The pathogenic mechanism of oral bacteria and treatment with inhibitors.

OBJECTIVES: The objective of this study was to introduce the evidence obtained through extensive research that periodontitis increases risk of many systemic diseases. METHOD: Analysis of some oral bacteria (P. gingivalis, T. denticola, T. forsythia, A. actinomycetemcomitans, and F. nucleatum) and its related treatments and mediators by the specific methods (western blot, ELISA, etc). RESULTS: This article reviews in detail the evidence obtained through extensive research that periodontitis increases risk of many systemic diseases, including cardiovascular disease, rheumatoid arthritis, and Alzheimer's disease. These diseases are known to be associated with some certain specific gram-negative bacteria as periodontal pathogens, which induce inflammation and related diseases through TLR receptors, kinases, transcriptional factors and other cytokines. We also reviewed the latest research for inhibitors against inflammation and related diseases that have potential to be further applied clinically. In addition, based on a large amount of research evidence, we draw two tables about the mechanism of disease caused by periodontal bacteria, so that readers can easily search and analyze these research results. DISCUSSION: This review details how the periodontal bacteria and their virulence factors can trigger host immune defense and induce many systemic diseases via inflammation and invasion. This Review also addressed the latest research around inhibitors against inflammation.

The role of TNF-α induced protein 1 in the activation of pro-apoptotic proteins.

It is known that Porphyromonas gingivalis/lipopolysaccharide (P. gingivalis/LPS) induces inflammatory diseases via TNF-α-mediated transcription factors. Our recent data shows that TNFAIP1 (TNF-α induced protein 1) is related to TNF-α. However, little is known regarding how TNFAIP1 is involved in the TNF-α-dependent pathway. We therefore focused on the biological function of TNFAIP1 and examined how TNFAIP1 mediates TNF-α and other genes. We found that TNF-α was upregulated and peaks before the upregulation of apoptotic genes such as Bad, Bcl-x, Caspase 3, Catalase, Claspin, Cytochromic, Ho-1/HMOX1/HSP32, or MCI-1 in our time course with TNFAIP1-treated cells. Our findings here may serve as the foundation for future studies linking regulation of TNFAIP1 and intervention of inflammatory disease.