The Effects Of Crack Cocaine On Teeth
Lloyd Villasenor
You may have noticed that many drug addicts have bad teeth. That's because drugs such as methamphetamine (meth), heroin, cocaine, ecstasy, and even marijuana can cause problems for your teeth and gums. Here are a few of the main reasons:
Methamphetamine (Meth)
In one study, 96% of people who used meth had cavities and 58% had untreated tooth decay. People use the term "meth mouth" to describe this condition of stained, badly damaged teeth.
Cocaine
This drug can have different effects on your mouth, depending on how you take it. When you snort it, cocaine can damage the tissue between your nose and the roof of your mouth, eventually causing a hole and making it hard to talk or eat.
Like meth, it's very acidic. So when you smoke crack or put powdered cocaine in your mouth, the acids coat your teeth and can break down their protective enamel. This can cause gum disease and tooth decay. If you rub it on your gums, it can cause mouth sores.
In a 2008 research review covering anecdotal reports on cocaine and oral health, results found that consuming cocaine orally caused ulcerated lesions on the gums where the cocaine touched, usually near the front teeth.
Doctors sometimes prescribe medications to reduce cocaine withdrawal symptoms, such as antidepressants, lithium, and levodopa. These medications can cause dry mouth, alter taste perception, or cause involuntary facial movements.
In the UK almost one million individuals use cocaine on a regular basis, implying that dentists are likely to encounter individuals that use cocaine. Regular use of this drug may have several orofacial effects, such as perforation of the nasal septum and palate, gingival lesions and erosion of tooth surfaces. In addition, recent use of cocaine increases the risk of a medical emergency during dental treatment, especially when epinephrine-containing local anaesthetics or retraction cords are used. Therefore, dental treatment should be postponed for 6 to 24 hours after the use of cocaine.
In the UK, cocaine use is still increasing. Currently, approximately 910,000 people are using cocaine, resulting in Europe's second highest cocaine prevalence rate. The highest prevalence levels are reported in London (4.1%) and the lowest in Wales (1.6%) and Yorkshire (1.8%).1
The main method of administration is snorting cocaine.2 Within a few minutes after inhalation, an euphoric high feeling occurs which lasts for 20 to 90 minutes. For smoking of cocaine, the cocaine powder must first be converted into a smokeable form, eg by utilising sodium bicarbonate. This form is known as 'crack' because of the cracking sound made during heating.3 The popularity of crack has made intravenous injection of cocaine rather obsolete.2,4,5 Application of cocaine powder to the gingiva is mainly restricted to testing the purity of the cocaine.3
In its non-ionised form, cocaine diffuses across the lipid membranes of neurons. In the axoplasm, it returns to the active cationic form, which binds to the sodium channels. This interaction prevents the generation of an action potential, resulting in a reversible anaesthetic effect.2 In addition, cocaine blocks the re-uptake of norepinephrine and dopamine, which prolongs and increases the effects of these neurotransmitters.6
With increasing doses of cocaine, these initial signs of central nervous system excitation are rapidly followed by a generalised state of central nervous system depression, resulting in a decreased respiration rate with periods of apnoea.2,6
The sympathomimetic effect of cocaine results in an increased heart rate and an increased oxygen demand of the myocardium. However, cocaine simultaneously induces vasoconstriction of the coronary arteries, decreasing the oxygen supply. This combination of increased myocardial oxygen demand and decreased coronary artery perfusion may lead to angina, myocardial infarction or cardiac dysrhythmias.2,5,6,7 Peripheral vasoconstriction increases the arterial blood pressure 15-20% above normal levels, further increasing the cardiac workload.4 Acute hypertension may lead to aortic dissection or rupture of an intracranial aneurysm.2
Cocaine and its metabolites cross the placenta to the foetus. Several human and animal studies indicate that use of cocaine during pregnancy reduces the occipital-frontal head circumference at birth and has a small negative effect on speech development.8,9 In mice, cocaine increases the risk of a foetus with a cleft palate, especially in combination with alcohol.10 In a cocaine-using pregnant woman, a foetus with bilateral cleft lip and palate was detected at 14 weeks of gestation.11
More than half of the people who snort cocaine have recurrent epistaxis, intranasal crusting, rhinitis and chronic sinusitis.12,13 Nasal septum perforation (Fig. 1) is a frequently reported complication, observed in approximately 5% of cocaine snorters.14,15 The perforation of the nasal septum reduces the nasal support and results in a broad, flat nose, the so-called saddle nose deformity12,14,15,16,17,18 (Fig. 2).
