Community Deni Oral Epidemiol 1993: 21: 78-81Prinied in Denmark . All righis reserved

Copyright © Munksgaard 1993

Communify Dentistryand Oral Epidemiology

ISSN 0301-5661

Effects of cannabis smoking on oralsoft tissues

M. R. Darling and T. i\1. ArendorfFaculty of Dentistry. University of the WesternCape, Mitctiells Plain, Soutti Africa

Darling MR, Arendorf TM: Effects of eannabis smoking on oral soft tissues.Community Dent Oral Epidemiol 1993; 21: 78-81. © Munksgaard, 1993

Abstract - The oral effects of cigarette smoking have been well documented butthe effects of cannabis smoke on the oral environment have been poorly documented.Three-hundred cannabis/tobacco/methaqualone smokers were examined. Two con-trol groups consisting of 152 tobacco- and 189 non-smokers respeetively were exam-ined similarly. Health of the oral tissues and oral dryness was recorded. Lesionspresent included leukoedema, leukoplakia and numerous others. The only significantdifferenees between lesions and conditions noted in cannabis users and controlsoccurred with respect to leukoedema, dry mouth and traumatic ulcer.

Key words: cannabis: oral soft tissues '

M. H. Darling, Faculty of Dentistry. Universityof the Western Cape, Private Bag X08, MitchellsPlain, 7785, South Africa - .?

Accepted for publication 12 August 1992

Cannabis is a drug of plant origin (1-3)and is abused worldwide (1, 4-7). It isalso the most widely used illicit drug inSouth Africa (8-10). Prevalence figuresfor use amongst young men range from12 to 19% (9). The abuse of cannabis iswell known in the Western Cape regionof South Afriea partieularly (3, 11, 12),with a prevalenee figure of 26% amongadolescents (II). An exclusively SouthAfrican feature is the smoking of the"white pipe", a mixture of eannabis andsmall quantities of eigarette tobaeeo andcrushed methaqualone tablets in a bottleneek (3).

The objeetive of this study was to de-termine the effects of cannabis smokingon the oral soft tissues. Cigarette smok-ing is known to eause lesions of the oralsoft tissues (13) and changes in humanlingual epithelium (14). Cannabis use hasalso been associated with oral soft tissuelesions (15, 16).

Material and methods

Three hundred eannabis/methaqualone/tobacco smokers attending a rehabilita-tion centre were examined by a single(dentally qualified) examiner using a

mouth mirror, probe and eheek retrac-tors in natural light. Two race-, age- andsex-matched eontrol groups consisting of152 tobacco smokers and 189 non-smokers (who had never smoked) wereexamined similarly. These control groupswere drawn from randomly selected pa-tients attending the dental hospital of theUniversity of the Western Cape and twogeneral dental practices in Cape Town.Patients and eontrols were representativeof all soeio-eeonomie classes.

Health of the oral tissues was recorded.The presence of oral mueosal lesions in-cluding severe gingivitis was noted, usingthe elinieal diagnostic eriteria as detailedin the World Health Organization ( WHO)Guide to Epidemiology and Diagnosis ofOral Mueosal Diseases and Conditions(17). This information was detailed on theWHO assessment form/questionnaire fororal mucosal diseases (17). Severe gin-givitis was recorded when the gingiva ex-hibited redness, swelhng and spontaneousbleeding. A photographic record of alllesions found was kept. Where necessary,patients were eneouraged to have a biopsytaken.

In addition to the information requiredon the assessment form, patients werequestioned with respect to cannabis, me-

thaqualone, tobacco and alcohol usage.This information was recorded in the sec-tions on Smoking Habits and OtherHabits.

Results

Participants who were female. Black orused eannabis only were exeluded as thenumbers were too small to have statisticalsignificance. These ineluded 34 of thestudy group, 7 tobaeeo-smoking and 21non-smoking eontrols.

Cannabis / methaqualone / tobaccosmokers numbered 266, with a mean ageof24.7yr(SD = 8.9; range 13-51 yr). Themean number of pipes smoked per daywas 4.7 (SD = 4.5). Of the study group 237also smoked cigarettes and 123 used alco-hol. The non-smoking contols numbered168 and the eigarette smoking eontrolsnumbered 145. There was no signifieantdifferenee between the study group andeontrols with respeet to age and alcoholusage (Table 1).

