periodontal health to periodontitis is formed by biofilm pathogens and host immune responses activated by these microorganisms. Intercellular communication is crucial during the progression of chronic inflammatory diseases, such as periodontitis. Cytokines, one of these ways of communication, are soluble proteins produced by various types of cells, such as structural and inflammatory cells, responsible for maintaining a complex network of communication between homotypic and heterotypic cell groups.
Interleukin-17 (IL-17) is a pro-inflammatory cytokine mostly stimulated from Th17 cells, stimulating inflammatory processes with many different mechanisms.
IL-35 inhibits the differentiation of Th17 cells and suppresses IL-17 production and therefore plays a protective role in Th17-related diseases.
There are many studies evaluating the effect of non-surgical periodontal treatment on individuals with smokers with periodontitis. However, the obtained results do not allow a clear data to be revealed. To exemplify, when the studies which investigates the evaluation of non-surgical periodontal treatment on IL-17 levels were evaluated, contradictory results were determined. In addition, as a result of our research, no studies evaluating the effects of non-surgical periodontal treatment on IL-35 levels in smokers with periodontitis have not been found.
- Conditions
- Periodontitis, Periodontal Diseases, Smoking, Smoking, Tobacco
- Being tested
- Non-surgical periodontal treatment
- Keywords
- periodontitis, non-surgical periodontal treatment, IL-17, IL-35, saliva, gingival crevicular fluid
- Medical subject headings
- Periodontitis, Periodontal Diseases, Smoking, Tobacco Smoking
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Non-surgical periodontal treatmentProcedure or surgery
Non-surgical periodontal treatment includes periodontal prophylaxis and root planning. No other methods or any of drugs will be used.
| Study group | Role | What they receive |
|---|---|---|
| Smoker-Periodontitis; Non-surgical periodontal treatment | Active comparator | Not described Receives: Procedure: Non-surgical periodontal treatment |
| Nonsmoker-Periodontitis;Non-surgical periodontal treatment | Active comparator | Not described Receives: Procedure: Non-surgical periodontal treatment |
| Healthy | No intervention | Not described |
What is being measured
The primary outcome is the main question the study is designed to answer.
IL-17 levels in gingival crevicular fluid
by ELISA method
Measured: Change from baseline to 1st month after non-surgical periodontal treatment
IL-17 levels in saliva
by ELISA method
Measured: Change from baseline to 1st month after non-surgical periodontal treatment
IL-35 levels in gingival crevicular fluid
by ELISA method
Measured: Change from baseline to 1st month after non-surgical periodontal treatment
IL-35 levels in saliva
by ELISA method
Measured: Change from baseline to 1st month after non-surgical periodontal treatment
Secondary outcomes (5)
Plaque Index (PI)
by using Williams periodontal probe; Scores from 0 to 3, 0 is no visible plaque, 3 is visible plaque or dental calculus.
Measured: Change from baseline to 1st month after non-surgical periodontal treatment
Gingival Index (GI)
by using Williams periodontal probe; Scores from 0 to 3, 0 is healthy gingiva, 3 is diseased gingiva with spontaneous bleeding.
Measured: Change from baseline to 1st month after non-surgical periodontal treatment
Pocket Depth (PD)
by using Williams periodontal probe with milimeter signs; Pocket Depth is registered by milimeters.
Measured: Change from baseline to 1st month after non-surgical periodontal treatment
Bleeding in Probing Index (BOP)
by using Williams periodontal probe; BOP is registered with + or - according to the presence of bleeding on probing.
Measured: Change from baseline to 1st month after non-surgical periodontal treatment
Clinical Attachment Loss (CAL)
by using Williams periodontal probe with milimeter signs; CAL is registered by milimeters.
Measured: Change from baseline to 1st month after non-surgical periodontal treatment
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted16 Mar 2022
- Study start1 Jan 2018
- Primary completion1 Jun 2019
- Study completion7 Mar 2022
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (13)Papers the sponsor has linked to this study.
- Other trials for PeriodontitisStudies of the same condition, open and under way.
