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Effect of dental plaque control on gingival lichen planus
oral pathology Editor: Lewis R. Eversole,
DDS, MSD, MA
Scripps Oral Pathology Service P. 0. Box 1965 La Jolla, California 92038
Effect of dental plaque control on gingival lichen planus Palle Holmstrup, DDS, PhD, Dr Odont,“, b*c Annette Westborg Schiqtz, Dent Hy$ and Jytte Westergaard, DDS, PhD,a Copenhagen, Denmark ROYAL
DENTAL
COLLEGE
AND UNIVERSITY
HOSPITAL
Eleven patients, all women, aged 43 to 76 years, with atrophic or ulcerative lichen planus lesions of gingiva were included in this preliminary study. After initial examination, the patients received an intensive individual hygiene treatment. The patients continued using the most appropriate, atraumatic method resulting in the best possible oral hygiene over a 1 year period during which they were seen for follow-up examinations at 3-month intervals. The mean plaque scores decreased after the initial treatment followed by an increase. The mean scores for severity of subjective symptoms and for type and extension of lesions initially decreased with the plaque scores and remained lower throughout the study. It is concluded that in some cases both subjective and objective improvement of atrophic and ulcerative gingival lichen planus may be obtained by means of intensive oral hygiene procedures although such procedures do not remove the basic cause of lichen planus. However, further studies are needed to examine the role of dental plaque control in patients with oral lichen planus.
(ORALSURGORALMEDORAL PATHOL1990;69:585-90)
L
ichen Planus is a chronic mucocutaneous disorder of unknown cause (for review, see reference 1). Recently, on the basisof a prospective follow-up study of 611 patients, we have reported on the course of the various clinical forms2 and the malignant development of intraoral lesions.3 The intraoral lesions can affect all locations of the mucosal lining, including the gingiva. 4,5When gingival lichen planus affections are atrophic or ulcerative they possessparticular therapeutic problems because toothbrushing is complicated by pain and bleeding. The resulting condition frequently comprises major accumulations of dental
Department of Periodontologya and Department of Oral Pathology and Medicine,b Royal Dental College; Department of Oral Medicine and Oral Surgery,c University Hospital, Copenhagen, Denmark. 7/14/15045
plaque, which again may influence the course of lichen planus. The therapeutic possibilities of oral lichen planus so far described have focused on topical administration of steroids in various form&*’ and vitamin A Since these drugs have side effects and analogues.12-20 recurrence is common after cessation of therapy, the need for therapeutic alternatives is obvious. The effect of dental plaque control in patients with atrophic or ulcerative lichen planus has not received much attention in the literature. The purpose of the present preliminary study was, therefore, to evaluate the effect of dental plaque control on lesions and subjective symptoms in patients with atrophic or ulcerative lichen planus lesions of gingiva. MATERIAL
AND METHODS
Eleven patients with oral lichen planus, all women, aged 43 to 76 years, mean 59.8 years, (Table I) seen
Holmstrup,
506
Table
Schi$tz, and Westergaard
I. Clinical data of patients* with gingival lichen planus
Tobacco smoking
Patient no. 1 2 3 4 5 6 7 8 9 10 11 *All Type A: B: C: D:
ORAL SURG ORAL
48
-
16
-
64 61 56
15 52 63 43
patients were women. TEvaluated of gingival lichen planus: reticular atrophic ulcerative plaque
Type of gingival lichen planus
27 23 21 21 22 22 14 23 26 21 21
APB
+ + + on intraoral
-
Total no. of teeth
53 61
MED ORAL PATHOL May 1990
Depth <5 <6 <5 <5 <5 <5
B B
A,B &W B,D A,B A&C &B AB AB
Range of
Periodontal pockets (mm)
<4 <6 <4 <6 <3
lossof x
approximal attachment? (mm)
2.8 2.6 2.2 2.4 2.2 2.2 2.2 2.4 2.4 2.2 2.1
2-3 3-4 2-3 l-2 3-4 2-5 2-3 3-5 l-2 l-3 o-1
radiographs.