The distribution of oral mucosallesions in eannabis/methaqualone/to-bacco smokers and control groups isshown in Table 2. The prevalence of leu-koedema was signifieantly greater, andtraumatic ulcer significantly less, in the

Cannabis effeet on oral soft tis.wes 79

Table 1. Epidemiologic data: cannabis/methaqualone/tobacco smokers (GI), cigarette-smokingcontrols (Cl) and non-smoking controls (C2)

GI Cl C2

1. Number2. Mean age3. Mean number of cannabis pipes smoked/day4. Mean duration of cannabis smoking (years)5. Mean number of cigarettes smoked/day6. Mean duration of cigarette smoking (years)7. Number of alcohol users8. Race distribution:

Caucasian•Coloured

26624.74.78.98.26.9

123

54212

14528.3

--

10.79.2

60

!5130

16825.3

-.---

47

19149

* South African category for people of mixed origin.

Table 2. Distribution of lesions by percentage in cannabis/methaqualone/tobacco smokers (GI),cigarette smoking controls (Cl) and non-smoking controls (C2)

GI Cl C2

1. Leukoedema2. Leukoplakia3. Dry mouth after smoking4. Nicotinic stomatitis5. Erythroplakia6. Denture stomatitis7. Angular cheilitis8. Median rhomboid glossitis9. Hypopigmented lower lip

10. Fordyce's granules11. Hyperkeratosis12. Recurrent herpes13. Cheek chewer's lesion14. Traumatic inflammation15. Traumatic ulcer16. Mucocoele17. Geographic tongue18. Fibromatosis gingivae19. Lip burns20. Severe gingivitis21. Haematoma22. Papilloma/wart23. Numb lips after smoking24. Chemical burn25. Brown stained tongue26. Aphthae27. Atrophic tongue

57.1L5

69.610.52.33.43.00.82.31.51.10.80.80.8

0.80.40.4

0.40.40.40.40.40.80.4_

51.70.7

18.611.00.72.1-1.41.42.10.7_-—_...1.4-

0.7.-

2.8_ •

1.40.71.40.7

20.20.6

Not assessed--1.20.6-

0.64.2-

0.61.2-

2.4-——

1.2--

Not assessed----

Table 3. Significant differences in the prevalence of oral mucosal lesions and dry mouth betweencannabis/methaqualone/tobacco smokers (GI), cigarette-smoking controls (Cl) and non-smok-ing controls (C2)

GI V C2 GI VCl Cl VC2

Leukoedema

Dry mouth

Traumatic ulcer

/> = 0.000chi-square

P = 0.022Fisher's exact

P = 0.000chi-square

Study group than in the non-smoking eon-trols (Table 3). There were no raee relateddifferences in the prevalence of leukoede-ma. The prevalence of dry mouth wassigniftcantly greater in the study group

than in the eigarette-smoking eontrols(Table 3). These were the only differeneesbetween the study group and controls.

Of the four leukoplakias present in themouths of cannabis users examined in this

study, three involved the bueeal mueosaand one the mandibular alveolar mueosa.All the lesions were homogeneous. Therewere no significant differences from thecontrol groups.

Erythroplakia occurred in six cannabisusers and one eigarette smoker, but innone of the non-smoking controls. Of thecannabis users who had red lesions, threedid not smoke cigarettes and four did notuse aleohol. None of these variables weredifferent in the eontrols.

Nine patients had denture stomatitis,of whom two had an assoeiated angularcheilitis and one had reeurrent herpes la-bialis. None of these patients had medianrhomboid glossitis, which had previouslybeen associated with denture stomatitis(18). A total of eight patients had angularcheilitis, of whom two had an associatedmedian rhomboid glossitis. Both patientswith median rhomboid glossitis were den-tate. There was no differenee between thestudy group and eontrols with regard tothese lesions and denture wearing.

Six of the study group had depigmen-tation of the lower lip. Of these, threesmoked cigarettes and two used alcohol.

Two cannabis users had reeurrent her-pes labiahs involving the lower lip. Oneof these patients had an associated den-ture stomatitis. No significant differencesexisted between the study group and thecontrols.

Four of the non-smoking controls hadtraumatic oral ulcers, signifieantly great-er than the study group. Two of theselesions were assoeiated with trauma dueto mastication and two with denturetrauma.

Statistical methods used to analyseand compare the data ineluded Chi-square and Fisher's exact tests.

