Nicotine and its effects on periodontal tissue
Absztrakt
Nicotine, the chief active ingredient of tobacco, has been known since the introduction of the plant in Europe in the middle sixteenth century. Nicotine can be found in some vegetables consumed in every-day life such as eggplant, cauliflower, green tomatoes, and potatoes. Tobacco, which is the main source of nicotine, has two main forms: combustible tobacco (e.g. cigarettes) and smokeless tobacco (e.g. chewing tobacco). An average cigarette contains about 0.5 to 1.0 g of tobacco and 10 mg nicotine. On the other hand, the nicotine content of the bidis (21.2 mg/g) is much higher than the conventional cigarette. Nicotine is an alkaloid that is able to spread quickly to every part of the body as soon as it enters the circulation and can pass the blood brain barrier in just 7 seconds. The liver, lungs and the kidneys metabolizes majority of the inhaled nicotine. Pharmacological characteristics of nicotine present in cigarettes increases its addictive effect unlike the medically used nicotine products. Nicotine metabolites play a role in its addictive nature. Nicotine imposes its effect in 3 major ways, and creates physiological and pathological results in different body organs: ganglionic transmission, nicotinic acetylcholine receptors and stimulation of central nervous system. Poisoning from nicotine may occur by the ingestion of the products containing nicotine accidentally, or by ingestion of the actual tobacco by the children. 60 mg of nicotine is the fatal dose for an adult. The symptoms of nicotine poisoning can be acute and fast acting; they include nausea, abdominal pain, salivation, cold sweat, vomiting, diarrhea, and severe weakness. Other than these negative effects, nicotine will also alter the taste sensation and cause halitosis, smell impairments, attrition, and damage the wound healing process and delay it. According to the extensive studies done over the past 15 years to investigate the effects of the nicotine on periodontal damage, the odds of periodontitis occurring among smokers is much greater than non-smokers, with a ratio of 2.5 to 7 or even higher. Smokeless tobacco is not an exception from this result, and they can cause diseases such as oral carcinomas and white oral mucosal lesions. The nicotine concentration around the gingival tissue can get up to 300 times higher than in the plasma cells of a smoker (20 ng/ml), which in turn will damage the cell population of the oral cavity. Smoking produces harmful chemicals and carbon monoxide, which cause a decrease in the blood flow of the oral cavity capillaries. Nicotine can cause vasoconstriction and further halt the circulation. In smokers, dry socket develops easier than non-smokers. Although the result of the oral implant treatment is mainly under the effect of inflammation triggered by the plaque and occlusal load, smoking is also a major risk factor for the soft tissue alteration and loss in the implant area. This highlights the importance of dental professionals to educate their patients on smoking cessation.