for follow-up examination as part of a prospective study293 were included in the present investigation. The diagnosis of oral lichen planus was confirmed 3 to 14 years previously on the basis of both clinical and histologic features. 2 The clinical features were reticular and/or papular affections in any location of the oral mucosa. The histologic features were hyperkeratosis, degenerative changes of basal cells, and a bandlike, subepithelial inflammatory infiltrate composed of lymphocytes and histiocytes (Figs. 1 and 2 and Table I). All 11 patients had lichen planus affections of the vestibular gingiva and a few also had affections of the lingual gingiva. In all patients, atrophic or ulcerative lichen planus lesions of gingiva were related to at least 10 teeth and the lesions were associated with subjective symptoms. Gingiva affected by atrophic lichen planus commonly showed areas of a normal margin without erythema (Figs. 1 and 2). All patients except one had dental crowns, the number ranging from 1 to 16. Furthermore, three patients had two bridges each and one had two partial dentures. The periodontal pocket depths (Table I) varied from 2 to 5 mm, the individual means in all casesbeing between 2 and 3 mm and the ranges of loss of periodontal attachment (Table I) as evaluated on intraoral radiographs varied from 0 to 5 mm. None of the patients had received treatment with steroids or antibiotics within 3 months before the study. Three patients were daily tobacco smokers (Table I). The initial examination of the patients included registration of subjective symptoms and oral hygiene procedures. The type and extension of oral lichen
planus lesions were recorded on a diagram and photographed. The severity of subjective symptoms and of type and extension of lesions was registered on a point scale at which the condition at time of admission was rated 3 points. In case of changes, the following scale was used: improvement was rated -% point; marked improvement - 1 point; aggravation +% point; marked aggravation +l point. Improvement of lesions was recorded in casesof healed ulcers, decreasederythema, and decreasedsize of lesions.To ensure the most objective registrations, scoring of symptoms and lesions and scoring of dental plaque were never performed by the same examiner. The lesions were examined for secondary candidal infection, which was diagnosed on the basis of hyphae or pseudohyphae in smears stained with periodic acidschiff from the lesions. After staining with erythrosine, the coronal extension of the dental plaque was recorded at six sites around each tooth according to the method of Quigley and Hein21 Intraoral radiographs of all teeth present were examined for loss of proximal bone attachment by measuring the distance from the cementum-enamel junction to the marginal alveolar bone. initial
treatment
The initial treatment comprised an intensive individual hygiene program with the possibility of frequent professional assistancein establishing the most appropriate atraumatic procedures for obtaining the best possible oral hygiene by the use of toothbrushes
Dental plaque and gingival
Volume 69 Number 5
lichen planus
587
Fig. 1. Ginglval lichen planus with atrophic lesions demonstrating areas of unaffected margin (arrows), patient 4.
Fig. 2. Gingival lichen planus with atrophic lesions in upper incisor region, patient 3.
and toothsticks, floss, and chlorhexidine for mouthrinsing (0.2% solution) or for toothbrushing (Hibitane toothpaste) as needed. In the initial treatment period, the oral hygiene procedures were changed in all patients. The changes included number and method of toothbrushings, additional use of interdental brushes, toothsticks, and dental floss. In five patients this was further supplemented by mouthrinsing or toothbrushing with chlorhexidine; one patient used an electric toothbrush. The program included scaling, treatment of caries, and renewing of insufficient fillings. The initial treatment was terminated when the method resulting in the best oral hygiene had been identified. Thereafter, the patients continued using this method over the entire l-year period of the study. Follow-up recording
and treatment
At completion of the initial treatment and 3, 6, 9, and 12 months thereafter, the following recordings were performed: subjective symptoms, type and extension of lichen planus affections, plaque index,
probing pocket depths (only at 3-month follow-up), and the presence of secondary candidal infection. Scoring of symptoms and lesions as well as plaque scoring was performed blindly by two different examiners. After registration, the patients received a professional oral hygiene treatment and reinstruction was performed at the follow-up examinations if needed. One of the eleven patients left the study after the 3-month follow-up examination. Four patients who had not previously used chlorhexidine for toothbrushing did so for 3 months after the 12-month follow-up registration to examine a possible additional effect. The mean plaque scores for all surfaces and separately for vestibular surfaces were calculated for each follow-up examination and transferred to a diagram with the mean scores for symptoms and type and extension of lesions. RESULTS
In Fig. 3, the mean dental plaque scoresfor all surfaces and for vestibular surfaces alone are shown in
58% Holmstrup, Schi#tz, and Westergaard
L *
, 0
ORAL SURG ORAL MED ORAL PATHOL May 1990
I 5
I 6
I e
1 11
I * 16 aolmm
Fig. 3. Mean scores for dental plaque, subjective symptoms, and type and extension of oral lichen planus lesions. The 15-month data only involve four patients.