Discussion

Leukoedema was found to oeeur morefrequently in cannabis users than in eon-trols. This compares favourably with thefindings of previous studies (15, 19). Leu-koedema is regarded by some to be avariant of normal (20, 21), and tnanyrelate the presence of leukoederna to hab-its, including smoking (22-26), eheeksucking (25), betel nut chewing (22) andcoca leaf chewing (27).

VAN WYK & AMBROSIO (1983) suggestthat leukoedema is a pathological entityand that eellular damage results in mani-festation of the lesion (28). They further

80 DARLING AND ARENDORF

speculate that there is a threshold forsmoking and when exceeded, leukoede-ma develops. It is therefore conceivablethat eannabis smoking, in a similar fash-ion to tobaeeo smoking, along with otherfactors such as alcohol use and irritation,may produce leukoedema. It is probablethat the aetiology of leukoedema is mul-tifactorial (caused by both tobacco andcannabis smoking in the current study),a view supporting that of VAN WYK (29).

Cannabis users did not show greaterprevalenee of leukoplakia when eotn-pared with control groups. Cannabis con-tains numerous carcinogens (30) and oralleukoplakia in a cannabis user shouldtherefore be closely tnonitored as the ma-lignant potential of leukoplakia is wellknown (22, 31-33). DONALD (1986) re-ported the oeeurrenee of head and neekcarcinoma in a group of young cannabissmokers (30). It seems reasonable to spec-ulate that the lesions in the mouths of thecannabis smokers were probably of lowmalignant potential as all were hotnoge-neous. Unfortunately, due to the relue-tanee of these patients to cooperate, biop-sies were refused and follow-up was poor.

The majority (69.6%) of eannabis us-ers experienced a dry tnouth almost im-mediately after cannabis usage. Cannabisis a drug with parasympatholytic proper-ties (34, 35) and hence could produce theclinical symptom of xerostornia. The drymouth experieticed was transient and noparticipant could accurately determinethe duration.

It is noteworthy that nicotinie stomati-tis was present in four cannabis users whodid not smoke cigarettes. This suggeststhat the lesion can be eaused by cannabissmoke. This has not been mentioned pre-viously in the available literature.

The differenee between the groups wasnot significant but it appears evident thatthe condensate of eannabis smoke hasthe potential to eause red lesions of theoral mucosa. Dietary and other factorsmay have played a role in the aetiologyof these lesions, but the role of cannabissmoke eannot be discounted.

Inhibition of the irnmune response incannabis smokers has been reported (36,37) and has been associated with a recur-rent genital herpes simplex (38). Simi-larly, it would not be surprising for oralcandidosis to be a eommon fmding, withan additional predisposing factor beingthe xerostomia reportedly experieneed bycannabis users. ARENDORF & WALKER

(39) have suggested that tobaeeo smok-ing and denture wearing may play a rolein the development of median rhomboidglossitis by favouring the loeal prolifera-tion of Candida albieans on the dorsumof the tongue. It is likely that a combina-tion of poor denture hygiene, deficientnutritional factors and cannabis use con-tributed to the manifestation of can-didosis (multifocal in four cases) and me-dian rhomboid glossitis in these patients(40). Interestingly, none of (he controlsin the present study exhibited the ehronicmultifoeal form of the disease.

Depigtnented lesions of the lips relatedto smoking habits and alcohol usagehave been deseribed by VAN WYK et al.(25, 41). The intense heat generated with-in the cannabis pipe during smoking wasthe likely cause of the hypopigmentedlower lip in the patients examined in theeurrent investigation, a theory whieheoncurs with that of VAN WYK et al. (25).

In the current study group and con-trols, the oeeurrenee of severe gingivitiswas assoeiated with poor oral hygienewhich was the likely tnajor causativefaetor.

An assoeiation between cannabis useand oral papilloma has beeti deseribed(42). It is difficult to ascribe the presenceof oral papilloma to cigarette or cannabissmoking, and the possible role of humanpapilloma virus eannot be ignored(43^5). In 1980, COLON (42) discountedthe role of venereal disease and viral in-volvement without providing evideneefor doing so.

Smoking, both eannabis and tobacco,may inhibit aphthous uleeration by in-ereasingkeratinisation of the oral mueosa(46, 47). This may explain the low inei-denee of aphthae in the present study.

Further long-term elinieal and histo-logieal investigations of the oral effectson eannabis smokers would be worth-while as our study has shown that theoral health of users is sotnewhat compro-mised.

