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Phagocytic Function of Salivary PMN After Smoking or Secondary Smoking
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AbstractAlterations in polymorphonuclear leukocyte (PMN) functions, such as phagocytosis, Chemotaxis, and oxidative burst, play a pivotal role in periodontal pathogenesis. In addition, previous studies have demonstrated a strong relationship between smoking and periodontal disease. In the present study, the effect of cigarette smoking or passive smoking (secondary smoking) on the phagocytic function of salivary PMN (SPMN) was investigated. Twenty volunteers with clinically healthy gingiva (10 smokers, 10 non‐smokers) participated in this study. In a small room, the smokers and passive smokers (non‐smokers) were instructed to smoke and breathe, respectively, in an identical, specific way for about 4 minutes. SPMN was isolated immediately before and after smoking or passive smoking. PMN was then incubated with fluoresbrite beads for 45 minutes at 37°C and the phagocytic status estimated by using a flow cytometer. Cell viability was determined by trypan blue exclusion (smokers before smoking: 88.3%; smokers after smoking: 89.6%; non‐smokers before passive smoking: 89.0%; non‐smokers after passive smoking: 89.4%). In both smokers and passive smokers, the proportion of phagocytic cells increased between before and after smoking (smokers before: 33.2%; after: 42.1%; passive smokers before: 36.2%; after: 44.1%). Both increases were statistically significant (P < 0.01). These results demonstrate that the phagocytic activity of SPMN intensifies after smoking and passive smoking. They also suggest that certain substances in cigarette smoke, perhaps nicotine, overstimulate the host response in the oral cavity. Ann Periodontol 1998;3:102–107.
Title: Phagocytic Function of Salivary PMN After Smoking or Secondary Smoking
Description:
AbstractAlterations in polymorphonuclear leukocyte (PMN) functions, such as phagocytosis, Chemotaxis, and oxidative burst, play a pivotal role in periodontal pathogenesis.
In addition, previous studies have demonstrated a strong relationship between smoking and periodontal disease.
In the present study, the effect of cigarette smoking or passive smoking (secondary smoking) on the phagocytic function of salivary PMN (SPMN) was investigated.
Twenty volunteers with clinically healthy gingiva (10 smokers, 10 non‐smokers) participated in this study.
In a small room, the smokers and passive smokers (non‐smokers) were instructed to smoke and breathe, respectively, in an identical, specific way for about 4 minutes.
SPMN was isolated immediately before and after smoking or passive smoking.
PMN was then incubated with fluoresbrite beads for 45 minutes at 37°C and the phagocytic status estimated by using a flow cytometer.
Cell viability was determined by trypan blue exclusion (smokers before smoking: 88.
3%; smokers after smoking: 89.
6%; non‐smokers before passive smoking: 89.
0%; non‐smokers after passive smoking: 89.
4%).
In both smokers and passive smokers, the proportion of phagocytic cells increased between before and after smoking (smokers before: 33.
2%; after: 42.
1%; passive smokers before: 36.
2%; after: 44.
1%).
Both increases were statistically significant (P < 0.
01).
These results demonstrate that the phagocytic activity of SPMN intensifies after smoking and passive smoking.
They also suggest that certain substances in cigarette smoke, perhaps nicotine, overstimulate the host response in the oral cavity.
Ann Periodontol 1998;3:102–107.
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