Table
II. Type of subjective symptoms initially (I) and at the final examination (F) Smarting pain or tenderness Spontaneous
Patient No. 1 2* 3 4 5 6 1 8 9 10 11
I
When eating
F
I
-
+ + + + +
+ -
When toothbrushing I
-
+ -
F
Bleeding
-
-
+ + -
+ -
-
+ +
+ +
+ + + + + + + + + +
When toothbrushing
F
I
F
-
+ + + +
+ +
+ + + + + +
-
-
*Patient left the study after 3 months.
relation to the mean scores for subjective symptoms and for type and extension of gingival lesions. As can be seen, the vestibular plaque scores were lower than the scores for all surfaces. Both scores decreased after the initial treatment followed by an increase. The mean scores for severity of subjective symptoms and the scoresfor type and extension of lesions initially decreased with the plaque scores and remained lower throughout the study (Fig. 3). The mean plaque score for all surfaces after 12 months was 2.2, for vestibular surfaces 1.9. The corresponding score for subjective symptoms was 2.4, for type
and extension of lesions 2.5. At the individual level, a prominent feature in several caseswas aggravation of lichen planus affections in relation to dental crowns. In the vast majority of patients, both the plaque scoresand the scores for severity of subjective symptoms and for severity of type and extension of lesions had decreased at termination of the study as compared with the initial examination. At the initial recording, the patients reported on various symptomsas shown in Table II. Most of these were associatedwith eating and toothbrushing, and in six patients they were reported to be severe.At the end of the study, an
Volume 69 Number 5
improvement of the symptoms was obtained in 9 of the 11 patients, and 4 patients had no symptoms. No patients had increased symptoms (Table II). Hyphae or pseudohyphae were observed in smears from lesions of five patients at the initial examination but in only one patient after the initial treatment. There was no relationship between presence of yeast organisms in smears from the lesions and their severity. DISCUSSION
The present preliminary results indicate that it may be possible by means of controlled oral hygiene procedures to obtain improvements in symptoms and lesions associated with gingival lichen planus. This finding is in accordance with a previously reported improvement in a patient with lichen planus treated with optimum plaque control and periodontal therapy.** The mechanism by which factors in dental plaque may influence the course of gingival lichen planus affections is unknown. However, experimental external damage to clinically normal skin in patients with lichen planus has resulted in lichen planus-like features,23and we have seen reversible aggravation with atrophic gingival lichen planus lesions arising after electric toothbrushing in areas affected by reticular lichen planus (data not shown). Others have reported on a case of oral lichen planus evoked by periodontal surgery.24The latter authors have proposed an explanation of their observation by a possible secretion of interleukin I from epithelium stimulated by factors such as endotoxin, silica particle, ultraviolet radiation, and mechanical trauma. Interleukin I is involved in lymphocyte and macrophage activation and the authors further speculate on a genetic factor predisposing to the development of lichen planus. Thus somedata support that the diseaseprocessin lichen planus can be influenced by external factors. Similar mechanisms may be responsible for dental plaque-induced aggravation of already established gingival lesions. The plaque reduction obtained among the present patients was not very prominent. This could be due to symptoms associated with the lichen planus lesions. These lesions were almost exclusively located at the facial aspect and if symptoms from the lesions compromised toothbrushing, plaque scores of vestibular surfaces should be expected to be higher than the overall scores. However, in general, the vestibular scoreswere lowest and, therefore, do not support such a hypothesis for the present patients. The large number of dental restorations in these patients may also explain the minor reduction in plaque score.
