in mon- s linical and characteristic histopathologic features

Richard L. bfiller, DDS, PhD,a Alan R. Gould, DDS, MS,’ and Mark L. Bernstein, DDS,a Louisville, Ky.

DEPARTMENT OF SURGICAL AND HOSPITAL DENTISTRY, UNIVERSITY OF LOUISVILLE SCHOOL OF DENTISTRY

Fourteen new cases of cinnamon-induced stomatitis are reported. Ten of these fourteen cases ‘were first detected on the basis of histopathologic changes, which included hyperkeratosis, chronic lichenoid mucositis with plasmacytic infiltration, and marked chronic perivasculitis. Six cases of false-positive histopathologic findings are presented for comparison. It is recommended that when the histopathologic features described are recognized, cinnamon stomatitis should be considered. (ORAL SURC ORAL MED ORAL PATHQL 1992;73:708-16)

innamon-induced contact dermatitis and mucosi- tis have been sporadically reported in the medical and dental literaturele3 and have received increased at- tention in recent years. 4-12 Exposure to cinnamon- flavoring agents that result in adverse reactions has occurred with candy,‘O chewing gum,‘O cinnamon toast,7 mouthwash,7 lip sunscreen9 toothpaste,3‘6, 8, l2 prophylaxis preparations,’ and volatile oils.2 The pathogenesis that underlies these responses may in- volve both immunologic and nonimmunologic mech- anisms. Clinical presentation of oral lesions is heter- ogeneous and can include pain or burning with urticarial swelling,‘> 2, 7-9, l2 erythema,‘, 2, lo, l2 fis- sures, 2, 8, 9 ulceration,8, l2 adherent and peeling white patches, lo sloughing,*, l2 and vesicular lesions.3, 6 Combined red and white lesions with or without ulceration have been described, which suggests a clinical resemblance to oral lichen planus and lupus erythematosus. lo Oral anatomic distribution has on occasion been described as somewhat generalized, l, 6 8 although the more common focal involvement of the buccal mucosa,rO tongue,7, lo lip,‘, 3, 7,9, t2 floor of the mouth,‘O and gingiva 1 1, 1 2 has been reported. Perioral skin’, 3, 8 as well as distant skin involvement6 (e.g., hands) concurrent with oral lesions has also been re- ported. Lesions typically develop at sites of direct ex- posure to cinnamon agents, which is consistent with contact sensitivity. However, oral lesion distribution appears restricted, which suggests anatomic variation

“Professor of Oral Pathoiogy. 7/M/35643

708

in the level of sensitivity to cinnamon-containing agents.

During recent years we have encountered a number of patients with cinnamon-induced oral mucosal dis- ease. The clinical and histologic features demon- strated in these cases are described herein. It is our observation that the microscopic findings are suffi- ciently characteristic to permit a useful degree of ac- curacy in identifying patients with cinnamon-induced oral mucositis.

METHODS OF EVALUATION

Twenty-seven cases of possible cinnamon-related stomatitis venenata were retrieved from our clinical and histopathologic records and from review of biopsy records at the University of Louisville School of Den- tistry (ULSD) from 198 1 through 1990. All histo- pathologic and clinical cases with cinnamon men- tioned in the pathologists’ comments were included in the series. Patient follow-up data were obtained either by our direct examination (8) of the patients, tele- phone follow up (2) by the referring dentist, or tele- phone follow up (10) directly by us. Clinical photo- graphs were taken by us or by the referring practi- tioner. Seven cases were excluded from the study because the patients could not be contacted for follow-up and the practitioners had no follow-up data (5) or because the practitioners did not notify the pa- tient of a possible association of cinnamon to the le- sions (2). The twenty cases included in the study were subdivided into group A-12 patients who used cin- namon, whose lesions were biopsied, and who demon-

