OBJECTIVE: Periodontitis is a chronic inflammatory disease caused by microbial dental plaque which leads to the destruction and loss of supporting tissues of the tooth. Microbial plaque alone, however, is not enough to cause the disease. The body's response plays an important role, in which an imbalance between the pro-inflammatory and anti-inflammatory effects of cytokines leads to an inflammatory reaction. PATIENTS AND METHODS: We detected changes in mRNA expression and protein levels of MIP-1alpha, and metalloproteinases (MMP-2, MMP-9) contributing to cascades in the initiation and progression of inflammatory bone resorption and destruction of periodontal soft tissues in patients with aggressive (AP) or chronic (CP) forms of periodontitis in comparison with healthy individuals (control). RESULTS: MIP-1alpha mRNA levels were highest in AP (280 +/- 23% higher than the control) also in comparison with CP. The difference in protein level was less pronounced. MMP-2 mRNA expression values were similar (300 +/- 12% higher in comparison with control), but protein levels were lower, also when compared to CP. Only in CP MMP-9 mRNA levels were significantly higher than the control (30 +/- 8%), while protein levels were again higher in AP. Both AP and CP showed a positive correlation between the level of MIP-1a and MMP-2 (0.879, and 0.954 respectively). However, a strong positive correlation was only found between the levels of MMP-2 and MMP-9 in CP (0.812). CONCLUSIONS: MIP-1alpha, MMP-2 and MMP-9 mRNA expression, along with the concentration of proteins in saliva in patients with periodontal disease, is higher than in healthy individuals and correlates with the severity of the disease.
No clinical trial protocols linked to this paper
Clinical trials are automatically linked when NCT numbers are found in the paper's title or abstract.PICO Elements
No PICO elements extracted yet. Click "Extract PICO" to analyze this paper.
Paper Details
MeSH Terms
Associated Data
No associated datasets or code repositories found for this paper.
Related Papers
Related paper suggestions will be available in future updates.