Acute Coronary Artery Disease, Periodontal Diseases
Conditions
Brief summary
The Klotho gene was initially identified as an aging suppressor gene, but subsequent research revealed its multifaceted functions, encompassing antioxidant defense, anti-inflammatory effects, calcium and phosphorus balance, metabolic regulation, and anti-apoptotic activity. It encodes a single pass transmembrane protein and is expressed primarily in renal tubules. The Klotho protein exists in two forms: membrane-bound and secreted. Membrane Klotho acts as a co-receptor for FGF23, a bone-derived hormone, while secreted Klotho regulates various cell surface glycoproteins, including ion channels and growth factor receptors. Klotho has recently emerged as a potential biomarker for coronary heart disease, with evidence suggesting its involvement in the disease's pathophysiology. The red complex, comprising Porphyromonas gingivalis, Treponema denticola and Tannerella forsythia harbors key pathogens in adult periodontal disease. These bacteria possess various virulence factors, including fimbriae, lipopolysaccharides, and proteases in P. gingivalis, which disrupt inflammatory and immune responses and degrade connective tissue proteins. T. forsythia produces a trypsin-like protease, sialidase, hemagglutinin, and BspA, contributing to alveolar bone loss. Meanwhile, T. denticola disrupts the host cell extracellular matrix, penetrates tissue, and dysregulates immunoregulatory factors, further exacerbating periodontal disease. Similarly, Herpes Simplex Virus 1 (HSV-1), human Cytomegalovirus (HCMV) and Epstein Barr Virus (EBV) have been implicated in the pathogenesis of periodontal disease. The expressions of viruses along the red complex bacteria would provide further evidence of periodontal risk in progression of acute coronary artery disease.
Detailed description
The selected subjects will be categorized into the following groups: GROUP I: Healthy volunteers. GROUP II: Periodontitis patients without acute coronary syndrome. GROUP III: Acute coronary syndrome without periodontitis GROUP IV: Periodontitis and acute coronary syndrome
Interventions
None listed
Sponsors
Study design
Eligibility
Inclusion criteria
1. Patients willing to participate in the study. 2. Male and female patients within the age group of 30-65 years. 3. Patients having ≥ 10 remaining natural teeth. 4. No history of long-term antibiotic use in past 6 months.
Exclusion criteria
1. Subjects with systemic conditions such as type I and type I diabetes mellitus, respiratory diseases, renal disease, liver disease, rheumatoid arthritis, allergy, advanced malignancies/neoplasm and HIV infection will be excluded from the present investigation. 2. 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. 3. Pregnant women (pregnancy may alter the oral flora). 4. Current smokers and individuals who quit smoking less than 6 months. 5. Patients who have undergone periodontal therapy within the previous 6 months
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Changes in periodontal parameters | Baseline-24 months | Change in periodontal probing depth (measured in mm higher value indicate disease progression) |
| Change in periodontal variables | Baseline - 2 years | Change in Clinical attachment level (measured in mm higher value indicate disease progression) |
| Change in periodontal criteria | Baseline - 2 years | Change in plaque index (measured as a ratio, range: 0 to 3, maximum value indicates worse outcome and minimum value indicates better outcome) |