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Cinnamon stomatitis 709

Table I. Histopathologic changes

Epithelial Injammatory resolution

Al 55, F Buccal mucosa A2 37, F Buccal mucosa A3 56, F Buccal mucosa A4 37, M Buccal mucosa A5 71, M Tongue A6 62, F Tongue Al 34, M Buccal mucosa A8 62, M Buccal mucosa A9 73, F Buccal mucosa A10 60, M Buccal mucosa A 11 49, M Buccal mucosa Al2 40, M Buccal mucosa Cl 57, M Buccal mucosa C2 59, M Tongue C3 54, F Buccal mucosa C4 39, F Buccal mucosa C5 58, M Lip C6 76, F Buccal mucosa

Parakerafosis

Parakeratosis

Parakeratosis

Parakeratosis*

Acanthosis

Parakeratosis*

Parakeratosis orthokeratosis

Parakeratosis

Parakeratosis

Parakeratosis

Parakeratosis

Parakeratosis

Orthokeratosis

Parakeratosis Monilia

Parakeratosis

Orthokeratosis

Orthokeratosis

Parakeratosis

L, PC

L, PC

L, PC

L*

L, PC, PMN

L, PC *

L, H

L, PMN

L

L, PC H

L

PC, L

L

PC, L

PC, L

L

L

L, PC

strated lesion regression after discontinuance of cin- namon; group B-two patients who used cinnamon, whose lesions were not subjected to biopsy, and who showed lesion regression after discontinuance of cin- namon agents; and group C-six patients whose lesions were subjected to biopsy, and who did not ac- knowledge the use of cinnamon as a possible etiologic agent.

We reviewed all histopat.hologic slides and reports and developed a consensus on the histopathologic cri- teria. Summary charts of histopathologic changes

- *Biopsy 3 weeks after discontinuance of cinnamon + Present. - Absent. L = Lymphocytes. PC = Plasma cells. H = Histiocytes. PMN = Neutrophils. Y = Yes. N = No.

+

+

Y

Y

Y

Y

Major

Y

Y

Y

Y

Y

Y

Y

Y Mycostatin

N

Y Amalgam

Y Vitamins

N

(Table I) and clinical features (Table II) were devel- oped. Clinical data were based on chart entries, information from biopsy clinical data sheets, and personal observations.

CASE REPORTS Group A-Patients with histopathologic lesions who used cinnamon and achieved a degree of resolution when cinnamon was removed.

Case Al. A 55-year-old white woman was referred to ULSD with blistering, sloughing lichenoid mucositis of the bilateral palate, buccal mucosa, and retromolar areas (Fig.

71 M iller, Could, and Berm&in ORAL %RG ORAL ht%D ORAL PATHOL June 1992

Table II. Clinical features -.

Clinical Cinnamon Degree of Case Location Duration presentation Tobacco form response

Al Buccal mucosa (L,R) 6 months Sloughing, pain, None Gum 100% resolution palate white lichenoid in weeks

A2 Buccal mucosa (L) months White plaque, Unknown Hard candy, 100% resolution discomfort, gum in months swelling

A3 Buccal mucosa (L) 3 weeks White lichenoid Cigarettes-41 Sugarless gum 100% resolution pack years in 2 weeks

A4 Buccal vestibule (R) 5 years White plaque Smokeless, Stick bark 100% resolution cessation-5 years 2 months

A5 Posterior dorsal 4 months Red & white patches, Unknown Jaw breakers 100% resolution tongue (R,L) slight pain

A6 Buccal mucosa (L,R), 3 months White Iichenoid gingiva (L,R), ulcerations ventral tongue

Al Buccal macosa (L,R) 6-8 weeks White Lacy ulcerated

A8 Buccal mucosa (R) 2 months Red/white/ulcers vestibule (R) lichenoid

A9 Buccal mucosa (L) 4 months Red/white lupus-like

A10 Buccal mucosa (R) 4 months White fissured vestibule (R) recurrent

All Buccal mucosa (R,L) Chronic White, lacy

A12 Buccal mucosa (R,L) 6 weeks White striated

B1

B2

Buecal mucosa (R) gingiva (R)