Dental plaque and gingival
lichen planus
589
A characteristic feature of oral lichen planus is fluctuations in type and extension of the affections.2 Such fluctuations might call for future controlled studies to elucidate the significance of a possible treatment. The scoring system used for severity of symptoms and for type and extension of lesions is a coarse semiquantitative system which, obviously, was not intended to pick up minor differences. It is, however, noteworthy that with this system the mean scoresfor symptoms and lesions after 12 months were reduced according to a registration of improvement. The corresponding recordings for the four patients with supplementary use of chlorhexidine were reduced according to a marked improvement. It should be noted that dental plaque control did not remove the basic cause of oral lichen planus, which persisted in all the treated patients. However, in some casesit may be possible to obtain an improvement of subjective symptoms and objective changes in gingival lichen planus affections by means of intensive oral hygiene procedures. Future additional, controlled studies are needed to further examine the role of dental plaque control in patients with oral lichen planus. REFERENCES 1. Scully C, El-Kom M. Lichen planus: review and update on pathogenesis. J Oral Path01 1976;14:43 1-58. 2. Thorn JJ, Holmstrup P, Rindum J, Pindborg JJ. The course of various clinical forms of oral lichen planus. A prospective follow-up study of 61 1 patients. J Oral Path01 1988;17:213-8. 3. Holmstrup P, Thorn JJ, Rindum J, Pindborg JJ. Malignant development of lichen planus affected oral mucosa. J Oral Pathoi 1988;17:219-25. 4. Andreasen JO. Oral lichen planus. I. A clinical evaluation of I 15 cases. ORAL SURG ORAL MED ORAL PATHOL 1963;25:3 I42. 5. Jandinski JJ, Skhlar G. Lichen planus of the gingiva. J Periodontol 1976;47:724-33. 6. Mumford PB, Morgan JK. The use of cortisone in lichen planus. Br J Dermatol 1956;68:258-60. 7. Kovesi G, Banoczy J. Follow-up studies in oral lichen planus. Int J Oral Surg 1973;2:13-9. ii. Randell S, Cohen L. Erosive lichen planus. Management of oral lesions with intralesional corticosteroid injections, J Oral Med 1974;29:88-9 1. I. i‘yidesiey WR, Harding SM. Betamethaaone vaierate aerosoi tn the treatment of oral lichen planus. Br J Dermatol 1977: 96165962. IO. Greenspan JS, Yeoman CM, Harding SM. Oral lichen planus. A double-blind comparison of treatment with betamethasone valerate aerosol and- pellets. Br Dent J 1978;144:83-4. il. Silverman S. Lozada-Nur F. Maaliorati C. Clinical efficacv of prednisone in the treatment of patients with oral inflamma;ory ulcerative diseases. A study of 55 patients. ORAL SURG ORAL MED ORAL
PATHOL
1985;59:360-3.
12. Gunther SH. Vitamin A acid in the treatment of oral lichen planus. Arch Dermatol 1973;107:277. I?. Hersle K. Mobacken H. Sloberg K. Theilander E. Severe oral lichen planus: treatment with an-aromatic retinoid (etretinate). Br J Dermatol 1979;106:77-80.
590
Holmstrup,
14. Sloberg K, Hersle
15.
16.
17. 18. 19. 20. 21.
Schi$tz, and Westergaard
K, Mobacken H, Theilander H. Topical tretinoin therapy and oral lichen planus. Arch Dermatol 1979;115:716-8. Sloberg K, Hersle K, Mobacken H, Theilander H. Severe oral lichen planus. Remission and maintenanace with vitamin A analoaues. J Oral Pathol 1983:12:473-7. Ferguion MM, Simpson NB, Hammcrsly N. The treatment of erosive lichen planis with a retinoid-etietinate. ORAL SURG ORAL MED ORAL PATHOL 1984:58:283-7. Handler AL. Isotretinoin for oral lichen planus. J Am Acad Dermatol 1984;10:674. Stans ME, Bergfeld WF. Treatment of oral lichen planus with low-dose isotretinoin. J Am Acad Dermatol 1984;11:527-8. Zegarelli D. Treatment of oral lichen planus with topical vitamin A acid. J Oral Med 1984;39:186-90. Woo TY. Systemic isotretinoin treatment of oral and cutaneous lichen planus. Cutis 1985;35:385-93. Quigley GA, Hein JW. Comparative cleansing efficiency of manual and power brushing. J Am Dent Assoc 1962;65:26-9.