- More trials run by Gazi UniversityThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Model description
- A total of 55 subjects will be grouped as: 18 non-smoker patients with periodontitis (Group 1), 19 smoker patients with periodontitis (Group 2), 18 non-smoker and periodontally healthy individuals who will refer to our department. Spitting method will be used for collecting saliva samples. The paper strip method will be used for gingival crevicular fluid (GCF) sample collection. Samples will be taken from the mesial and distal surfaces of the teeth (healthy or have greater than or equal to 5mm pocket depth) after isolation from the saliva. Paper strips will be transferred to polypropylene tubes and stored at -30 ° C until inspection. After collecting samples, non-surgical periodontal treatment will be performed to all individuals which are classified as Group 1 and Group 2. Collection of saliva and GCF samples will be repeated at the 1st month after the end of treatment. ELISA kits will be used for the detection of saliva and GCF's IL-17 and IL-35.
- Masking
- None (open label)
- Enrolment
- 55 participants (actual)
Sponsor and investigators
- Lead sponsor
- Gazi University
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Ezgi Sıla Taşkaldıran, Gazi University
- Investigators
- Gülay Tüter, Professor, Study director, Gazi University Dentistry Faculty Department of Periodontology
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT05281848
- Sponsor's protocol ID
- 21071282-050.99
- Status last verified
- Mar 2022
- First submitted
- 2 Mar 2020
- Last updated
- 16 Mar 2022
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Page RC, Kornman KS. The pathogenesis of human periodontitis: an introduction. Periodontol 2000. 1997 Jun;14:9-11. doi: 10.1111/j.1600-0757.1997.tb00189.x. No abstract available.
PubMed 9567963Papapanou PN, Sanz M, Buduneli N, Dietrich T, Feres M, Fine DH, Flemmig TF, Garcia R, Giannobile WV, Graziani F, Greenwell H, Herrera D, Kao RT, Kebschull M, Kinane DF, Kirkwood KL, Kocher T, Kornman KS, Kumar PS, Loos BG, Machtei E, Meng H, Mombelli A, Needleman I, Offenbacher S, Seymour GJ, Teles R, Tonetti MS. Periodontitis: Consensus report of workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018 Jun;89 Suppl 1:S173-S182. doi: 10.1002/JPER.17-0721.
PubMed 29926951Kinane DF, Stathopoulou PG, Papapanou PN. Periodontal diseases. Nat Rev Dis Primers. 2017 Jun 22;3:17038. doi: 10.1038/nrdp.2017.38.
PubMed 28805207Page RC, Schroeder HE. Pathogenesis of inflammatory periodontal disease. A summary of current work. Lab Invest. 1976 Mar;34(3):235-49.
PubMed 765622Preshaw PM. Host modulation therapy with anti-inflammatory agents. Periodontol 2000. 2018 Feb;76(1):131-149. doi: 10.1111/prd.12148. Epub 2017 Nov 29.
PubMed 29193331Okada H, Murakami S. Cytokine expression in periodontal health and disease. Crit Rev Oral Biol Med. 1998;9(3):248-66. doi: 10.1177/10454411980090030101.
PubMed 9715365Zhang JM, An J. Cytokines, inflammation, and pain. Int Anesthesiol Clin. 2007 Spring;45(2):27-37. doi: 10.1097/AIA.0b013e318034194e.
PubMed 17426506Qiu F, Liang CL, Liu H, Zeng YQ, Hou S, Huang S, Lai X, Dai Z. Impacts of cigarette smoking on immune responsiveness: Up and down or upside down? Oncotarget. 2017 Jan 3;8(1):268-284. doi: 10.18632/oncotarget.13613.
PubMed 27902485Cua DJ, Tato CM. Innate IL-17-producing cells: the sentinels of the immune system. Nat Rev Immunol. 2010 Jul;10(7):479-89. doi: 10.1038/nri2800. Epub 2010 Jun 18.
PubMed 20559326Yao Z, Painter SL, Fanslow WC, Ulrich D, Macduff BM, Spriggs MK, Armitage RJ. Human IL-17: a novel cytokine derived from T cells. J Immunol. 1995 Dec 15;155(12):5483-6.
PubMed 7499828Vignali DA, Kuchroo VK. IL-12 family cytokines: immunological playmakers. Nat Immunol. 2012 Jul 19;13(8):722-8. doi: 10.1038/ni.2366.
