Alcohol consumption is accepted around the world. About 70% of the US population drinks alcohol, and 1 in 10 will suffer from problems of alcoholism,1 a statistic that is probably mirrored in the Canadian population. Patients who consume alcohol can be divided into 3 categories: those who consume alcohol in moderation, those who abuse alcohol and those with alcohol dependence.1,2
There is no agreed-upon definition of moderate drinking, but most authorities believe that less than 1 drink per day for women and less than 2 drinks per day for men can be considered moderate. People who abuse alcohol experience repeated episodes of alcohol intoxication severe enough to alter mood and impair judgment. Their alcohol consumption prevents them from fulfilling their societal obligations and often results in dangerous behaviour.3,4 Alcohol dependence is described as a physiological dependence resulting in tolerance and/or withdrawal symptoms (tremor, weakness, sweating and delirium tremens).3,5
The etiology of alcoholism is unknown, although both genetics and environment probably play a role. Whatever the cause, it is likely that every practising dentist will treat at least one alcoholic patient or recovering alcoholic patient in his or her career, so dentists must be aware of the special needs of these patients.4 Furthermore, dentists should be prepared to refer patients to appropriate centres or professionals for additional treatment when appropriate.
Effects on Teeth and Periodontium
Alcoholic patients frequently consume more than 50% of their daily caloric intake in the form of ethyl alcohol,3,6 with much of the remaining caloric intake coming from sweet drinks high in simple sugars.3 Alcohol is also the most common cause of sialadenosis of the parotid gland, a peripheral autonomic neuropathy occurring in 30%–80% of patients with cirrhosis. This condition manifests with noninflammatory swelling of the parotid gland and decreased secretion of saliva, which in turn reduces the ability to neutralize cariogenic acid.2,7,8
Decreased immune response secondary to alcoholic cirrhosis,6 combined with a cariogenic, nutritionally poor diet, poor oral hygiene, decreased salivary flow and a high incidence of smoking among these patients, provides an environment conducive to rapid progression of periodontal disease and caries.
Effects on Mucosa and Underlying Tissues
Nutritional deficiencies are detrimental to the immune system but also have orofacial presentations. Common nutritional deficiencies in alcoholic patients include deficiencies of protein, minerals, trace elements, folic acid (causing mucosal ulcers), riboflavin (causing glossitis, filiform atrophy, pallor of oral commissures and dry scaly skin), pyridoxine (causing anemia and mucosal ulcerations) and vitamin E.1,3,5,8 Altered absorption of nutrients exacerbates the poor diet. More specifically, alcohol decreases gastrointestinal absorption of folic acid, riboflavin, niacin, thiamine (causing neuropathologies), vitamin D (causing osteoporosis) and vitamin K (causing coagulopathies).1,3,5 Alcohol also enhances the excretion of magnesium and zinc. Poor intake and poor absorption combined with increased excretion frequently lead to glossitis, angular cheilitis, candidal infection, oral ulceration and acute necrotizing ulcerative gingivitis.3,5
Patients who consume alcohol are at increased risk of many cancers, including oral cancers. Among those who continue to drink after a diagnosis of oral cancer, the risk that a second primary tumour will develop increases by up to 50%.9 The exact mechanism by which alcohol increases the risk of oral cancer is still unclear. Alcohol is not itself a carcinogen, but acetaldehyde, produced when ethanol is metabolized by alcohol dehydrogenase (an enzyme produced locally by oral bacteria9), is a potent carcinogen. Acetaldehyde is also produced systemically by the breakdown of alcohol in the body and is subsequently secreted by the salivary glands.9 Smoking, the carcinogenic effects of acetaldehyde and the ability of alcohol to increase permeability of the mucous membranes and solubility of carcinogens3 may combine to promote tobacco-initiated tumours.5 Therefore, all oral ulcerations in alcoholic patients, including leukoplakia and erythroplakia, should be treated with suspicion, especially if the patient smokes.
The effect of ethanol on the liver can be viewed as a 3-stage phenomenon.4,7 The first stage, fatty liver (caused by steatosis), is the result of alcoholic insult to the liver. It usually has few signs or symptoms, is reversible after 2–4 weeks of abstinence4,7 and is seen histologically as the buildup of fat within the hepatocytes.4,7
The second stage, acute or chronic hepatitis, may occur if the patient has an exceptionally high intake of alcohol. Mild cases present without symptoms and may be diagnosable only by abnormalities on liver function tests. Severe cases may present with jaundice, hepatic encephalopathy, ascites, bleeding esophageal varices, abnormal clotting and coma. Although hepatitis is usually reversible, it may also progress to cirrhosis.3,5
The third stage is cirrhosis, the development of fibrous nodules within the liver, which occurs with repeated damage and healing with scar tissue. A cirrhotic liver is thus unable to perform its normal functions, and production of several clotting factors (V, VII, IX and X), synthesis of bile, control of glycemia, metabolism of cholesterol and detoxification are all impaired. Congestion or hypertension of the portal vein in cirrhosis leads to esophageal varices, rectal hemorrhoids and splenomegaly. Splenomegaly results in sequestration of blood cells, and sequestration combined with alcohol-related coagulopathies can lead to fatal bleeding.3
Long-term alcohol use can lead to mild hypertension and increases in both triglycerides and low-density lipoproteins. In people without alcoholism, this triad has been related to increased risk for coronary artery and cerebrovascular disease. No studies have examined these risks in people with alcoholism, but extrapolation of these risks to this population seems reasonable. Excessive ingestion of alcohol may also damage the myofibrillar architecture, which could eventually lead to congestive heart failure. An evaluation of the cardiovascular system may therefore be warranted before any dental treatment is undertaken.3
Alcoholic patients may seek treatment for pain or infection only in emergency situations. Immune deficits, including deficiency of complement, impaired adherence of Kupffer cells and neutrophils, and impaired motility and phagocytotic activity,5 leave these patients at greater risk for infection and necessitate aggressive management while limiting the portals of entry. For example, osteomyelitis of the mandible following simple dental extractions has been documented.10
In alcoholic patients, the liver’s ability to metabolize drugs is usually impaired, which may result in subtherapeutic or toxic doses of prescribed medications.6,11 Dentists should be aware of several direct drug–alcohol interactions (Table 1).4,8 In addition to these problems, patients with cirrhosis have decreased albumin levels. The dosages of drugs that bind albumin in the blood are based on binding percentages. Therefore, if albumin levels are decreased, plasma levels of these drugs will be increased relative to patients with normal levels of albumin. This phenomenon is especially important for drugs such as warfarin, which have high protein-binding percentages.6,11