Smoking Effects on Gingival Crevicular Fluid Volume and Antioxidant Capacity

Gingival crevicular fluid (GCF) total antioxidant capacity (TAOC) is reduced in non-smoking periodontitis patients compared to healthy controls reflecting local oxidative damage (Chapple et al. J Clin Perio 34:103-110,2007). Smoking is a major risk factor for periodontitis and cigarette smoke contains damaging free-radicals. Objective: This study examined the effects of smoking 1 cigarette (6mg tar, 0.5mg nicotine, 7mg CO) upon GCF volume and TAOC in periodontally healthy individuals, classified by expired air CO analysis as light (≤20ppm CO; n=20), heavy (≥21 ppm CO; n=20) or non-smokers (n=20). Methods: 30-second GCF samples were collected on Periopapers from the mesio-buccal sites of 3 teeth before, immediately, 10 and 60 minutes after smoking. Fluid volumes and TAOC were determined as for non-smoking periodontitis patients and controls (Brock et al. J Clin Perio 31:515-521,2004; Chapple et al. 2007). Results: Baseline GCF volumes for smokers (0.22±0.19ul, light; 0.23±0.17ul, heavy) were similar to those of non-smokers (0.24±0.31ul). In light smokers GCF volume decreased at 10 minutes (p=0.034) post-smoking but recovered to baseline levels at 60 minutes. Smoking had no effect on GCF volume in heavy smokers. Non-smokers showed reduced GCF volume immediately after smoking (0.1±0.08ul) which remained reduced at 60 minutes (0.05±0.04ul; p=0.001). Mean baseline levels of GCF TAOC in heavy smokers were higher than those of light smokers and significantly higher than those reported for non-smokers (TAOC/30sec, p=0.001). GCF TAOC of light smokers was unaffected by smoking whereas a transient reduction in GCF TAOC (concentration and amount/30seconds; p<0.006) was seen immediately post smoking in heavy smokers. Conclusion: GCF volumes are unaffected by smoking status, but GCF TAOC is higher in chronic smokers, thereby increasing local anti-radical scavenging. The decrease in GCF volume in non-smokers after smoking is not replicated in chronic smokers. These data imply compensatory mechanisms develop in smokers to protect against smoke-derived radicals.