PubMed 22814351Eshghipour B, Tofighi H, Nehal F, Vohra F, Javed F, Akram Z. Effect of scaling and root planing on gingival crevicular fluid cytokine/chemokine levels in smokers with chronic periodontitis: A systematic review. J Investig Clin Dent. 2018 Aug;9(3):e12327. doi: 10.1111/jicd.12327. Epub 2018 Feb 15.
PubMed 29450974Ezgi Sila T, Gulay T, Aysegul AY, Melek Y. Non-surgical periodontal treatment effects on IL-17 and IL-35 levels in smokers and non-smokers with periodontitis. Odontology. 2026 Jul;114(3):1481-1492. doi: 10.1007/s10266-025-01207-0. Epub 2025 Sep 19.
PubMed 40971113
Study at a glance
From the registry record, last updated by the sponsor on 16 Mar 2022. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Evaluation of the Effect of Non-surgical Periodontal Treatment on Salivary and Gingival Crevicular Fluid Levels of IL-17 and IL-35 in Periodontitis Patients as Smoker and Non-smoker
- ClinicalTrials.gov ID
- NCT05281848
- Acronym / sponsor ID
- 21071282-050.99
- Conditions
- Periodontitis, Periodontal Diseases, Smoking, Smoking, Tobacco
- Keywords
- periodontitis, non-surgical periodontal treatment, IL-17, IL-35, saliva, gingival crevicular fluid
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 55 participants (actual)
- Lead sponsor
- Gazi UniversityUniversity, hospital or other
- Study start
- 1 Jan 2018 (actual)
- Primary completion
- 1 Jun 2019 (actual)
- Study completion
- 7 Mar 2022 (actual)
- First posted
- 16 Mar 2022 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Periodontal diseases are among the major causes of tooth loss. Smoking may play a role as a contributing factor in the development of periodontitis by reducing the immune response. The role of cytokines in the pathogenesis of periodontal disease is clearly indicated in the literature; it has been shown that microorganisms that cause periodontal disease cause cytokine increase in saliva, gingival tissue and gingival crevicular fluid. Among these cytokines, interleukin (IL) -17 is proinflammatory and IL-35 is antiinflammatory and has been associated with periodontal disease.
Detailed description
Periodontal diseases are among the complex inflammatory diseases that are considered among the leading causes of tooth loss, mostly observed with multiple etiological factors. The complexity of periodontal disease is due to the presence of the biofilm and the accompanying host response together.
Smoking, which is considered as one of the risk factors in terms of periodontitis, is one of the most preventable risk factors that affect the periodonium with many different mechanisms. Smoking plays a role in the etiopathogenesis of periodontitis, with its physiological changes in gingival tissue and its effects on host response and is considered to be an established risk factor. Although the effects of smoking on host response and its role in increasing the risk of periodontal disease are still being investigated, its effects on natural and acquired immune response cells have been studied separately. Consequently, components of cigarette suppress the immune system's defense responses; however, it has been reported to exacerbate pathological reactions.
The process of progression from periodontal health to periodontitis is formed by biofilm pathogens and host immune responses activated by these microorganisms. Intercellular communication is crucial during the progression of chronic inflammatory diseases, such as periodontitis. Cytokines, one of these ways of communication, are soluble proteins produced by various types of cells, such as structural and inflammatory cells, responsible for maintaining a complex network of communication between homotypic and heterotypic cell groups.
Interleukin-17 (IL-17) is a pro-inflammatory cytokine mostly stimulated from Th17 cells, stimulating inflammatory processes with many different mechanisms.
IL-35 inhibits the differentiation of Th17 cells and suppresses IL-17 production and therefore plays a protective role in Th17-related diseases.
