16 The Journal of the Greater Houston Dental Society • October 2009

The Abused Mouth, Part I: Cocaine-AssociatedOral Damage (Review and Case Reports)

Feature

by J.E. Bouquot, D.D.S., M.S., C.D. Johnson, D.D.S., M. S., Azideh Afshari, D.D.S.

This is the first in a series of brief reviews of the oral and maxillofacialeffects of drug abuse and drug use; it is not intended as an in-depth summary of drug physiology or pharmacokinetics. The drugsto be discussed may be illegal or legal, recreational, over-the-counteror prescribed. A recent survey of private dental offices shows thatdentists estimate that 5-10% of their patients are drug abusers,based on oral manifestations or in-office behavior, aftermethamphetamine, cocaine is the most often suspected drug.1 Ofcourse, numerous past surveys have made it perfectly clear thatthe U.S. population has shown a strong penchant for recreationaldrug use and off-use of prescription and OTC drugs. Our reviewstarts with cocaine because there is so very little in the literatureabout its effects on the oral environment.

Cocaine - What Is It?Cocaine is an alkaloid extracted from the leaf of the coca plant,

Erythroxylum coca, indigenous to South America and grown mostextensively in Columbia, Peru and Bolivia. Two chemical forms ofcocaine exist, the hydrochloride salt and the “freebase” form. Thehydrochloride salt, or powdered form dissolves in water and can beinjected or made into a paste. It is usually snorted as a powder(Figure 1), but is frequently injected (intravenously) or placedagainst the oral mucosa. Freebase refers to a compound that hasnot been neutralized by an acid to make the hydrochloride salt.

The freebase form of cocaine, typically called crack cocaine orsimply crack, is smokable, chewable and injectable, and can beformed into crystalline blocks (rocks); it is also much less expensive.The term “crack” refers to the crackling sound heard when themixture is smoked. Regardless of the type used, when in closecontact with oral or nasal mucosa, cocaine is easily transportedacross the membrane. It should be noted that most purchasedcocaine is not pure; street dealers dilute or “cut” it with cornstarch,talcum powder, sugar, procaine or amphetamines (especially OTCdiet pills). Numerous street names are applied to these products:

Coke C SnowSnowflake Flake# BlowBump Candy CharlieCrack Toot

Cocaine blocks the reuptake of norepinephrine and dopaminein the sympathetic nervous system by altering dopamine receptorsin the pleasure center, allowing excess dopamine to build up.2 It isthis excess of dopamine that is responsible for cocaine’s euphoric

effects. It produces pleasant feelings of euphoria or “joy,” theamplification of sensations and increased motor activity or“excitability,” giving a feeling of “being sharp” (cocaine was theaddiction of Sherlock Holmes). The effects typically last from a fewminutes to two hours.2 With repeated use, unfortunately, cocainecan cause long-term changes in the brain’s reward system and inother brain systems as well, eventually leading to addiction. Withrepeated use, tolerance to the cocaine high often develops, forcinglarger amounts to be used more frequently over time.2

PopularityCurrent use and abuse. Estimates of current cocaine use vary

widely, as one would expect from self reports of illegal activity, butthe U.S. government’s National Survey on Drug Use and Health(NSDUH) estimates that 35.9 million American adults and teenshave used cocaine, and 8.6 million have used crack.3 Almost amillion Americans per year use cocaine for the first time (crackrepresents about 1/3 of this number). Only marijuana, among theillegal drugs, is more popular than this. The majority of regularusers are 18-34 years of age and among 18-25 year olds, the regularuse rate is more than 6%.3 Regular use among high school seniorsis approximately 2%. A recently noted phenomenon is increaseduse among the older baby boomers: regular use is almost 10% forthe 50-59 year age group, almost double that of any other age.3

Historical use and abuse. Recreational cocaine use has a verylong history, and it also has had a limited but important medicinalvalue. In 1884, for example, Köller first used it as a local anesthetic,and cocaine sprays are still used by otolaryngologists for topicalanesthesia of the oropharynx, the larynx, even the mouth.4

Additionally, it was the active ingredient in many intestinal potionsand even in toothache drops of the eighteenth and nineteenthcenturies. Today, of course, its recreational use greatly eclipses itsmedicinal use, allowing contemporary health professionals todocument a large number of medical, psychological and socialproblems from abuse and addiction (Table 1). These problems, alongwith those produced by other narcotics, were severe enough thatin 1914 Congress included cocaine as a narcotic in the HarrisonAct, essentially outlawing its recreational use.

