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.
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.
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.
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.
GROUP I * 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 * Systemically healthy subjects with periodontitis having interdental clinical attachment loss ≥ 3-5mm (stage II/III periodontitis) and probing pocket depth (PPD) ≥ 5mm (stage I/III periodontitis) and bleeding on probing ≥ 10% of sites. GROUP III * Patients diagnosed with acute coronary syndrome with healthy periodontium having probing pocket depth (PPD) ≤ 3mm, no clinical attachment loss (CAL=0) and bleeding on probing ≤ 10% of sites GROUP IV * Acute coronary syndrome 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%.
Case-control
Other
Not listed
Changes in periodontal parameters
Change in periodontal probing depth (measured in mm higher value indicate disease progression)
Change in periodontal variables
Change in Clinical attachment level (measured in mm higher value indicate disease progression)
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)
Change in periodontal variables
Changes in Gingival index (measure as a ratio, (0-3)higher value indicates severity of gingival inflammation)
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