ORAL SURC; ORAL MED ORAL PATHOL May 1990 22. Erpenstein H. Periodontal and prosthetic treatment in patients with oral lichen planus. J Clin Periodontol 1985;12:104-12. 23. Stankler L, Ewen SWB. The effects of experimental skin damage in patients with lichen planus. Br J Dermatol 1974: 90:25-8. 24. Katz J, Goultschin
J, Benoliel I, Pisanty S. Lichen planus evoked by periodontal surgery. J Clin Periodontol l988;15: 263-5.
Reprint requests to. Palle Holmstrup Department of Periodontology Royal Dental College 20 Nprre Alle DK-2200 Copenhagen N Denmark
DDS, MSD, MA
Scripps Oral Pathology Service P. 0. Box 1965 La Jolla, California 92038
Effect of dental plaque control on gingival lichen planus Palle Holmstrup, DDS, PhD, Dr Odont,“, b*c Annette Westborg Schiqtz, Dent Hy$ and Jytte Westergaard, DDS, PhD,a Copenhagen, Denmark ROYAL
DENTAL
COLLEGE
AND UNIVERSITY
HOSPITAL
Eleven patients, all women, aged 43 to 76 years, with atrophic or ulcerative lichen planus lesions of gingiva were included in this preliminary study. After initial examination, the patients received an intensive individual hygiene treatment. The patients continued using the most appropriate, atraumatic method resulting in the best possible oral hygiene over a 1 year period during which they were seen for follow-up examinations at 3-month intervals. The mean plaque scores decreased after the initial treatment followed by an increase. The mean scores for severity of subjective symptoms and for type and extension of lesions initially decreased with the plaque scores and remained lower throughout the study. It is concluded that in some cases both subjective and objective improvement of atrophic and ulcerative gingival lichen planus may be obtained by means of intensive oral hygiene procedures although such procedures do not remove the basic cause of lichen planus. However, further studies are needed to examine the role of dental plaque control in patients with oral lichen planus.
(ORALSURGORALMEDORAL PATHOL1990;69:585-90)
L
ichen Planus is a chronic mucocutaneous disorder of unknown cause (for review, see reference 1). Recently, on the basisof a prospective follow-up study of 611 patients, we have reported on the course of the various clinical forms2 and the malignant development of intraoral lesions.3 The intraoral lesions can affect all locations of the mucosal lining, including the gingiva. 4,5When gingival lichen planus affections are atrophic or ulcerative they possessparticular therapeutic problems because toothbrushing is complicated by pain and bleeding. The resulting condition frequently comprises major accumulations of dental
Department of Periodontologya and Department of Oral Pathology and Medicine,b Royal Dental College; Department of Oral Medicine and Oral Surgery,c University Hospital, Copenhagen, Denmark. 7/14/15045
plaque, which again may influence the course of lichen planus. The therapeutic possibilities of oral lichen planus so far described have focused on topical administration of steroids in various form&*’ and vitamin A Since these drugs have side effects and analogues.12-20 recurrence is common after cessation of therapy, the need for therapeutic alternatives is obvious. The effect of dental plaque control in patients with atrophic or ulcerative lichen planus has not received much attention in the literature. The purpose of the present preliminary study was, therefore, to evaluate the effect of dental plaque control on lesions and subjective symptoms in patients with atrophic or ulcerative lichen planus lesions of gingiva. MATERIAL
AND METHODS
Eleven patients with oral lichen planus, all women, aged 43 to 76 years, mean 59.8 years, (Table I) seen
Holmstrup,
506
Table
Schi$tz, and Westergaard
I. Clinical data of patients* with gingival lichen planus
Tobacco smoking
Patient no. 1 2 3 4 5 6 7 8 9 10 11 *All Type A: B: C: D:
ORAL SURG ORAL
48
-
16
-
64 61 56
15 52 63 43
patients were women. TEvaluated of gingival lichen planus: reticular atrophic ulcerative plaque
Type of gingival lichen planus
27 23 21 21 22 22 14 23 26 21 21
APB
+ + + on intraoral
-
Total no. of teeth
53 61
MED ORAL PATHOL May 1990
Depth <5 <6 <5 <5 <5 <5
B B
A,B &W B,D A,B A&C &B AB AB
Range of
Periodontal pockets (mm)
<4 <6 <4 <6 <3
lossof x
approximal attachment? (mm)
2.8 2.6 2.2 2.4 2.2 2.2 2.2 2.4 2.4 2.2 2.1
2-3 3-4 2-3 l-2 3-4 2-5 2-3 3-5 l-2 l-3 o-1
radiographs.