Maxillofacial Effects of CocaineNasal and nasopharyngeal damage. The most notorious

and well documented of maxillofacial damages from cocaine is theperforation of the nasal septum from snorting the powder, usuallyaccompanied by a “runny nose,” nosebleeds and a diminished

17 The Journal of the Greater Houston Dental Society • October 2009

Table 1: Deleterious effects of cocaine abuse, excludingmaxillofacial problems.

Adverse Effect Comment

Physical effects:Myocardial ischemia May lead to infarction, sudden

death

Atherosclerosis Accelerates its developmentVasoconstriction Causes local ischemia in are of

mucosal contact; systemicvasoconstriction also occurs

Aortic dissection May lead to death from rupture

Malignant hypertension May lead to ruptured blood

vesselsExcess thrombus formation May produce stroke, infarction,

etc.Seizures, tremors

Facial muscle activity From abnormal synapsis anddelayed signal transmission

Headache Usually anterior, centered

Tinnitus Progressively increasing with

cocaine use

Respiratory depression May lead to respiratory death

Tachycardia, arrhythmia May lead to cardiac death

Loss of appetite

Abdominal pain, nausea

Hyperthermia May lead to death

Stained, calloused fingers From holding crack pipe

Psychological effects:Hallucinations Especially “coke bugs”(formication, Magnan’s sign; sensation oftiny insects crawlingover the skin; also seen in amphetamine abusers)ParanoiaTalking nonsense Illogical topics, jumbling ofwords, inappropriate use of words

Figure 1 - Telltale sign of cocaine crystals in nostril of a dentalpatient who snorted just before entering dental office.

Figures 2a/2b -Palatalperforation fromcocaine-inducedosteonecrosis ina cocaine snortercan occur withlittle or no pain.

sense of smell.5,6 This septal necrosis results from repeatedischemia in a region with only a thin mucosal covering a cartilagestructure (septum) which, by nature, gets its blood supply fromthe surface. Once perforated, the septum will not regenerate orheal itself, even if cocaine use were to be stopped. Severe casesinvolve extended necrosis of the midline of the hard palate(cocaine-induced perforating osteonecrosis) at the attachmentwith the cartilage (Figure 2). This is less easily explained becauseof the better blood supply in bone compared to cartilage, but itremains likely that continued ischemic contact with the powder isthe salient process. Other extraoral upper aerodigestive tracteffects include dysphagia (difficulty swallowing), vocalhoarseness and necrotic sloughing of nasopharyngeal mucosa.6

A telltale sign of cocaine smoking, uvular angioedema (Quink’sedema), has been recently reported, but evidence of progressionto palatal destruction is lacking.7,8

Oral mucosal damage. Our Urgent Care Clinic experience hasuncovered several different, usually unreported types of oralchange from cocaine abuse. Some individuals, for example, preferto repeatedly place or “rub” the powder or rock crystals against the

alveolar mucosa, holding it in place with the lip or cheek. This mayinitially (or only) produce a region of mild erythema (cocaineerythema), but may also produce a relatively painless, somewhatgray-based ischemic ulcer with minimal inflammatory erythemasurrounding it, called a cocaine ulcer in our Clinic (Figure 3).9-12

Also, at least one case of deep soft tissue ulceration of the hardpalate, without perforation, has been reported as necrotizingsialometaplasia, a rare lesion with an apparent ischemic etiology.13

Additionally, some individuals experience an odd combinationof hyperkeratosis, from the rubbing or physical/chemical contact,and small focal irregularities and erythemas, imparting an appearanceof abrasive or “moth-eaten” damage. For want of a better name, wehave been calling this cocaine excoriation (Figure 4). This onlyoccurs on well keratinized surfaces, in our experience, on lesskeratinized surfaces the placement is more likely to produce an areaof white hyperkeratosis which mimics leukoplakia (Figures 5a and5b). Again, for want of an established diagnostic name, we havebeen calling this cocaine keratosis. Sometimes, this white plaque

18 The Journal of the Greater Houston Dental Society • October 2009

Figure 3 - Gray based ischemia-inducedcocaine ulcer may be found in area ofchronic crystal or rock placement.

Figure 4 - On heavily keratinizedsurfaces, cocaine produces anirregular white keratotic change witha “moth-eaten” appearance, calledcocaine excoriation.

Figure 5a - Cocaine Keratosis ofalveolar mucosa where cocaine ischronically placed.