The major pathological factor seems to be the vasoconstrictive activity of cocaine, inducing local ischaemia which may lead to necrosis of the nasal septum and surrounding tissues. This process can be exacerbated by chemical irritation from adulterants in 'cut' cocaine such as quinine, caffeine, talc, plaster of Paris or amphetamines.19,20 Addition of lidocaine and procaine can cause facial numbness.20 Some patients use instruments such as pens and pencils to remove intranasal crusting, which increases the risk of nasal perforation.17,20 Finally, snorting of cocaine impairs the nasal mucociliary transport system that removes particles from the nose, thereby decreasing the nasal defence against infection.20 In a recent study, all patients with nasal septum perforation caused by cocaine abuse were nasal carriers of Staphylococcus aureus, suggesting that this micro-organism may contribute to the tissue damage.21
Chronic use of cocaine seems to have similar effects on the palate. Since 1989, at least 45 cases of cocaine-induced oronasal perforations have been reported in the literature,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41 suggesting that this complication is much less rare than previously thought. In general, perforation of the nasal septum occurs first and is followed several months later by a slowly enlarging palatal perforation.
The majority of the patients with cocaine-induced palatal necrosis are female (72%), despite the fact that more men than women use cocaine.13 Therefore, it has been suggested that women are more susceptible to this complication of cocaine usage.14
The initial treatment of a cocaine-induced palatal defect is complete abstinence from the drug, and the exclusion of other potential causes of midline palatal necrosis such as a tumour, Wegener's granulomatosis, trauma, chronic (fungal) infection and tertiary syphilis.40
It is advised that definitive reconstruction of the palatal defect should only be attempted after a long period of complete cocaine abstinence, at least for one year.14 The palatal defect can surgically be closed with a unilateral or bilateral pedicle flap, an anterior based tongue flap or a microvascular free flap with or without bone transfer.12,15,26,35,37,40
Long term use of a maxillary obturator for a cocaine-induced palatal defect was described by five patients as comfortable or at least acceptable.15,18,19,23,38 Considering the relatively poor outcome from surgical repair of cocaine-induced palatal defects, the non-surgical conservative approach seems the better option.
Cocaine users frequently suffer from bruxism, commonly giving rise to pain in the temporomandibular joint and masticatory muscles.7 Mild attrition affecting all canines and first premolars as well as the upper lateral incisors was observed in a patient with a two-year history of regular use of cocaine and other drugs.3 Administration of cocaine to rats also induced a significant increase in attrition rate and non-functional masticatory activity.42 The increased risk of cervical abrasion is probably related to excessive vigorous tooth brushing.7
Dissolved in saliva, cocaine powder results in a substantial decrease of the salivary pH. This increases the risk of dissolving the tooth mineral calciumhydroxyapatite. In some chronic users loss of facial and occlusal tooth enamel was indeed observed, which gave the tooth surfaces a smooth and glassy appearance.43 A cocaine-induced decrease in salivary pH could also explain the rapid tarnishing of gold crowns in crack' users.44
A 14-year-old boy who rubbed cocaine on his gingivae had carious lesions on his incisors and canines.3 Another patient presented with three carious teeth which needed extraction.38 This suggests that the caries risk may be increased, due to sugar used to 'cut' pure cocaine.45
After oral use of cocaine, several individuals developed gingival lesions at the site of application, usually the maxillary anterior teeth. The gingivae were coated with a white slough, which could easily be removed, showing underlying ulceration and erythema. The patients reported painful, retracted gingivae.3,46,47,48 Full mouth radiographs revealed severe alveolar bone loss in one patient.45 These complications are probably related to the strong vasoconstrictive properties of cocaine.46 In addition, gingival laceration may be aggravated by excessively vigorous toothbrushing during a 'high' period.3
After abstaining from cocaine, in most subjects the gingival lesions disappeared spontaneously within two weeks to 18 months.3,46,47,48 However, in one patient a necrotic lesion of the alveolar mucosa led to exposure of the bone. Despite antibiotic treatment the lesion worsened, eventually leading to loss of both upper left incisors.48
Several individuals have been described with orofacial pain compatible with cluster headache. Cocaine triggered pain in the premolar zone of the maxilla, followed by spread to the periorbital zone on the same side.48,50 Medication used to reduce symptoms of cocaine withdrawal may also have oral side effects. This medication includes antidepressants, lithium and levodopa.7 Antidepressants are a well-known cause of xerostomia. Levodopa and lithium may alter taste perception, induce a red discoloration of saliva, or induce involuntary facial movements.51
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