Buccal mucosa (R,L) tongue

8 months Red in white recurrent sloughing

painful 5 months White plaques

peeling

1). The lesions were painful, of 6 months’ duration, and seemed to worsen when the patient ate egg and tuna salad. The patient’s dentition was in good repair, and she admit- ted to no oral habits. The health history was positive for al- lergies to metallic jewelry, strawberries, tomatoes, and penicillin. A biopsy of the buccal mucosa revealed lichenoid mucositis with perivascular infiltrates. The patient was re- ferred to an allergist, who performed skin tests that were positive for 27 of 200 allergens. Working with the allergist, we fabricated a palatal acrylic stent so that we could con- duct tests for three formulations of amalgam, corroded amalgam from the patient’s fillings, and zinc oxide eugenol. Placement of the stem revealed no contact mucositis, and there was paradoxical resolution of all oral lesions within I week. Removal of the stent triggered recurrence of lesions within days. Reinsertion of the stem again produced the ie- sion resolution. After 1 month of resolution while she was wearing the stent, the patient complained that she was “un- able to chew my cinnamon gum” when she wore the appli- ance. Further investigation revealed a history of chewing two to three packages of cinnamon chewing gum per day for the previous 6 months. Subsequent withdrawal of the gum yielded resolution of lesions and contact with cinnamon gum replicated the lesions (Fig. 2).

-

Unknown Gum in 6 weeks

Major resolution in 3 years

None Gum, toothpaste 100% resolution 4 months

Cigars Gum 100% resolution months

Unknown Antacid 100% resolution 6 weeks

Cigars, cessation- GUllI 100% resolution 4 months months

Pipe Breath savers 100% resolution months

Cigarettes, Gum 100% resolution cessation-6 weeks months

Cigarettes Gum 100% resolution (menthol) 3 weeks

None Gum, candy 100% resolution in 3 weeks

Case AZ. A 37-year-old white woman consulted her gen- eral dentist regarding a 3.5 X 2.0 cm white plaque of the left buccal mucosa (Fig. 3.) She had noted episodes of swelling, discomfort and numbness in the area for 2 months. A biopsy revealed chronic mucositis with marked perivascular in% trate. A note with the biopsy report suggested lupus erythe- matosus, lichen planus, and contact allergy as possible causes (Fig. 4.) The patient was referred to ULSD for eval- uation. She revealed a history of Barlow syndrome, rheu- matic heart murmur, and previous psychiatric disease treated with Compazine. The patient was presently taking no medications. Tests for lupus erythematosus wrere nega- tive. The patient admitted the use of cinnamon-flavored “red hots” and cinnamon chewing gum. Reduction in con- sumption of the gum and candy resulted in regression of the lesions after 1 month and subsequent resolution of lesions. The patient has had no oral lesions for the past 5 years with reduced consumption of cinnamon-flavored gum.

Case A3. A 56-year-old white woman visited an ora! sur- geon for an incisional biopsy of a white 2.0 x 2.0 cm lichenoid lesion of the left buccal mucosa of 3 weeks’ dura- tion. The patient was in good general health and had smoked cigarettes for 41 years. A biopsy of the lesion revealed chronic mucositis with findings characteristic of those

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Cinnamon stomatitis 711

Fig. 1. Case Al. Representative red and white linear lesion of buccal mucosa at level of occlusal line, in- cluding retromolar mucosa.

Fig. 2. Case Al. Resolution of lesions after discontinuance of cinnamon.

caused by cinnamon-flavoring agents. The patient was no- tified and admitted to heavy use of sugarless cinnamon chewing gum for at least 3 weeks. Discontinuance of the gum resulted in resolution of lesions within a 2-week period. The patient complained of previous medical expenses asso- ciated with attempts to (diagnose the lesion and, on retention of an attorney, settled fior compensation from the manufac- turer of the chewing gum.

Case A4. A 37-year-old white man visited the ULSD clinics with a 3.0 X 3.0 cm white demarcated lesion of the mandibular right bucca.1 vestibule. The patient reported the use of smokeless tobacco in this area for 7 years with ces- sation 5 years before. The patient had substituted the use of stick cinnamon in the affected area for the past 5 years.