Figure 5b - Cocaine Keratosiswith a central cocaine ulcer isfound in the region of chroniccocaine placement.

Figure 6 - Partially sloughingcocaine pseudomembrane in regionof cocaine placement.

Figure 7a - Smooth erosion concavi-ties are admixed with angular areasof enamel abrasion on the right, theregion of chronic cocaineplacement(cocaine erosion/abra-sion).

can be partially or completely scraped off to reveal an erythematous,perhaps ulcerated surface, which we call a cocaine pseudomembrane(Figure 6); this has been previously reported.10,14 To the best of ourknowledge, none of the leukoplakia look-alike lesions isprecancerous, although at least one investigation has found nuclearatypia in cytologic smears taken from clinically normal oral mucosaof cocaine addicts.15

Tooth damage. The teeth may also be affected. We have noticeda relatively unique combination of abrasion and erosion of theteeth in the region of chronic cocaine placement, called cocaineerosion (Figure 7a).16-18 In some addicts, the pattern fits better forthe erosion seen in gastric reflux patients, presumably because ofthe nauseous problems seen in some cocaine abusers (Figure 7b).However, the primary dental problem, as with so many seriousaddictions, stems from ignoring usual health care, including goodoral hygiene habits. This may result in severe, even rampant cariesin an individual who had been relatively stable in his or her cariesexperience prior to the addiction (Figure 8a), or in neglect of obviousdental infection (Figure 8b).

Gingival damage. The ischemic nature of topical cocaine usewould presume to cause local alveolar bone loss and tooth loss inthe region of chronic placement. Tobacco is well known to producelocal ischemia, and this is certainly the experience of smokelesstobacco users. We have occasionally seen this in our patient

population of cocaine users, and others have reported relativelyrapid and painless gingival erosion, sometimes called cocainegingivitis, in the area of drug contact.11,14, 17-19 We prefer the term,cocaine dehiscence, because the lesion is typically very localized(Figure 9).

Alveolar bone damage. A deeper ischemic effect of alveolarbone has been seen in our Clinic on several occasions, typicallypresenting as unhealing, exposed bone after trauma or extraction(Figure 10). We have been referring to this as cocaine-inducedalveolar osteonecrosis and presume the etiologic mechanisms tobe identical to those which produce a perforated septum and hardpalate. The microscopic features, however, are identical to those ofbisphosphonate-induced alveolar osteonecrosis orosteoradionecrosis, essentially demonstrating acute osteomyelitiswith bony sequestrum formation, often with bacteria coating thesequestra. Biopsy, therefore, cannot provide a complete diagnosis.It must be combined with appropriate clinical features and a historyof cocaine use.

Miscellaneous adverse maxillofacial effects. There are a fewfinal cocaine effects of importance to the dental profession. Recentuse of cocaine increases the risk of a medical emergency duringdental treatment, especially when epinephrine-containing localanesthetics or retraction cords are used. Because of this, someauthorities suggest that dental treatment should be postponed for

19 The Journal of the Greater Houston Dental Society • October 2009

Figure 7b - Posterior palatal erosionis seen in cocaine addict with gastricreflux (gastric reflex erosion).

Figure 8a - Rampant caries fromdental neglect in cocaine addict.

Figure 8b - Extensive facialdestruction from actinomycosis infacial fistula ignored by cocaineaddict.

Figure 9 - Cocaine dehiscence withgingival recession, root exposure andsuperficial chemical burn (white)

Figure 10a - Cocaine inducedalveolar osteonecrosis with spontane-ous bone exposure in area of cocaineplacement.

Figure 10b - Cocaine inducedalveolar osteonecrosis here repre-sented by exposed bone and poorlyhealing would after a bar brawl, mayremain relatively painless..

six to 24 hours after the use of cocaine.12,18 Also, surgical healing,especially after extraction or gingival graft procedures, may beprolonged by the ischemic effects of cocaine on local, or evendistant tissues, and may prevent healing entirely or may extendbleeding time to an alarming degree.18,20

Unfortunately, the dentist is more likely than not to be unawareof a cocaine addiction in his or her dental patient, since more than65% of all cocaine addicts hide their addiction from their health careproviders.21 Along this line, it is very interesting to know thatrecent research has found a very high sensitivity rate, approaching100%, for the identification of cocaine in saliva, and that forensicinvestigators can identify chronic cocaine abuse via spectrographicanalysis of human teeth.22,23 Perhaps someday, dentists will bequickly checking saliva for evidence of use prior to oral surgery?For completeness, we should mention that cocaine use by a pregnantmother has been associated with an increased risk of cleft lip, cleftpalate and ankyloglossia in the infant.12,24

