DKK-3 rs11544814 and CFH rs10737680 Polymorphism and Protein Levels With Non Surgical Periodontal Therapy in Periodontitis Patients With and Without CAD

NCT05828368 | Unknown

• 1 other identifier: 000
• Study Type: interventional
• Target: 160
• Locations: 1 country
• Sites: 2

Brief Summary

Untreated periodontal infection may result in transient bacteremia and toxaemia which may be the cause of adverse systemic events, leading to various systemic disorders. Amongst all the systemic diseases, cardiovascular disease has been recognized as a major systemic inflammatory condition that present similarities with periodontal disease. Increased systemic biomarkers of inflammation associated with periodontal disease have been interpreted as a mechanistic link between periodontitis and cardiovascular diseases. Genetic factors are also known to play a pivotal role in influencing the inflammatory and immune response. Genetic polymorphisms are alterations in the DNA sequence found in general population. Most forms of periodontitis represent a life-long account of interactions between the genome and the environment. The previous literature has stated a strong association of genetic polymorphisms in periodontitis and coronary artery diseases. Identifying these polymorphisms can potentially lead to a better understanding of the mechanisms modulating the expression of inflammatory mediators as well as provides potential therapeutic targets in the prevention of periodontal disease. Two such novel polymorphisms have gained attention recently, namely the Dickkopf-3 and complement factor H polymorphisms. Dickkopf-3 belongs to Dickkopf family of glycoproteins. Dickkopf-3 has been mainly investigated in oncology for its role as a tumor suppressor gene and as a therapeutic target in several types of human carcinomas. Recently, Dickkopf-3 gained attention as an emerging biomarker for cardiovascular and renal diseases. Dickkopf-3 has shown to play a role in pathophysiology of arterial wall thickening and abnormality implicated in atherosclerosis. However, genetic polymorphism of Dickkopf-3 rs11544814 and complement factor H rs10737680 its protein levels have never been investigated in subgingival plaque samples of periodontitis patients with coronary artery disease specifically before and after non-surgical therapy. This may further improve our understanding of the influence of this polymorphism on the above mentioned systemic diseases.

Conditions

Periodontal Diseases

Keywords

Periodontitis; Cardiovascular disease; Non surgical periodontal therapy; Biomarker

Outcome Measures

Primary Outcomes (4)

• Change in periodontal parameters

  Change in Periodontal Probing Depth (measured in mm higher value indicate disease progression)

  Two years

• Change in periodontal variables

  Change in Clinical Attachment Level (measured in mm higher value indicate disease progression)

  Two years

• Change in periodontal criteria

  Change in Plaque Index (measured as a ratio, range: 0 to 3, maximum value indicates worse outcome and minimum value indicates better outcome )

  Two years

• Change in periodontal variables

  Change in Gingival index (measured as a ratio, higher value indicates severity of gingival inflammation )

  Two years

Study Arms (4)

GROUP I: 40 systemically healthy subjects with healthy periodontium.

NO INTERVENTION

Systemically healthy subjects with healthy periodontium having probing pocket depth (PPD) ≤3mm, no clinical attachment loss (CAL=0) and bleeding on probing ≤ 10% of sites.

GROUP II: 40 periodontitis patients without coronary artery disease

EXPERIMENTAL

Systemically healthy subjects with periodontitis having interdental clinical attachment loss ≥ 3-5mm (stage II/III periodontitis) and probing pocket depth (PPD) ≥5mm (stage II/III periodontitis) and bleeding on probing ≥10% of sites.

Procedure: Non surgical periodontal therapy

GROUP III: 40 coronary artery disease patients without periodontitis.

EXPERIMENTAL

Patients diagnosed with coronary artery disease with healthy periodontium having probing pocket depth (PPD)≤3mm, no clinical attachment loss (CAL=0) and bleeding on probing ≤ 10% of sites (CAD).

Procedure: Non surgical periodontal therapy

GROUP IV: 40 periodontitis patients with coronary artery disease.