The health history was negative. An incisional biopsy per- formed 3 weeks after discontinuance of cinnamon use resulted in a diagnosis of chronic lichenoid mucositis secondary to cinnamon. The patient was advised to discon- tinue use of cinnamon in any form. A follow-up clinical ex- amination 2 months after the biopsy revealed normal mu- cosa of the area.

Case A5 to Al 2. This series of eight patients visited their dentists with white, red and white, and lichenoid lesions (Table II). A biopsy of each lesion was interpreted as con- sistent with stomatitis venenata versus lupus erythematosus based on the histopathologic features described in this ar- ticle (Table I). Oral cinnamon product usage was identified and withdrawn with subsequent lesion reduction (Case A6)

712 Miller, Gould, and Bernstein ORAL SURG ORAL k&D ORAL PATHaL June 1992

Fig. 9. Case A2. Well-defined, white, roughened plaque extending length of buccal mucosa at level of oc- clusal line. Note biopsy site at middle inferior aspect of lesion.

or total resolution (Cases A5 and A7 to Al2). Patient AS was rechallenged with cinnamon gum and the lesions recurred.

Group B-Patients with ciinicai mucositis that resolved when cinnamon was removed (biopsies not performed)

Case Bl. A 53-year-old white woman was referred to ULSD for evaluation of recurrent painful buccal mucosa of 8 months’ duration. Oral inspection revealed red and white sloughing lesions of the right buccal mucosa and gingiva. The right buccal mucosa appeared erythematous and atrophic. She had a history of previous carcinoma of the cervix with no sequelae after a hysterectomy, sinusitis treated with a Caldwell-Luc operation, previous alcoholism, and osteoarthritis. She was taking an antihypertensive di- uretic and Synthroid. The patient smoked one pack of men- thol-flavored cigarettes per day. The patient admitted to chronic use of cinnamon-flavored chewing gum on the right side of her mouth. A clinical diagnosis of cinnamon mucositis was rendered, and the patient discontinued the use of cinnamon gum. A follow up 3 weeks later revealed the absence of any clinical lesions.

Case B2. A 42-year-old white woman was referred to ULSD for evaluation of peeling of the tongue. The patient complained that her buccal mucosa was irritated and had peeled for 5 months, and she correlated the onset with an- tibiotic therapy. Previous antifungal therapy was not effec- tive. An oral examination revealed multiple raised, non- painful white plaques of the buccal mucosa bilaterally, which somewhat resembled lesions caused by cheek biting (Fig. 5). Her health history was not remarkable. The patient was not aware of cheek chewing and admitted to chronic use of cinnamon-flavored candy and chewing gum. An exfolia- tive cytology study was negative for fungus. The patient was

advised to discontinue the use of cinnamon and the lesions resolved at 3-week fallow up.

Croup C-Patients with clinical mucositis and histopathologic lesions and no history of significant cinnamon use

Case Ci. A 57-year-old healthy white man was referred to an oral surgeon for a biopsy of the buccal mucosa. A chronic lesion of the left buccal mucosa appeared flat and white. The patient denied tobacco or alcohol use but admit- ted to chronic cheek biting. A biopsy revealed lichenoid mucositis with chronic perivascular inflammation. A com- ment suggested cinnamon as a cause of the mucositis. The patient denied the use of any cinnamon- or mint-flavored products or agents. A telephone follow up revealed that the lesion did not recur after an excisional biopsy without any other form of treatment. There was no further recurrence or development of new lesions.

Case CZ. A 59-year-old white man had a biopsy per- formed on a white lesian with red periphery of the left ven- tral tongue. The lesion had been present for 3 years. The patient had stopped smoking 3 years earlier. The biopsy re- vealed severe chronic mucositis and vasculitis with focal se- vere monilial colonizations. A biopsy comment speculated on evaluation of cinnamon and lupus erythematosus as causes. The patient denied use of cinnamon products. Eigh- teen months later, during a telephone follow up, he reported the disappearance of the lesion after use of an antifungal mouthrinse. No lesions had recurred in the 17-month interim.

