The involvement of nervous and some inflammatory response mechanisms in the acute snuff-induced gingival hyperaemia in humans.
OBJECTIVE
Tobacco users and especially cigarette smokers are at higher risk than non-smokers for periodontal disease. The pathogenic mechanism has been proposed to be the vasoconstrictive properties of nicotine, with reduced gingival blood flow (GBF) as a contributing factor in the development of periodontal disease. However, in a previous study in humans, we found GBF to increase in response to acute exposure to snuff. The present study was designed to investigate whether the tobacco-induced acute GBF increase is dependent on intact nervous conduction. We further investigated the effect of piroxicam (NSAID) and dexchlorpheniramin (DCPA) (antihistamine) on the snuff-induced responses in the gingiva, to see if chemical mediators of inflammation also influenced the response.


METHODS
Laser Doppler flowmetry (LDF) was used to measure gingival blood flow bilaterally in the buccal maxillary gingiva, in the forehead skin and in the thumb. Also arterial blood pressure (BP) and heart rate (HR) were monitored. Infraorbital nerve block anaesthesia (INB), superficial mucosal anaesthesia, 20 mg piroxicam or 2 mg DCPA were used in combination with snuff to study the vascular responses to 500 mg snuff (1% nicotine).


RESULTS
Snuff induced a rapid increase in GBF that was higher than the increase in BP, indicating an active vasodilatation. The snuff-induced vasodilatation was partly blocked by INB and more so by superficial mucosal anaesthesia. Piroxicam and DCPA exerted diverse effects on vascular homeostasis but had no effect on the snuff-induced vasodilatation in the gingiva.


CONCLUSIONS
The results of this study confirm that snuff induces local gingival vasodilatation, and imply that this vasodilatation most likely is a summation of responses due to both autonomic and antidromic reflex mechanisms. We further discuss the possible involvement of the nervously mediated effects of tobacco and nicotine on vascular homeostasis and in tobacco-associated periodontitis.
Mavropoulos
Antonios
A
Department of Oral Biology, Faculty of Dentistry, University of Oslo, Blindern, Norway.
Aars
Harald
H
Brodin
Pål
P
D000293:Adolescent; D000328:Adult; D000779:Anesthetics, Local / Q000494:pharmacology; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D002744:Chlorpheniramine / Q000494:pharmacology; D005260:Female; D005881:Gingiva / Q000098:blood supply*; D006634:Histamine H1 Antagonists / Q000494:pharmacology; D006801:Humans; D006940:Hyperemia / Q000209:etiology; D018836:Inflammation Mediators / Q000378:metabolism; D017078:Laser-Doppler Flowmetry; D008297:Male; D009431:Neural Conduction / Q000187:drug effects; D020078:Neurogenic Inflammation / Q000209:etiology*; D009538:Nicotine / Q000031:analogs & derivatives / Q000494:pharmacology; D018722:Nicotinic Agonists / Q000494:pharmacology; D010894:Piroxicam / Q000494:pharmacology; D011109:Polymethacrylic Acids / Q000494:pharmacology; D011145:Polyvinyls / Q000494:pharmacology; D018709:Statistics, Nonparametric; D061485:Tobacco Use Cessation Devices; D014030:Tobacco, Smokeless / Q000009:adverse effects*; D014664:Vasodilation / Q000187:drug effects*
D000779:Anesthetics, Local; D000894:Anti-Inflammatory Agents, Non-Steroidal; D006634:Histamine H1 Antagonists; D018836:Inflammation Mediators; D018722:Nicotinic Agonists; D011109:Polymethacrylic Acids; D011145:Polyvinyls; D010894:Piroxicam; C018904:dexchlorpheniramine; D002744:Chlorpheniramine; D009538:Nicotine