EXPERIMENTAL

Coronary artery disease (CAD) patients with periodontitis having interdental clinical attachment loss ≥3-5mm (stage II/III periodontitis) and probing pocket depth (PPD) ≥5mm (stage II/III periodontitis) and bleeding on probing ≥ 10%.

Procedure: Non surgical periodontal therapy

Interventions

Non surgical periodontal therapy PROCEDURE

Scaling and root planing is a deep cleaning below the gumline used to treat gum disease. Gum disease is caused by a sticky film of bacteria called plaque. Plaque is always forming on your teeth, but if they aren't cleaned well, the bacteria in plaque can cause your gums to become inflamed.

Also known as: Scaling and root planing

GROUP II: 40 periodontitis patients without coronary artery disease; GROUP III: 40 coronary artery disease patients without periodontitis.; GROUP IV: 40 periodontitis patients with coronary artery disease.

Eligibility Criteria

• Age: 30 Years - 65 Years
• Sex: all
• Healthy Volunteers: Yes
• Age Groups: Adult (18-64), Older Adult (65+)

You may qualify if:

• Patients willing to participate in the study.
• Male and female patients within the age group of 30-65 years.
• Patients having ≥ 10 remaining natural teeth.
• No history of long term antibiotic use in past 6 months.

You may not qualify if:

• Subjects with systemic conditions such as type I and type II diabetes mellitus, respiratory diseases, renal disease, liver disease, rheumatoid arthritis, allergy, advanced malignancies/neoplasm and HIV infection will be excluded from the present investigation.
• Subjects on drugs such as corticosteroids or antibiotics within 6 months of investigation or antiepileptic drugs (phenytoin or cyclosporine) having an impact on periodontal tissues will be excluded.
• Pregnant women (pregnancy may alter the oral flora).
• Current smokers and individuals who quit smoking less than 6 months.
• Patients who have undergone periodontal therapy within the previous 6 months.

Sponsors & Collaborators

• Meenakshi Ammal Dental College and Hospital: lead

Study Sites (2)

Meenakshi Ammal Dental college and hospital

Chennai, Tamil Nadu, 600095, India

Location

Frontier lifeline Hospital

Chennai, Tamil Nadu, 600101, India

Location

Related Publications (1)

• Cheng WL, Yang Y, Zhang XJ, Guo J, Gong J, Gong FH, She ZG, Huang Z, Xia H, Li H. Dickkopf-3 Ablation Attenuates the Development of Atherosclerosis in ApoE-Deficient Mice. J Am Heart Assoc. 2017 Feb 20;6(2):e004690. doi: 10.1161/JAHA.116.004690.

  PMID: 28219919 BACKGROUND

MeSH Terms

Conditions

Periodontal Diseases; Periodontitis; Cardiovascular Diseases

Interventions

Tooth Exfoliation; Root Planing

Condition Hierarchy (Ancestors)

Mouth Diseases; Stomatognathic Diseases

Intervention Hierarchy (Ancestors)

Dental Physiological Phenomena; Digestive System and Oral Physiological Phenomena; Dental Scaling; Dental Prophylaxis; Periodontics; Dentistry; Subgingival Curettage; Preventive Dentistry

Central Study Contacts

Jaideep Mahendra, MDS, Ph.D Post Doc(USA)

CONTACT

9444963973; jaideep_m_23@yahoo.co.in

Bawatharani M, BDS

CONTACT

9043365789; bawa1397@gmail.com

Study Design

• Study Type: interventional
• Phase: not applicable
• Allocation: NON RANDOMIZED
• Masking: NONE
• Purpose: TREATMENT
• Intervention Model: PARALLEL
• Sponsor Type: OTHER
• Responsible Party: PRINCIPAL INVESTIGATOR
• PI Title: Professor department of periodontology

Study Record Dates

• First Submitted: April 12, 2023
• First Posted: April 25, 2023
• Study Start: June 1, 2023
• Primary Completion: January 31, 2025
• Study Completion: April 30, 2025
• Last Updated: May 22, 2023

Record last verified: 2023-05

Data Sharing

• IPD Sharing: Will not share

Locations

IN (2)