Cases C3 to C6. Four patients visited their dentists with white, red and white, and lichenoid lesions. A biopsy of each lesion was interpreted as consistent with stomatitis venenata versus lupus erythematosus on the basis of the histopatho- logic features described in this article (Table I). No cinna-

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Cinnamon stomatitis 713

Fig. 4. Case 1~2. Photomicrograph showing hyperparakeratosis, subepithelial, and prominent perivascular chronic inflammatory infiltrates. (Hematoxylin-eosin stain; original magnification x40.)

Fig. 5. Case B2. White, macerated, linear lesion of buccal mucosa at occlusal plane and white lesion in cor- responding area of lateral tongue.

mon-product usage was identifiable in any of these patients. The patient in Case C4 reported subsequent lesion resolu- tion after replacement of broken adjacent amalgam resto- rations, and the patient in Case C5 reported lesion resolu- tion after commencement of multivitamin prophylaxis. ‘In Cases C3 and C6 lesions remained after incisional biopsy.

Results

Analysis of the 12 g:roup A patients showed that the fol- lowing criteria were most apparent in the majority of cases. All cases showed a degree of mucosal hyperparakeratosis, hyperorthokeratosis, and/or acanthosis. Basal layer lique- faction and basement membrane dissolution were often noted (Fig. 6). Superficial ulcerations of the mucosa with

fibrinous exudates were not uncommon. A predominance in lymphocytes with plasma cells were usually mixed and fre- quently arranged in a lichenoid bandlike infiltration of the lamina propria and superficial submucosa. In most cases plasma cell infiltrates exceeded those usually expected in li- chen planus, and in some cases plasmacytic infiltrates pre- dominated. Edema and granulocyte infiltrates, histiocytic infiltrates, and granulation tissue formation were apparent to some degree in the submucosa of most cases. In several cases, lichenoid changes such as Civatte bodies, predomi- nant lymphocytic infiltrates, sawtooth rete ridges, and leu- kocytic exocytosis were noted. Fibrin deposits or fibrinoid change was noted in the submucosa of two cases. A char- acteristic feature noted in all group A patients was the

714 AfilLer, Gould, and Bernstein ORAL SUKG ORAL.MEDQRAL PATHOL June 1992

Case A7. Histologic appearance of buccal mucosal Iesion with mild hyperparakeratosis, lichenoid infiltrate (with sawtoothing of rete ridges and obscuring of basal layer), and perivascular cuffing. (Hemotox- ylin-eosin stain; original magnification X40.)

Fig. 7. Case A8. Photomicrograph shows striking perivascular infiltrate deep within submucosa and isoiated from other inflammatory foci. (Hemotoxylin-eosin stain; original magnification X 100.)

presence of a perivascular chronic inflammatory infiltrate that involved discrete dense infiltrates of lymphocytes, oc- casional plasma cells, and rare eosinophils that extended deep into the submucosa well below the base of the lichenoid infiltrate (Figs. 6 and 7). This cuffing was often striking and was apparent when the slide was viewed with the unaided eye. A somewhat reduced infiltrate was noted in two cate- gory A patients whose lesions were submitted to biopsy 3 weeks after discontinuance of cinnamon when compared to the results of those whose biopsies corresponded to active cinnamon use. No attempt was made to correlate the

amount of cinnamon use or the type of agent with degree of histopathologic change.

DISCUSSION

Chronic allergic contact dermatitis and primary irritant dermatitis and mucositis have been found to be secondary to use of cinnamon, cinnamon com- pounds, and cinnamic aldehyde in numerous re- ports.‘-16 These reactions to cinnamon agents in salves, ointments, deodorants, and fragrances are not

Volume 73 Number 6

Cinnamon stomatitis 715

uncommon”~ l5 and tare frequently overlooked as causative agents by health care diagnosticians.16 The flavor and odor of cinnamon are considered pleasing; therefore the use of these compounds is ubiquitous. Common oral preparations such as foods (pies, rolls, candies), mouthwash, toothpaste, chewing gum, and mouth fresheners often include cinnamon for flavor or fragrance. Some persons have a special preference for this flavor and therefore frequently use such prepara- tions excessively. Smoking cessation frequently in- cludes substitutian of candies, fresheners, or chewing gum for tobacco. Cinnamon-flavored substitutes are often chosen.