There are many studies evaluating the effect of non-surgical periodontal treatment on individuals with smokers with periodontitis. However, the obtained results do not allow a clear data to be revealed. To exemplify, when the studies which investigates the evaluation of non-surgical periodontal treatment on IL-17 levels were evaluated, contradictory results were determined. In addition, as a result of our research, no studies evaluating the effects of non-surgical periodontal treatment on IL-35 levels in smokers with periodontitis have not been found.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- None (open label)
- Number of arms
- 3
- Model description
- A total of 55 subjects will be grouped as: 18 non-smoker patients with periodontitis (Group 1), 19 smoker patients with periodontitis (Group 2), 18 non-smoker and periodontally healthy individuals who will refer to our department. Spitting method will be used for collecting saliva samples. The paper strip method will be used for gingival crevicular fluid (GCF) sample collection. Samples will be taken from the mesial and distal surfaces of the teeth (healthy or have greater than or equal to 5mm pocket depth) after isolation from the saliva. Paper strips will be transferred to polypropylene tubes and stored at -30 ° C until inspection. After collecting samples, non-surgical periodontal treatment will be performed to all individuals which are classified as Group 1 and Group 2. Collection of saliva and GCF samples will be repeated at the 1st month after the end of treatment. ELISA kits will be used for the detection of saliva and GCF's IL-17 and IL-35.
| Arm | Type | Receives |
|---|---|---|
| Smoker-Periodontitis; Non-surgical periodontal treatment | Active comparator | Procedure: Non-surgical periodontal treatment |
| Nonsmoker-Periodontitis;Non-surgical periodontal treatment | Active comparator | Procedure: Non-surgical periodontal treatment |
| Healthy | No intervention | – |
Who may qualify
- Ages
- 18 to 70 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (7 listed)
- To be volunteer to participate in the study
- To be over 18
- Being systemically healthy
- Having greater than or equal to 15 teeth out of 3rd molar teeth
- To have localized or generalized periodontitis for the experimental group (clinical attachment loss in at least 6 surrounding areas and presence of greater than or equal to 5 mm periodontal pocket)
Key exclusion criteria (6 listed)
- Have any systemic disease affecting periodontal condition
- To receive periodontal treatment in the last 6 months
- Use any medication that may affect the inflammatory process in the last 3 months
- Use local or systemic antibiotics in the last 3 months
- Pregnancy or lactation for female patients
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Non-surgical periodontal treatmentNon-surgical periodontal treatment includes periodontal prophylaxis and root planning. No other methods or any of drugs will be used. | Procedure or surgery | Nonsmoker-Periodontitis;Non-surgical periodontal treatment, Smoker-Periodontitis; Non-surgical periodontal treatment |
Primary outcome
IL-17 levels in gingival crevicular fluid
Time frame: Change from baseline to 1st month after non-surgical periodontal treatment
by ELISA method
IL-17 levels in saliva
Time frame: Change from baseline to 1st month after non-surgical periodontal treatment
by ELISA method
IL-35 levels in gingival crevicular fluid
Time frame: Change from baseline to 1st month after non-surgical periodontal treatment
by ELISA method
IL-35 levels in saliva
Time frame: Change from baseline to 1st month after non-surgical periodontal treatment
by ELISA method
5 secondary outcomes
Plaque Index (PI)
Time frame: Change from baseline to 1st month after non-surgical periodontal treatment
Gingival Index (GI)
Time frame: Change from baseline to 1st month after non-surgical periodontal treatment
Pocket Depth (PD)
Time frame: Change from baseline to 1st month after non-surgical periodontal treatment
Bleeding in Probing Index (BOP)
Time frame: Change from baseline to 1st month after non-surgical periodontal treatment
Clinical Attachment Loss (CAL)
Time frame: Change from baseline to 1st month after non-surgical periodontal treatment
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 16 Mar 2022.
- Background: PubMed 9567963Page RC, Kornman KS. The pathogenesis of human periodontitis: an introduction. Periodontol 2000. 1997 Jun;14:9-11. doi: 10.1111/j.1600-0757.1997.tb00189.x. No abstract available.
- Background: PubMed 29926951Papapanou PN, Sanz M, Buduneli N, Dietrich T, Feres M, Fine DH, Flemmig TF, Garcia R, Giannobile WV, Graziani F, Greenwell H, Herrera D, Kao RT, Kebschull M, Kinane DF, Kirkwood KL, Kocher T, Kornman KS, Kumar PS, Loos BG, Machtei E, Meng H, Mombelli A, Needleman I, Offenbacher S, Seymour GJ, Teles R, Tonetti MS. Periodontitis: Consensus report of workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018 Jun;89 Suppl 1:S173-S182. doi: 10.1002/JPER.17-0721.
