Wu et al1 have shown that periodontal disease is another putative and independent risk factor for cerebrovascular disease, particularly for ischemic stroke. Presently, it is unknown whether the association between periodontal disease and stroke is causal. Several pathogenic pathways make a causal linkage possible. Beck at al2 hypothesized that subjects with genetically determined strong monocytic response to bacterial antigens could be at high risk for developing both periodontal disease and atherosclerosis. It is also possible that a susceptibility to strong inflammatory response could increase the risk of both periodontitis and stroke. Inflammation in the vessel wall plays an essential role not only in the initiation and progression of atherosclerosis but also in the erosion or fissuration of plaques and eventually in the rupture of plaques.3
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Probability of death within 1 year according to different patterns of changes in serum c-reactive protein levels from admission through discharge. The patients were grouped according to different patterns of c-reactive protein levels from admission to discharge. Group 1 indicates a persistently normal pattern (n = 34 [17.6%]); group 2, an increasing pattern (n = 13 [6.8%]); group 3, a decreasing pattern (n = 57 [29.5%]); and group 4, a pattern of persistent elevation (n = 89 [46.1%]) (log-rank test, P<.001; χ2 test for trend, P<.001). The risk of death at 1 year was derived from Kaplan-Meier curves. The risk was 2.2% (95% confidence interval [CI], 0.3%-13.8%) for patients with a persistently normal pattern; 20.0% (95% CI, 6.6%-47.1%) for those with an increasing pattern; 0% (95% CI, 0%-6.3%) for those with a decreasing pattern; and 27.8% (95% CI, 19.6%-37.9%) for those with a pattern of persistent elevation.
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