Previous authors have reported clinical mucositis caused by cinnamon contact as either acute or chronic. Acute mucositis tends to be swollen, vesicu- lobullous, ulcerative, red, and painful.7x *, 12. Chronic mucositis tends to be keratotic, desquamative, li- chenoid, or erytbematous. lo Our cases confirm these findings. The clinical differential diagnoses often in- cluded lichen planus, lupus erythematosus, cheek bit- ing, hyperkeratosis, snuff-dipper lesion, candidiasis, premalignancy, carcinoma, and lichenoid rnucositis. The location of lesions tended to be focal. Lesions commonly were situated on the buccal mucosa, the vestibule, and the lateral part of the tongue. Such cases were frequently associated with the use of solid cinnamon agents with the lesion location correspond- ing to areas of contact. Patients who used prepara- tions such as toothpaste or mouthwash tended to have more diffuse lesions. Since lesion distribution and ap- pearance are variable, the clinical diagnosis can best be made after (careful questioning of the patient, withdrawal of the suspected compound with disap- pearance of lesions, and reappearance of lesions by reintroduction of cinnamon compounds. A biopsy is frequently indicated since such conditions as lupus erythematosus, lichen planus, dysplasia, and carci- noma may appear in the clinical differential diagno- sis.

The histopathologic characteristics of oral cinna- mon-induced mucositis’O and dermatitis have been reported in only a -few cases. Allen and Blozis” described histopathologic changes in two of their cases as psoriasiform mucositis with occasional Mu- nro-type intraepithelial microabscesses. They further noted a lymphocytic predominant infiltrate of the submucosa that involved the lamina propria and basal layer in a lichenoid pattern. Submucosal perivascular infiltrates were reported. Our results share some fea- tures with those reported. Most of our proven cases featured hyperorthokeratosis or hyperparakeratosis. Psoriasiform changeis were not apparent. The con- nective tissue infiltrates were lichenoid in distribution;

however, the frequent presence of plasma cells often militated against a diagnosis of lichen planus. All of our group A cases showed prominent to striking perivascular chronic inflammatory (lymphocytes and plasma cells) infiltration. These changes seem analo- gous to those reported by Lever17 for contact derma- titis (allergic and nonallergic) and quite similar to those of discoid lupus erythematosus.‘8, l9 Tests for lupus erythematosus were frequently suggested in notes after microscopic evaluation. The histopatho- logic findings in all 12 group A patients were consid- ered suggestive of contact stomatitis. Ten of these clinical cases elicited no suspicion of cinnamon-com- pound usage before the biopsy; however, when inves- tigated on the basis of notes that accompanied the histopathology reports, these cases were proved pos- itive. It is our contention that such histopathologic changes described herein are highly suggestive of cinnamon-induced mucositis. The recognition of this clinical-histopathologic relationship may prevent fur- ther unnecessary tests. In at least one instance (Case A3), attorneys seemed to agree. It is noteworthy that the presence of cinnamon20 products in foodstuffs is sometimes subtle; therefore, patients may unknow- ingly consume significant amounts of cinnamon. For example, locally popular commercial recipes for chili include significant amounts of cinnamon.

The histopathologic changes described herein are not pathognomonic for cinnamon-induced mucositis. Other essential oils, fragrances, topical allergens, and irritants might produce similar changes. Our six group C patients had histopathologic changes sug- gestive of cinnamon reaction, but these patients denied significant use of cinnamon. In one of these false-positive cases, chronic candidiasis was probably the etiologic factor. In a second Group C case, either metal allergy or local irritation played a causative role. Several lesions persisted as lichen planus or as lichenoid mucositis. Some patients showed spontane- ous regression or had no recurrence after biopsies were performed.

