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Background: The acute-phase response involves molecules including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and C-reactive protein (CRP). This study aimed to determine whether subgingival scaling resulted in rapid changes in plasma concentrations of these molecules. Methods: Twenty-three non-smoking adults with chronic periodontitis received subgingival scaling for 60 minutes. Venous blood samples were taken at 0, 15. 30, 60, and 120 minutes. TNF-α and IL-6 were assayed from all samples and CRP From the baseline and final samples. Lipopolysaccharide (LPS) was assayed at 0, 15, and 30 minutes using limulus lysate assay (LAL) and EndoCAb Ig assays. Results: LPS assays were suggestive of a transient low-grade bacteremia, but changes in LPS approaching significance (P = 0.061) were seen with LAL only. There was a significant increase in circulating TNF-α (P = 0.0387) and IL-6 (P <0.0001), and the degree of charge in TNF-α was correlated with the severity of periodontal breakdown (P = 0.001). There was also a significant correlation between levels of IL-6 and TNF-α (P <0.001). Conclusions: Chronic periodontitis patients undergoing an episode of subgingival scaling show a significant elevation in circulating TNF-α and IL-6. This may account for anecdotal reports of pyrexia following treatment and may be significant in terms of the relationship between periodontal disease, bacteremia, and cardiovascular disease. [ABSTRACT FROM AUTHOR]

Soluble CD44 isoforms have been reported as markers of specific malignancies and inflammatory diseases. However, recent reports suggest tobacco smoking may lead to an elevation in the circulating concentration of specific CD44 variants. We, therefore, investigated the effect of smoking status on circulating levels of total sCD44. Total soluble CD44 was measured by enzyme-linked immunosorbent assay in the serum of two age- and gender-matched groups consisting of smokers (n= 19) and non-smokers (n= 20). Smoking status was confirmed by analysis of serum cotinine. The concentration of total sCD44 was found to be significantly elevated in smokers compared with non-smokers (p= 0.025). The observation that total sCD44 concentration is raised in smokers may have relevance to the aetiology of smoking-associated diseases. The effect of smoking on sCD44 concentrations should be considered when assessing the role of sCD44 as a marker of inflammatory disease, cancer, or other disease processes. [ABSTRACT FROM AUTHOR]