Discussion - References.
Microorganisms from oral focal infections may disseminate throughout the body and subsequently colonize extraoral tissues. During septicaemia, microorganisms from the oral cavity may attach to and invade sites along the arterial tree. This theory was originally formulated to address the putative association between periodontal disease and cardiovascular disease. The theory could also apply to microorganisms associated with endodontic infections due to bacteraemia after endodontic therapy (Debelian et al . 1995, Debelian et al . 1998). The interactions between the bacteria and the vascular cells could initiate, or more likely, exacerbate the inflammatory lesion of atherosclerosis (Ross 1999).
In contrast to the focal infection theory, microorganisms from endodontic infections may not be seeding distant sites in the body, but rather the dental pulp may be infected by a general bacteraemia (Drancourt et al . 1998, Aboudharam et al. 2000). Therefore, bacteria found in the dental pulp could be a reflection of microorganisms found systemically. These bacteria may be indicators of pathogens causing morbidity at extraoral sites. More specifically, invasive bacteria in the dental pulp may be indicative of bacteria causing disease at the endothelium.
Figure 3. Invasion of human coronary artery endothelial cells by clinical isolates. Bacteria were isolated from infected root canals and tested using the antibiotic protection assay. Error bars represent the standard deviation (n = 3).
The invasion ability of strains of P. endodontalis in this study was heterogeneous. Of the three strains tested, only P. endodontalis ATCC 35406 was invasive. This finding was not unexpected, since previous studies have demonstrated that the invasion abilities of both P. gingivalis and P. intermedia vary amongst the different strains (Dorn et al. 1998). Conversely, certain strains of P. loeschii, P. nigrescens, and P. tannerae that were not tested in this study may be invasive. The different strains of BPBs from the oral cavity vary in their ability to invade nonphagocytic cells. The intracellular location of P. endodontalis was different from that of P. gingivalis. Although both are invasive, the two microorganisms have evolved different mechanisms of controlling their intracellular environment in order to survive (Hackstadt 2000).
In summary, we have demonstrated that some, but not all, microorganisms associated with endodontic infections can invade human coronary artery endothelial cells (HCAEC) and coronary artery smooth muscle cells (CASMC). A next step would involve animal models to determine whether the bacteraemic conditions would produce the same effect in vivo. If the hypothesis regarding atherosclerotic exacerbations caused by the direct interactions between oral bacteria and vascular cells is correct, then microorganisms in the pulp chamber may represent a source of infectious organisms that contribute to the pathogenesis of CHD.
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