Some reactions to cinnamon are allergic, and patch tests might confirm these cases.2o However, dermato- logic skin tests or patch tests may yield misleading or equivocal results. It has been reported that some pa- tients with cinnamon-induced dermatitis test nega- tive. We recommend consultation with an allergist and agent withdrawal with clinical follow-up as a simple, inexpensive, and accurate method of diagno- sis.

We thank Drs. William Massey, Statesboro, Georgia; Edgar DeJean, Salem, Indiana; Dennis Perry, Cincinnati, Ohio; William D. Shaver, Owensboro, Kentucky; David

‘816 Miller, Gould, and Bernstein

Graves, Elizabethtown, Kentucky; Stephen Schuler, Flo- rence, Kentucky; and Ralph Green, F. Richard Schmitt, Ivan Marks, William Epstein, and W. Ron Harris of Lou- isville, Kentucky, for their help in obtaining patient infor- mation and follow-up.

i. Silvers SH. Stomatitis and dermatitis venenata with purpura resulting from oil of cloves and oil of cassia. Dent Items Inter- est 1939;61:649-51.

2. Miller J. Cheilitis from sensitivity to oil of cinnamon present in bubble gum. JAMA 1941;116:131-2.

3. Laubach JL, Malkinson FD, Ringrose EJ. Cheilitis caused by cinnamon (cassia) oil in toothpaste. JAMA 1953;152:404-5.

4. Kirton V, Wilkinson DS. Contact sensitivity to toothpaste. Br Med J 1973;2(5858):115-6.

5. Magnusson B, Wilkinson DS. Contact sensitivity to cinnamon aldehyde in toothpaste. I. clinical aspects and patch tests. Contact Dermatitis 1975;1:70-6.

6. Drake TE, Maibach HI. Allergic contact dermatitis and sto- matitis caused by a cinnamic aldehyde-flavored toothpaste. Arch Dermatol 1976;112:202-3.

7. Mathias CGT, Chappler RR, Maibach HI. Contact urticaria from einnamic aldehyde. Arch Dermatol 1980;116:74-6.

8. Millard L. Acutecontact sensitivity to a new toothpaste. J Dent 1973;1:168-70.

9. Maibach HI. Cheilitis: occult allergy to cinnamic aldehyde. Contact Dermatitis 1986;15:106-7.

10. Allen CM, Blozis GG. Oral mucosal reactions to cinnamon- flavored chewing gum. J Am Dent Assoc 1988;116:664-7.

ORAL Sum ORAL Mm ORAL PATtim June 1992

11. Rademaker M, Forsyth A. Contact dermatitis in children. Contact Dermatitis 1989;20:104-7.

12. Thyne G, Young DW, Ferguson MM. Contact stomatitis caused by toothpaste. N Z Dent J I989;85: 124-6.

13. Kligman AM. The spectrum of contact urticaria. wheals, erythema, and pruritus. Dermatol Clin 1990;8:57-60.

14. Schorr WF. Cinnamic aldehyde allergy. Contact Dermatitis 1975;1:108-11.

15. Dooms-Goosens A, Dubelloy R, Degeerf H. Contact and sys- temic contact-type dermatitis to spices. Dermatol Clin 1990; 8:89-93.

16. Storrs FJ, Rosenthal LE, Adams RM, et al. Prevalence and relevance of allergic reactions in patients patch tested in North America-1984 to 1985. J Am Acad Dermatol 1989;20:1038- 45.

17. Lever WF, Schaumburg-Lever G. Histopathology of the skin. 7th ed. Philadelphia: JB Lippincott, 1990:106-10.

18. Sch$dt M. Oral discoid lupus erythematosus. III. A histo- pathologic study of 66 patients. ORAL SURG ORAL MED ORAL PATHOL 1984;51:281-93.

19. Karjalainen TK, Tomich CE. A histopathologic study of oral mucosal lupus erythematosus. ORAL SURG ORAL MED ORAL PATHOL 1989;67:547-54.

20. Fisher A ed. Contact dermititis. 3rd ed. Philadelphia: Lea & Febiger, 1986:776-g.

Reprint requests. Richard L. Miller, DDS, PhD Department of Surgical and Hospita! Dentistry University of Louisville Louisville, KY 40292

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