for follow-up examination as part of a prospective study293 were included in the present investigation. The diagnosis of oral lichen planus was confirmed 3 to 14 years previously on the basis of both clinical and histologic features. 2 The clinical features were reticular and/or papular affections in any location of the oral mucosa. The histologic features were hyperkeratosis, degenerative changes of basal cells, and a bandlike, subepithelial inflammatory infiltrate composed of lymphocytes and histiocytes (Figs. 1 and 2 and Table I). All 11 patients had lichen planus affections of the vestibular gingiva and a few also had affections of the lingual gingiva. In all patients, atrophic or ulcerative lichen planus lesions of gingiva were related to at least 10 teeth and the lesions were associated with subjective symptoms. Gingiva affected by atrophic lichen planus commonly showed areas of a normal margin without erythema (Figs. 1 and 2). All patients except one had dental crowns, the number ranging from 1 to 16. Furthermore, three patients had two bridges each and one had two partial dentures. The periodontal pocket depths (Table I) varied from 2 to 5 mm, the individual means in all casesbeing between 2 and 3 mm and the ranges of loss of periodontal attachment (Table I) as evaluated on intraoral radiographs varied from 0 to 5 mm. None of the patients had received treatment with steroids or antibiotics within 3 months before the study. Three patients were daily tobacco smokers (Table I). The initial examination of the patients included registration of subjective symptoms and oral hygiene procedures. The type and extension of oral lichen
planus lesions were recorded on a diagram and photographed. The severity of subjective symptoms and of type and extension of lesions was registered on a point scale at which the condition at time of admission was rated 3 points. In case of changes, the following scale was used: improvement was rated -% point; marked improvement - 1 point; aggravation +% point; marked aggravation +l point. Improvement of lesions was recorded in casesof healed ulcers, decreasederythema, and decreasedsize of lesions.To ensure the most objective registrations, scoring of symptoms and lesions and scoring of dental plaque were never performed by the same examiner. The lesions were examined for secondary candidal infection, which was diagnosed on the basis of hyphae or pseudohyphae in smears stained with periodic acidschiff from the lesions. After staining with erythrosine, the coronal extension of the dental plaque was recorded at six sites around each tooth according to the method of Quigley and Hein21 Intraoral radiographs of all teeth present were examined for loss of proximal bone attachment by measuring the distance from the cementum-enamel junction to the marginal alveolar bone. initial
treatment
The initial treatment comprised an intensive individual hygiene program with the possibility of frequent professional assistancein establishing the most appropriate atraumatic procedures for obtaining the best possible oral hygiene by the use of toothbrushes
Dental plaque and gingival
Volume 69 Number 5
lichen planus
587
Fig. 1. Ginglval lichen planus with atrophic lesions demonstrating areas of unaffected margin (arrows), patient 4.
