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Nonsurgical Periodontal Treatment Combined With Anti-TNF-α in Patients With Rheumatoid Arthritis and Periodontitis

Investigation of the Effect of Nonsurgical Periodontal Treatment Applied Together With Anti-TNF-α on Alveolar Bone Loss and Oxidative Stress in Patients With Rheumatoid Arthritis and Periodontitis

Status
Completed
Phases
NA
Study type
Interventional
Source
ClinicalTrials.gov
Registry ID
NCT06818045
Enrollment
46
Registered
2025-02-10
Start date
2024-03-01
Completion date
2025-04-18
Last updated
2025-04-23

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Peridontal Disease, Rheumatic Arthritis

Keywords

rheumatoid arthritis, periodontal disease, inflammation

Brief summary

Periodontitis is a multifactorial disease of the periodontium that can lead to destruction of the alveolar bone and supporting connective tissue and subsequent tooth loss. Recent studies have shown that periodontitis is associated with age, smoking habits, genetic predisposition, socioeconomic status, and various systemic diseases such as diabetes mellitus, atherosclerosis, obesity, osteoporosis, and rheumatoid arthritis (RA). RA is a chronic, systemic inflammatory disease of unknown etiology that primarily affects the joints. Periodontitis and RA have similar clinical and pathogenic features. Clinically, both diseases are characterized by local destruction of hard and soft tissues. Their pathogenesis involves the release of cytokines and matrix metalloproteinases (MMPs) from inflammatory cells. Expression of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) leads to the release of high levels of inflammatory mediators that cause bone destruction and the spread of inflammation. TNF-α is the main regulatory cytokine in both RA and periodontitis. TNF-α inhibitors (anti-TNF-α) reduce the number of inflammatory cells, osteoclast formation and bone loss. In addition, many immunological processes have been identified that are similar to both diseases. Autoreactive T cells, natural killer cells, heat shock proteins, autoantibodies and genetic factors are reported to play an important role in the inflammatory pathway of RA and periodontitis. Recently, TNF-α blocking agents (anti-TNF-α) have been developed and used for the treatment of RA. Animal and human studies have suggested that anti-TNF-α treatment may reduce the severity of periodontitis. The aim of this study was to investigate the effect of nonsurgical periodontal treatment combined with anti-TNF-α on alveolar bone loss and oxidative stress in individuals with RA and periodontitis.

Interventions

This procedure will be applied to all patients. All patients received nonsurgical periodontal treatment. Scaling root planing and subgingival debridement were performed.

OTHERPeriodontal measurements will be performed

Periodontal measurements will be performed on all patients (plaque index, gingival index, bleeding on probing, periodontal pocket depth, clinical attachment loss).

Serum and gingival crevicular fluid (GCF) samples will be collected from patients for biochemical evaluations.

OTHERNo medication will be administered to patients.

No medication will be administered to patients.

Sponsors

Hatice Yemenoğlu
Lead SponsorOTHER

Study design

Allocation
NA
Intervention model
SINGLE_GROUP
Primary purpose
PREVENTION
Masking
NONE

Eligibility

Sex/Gender
ALL
Age
18 Years to 65 Years
Healthy volunteers
No

Inclusion criteria

* Being between the ages of 18-65, * Having a confirmed diagnosis of Rheumatoid Arthritis (RA), * Having a diagnosis of Stage III-IV periodontitis, * Having at least 20 teeth,

Exclusion criteria

* Having used antibiotics for the 3 months before the study, * Being pregnant and lactating, * Having received periodontal treatment in the last 6 months, * Being diabetic. * Smoking.

Design outcomes

Primary

MeasureTime frameDescription
Periodontal pocket depthbaseline, 3rd month after non-surgical periodontal therapy, 6th month after non-surgical periodontal therapyThe distance between the pocket base and the gingival margin is measured
clinical attachment lossbaseline, 3rd month after non-surgical periodontal therapy, 6th month after non-surgical periodontal therapyThe distance between the pocket base and the cementoenamel junction is measured

Secondary

MeasureTime frameDescription
serum and GCF matrix metalloproteinase 8 (MMP8) levelbaseline, after non-surgical periodontal therapy at 3 months, after non-surgical periodontal therapy at 6 months,MMP-8 levels in serum and GCF will be measured with biochemical kits.
serum and GCF receptor activator nuclear kappa B ligand (RANKL) levelbaseline, after non-surgical periodontal therapy at 3 months, after non-surgical periodontal therapy at 6 months,RANKL levels in serum and GCF will be measured with biochemical kits.
serum total oxidant status (TAS) levelbaseline, after non-surgical periodontal therapy at 3 months, after non-surgical periodontal therapy at 6 months,TOS levels in serum will be measured with biochemical kits.
serum total antioxidant status (TAS) levelbaseline, after non-surgical periodontal therapy at 3 months, after non-surgical periodontal therapy at 6 months,TAS levels in serum will be measured with biochemical kits.
serum and GCF osteoprotegrin (OPG) levelbaseline, after non-surgical periodontal therapy at 3 months, after non-surgical periodontal therapy at 6 months,OPG levels in serum and GCF will be measured with biochemical kits.

Countries

Turkey (Türkiye)

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: May 15, 2026