References

1. GRINSPOON L. Marihuana. Sci Am 1969:221: 17-25.

2. MiiCHOL/LAM R. Marihuana chemistry.Science 1970; 168: 1159-66.

3. DH MIRANDA S. Drugs and di-ug abuse inSouthern Africa. Pretoria: J. L. vanSchaik, 1987: 8^9 .

4. JoACHtMOGLU G. Natural and smoked

hashish. In: WoLSTiiNHOLME GEW.KNtGHT J, eds. Hashish: its chemistry andpharmacology. London: J. & A. Churchill.1965: 2-11. '

5. NORTON LE, GARRIOT JC. Detection ofmarihuana use by gas chroniatography/mass spectrometry analysis of mouthswabs. Am J Forensic Med Pathol 1983;4: 185-8.

6. KRAMER JM. Drug abuse in the SovietUnion. Pivhl Communism 1988: 37:28-40.

7. PLANT MA. The epidemiology of alcoholand illicit drug abuse. Meil Ini (South Af-rican Edn.). 1989; 62: 2538-42.

8. LEVIN S M . BBRMAN C , Conn H, MCIL-RAtTH J. Dagga (cannabis) usage amongmedical students in Johannesburg. S AfrMed J 1983; 63: 607-9.

9. VAN DER BURGH C . Some epidemiologicalaspects of dagga use in South Africa. In:Report on the South African Conferenceon Dagga. Pretoria: Government Printer,1983; 13-5.

10. LAMONT DL, DuFLOu JALC, COATBS D.Dagga-smoker's hand - a new physicalsign? S Afr Med J 1988; 73: 356-8.

11. DisuiK SA, EPSTEIN L M , DISLHR PB, RipMR, Kt,OPPER JM, KtnEL MA. Lifestylesof adolescents - a study in a Cape TownHigh School. Communiiy Healih in South-cm Africa 1989; 4: 8-12.

12. FuRMAN S. On dagga and mandrax abusein the Western Cape. SA Eamily Practice1989;/O. 28-9.

13. PALMER RM. Tobacco smoking and oralhealth. Brit Dcni J 1988; 164: 258-60.

14. VALENTINE JA, SCOTT J, WEST CR, ST.HILL CA. A histological analysis of theearly effects of alcohol and tobacco usageon human lingual epithelium. J Oral Pa-thol 1985; 14: 654-65.

15. EnLiNG H, NESI W, WAGNER EM. Leu-koedema in marijuana {Cannabis sativa-lin) smokers (translated). Rev Fac OdontolPorto Alegrc 1968/69; 10/11: 35-9.

16. DARLING MR, At<tiNDORF TM. Review ofthe effects of cannabis smoking on oralhealth. lnt Dent J 1992; 42: 19-22.

17. KRAMER I R H , PINDHORG JJ, BEZROUKOVV, SARDO-INITRRI J. World Health Orga-nization Guide to Epidemiology and Diag-nosis of Oral Mucosal Diseases and Condi-tions. Vojens, Denmark: P. J. SchmidtTryk (Reprinted from Community DentOral Epidemiol 1980; 8: 1-26).

18. BuDTZ-JORGENStiN E. Denture stomatitis(V). Candida agglutinins in human sera.Acta Odontol Scand 1972; 30: 313-25.

19. NE.SI W. Oral manifestations due to thehabit of smoking "Cannabis sativa" (Mar-ijuana) (translated). Rev Bras Odonlol1970; 27: 81-92.

20. ARCHARn HO, CARt..soN KP, STANLEYHR. Leukoedema of the human oralmucosa. Orat Siu-g 1968; 25: 717-28.

21. MARTtN JL, Ct<uMP EP. Leukoedema ofthe buccal mucosa in Negro children andyouth. Oial Swg Oial Med Oral Pathol1972; i^.-49-58.

22. PtNDliOtlG JJ, BARMtiS DE, RO0.D-PE-TERSEN B. Epidemiology and histology oforal leukoplakia and leukoedema amongPapuans and New Guineans. Caneer 1968;22: 379-84.

Cannabis effeet on oral soft tissues 81

23 . HAMNER JE, MEtiTA FS, PtNDBORG JJ,

DAFTARY DK. An epidemiologic and his-topathologic study of leukoedema among50,915 rural Indian villagers. Oial SurgOral Med Oral Pathol 1971; 32: 58-65.