Maxillofacial Effects of CrackCrack rocks or crystals may be placed against the oral mucosa,

producing the same adverse effects as cocaine powder, but crack isusually smoked and this produces several unique oral damages.Crack pipes are often inexpensive and the stem becomes quite hotduring use. The region of repeated placement of the stem on the lipbecomes pale, keratinized, fissured, possibly chronically ulcerated

(Figure 11), a lesion which we refer to as crack pipe cheilitis. Asimilar combination of hyperkeratosis, reactive melanosis anderythema may also be seen on the fingers which hold the hot crackpipe (Figure 12), sometimes called crack fingers. Occasional acutethermal burns with ulceration (crack burn) may also result from lipcontact with a hot pipe stem (Figure 13).14,17 Also, occasional incisalfractures occur from holding the pipe stem in the mouth (Figure 14),a problem we have been referring to, with a certain sense of humor,as a crack pipe crack. With extended use, even in the absence offracture, incisal edge abrasion may develop, producing a roundedconcavity of the same diameter as the pipe stem (crack pipeabrasion).

Occasionally, small, very hot particles of crack are inadvertentlysucked into the mouth, producing acute thermal burns of the oralmucosa, usually the tongue (Figure 15); we have been referring tothese as crack burns; they have been reported by others.17 Theindrawn airstream of the pipe may be extremely hot and focusedlocally, producing a similar acute thermal burn, usually of the hardpalate, which may actually be ulcerated, a sign which we refer to asan airstream burn (Figure 16). This phenomenon may also be seenin tobacco pipe smokers.

Treatment or management. While an experimental vaccineagainst cocaine is partially successful, behavior modification, i.e.psychiatry, is the only effective treatment for cocaine addiction;

20 The Journal of the Greater Houston Dental Society • October 2009

Figure 11 - Cocaine cheilitis is seenon lower vermilion in region ofrepeated crack pipe placement. Acutethermal burn of the lip vermilion(pipe stem burn) may occur from heatof the crack pipe stem.

Figure 12 - Discolored, callousedfingers (crack fingers) in region wherecrack pipe is chronically held.

Figure 13 - Acute thermalburns, called crack burns, arefrom hot rock embers suckedonto the tongue..

Figure 14 - Incisal fracture (crack pipecrack) of the maxillary right lateralincisor. .

Figure 15 - Acute thermal burn,in healing phase, resulting from excessintake of hot pipe airstream onto thehard palate (airstream burn).

Figure 16 - Crack pipe airstreamburn.

there is no proven medication available.2 The literature providesscant guidance on the diagnosis and management of the oral andmaxillofacial effects of cocaine abuse.12,14 The lifestyle and possiblenoncompliance issues associated with chemical abuse may onlyallow supportive or palliative treatments. To the best of ourknowledge, the exposed bone of alveolar osteonecrosis willeventually heal over, usually within a three to six month period,provided that the cocaine is no longer placed in that vestibular site.Removal of damaged bone should be helpful, since the problem isfocal and there should be unaffected bone surrounding the area ofcocaine-induced osteonecrosis, as with the bone inosteoradionecrosis, but we have no more than our anecdotalexperience as a basis for this belief. At the very least, moving thecocaine contact point intermittently should reduced the risk oftissue damage from ischemia, although it may produce more diffusecocaine gingivitis. Obviously, the best outcome would come fromstopping the habit completely and permanently. Along this sameline, the palatal perforation can be surgically covered by softtissues, or prosthetically covered with an obturator, but the diseaseis likely to progress while the habit continues.5,6

Other than bone destruction, tooth destruction from neglectand erosion/abrasion is the most likely serious oral problem incocaine abuse, possibly leading to severe occlusal and infectiveissues. Since most of the addicts in our Clinic have financial

difficulties, this too often leads to full mouth extraction. However,in a patient with better financial capabilities, and a willingness toalter his or her lifestyle, routine, albeit extensive, dental care shouldbe no different from that of a non-addicted patient, although itshould be noted that cocaine is apparently capable of discoloringsome dental materials.25

ConclusionThere are many, and often unreported, oral manifestations of

cocaine abuse or addiction. The clinician is likely, however, to viewthese as idiopathic or unexplained without knowledge of a potentialcocaine connection. It is hoped that this informal review of clinicalfeatures of addiction will aid in the identification of underlyingcauses of these lesions. It should be finally noted that the lesionsreported in this paper are presumed to be caused by cocaine use.Usually, this understanding is derived from discussions with addictsthemselves. However, we must emphasize, once again, that we onlyreport our anecdotal experience, not the results of a plannedinvestigation. Since we see no such investigation on the horizon,we offer the next best thing.