Fig. 2. Gingival lichen planus with atrophic lesions in upper incisor region, patient 3.
and toothsticks, floss, and chlorhexidine for mouthrinsing (0.2% solution) or for toothbrushing (Hibitane toothpaste) as needed. In the initial treatment period, the oral hygiene procedures were changed in all patients. The changes included number and method of toothbrushings, additional use of interdental brushes, toothsticks, and dental floss. In five patients this was further supplemented by mouthrinsing or toothbrushing with chlorhexidine; one patient used an electric toothbrush. The program included scaling, treatment of caries, and renewing of insufficient fillings. The initial treatment was terminated when the method resulting in the best oral hygiene had been identified. Thereafter, the patients continued using this method over the entire l-year period of the study. Follow-up recording
and treatment
At completion of the initial treatment and 3, 6, 9, and 12 months thereafter, the following recordings were performed: subjective symptoms, type and extension of lichen planus affections, plaque index,
probing pocket depths (only at 3-month follow-up), and the presence of secondary candidal infection. Scoring of symptoms and lesions as well as plaque scoring was performed blindly by two different examiners. After registration, the patients received a professional oral hygiene treatment and reinstruction was performed at the follow-up examinations if needed. One of the eleven patients left the study after the 3-month follow-up examination. Four patients who had not previously used chlorhexidine for toothbrushing did so for 3 months after the 12-month follow-up registration to examine a possible additional effect. The mean plaque scores for all surfaces and separately for vestibular surfaces were calculated for each follow-up examination and transferred to a diagram with the mean scores for symptoms and type and extension of lesions. RESULTS
In Fig. 3, the mean dental plaque scoresfor all surfaces and for vestibular surfaces alone are shown in
58% Holmstrup, Schi#tz, and Westergaard
L *
, 0
ORAL SURG ORAL MED ORAL PATHOL May 1990
I 5
I 6
I e
1 11
I * 16 aolmm
Fig. 3. Mean scores for dental plaque, subjective symptoms, and type and extension of oral lichen planus lesions. The 15-month data only involve four patients.
Table
II. Type of subjective symptoms initially (I) and at the final examination (F) Smarting pain or tenderness Spontaneous
Patient No. 1 2* 3 4 5 6 1 8 9 10 11
I
When eating
F
I
-
+ + + + +
+ -
When toothbrushing I
-
+ -
F
Bleeding
-
-
+ + -
+ -
-
+ +
+ +
+ + + + + + + + + +
When toothbrushing
F
I
F
-
+ + + +
+ +
+ + + + + +
-
-
*Patient left the study after 3 months.
relation to the mean scores for subjective symptoms and for type and extension of gingival lesions. As can be seen, the vestibular plaque scores were lower than the scores for all surfaces. Both scores decreased after the initial treatment followed by an increase. The mean scores for severity of subjective symptoms and the scoresfor type and extension of lesions initially decreased with the plaque scores and remained lower throughout the study (Fig. 3). The mean plaque score for all surfaces after 12 months was 2.2, for vestibular surfaces 1.9. The corresponding score for subjective symptoms was 2.4, for type
and extension of lesions 2.5. At the individual level, a prominent feature in several caseswas aggravation of lichen planus affections in relation to dental crowns. In the vast majority of patients, both the plaque scoresand the scores for severity of subjective symptoms and for severity of type and extension of lesions had decreased at termination of the study as compared with the initial examination. At the initial recording, the patients reported on various symptomsas shown in Table II. Most of these were associatedwith eating and toothbrushing, and in six patients they were reported to be severe.At the end of the study, an
Volume 69 Number 5
improvement of the symptoms was obtained in 9 of the 11 patients, and 4 patients had no symptoms. No patients had increased symptoms (Table II). Hyphae or pseudohyphae were observed in smears from lesions of five patients at the initial examination but in only one patient after the initial treatment. There was no relationship between presence of yeast organisms in smears from the lesions and their severity. DISCUSSION
The present preliminary results indicate that it may be possible by means of controlled oral hygiene procedures to obtain improvements in symptoms and lesions associated with gingival lichen planus. This finding is in accordance with a previously reported improvement in a patient with lichen planus treated with optimum plaque control and periodontal therapy.** The mechanism by which factors in dental plaque may influence the course of gingival lichen planus affections is unknown. However, experimental external damage to clinically normal skin in patients with lichen planus has resulted in lichen planus-like features,23and we have seen reversible aggravation with atrophic gingival lichen planus lesions arising after electric toothbrushing in areas affected by reticular lichen planus (data not shown). Others have reported on a case of oral lichen planus evoked by periodontal surgery.24The latter authors have proposed an explanation of their observation by a possible secretion of interleukin I from epithelium stimulated by factors such as endotoxin, silica particle, ultraviolet radiation, and mechanical trauma. Interleukin I is involved in lymphocyte and macrophage activation and the authors further speculate on a genetic factor predisposing to the development of lichen planus. Thus somedata support that the diseaseprocessin lichen planus can be influenced by external factors. Similar mechanisms may be responsible for dental plaque-induced aggravation of already established gingival lesions. The plaque reduction obtained among the present patients was not very prominent. This could be due to symptoms associated with the lichen planus lesions. These lesions were almost exclusively located at the facial aspect and if symptoms from the lesions compromised toothbrushing, plaque scores of vestibular surfaces should be expected to be higher than the overall scores. However, in general, the vestibular scoreswere lowest and, therefore, do not support such a hypothesis for the present patients. The large number of dental restorations in these patients may also explain the minor reduction in plaque score.
