Translation of Oral-Systemic Inflammation. Key Signaling Mechanisms
L. SHAPIRA, Hadassah and the Hebrew University Medical Center, Jerusalem, Israel
The effect of organ-specific inflammation resulted from infection on remote organs was documented in animals and humans, but the mechanism involved is still not clear. Using a mice model we had found that P. gingivalis infection in subcutaneous chambers can aggravate the course of viral infections. We hypothesize that the mechanism involved is related to the effect of the remote infection on T-cell functions. T-cells harvested from mice after sustained exposure to P. gingivalis were unable to mount a normal cytotoxic reaction. Furthermore, the immediate T-cell receptor (TCR) mediated signaling events were impaired, but the downstream machinery worked properly. Immunoblots and confocal microscopy revealed that the ζ-chain of the TCR in down-regulated by chronic exposure to P. gingivalis. This down regulation was only observed after long-term exposure to the bacteria, and was depended on the development of Th1-response, particularly the presence of IFNγ. IFNγ indirectly affects the T cells through a non-T cell population that were recruited to the spleen during chronic inflammation. The inflammation-induced immunosuppressive environment was found to be present in the spleen, but not in the lymph nodes. ζ-chain down regulation could be a physiological response in chronic inflammation that attenuates an exacerbated immune response, but this can acts as a “double-edged sword”, impairing immune responses to systemic diseases.
Bacterial Biofilms: A Role in Systemic Inflammation
M. SANZ, Complutense University, Madrid, Spain
It has been calculated that among individuals with chronic periodontitis, the surface area of the dento-gingival epithelium exposed to potential bacterial invasion and/or infiltration of antigenic microbial components is approximately 8 cm². Thus, it is not surprising that a breach of this epithelial barrier is a common occurrence in chronic periodontitis, and it is likely to result in systemic dissemination of microbes, antigens, and mediators of inflammation, which may constitute an independent risk factor for systemic inflammation and thus, to many systemic conditions, whose pathogenesis is based on chronic inflammation. In spite of the scientific evidence derived from many cross-sectional and cohort studies where these associations have been demonstrated, mostly between periodontitis and cardiovascular diseases, with pregnancy complications, with diabetes and with obesity, the role of bacterial serum dissemination and colonization at distant sites has not been fully proven. In this presentation we shall present available scientific evidence on the influence of periodontal treatment in the passage of periodontal pathogens derived from the subgingival biofilm into serum (bacteremia). We shall also present evidence on the colonization of these bacteria on atheroma plaques, derived from specimens collected from aortic arteries by endarterectomy and analysed by specific nested PCR against putative periodontal bacteria. With this available information, we shall try to develop possible clinical implications and directions for future research.
Translation of Oral-Systemic Inflammation to Preventive Outcomes
B. KLINGE, Karolinska Institutet, Huddinge, Sweden
In recent years the oral-systemic infection/inflammation link has gained renewed and increased interest. Several reports show an association between oral infection/inflammation and systemic disorders including cardiovascular diseases. Pneumonia mortality in the elderly seems to be related to poor oral health, with a prevalence of periodontal diseases.
Levels of some inflammatory markers has been found to be higher in individuals with periodontitis as compared to periodontally healthy controls, whereas levels of anti-inflammatory markers were lower. Following periodontal treatment, including preventive measures, it was shown that the local clinical signs of periodontal inflammatory burden were significantly reduced and the total body load of inflammation thus considerably decreased.
Provided a cause-relation effect of oral infection/inflammation to systemic diseases can be unquestionable established, preventive approaches to oral infection/inflammation also needs increased professional attention.