24. TYLDESLEY WR. Tobacco chewing in En-glish coal miners. A preliminary report.Brit J Oral Swg 1971; 9: 21-28.

25. VAN WYK CW, BREYTENBACH HS, DREYERWP. The epidemiology of preventable oralmucosal lesions in the Cape Peninsula. /Dent Assoc S Afr 1979; 34: 672-6.

26. AxELL T, HENRICSSON V. Leukoedema -an epidemiologic study with special refer-ence to the influence of tobacco habits.Community Dent Oral Epidemiol 1981; 9:142-6.

27. BoRGHELLi RF, STIRPARO M , ANDRADE J,BARROS R , CENTOFANTI M , DE ESTEVEZOT. Leukoedema in addicts to coca leavesin Humahuaca, Argentina. ComimmityDent Oral Epidemiol 1975; 3: 40-3.

28. VAN WYK CW, AMBROSIO SC. Leukoede-ma: ultrastructural and histochemical ob-servations. J Oral Pathol 1983; 12:319-29.

29. VAN WYK CW. An investigation into theassociation between leukoedema andsmoking. J Oral Pathol 1985; 14: 491-9.

30. DONALD PJ. Marijuana stTioking - Pos-sible cause of head and neck carcinomain young patients. Otolaryngol - Head andNeck Surg 1986; 94: 517-521.

31. SUGAR L, BANOCZY J. Follow-up studies

in oral leukoplakia. Bull World Health Org1969; 41: 289-93.

32. AXELL T, HOLMSTRUP P, KRAMER IRH,

PiNDBORG JJ, SHEAR M . Internationalseminar on oral leukoplakia and associ-ated lesions related to tobacco habits.Community Dent Oral Epidemiol 1984; 12:145-54.

33. LtND PO. Malignant transformation inoral leukoplakia. Scand J Dent Res 1987;95: 449-55.

34. HOROWITZ L G , NERSASIAN R R . A reviewof marijuana in relation to stress-responsemechanisms in the dental patient. JADA1978; 96: 983-6.

35. ASTON R. Drug abuse. Its relationship todental practice. Dent Clin North Am 1984;28: 595-610.

36. NAHAS GG, Suciu-FoCA N, ARMAND JP,

MORISHIMA A. Inhibition of cellular medi-ated immunity in marijuana smokers. Sci-ence 1974; 183: 419-20.

37. BARON JD. Kids and drugs. New York: ThePutnam Publishing Group, 1983; 15-27;36-7.

38. JUEL-JENSEN BE. Cannabis and recurrentHei-pes simplex. Biit Med J 1972; 4: 296.

39. ARENDORF TM, WALKER DM. Tobaccosmoking and denture wearing as local ae-tiological factors in median rhomboidglossitis. lnt J Oral Surg 1984; 13: 411-5.

40. DARLING MR, ARENDORF TM, COLDREY

N. Effect of cannabis use on oral candidalcarriage. / Oral Pathol Med 1990; 19:319-21.

41. VAN WYK CW, FARMAN AG, STAZ J. Oralhealth status of institutionalised elderlyCape Coloureds from the Cape Peninsulaof South Africa. Community Dent OralEpidemiol 1977; 5.- 179-84.

42. COLON PG JR. Oral papilloma in marijua-na users. Qidntessence lnt 1980; ;;.• 75-80.

43. SYRJANEN K, SYRJANEN S, LAMBERG M ,PYRHONEN S, NuuTtNEN J. Morphologicaland immunohistological evidence suggest-ing human papillomavirus (HPV) involve-ment in oral squamous cell carcinogenesis.lnt J Oral Surg 1983; 12: 418-24.

44. EvERSOLE LR, LAIPIS PJ. Oral squamouspapillomas. Detection of HPV DNA byin situ hybridization. Oral Surg Oral MedOial Pathol 1988; 65: 545-50.

45. PADAYACHEE A, VAN WYK CW. Humanpapillomavirus (HPV) in oral squamouscell papillomas. / Oral Pathol 1987' 16-353-5.

46. CHELLENI SJ, OLSON DL, SHAPIRO S. Theassociation between smoking and aph-thous ulcers. Oral Surg Oral Med OralPathol 1970; 29: 832-6.

47. RENNIB JS, READE PC, SCULLY C . Recur-rent aphthous stomatitis. Brit Dent J 1985-159: 361-7.