Alberto Pautassi
Paolo Lanzetti
Alberto Vecchiati

SMOKE AND ORAL CAVITY

A general vision of the effects of smoke dependence and of its pathogenetic mechanisms in the oral cavity.

INTRODUCTION

The inhalation of tobacco smoke causes an incredible amount of strain and malfunction within the human physiology. Just one cigarette leaves a significant amount of residue, or tar, in the lungs. By smoking on a regular basis, you are depriving your body of a significant amount of the oxygen it requires to function on a normal, healthy level.
Medical researchers from around the world have found that smokers are far more likely to develop cancer of the mouth and throat, bladder, kidney, liver, stomach, and pancreas. Smoking is also a known catalyst for breast cancer, cervical cancer, esophageal cancer, and leukemia.
Carbon Monoxide in cigarette smoke impairs the ability of your circulatory system to transport oxygen via the blood. This causes atherosclerosis, or hardening of the arteries, and can lead to any number of complications, from chronic fatigue to heart attack or stroke.
Smoking can also increase the level of low-density lipoprotein (or “bad”) cholesterol, while decreasing the level of high-density lipoprotein (or “good”) cholesterol within the blood. This poses yet another increase in your chances of suffering a heart attack or stroke.
Also, the electrical and chemical process by which the brain relays messages throughout the central nervous system is seriously disrupted by the numerous toxic chemicals inhaled through cigarette smoke. Research has demonstrated that smoking can alter, disrupt, and damage the structure and function of the human brain.

TOXIC SUBSTANCES

Cigarette smoke contains over 4,700 chemical compounds including 60 known carcinogens. No threshold level of exposure to cigarette smoke has been defined but there is conclusive evidence to indicate that long-term (years) smoking greatly increases the likelihood of developing numerous fatal conditions.

EFFECTS IN THE ORAL CAVITY

Perhaps the most serious oral condition that can arise is that of oral cancer. However, smoking also increases the risk for various other oral diseases, some almost completely exclusive to tobacco users. The National Institutes of Health, through the National Cancer Institute, determined in 1998 that "cigar smoking causes a variety of cancers including cancers of the oral cavity (lip, tongue, mouth, throat), esophagus, larynx, and lung." Pipe smoking involves significant health risks, particularly oral cancer. Roughly half of periodontitis or inflammation around the teeth cases attributed to current or former smoking. Smokeless tobacco causes gingival recession and white mucosal lesions. Up to 90% of periodontitis patients who are not helped by common modes of treatment are smokers. Smokers have significantly greater loss of bone height than nonsmokers, and the trend can be extended to pipe smokers to have more bone loss than nonsmokers. Smoking has been proven to be an important factor in the staining of teeth. Halitosis is common among tobacco smokers. Tooth loss has been shown to be 2 to 3 times higher in smokers than in non-smokers. In addition, complications may further include leukoplakia, the adherent white plaques or patches on the mucous membranes of the oral cavity, including the tongue, and a loss of taste sensation or salivary changes.

World Health Organization, Tobacco or oral health

SMOKING AND CANCER, Statistics for the U.S., Terry Martin

Interactions with bacterial flora

Effects of tobacco and P. gingivalis on gingival fibroblasts. 2010

NICOTINE EFFECT

A wide variety of mucosal changes have been noted in habitual users of smoked and smokeless tobacco. These changes most likely result from the many irritants, toxins, and carcinogens found naturally in cured or burned tobacco leaves, but may also arise from the mucosal drying effects, the high intraoral temperatures, intraoral pH changes, local alteration of membrane barriers and immune responses, or altered resistance to fungal and viral infections.
The LD50 of nicotine is 50 mg/kg for rats and 3 mg/kg for mice. 40–60 mg (0.5-1.0 mg/kg) can be a lethal dosage for adult humans. Nicotine therefore has a high toxicity in comparison to many other alkaloids such as cocaine, which has an LD50 of 95.1 mg/kg when administered to mice. It is unlikely that a person would overdose on nicotine through smoking alone, although intoxication can occur through the excessive use of nicotine patches, gum, nasal sprays or oral inhalers intended as smoking cessation aids. Spilling a high concentration of nicotine onto the skin can cause intoxication or even death, since nicotine readily passes into the bloodstream following dermal contact.
The carcinogenic properties of nicotine in standalone form, separate from tobacco smoke, have not been evaluated by the IARC, and it has not been assigned to an official carcinogen group. The currently available literature indicates that nicotine, on its own, does not promote the development of cancer in healthy tissue and has no mutagenic properties. However, nicotine and the increased cholinergic activity it causes have been shown to impede apoptosis, which is one of the methods by which the body destroys unwanted cells (programmed cell death). Since apoptosis helps to remove mutated or damaged cells that may eventually become cancerous, the inhibitory actions of nicotine may create a more favourable environment for cancer to develop, though this also remains to be proven.
Though the teratogenic properties of nicotine may or may not yet have been adequately researched, women who use nicotine gum and patches during the early stages of pregnancy face an increased risk of having babies with birth defects, according to a study of around 77,000 pregnant women in Denmark. The study found that women who use nicotine-replacement therapy in the first 12 weeks of pregnancy have a 60 percent greater risk of having babies with birth defects, compared to women who are non-smokers, the Daily Mail reported. The findings were published in the journal Obstetrics and Gynaecology.
Effective April 1, 1990, the Office of Environmental Health Hazard Assessment (OEHHA) of the California Environmental Protection Agency added nicotine to the list of chemicals known to the state to cause developmental toxicity, for the purposes of Proposition 65.

PHARMACOKINETICS

Side effects of nicotine.
As nicotine enters the body, it is distributed quickly through the bloodstream and can cross the blood-brain barrier. On average it takes about seven seconds for the substance to reach the brain when inhaled. The half life of nicotine in the body is around two hours.
The amount of nicotine absorbed by the body from smoking depends on many factors, including the type of tobacco, whether the smoke is inhaled, and whether a filter is used. For chewing tobacco, dipping tobacco, snus and snuff, which are held in the mouth between the lip and gum, or taken in the nose, the amount released into the body tends to be much greater than smoked tobacco. Nicotine is metabolized in the liver by cytochrome P450 enzymes (mostly CYP2A6, and also by CYP2B6). A major metabolite is cotinine.
Other primary metabolites include nicotine N'-oxide, nornicotine, nicotine isomethonium ion, 2-hydroxynicotine and nicotine glucuronide.
Glucuronidation and oxidative metabolism of nicotine to cotinine are both inhibited by menthol , an additive to mentholated cigarettes, thus increasing the half-life of nicotine in vivo.

BIBLIOGRAFIA/REFERENCES

http://www.smokefreereality.com/effects.php
http://www.helpwithsmoking.com/passive-smoking/contents-of-tobacco-smoke.php
http://quitsmoking.about.com/gi/dynamic/offsite.htm?site=http://www.csn.ul.ie/~stephen/reports/bc4927.html
http://en.wikipedia.org