- Background: PubMed 28805207Kinane DF, Stathopoulou PG, Papapanou PN. Periodontal diseases. Nat Rev Dis Primers. 2017 Jun 22;3:17038. doi: 10.1038/nrdp.2017.38.
- Background: PubMed 765622Page RC, Schroeder HE. Pathogenesis of inflammatory periodontal disease. A summary of current work. Lab Invest. 1976 Mar;34(3):235-49.
- Background: PubMed 29193331Preshaw PM. Host modulation therapy with anti-inflammatory agents. Periodontol 2000. 2018 Feb;76(1):131-149. doi: 10.1111/prd.12148. Epub 2017 Nov 29.
- Background: PubMed 9715365Okada H, Murakami S. Cytokine expression in periodontal health and disease. Crit Rev Oral Biol Med. 1998;9(3):248-66. doi: 10.1177/10454411980090030101.
- Background: PubMed 17426506Zhang JM, An J. Cytokines, inflammation, and pain. Int Anesthesiol Clin. 2007 Spring;45(2):27-37. doi: 10.1097/AIA.0b013e318034194e.
- Results publication: PubMed 27902485Qiu F, Liang CL, Liu H, Zeng YQ, Hou S, Huang S, Lai X, Dai Z. Impacts of cigarette smoking on immune responsiveness: Up and down or upside down? Oncotarget. 2017 Jan 3;8(1):268-284. doi: 10.18632/oncotarget.13613.
- Results publication: PubMed 20559326Cua DJ, Tato CM. Innate IL-17-producing cells: the sentinels of the immune system. Nat Rev Immunol. 2010 Jul;10(7):479-89. doi: 10.1038/nri2800. Epub 2010 Jun 18.
- Results publication: PubMed 7499828Yao Z, Painter SL, Fanslow WC, Ulrich D, Macduff BM, Spriggs MK, Armitage RJ. Human IL-17: a novel cytokine derived from T cells. J Immunol. 1995 Dec 15;155(12):5483-6.
- Results publication: PubMed 22814351Vignali DA, Kuchroo VK. IL-12 family cytokines: immunological playmakers. Nat Immunol. 2012 Jul 19;13(8):722-8. doi: 10.1038/ni.2366.
- Results publication: PubMed 29450974Eshghipour B, Tofighi H, Nehal F, Vohra F, Javed F, Akram Z. Effect of scaling and root planing on gingival crevicular fluid cytokine/chemokine levels in smokers with chronic periodontitis: A systematic review. J Investig Clin Dent. 2018 Aug;9(3):e12327. doi: 10.1111/jicd.12327. Epub 2018 Feb 15.
- Individual participant dataSharing planned: No
Related trials for Periodontitis
Recruiting
Effect of Cryotherapeutic and Nanotherapeutic Sodium Hypochlorite on Post-Operative Endodontic Pain.
Symptomatic Irreversible Pulpitis, Symptomatic Apical Periodontitis
Active, not recruitingObservational study
A Retrospective Comparative Evaluation of Omega-3 and Resveratrol Supplementation in Patients With Periodontitis
Periodontitis
Recruiting
Probiotics Versus Antibiotics as an Adjuvant to Non-surgical Periodontal Treatment Among Smokers With Stage II, Grade B Periodontitis
Probiotics, Antibiotics
Recruiting
Effects of Different Activation Techniques on Antimicrobial Photodynamic Therapy in Apical Periodontitis
Apical Periodontitis, Endodontic Retreatment
Recruiting
Ozone Gel Versus Chlorohexidine Gel as an Adjunct to Non-Surgical Treatment of Stage II Periodontitis Grade B Among Smokers Patients
Ozone Gel, Chlorohexidine Gel
Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Gülay Tüter, Professor study director
Gazi University Dentistry Faculty Department of Periodontology
2 sites in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Non-surgical periodontal treatment in people with Periodontitis and Periodontal Diseases, run by Gazi University at 2 sites in Turkey (Türkiye).
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 7 inclusion and 6 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 16 Mar 2022. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 2 sites in Turkey (Türkiye). Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
IL-17 levels in gingival crevicular fluid (time frame: Change from baseline to 1st month after non-surgical periodontal treatment). The study lists 4 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT05281848, which also lists 13 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 16 Mar 2022.