Dental plaque and gingival
lichen planus
589
A characteristic feature of oral lichen planus is fluctuations in type and extension of the affections.2 Such fluctuations might call for future controlled studies to elucidate the significance of a possible treatment. The scoring system used for severity of symptoms and for type and extension of lesions is a coarse semiquantitative system which, obviously, was not intended to pick up minor differences. It is, however, noteworthy that with this system the mean scoresfor symptoms and lesions after 12 months were reduced according to a registration of improvement. The corresponding recordings for the four patients with supplementary use of chlorhexidine were reduced according to a marked improvement. It should be noted that dental plaque control did not remove the basic cause of oral lichen planus, which persisted in all the treated patients. However, in some casesit may be possible to obtain an improvement of subjective symptoms and objective changes in gingival lichen planus affections by means of intensive oral hygiene procedures. Future additional, controlled studies are needed to further examine the role of dental plaque control in patients with oral lichen planus. REFERENCES 1. Scully C, El-Kom M. Lichen planus: review and update on pathogenesis. J Oral Path01 1976;14:43 1-58. 2. Thorn JJ, Holmstrup P, Rindum J, Pindborg JJ. The course of various clinical forms of oral lichen planus. A prospective follow-up study of 61 1 patients. J Oral Path01 1988;17:213-8. 3. Holmstrup P, Thorn JJ, Rindum J, Pindborg JJ. Malignant development of lichen planus affected oral mucosa. J Oral Pathoi 1988;17:219-25. 4. Andreasen JO. Oral lichen planus. I. A clinical evaluation of I 15 cases. ORAL SURG ORAL MED ORAL PATHOL 1963;25:3 I42. 5. Jandinski JJ, Skhlar G. Lichen planus of the gingiva. J Periodontol 1976;47:724-33. 6. Mumford PB, Morgan JK. The use of cortisone in lichen planus. Br J Dermatol 1956;68:258-60. 7. Kovesi G, Banoczy J. Follow-up studies in oral lichen planus. Int J Oral Surg 1973;2:13-9. ii. Randell S, Cohen L. Erosive lichen planus. Management of oral lesions with intralesional corticosteroid injections, J Oral Med 1974;29:88-9 1. I. i‘yidesiey WR, Harding SM. Betamethaaone vaierate aerosoi tn the treatment of oral lichen planus. Br J Dermatol 1977: 96165962. IO. Greenspan JS, Yeoman CM, Harding SM. Oral lichen planus. A double-blind comparison of treatment with betamethasone valerate aerosol and- pellets. Br Dent J 1978;144:83-4. il. Silverman S. Lozada-Nur F. Maaliorati C. Clinical efficacv of prednisone in the treatment of patients with oral inflamma;ory ulcerative diseases. A study of 55 patients. ORAL SURG ORAL MED ORAL
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Reprint requests to. Palle Holmstrup Department of Periodontology Royal Dental College 20 Nprre Alle DK-2200 Copenhagen N Denmark