Chemical dependency has many faces and takes many forms, including the use of depressants, stimulants, hallucinogens and alcohol. The most commonly abused substances are caffeine, alcohol and nicotine. There are a number of Central Nervous System Stimulants (CNSSs) commonly abused by chemically-dependent individuals, including over-the-counter diet pills, prescribed amphetamines, street amphetamines, methamphetamines and cocaine. Many other addictions with oral health implications exist and are highlighted in Table 1. This article will focus on the most common addictions we encounter, such as dependence on alcohol and nicotine, with a brief look at methamphetamines.
According to the Strategic Taskforce on Alcohol report there is convincing evidence to show that regular consumption of alcohol increases the risk of liver cirrhosis, as well as cancer of the mouth, pharynx, larynx, oesophagus and liver. In a comparison of alcohol consumption and alcohol-related mortality in Ireland over the last 30 years, increases in cancer, cirrhosis and cardiovascular disease are related to an increase in alcohol consumption.
The prevalence of periodontal disease and caries in alcohol and tobacco dependent patients is high and exacerbated by a lack of oral hygiene techniques and a diminished salivary flow. Xerostomia may occur due to nutritional deficiency, enhanced salivary gland apoptosis (Slomiany BL et al, 1997) and psychiatric medication.
Oral cancer has been identified as a significant public health threat. It has been defined by the World Health Organization International Classification of Diseases as a malignancy arising within the lips, oral cavity, oropharynx, nasopharynx, hypopharynx, and other sites within the lips, oral cavity and pharynx.
Oral cancer is the sixth most common cancer in the world, and its prevalence continues to increase globally (Moore SR et al, 2000). The British Dental Health Foundation reports that over the past four years cases of oral cancer in the UK have increased by 17%, an increase more rapid than any other cancer.
Oral cancer is largely a preventable disease, related to behavioural and lifestyle factors. The aetiology of oral cancer is multi-factorial, with alcohol, tobacco products, a diet low in fruit and vegetable intake, and possibly human papilloma virus, the main risk factors considered responsible for inducing this malignancy (Zain RB, 2001; La Vecchia C et al, 1997).
Concurrent abuse of tobacco and alcohol products worsens dental disease and heightens the risk of developing oral cancer. It is difficult to ascertain whether the high risk of periodontal breakdown and oral cancer is caused by the effect of general neglect and smoking or the effect of alcohol directly on the oral tissues.
One other aspect of alcohol abuse is loss of tooth surface due to erosion. There are two factors why this may be so: chemical damage to the tooth surface due to the acidity of the alcohol itself and erosion associated with alcoholism caused by frequent vomiting (Jarvinen V et al, 1992; Bebenius J, L’Estrange P, 1990).
A study of 37 alcoholic patients showed that their teeth had significantly more wear than age- and sex-matched controls (Robb ND, Smith BG, 1990). The tooth wear was most marked in males and those whose alcohol consumption was continuous rather than in the form of episodic binges. The wear appeared to be erosive in nature, and in 40% of the sample it affected the palatal surfaces of the upper anterior teeth. It is therefore suggested that dental professionals should bear in mind the possibility of chronic alcoholism in cases of unexplained dental erosion
There also appears to be an increased risk of mandibular osteomyelitis following extraction in the alcoholic patient (Davies HT, Carr RJ, 1990). It has been suggested that depression of the host’s defences, due to alcoholism, modifies the response to, and the spread of, this rare but serious infection.
Alcohol and bone density
Patients with alcoholic bone disease reveal a marked impairment in bone formation. Ethanol has been shown to reduce proliferation of osteoblasts. The precise mechanism of how alcohol impairs bone density remains to be clearly defined, but there is an increasing body of evidence emerging to suggest that in the human model, alcohol in large amounts is toxic to osteoblasts. Alcohol may also directly affect bone density by impairing liver function and altering both vitamin D and calcium metabolism. The consequences of alcohol intake during adolescence is particularly damaging, as peak bone mass is determined at this time.
There is evidence, however, for a positive effect of moderate alcohol consumption on bone. Social drinking has been associated with higher bone mass. Few studies have undertaken thorough investigations into the mechanisms of action of the proposed beneficial effect of moderate alcohol intake on bone density. Possible theories include the stimulation of calcitonin production and the effect of alcohol on endogenous hormone production. Alcohol may increase the adrenal production of androstnedione and its conversion to oestrogen. Whatever the beneficial effects of alcohol on bone density prove to be, they will only be related to moderate alcohol intake.
As dental professionals we are only too aware of the effects of smoking on the periodontium. Tobacco has long been linked to oral cancer and leukoplakia. Research over the last 20 years has established a firm association between tobacco use and periodontitis, alveolar bone loss and refractory periodontitis.
There is evidence that cigarette smoking exerts both systemic and local effects. The main effects of smoking on the oral tissues include:
• Tobacco smoke contains cytotoxic and vasoconstrictive substances, including nicotine, which have direct effects on the blood vessels supplying the gingival tissues (Raulin L et al, 1989)
• Nicotine adversely affects fibroblast function and readily penetrates the epithelium of the skin and oral mucosa, resulting in impaired tissue turnover, healing and maintenance of the periodontal attachment (Hanes P et al, 1991)
• Smoking exerts deleterious effects on bone formation and maintenance. Nicotine can suppress the proliferation of cultured osteoblasts while stimulating osteoblast alkaline phosphatase activity (Fang MA et al, 1991)
• The effects of smoking on the immune system are well documented. These include inhibition of oral neutrophil function, reduced antibody production, impaired phagocytic activity, and alteration of peripheral blood immunoregulatory T-cell ratios.
