Hyperaemic response to cigarette smoking in healthy gingiva.
OBJECTIVE
Cigarette smoking is currently considered as a risk factor for periodontal disease. Controversy exists as to whether the vasoconstrictive property of nicotine is one of the pathogenic mechanisms. To this end we tested the hypothesis that cigarette smoking is causing vasoconstriction in the healthy human gingiva.


METHODS
Gingival blood flow was continuously measured with laser Doppler flowmetry in healthy (n=13) casual consumers of tobacco. Simultaneously, recordings were made of skin blood flow in the forehead and the thumb as well as heart rate (HR) and blood pressure (BP). In another session infraorbital nerve block anaesthesia (INB) with 1.0 ml of Carbocain without vasoconstrictive additives was used to identify nervously mediated vascular responses to cigarette smoking (n=8).


RESULTS
Cigarette smoking induced a modest hyperaemic response in the gingiva that was lower than the relative increases in BP and HR, and the calculated gingival vascular conductance decreased. In the forehead, flow responses were similar to those in the gingiva, while in the thumb a powerful vasoconstriction was observed. During the later part of the 10-min recovery period, BP and HR tended to decrease while blood flow in the gingiva and forehead remained high. INB potentiated the hyperaemic response to cigarette smoking in gingiva.


CONCLUSIONS
The present results help to shed some light on the understanding of the vasoactive mechanisms induced by cigarette smoking, and to support the hypothesis that cigarette smoking causes nervously mediated vasoconstriction in the healthy human gingiva. However, the degree of vasoconstriction was far less than in the thumb skin, and in our subjects was overcome by the evoked rise in arterial perfusion pressure. As a consequence, gingival blood flow increased during smoking. It is speculated that small repeated vasoconstrictive attacks due to cigarette smoking may in the long run contribute to gingival vascular dysfunction and periodontal disease.
Mavropoulos
Antonios
A
Department of Oral Biology, Faculty of Dentistry, University of Oslo, Oslo, Norway. antoniom@odont.uio.no
Aars
Harald
H
Brodin
Pål
P
D000328:Adult; D001794:Blood Pressure / Q000502:physiology; D005260:Female; D005546:Forehead / Q000098:blood supply; D005881:Gingiva / Q000098:blood supply; D005882:Gingival Diseases / Q000209:etiology*; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D006940:Hyperemia / Q000209:etiology*; D017078:Laser-Doppler Flowmetry; D008297:Male; D009407:Nerve Block; D009538:Nicotine / Q000009:adverse effects; D009915:Orbit / Q000294:innervation; D012039:Regional Blood Flow / Q000502:physiology; D012307:Risk Factors; D012867:Skin / Q000098:blood supply; D012907:Smoking / Q000009:adverse effects*; D013223:Statistics as Topic; D013933:Thumb / Q000098:blood supply; D018924:Vascular Capacitance / Q000187:drug effects / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000009:adverse effects
D014662:Vasoconstrictor Agents; D009538:Nicotine