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Dr. Jerry Bouquot is Professor and Chair of the Department ofDiagnostic Sciences at the University of Texas Dental Branch inHouston. He is also an Adjunct Professor of the West VirginiaUniversity School of Dentistry, and is the Director of Research fora private research center, the Maxillofacial Center for Educationand Research. Dr. Bouquot has more than 220 published papers,abstracts and book chapters. Dr. Bouquot has been President ofthe American Board of Oral & Maxillofacial Pathology and anExecutive Counselor of the American Academy of Oral &Maxillofacial Pathology. He has been President of three regionaldental societies, President of his state’s American Cancer Society,a member of the national Board of Directors of the ACS and of theBoard of Trustees for the eight-state South Atlantic Division of theACS.

Dr. Cleverick D. “CD” Johnson earned his dental degree fromUniversity of Texas Dental Branch in 1986 following a Masters inBiology 1981 from Texas Southern University and completed aMinority Science Fellowship at the University of Houston Collegeof Pharmacy 1982. He is an Associate Professor at The Universityof Texas Health Science Center Dental Branch, department ofRestorative and Biomaterials, where he is the Director of theUrgent Care Dental Clinic. He has published extensively on theoral diagnosis and substance abuse. He has received many awardsand honors including the nationally recognized “Jefferson Award”for public and humanitarian in 2002 for his contributions toscience and dentistry.

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12. Brand HS, Gonggrijp S, Blanksma CJ. Cocaine and oral health.Br Dent J 2008; 204:365-9.13. Fava M, Cherubini K, Yurgel L, Salum F, Figueiredo MA.Necrotizing sialometaplasia of the palate in a cocaine-using patient.A case report. Minerva Stomatol 2008; 57:199-202.14. Blanksma CJ, Brand HS. Cocaine abuse: orofacial manifestationsand implications for dental treatment. Int Dent J 2005; 55:365-9.15. Woyceichoski IE, de Arruda EP, Resende LG, Machado MA,Grégio AM, Azevedo LR, de Lima AA. Cytomorphometric analysisof crack cocaine effects on the oral mucosa. Oral Surg Oral MedOral Pathol Oral Radiol Endod 2008; 105:745-9.16. Driscoll SE. A pattern of erosive carious lesions from cocaineuse. J Mass Dent Soc 2003; 52:12-4.17. Kapila YL, Kashani H. Cocaine-associated rapid gingivalrecession and dental erosion. A case report. J Periodontol 1997;68:485-8.18. Lee CY, Mohammadi H, Dixon RA. Medical and dentalimplications of cocaine abuse. J Oral Maxillofac Surg 1991; 49:290-3.19. Yukna RA. Cocaine periodontitis. Int J Periodontics RestorativeDent 1991; 11:72-9.20. Johnson CD, Brown RS. How cocaine abuse affects post-extraction bleeding. J Am Dent Assoc 1993; 124:60-2.21. Bernstein J, Bernstein E, Shepard DS, Valentine A, Heeren T,Winter M, Levenson S, Beaston-Blaakman A, Tassiopoulos K,Hingson R. Racial and ethnic differences in health and health care:lessons from an inner-city patient population actively using heroinand cocaine. J Ethn Subst Abuse 2006; 5:35-50.22. Allen KR, Azad R, Field HP, Blake DK. Replacement ofimmunoassay by LC tandem mass spectrometry for the routinemeasurement of drugs of abuse in oral fluid. Ann Clin Biochem.2005; 42:277-84.23. Pellegrini M, Casá A, Marchei E, Pacifici R, Mayné R, BarberoV, Garcia-Algar O, Pichini S. Development and validation of a gaschromatography-mass spectrometry assay for opiates and cocainein human teeth. J Pharm Biomed Anal 2006; 40:662-8.24. Harris EF, Friend GW, Tolley EA. Enhanced prevalence ofankyloglossia with maternal cocaine use. Cleft Palate Craniofac J1992; 29:72-6.25. Brown RS, Johnson CD. Corrosion of dental gold restorationsfrom inhalation of “crack” cocaine. Gen Dent 1994; 42:242-6.