Mavropoulos Antonios, Aars Harald, Brodin Pål
Department of Oral Biology, Faculty of Dentistry, University of Oslo, Oslo, Norway.
J Clin Periodontol. 2003 Mar;30(3):214-21. doi: 10.1034/j.1600-051x.2003.10284.x.
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.
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).
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.
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.
目前认为吸烟是牙周疾病的一个危险因素。关于尼古丁的血管收缩特性是否为致病机制之一，仍存在争议。为此，我们检验了吸烟会导致健康人牙龈血管收缩这一假设。
使用激光多普勒血流仪连续测量13名健康烟草偶尔使用者的牙龈血流量。同时，记录前额和拇指的皮肤血流量以及心率（HR）和血压（BP）。在另一组实验中，对8名受试者使用1.0毫升不含血管收缩添加剂的卡波卡因进行眶下神经阻滞麻醉（INB），以确定吸烟引起的神经介导的血管反应。
吸烟引起牙龈适度充血反应，低于血压和心率的相对升高幅度，计算得出的牙龈血管传导性降低。在前额，血流反应与牙龈相似，而在拇指观察到强烈的血管收缩。在10分钟恢复期的后期，血压和心率趋于下降，而牙龈和前额的血流量仍保持较高水平。INB增强了牙龈对吸烟的充血反应。
目前的结果有助于阐明对吸烟诱导的血管活性机制的理解，并支持吸烟会导致健康人牙龈神经介导的血管收缩这一假设。然而，血管收缩程度远低于拇指皮肤，并且在我们的受试者中被动脉灌注压的升高所克服。因此，吸烟期间牙龈血流量增加。据推测，长期来看，吸烟引起的反复小血管收缩发作可能会导致牙龈血管功能障碍和牙周疾病。