Tobacco smoking severely depletes the body of important antioxidant micronutrients needed for effective functioning of the host immune response. This is especially so in the case of vitamin C, beta-carotene and alpha tocopherol.
Deficiencies in antioxidant micronutrients result in reduced cell numbers in lymphoid tissue and produce functional abnormalities in the cell-mediated immune response (Grimble RF, 1997). Cigarette smoking impairs the antioxidant protective action of vitamin C, glutathione and other antioxidants at tissue level. This increased rate of lipid peroxidation and reduced antioxidant status will accelerate the rate of destruction of the periodontium and increase the incidence of oral cancer.
Recent study has suggested that dietary antioxidant intake is significantly lower in smokers than non-smokers (Zondervan KT et al, 1996; Schectman G et al, 1989). Smokers had the lowest dietary vitamin C, beta carotene and tocopherol intake and serum levels compared to those who had never smoked (Zondervan KT et al, 1996; Schectman G et al, 1989).
Methamphetamine is used in pill or powdered form, and can be injected, snorted, smoked or taken orally. It is a bitter tasting powder that readily dissolves in beverages. Another common form of the drug is a clear, chunky crystal. This is the form known as ‘ice’ or ‘crystal meth’ and it is smoked in a manner similar to crack cocaine.
Clandestine production accounts for most of the methamphetamine trafficked and abused world-wide. The illicit manufacture of methamphetamine can be accomplished in a variety of ways, but is produced most commonly using the ephedrine/pseudoephedrine reduction method.
Methamphetamine is also made from a mix of toxic substances, including over-the-counter cold medicine, fertiliser, battery acid, hydrogen peroxide, anhydrous ammonia (farm fertiliser), lithium (from batteries), paint thinner, ether, drain cleaner and lighter fluid. The oral effects of methamphetamine use, therefore, can be devastating.
The toxic and caustic ingredients involved in the making of the drug have devastating effects on the oral tissues. The main effects are rampant caries, increased wear associated with bruxism, xerostomia and, possibly, periodontal disease (Klasser GD, Epstein J, 2005).
Reports have described rampant caries that resembles early childhood caries, this being referred to as ‘meth mouth’. In 1995 Howe noted the incidence of gross caries was much higher in children receiving prescribed methamphetamine for obesity and attention deficit disorders. By 2002 Shaner was reporting a distinctive pattern of caries in methamphetamine users, involving the buccal smooth surface of the teeth and the interproximal surfaces of the anterior teeth. The teeth of methamphetamine users have also been described as ‘blackened, stained, rotting, crumbling or falling apart’ (American Dental Association, 2005).
The rampant caries associated with methamphetamine use has been attributed to the acidic nature of the drug, drug-induced xerostomia, its propensity to cause cravings for high calorie carbonated beverages and bruxism, and its long duration of action leading to extended periods of poor oral hygiene (Howe AM, 1995; Shaner JW, 2002; McGrath C, Chan B, 2005).
The type of carious lesions seen in these individuals resembles ‘radiation decay’. It is large, dark in colour and appears at the cervical one-third of the tooth at the gingival margin.
The xerostomic effects of methamphetamine have been attributed to the fact that as an sympathomimetic amine, it acts on a and b adrenergic receptors. The stimulation of a receptors in the vasculature of the salivary glands produces vasoconstriction and reduces salivary flow (Physicians’ Desk Reference, 1995). This reduces the availability of the protective factors found in saliva. Xerostomia has also been attributed to the elevated metabolism and over activity experienced with methamphetamine use (Shaner JW, 2002).
Other risk factors associated with methamphetamine use include increased bruxism and clenching. Methamphetamine is a neurotoxin and potent stimulant, which can also cause cerebral oedema and haemorrhage, paranoia and hallucinations. Short-term effects include insomnia, hyperactivity, decreased appetite, increased respiration and tremors, and drug-induced grinding (US National Institute on Drug Abuse).
A distinct pattern of tooth wear has been reported in methamphetamine users. Richards et al (2000) noted that users who preferentially snorted methamphetamine had significantly higher tooth wear in the anterior maxillary teeth than patients who injected, smoked or ingested it. It was suggested that patients who use methamphetamine have distinct patterns of wear based on route of administration, the difference being explained anatomically.
There is some debate whether these drugs directly contribute to periodontal disease, or whether patient neglect or apathy is the primary cause. The amphetamine cocaine is known to cause small vessel vasoconstriction, which retards the healing process and would, therefore, be a factor in the progression of periodontal disease. An increased risk of xerostomia and anorexia caused by the drugs are also deemed to be predominant factors in the development of periodontal disease.
Chemical abuse is a serious national problem that has the potential to affect all of our lives. As dental health professionals, we need to be aware of the systemic and oral health effects of drug abuse, as well as how to recognise the oral health risks and provide safe and adequate treatment.
Identification of the substance-abusing patient plus a cancer screening examination, preventive dental education, and use of saliva substitutes and anti-caries agents are indicated.
Special precautions must be taken when performing surgery and when prescribing or administering analgesics, antibiotics or sedative agents that are likely to have an adverse interaction with alcohol, drugs or psychiatric medications.