|
Clinical Evaluation of Iso Saudi Patients with Lichen Planus
Abdullah M. AlDosari, BDS, MSD, PhD, Maysara al Shawaf, BDS, MS,
Nii Otu Nartey, BDS, MSc, MRCD, Asma'a Faden, BDS
King Saud University College of Dentistry, P.O.Box 60169, Riyadh 11545, Saudi Arabia.
One hundred and fifty patients with oral lichen planus (LP) seen over a
period of about 12 years were retrospectively studied and evaluated.
Age, gender, site of lesion, presence of dental restorations and/or
appliances were recorded and analyzed. Findings showed a slight
preponderance of females (53%) to males (47%). The highest prevalence
was found to be between 41-50 years of age. Among the different
ciinical forms of oral LP, the reticular type was the most common (56%)
followed by erosive (26%), plaque (f 1%) atrophic (6%) and bullous
(0.4%) types. The buccal mucosa was the most commonly affected site
(83%) while the least affected was the ventrum of the tongue (5%).
Beside pathogenesis and premaiignant potential of lichen planus, local
and systemic findings are discussed.
Lichen planus (LP) is one of the
important mucocutaneous lesions that
should be of concern to dental clinicians. Its prevalence among the general population was reported to vary between
0.02% and 2%.'"3 A study of 981 patients with oral lesions referred to an oral medicine private practice
clinic showed that 20% of patients had oral LP.4 The
different clinical and histological features
of oral LP had been extensively discussed in several review reports.5"9 The literature
show that only two studies were
reported on oral LP among the Saudi populations with a prevalence of
0.6% and 1.7%, respectively.10"11
The purpose of this study was to present our clinical
experience with 150 Saudi patients who had oral LP and were seen over a period
of about 12 years.
One hundred and fifty patients with oral LP were examined in the Oral
Medicine Clinic at the College of Dentistry, King
Saud University
during the period 1981-1993. Some of these patients were referred by general
practitioners in the city of Riyadh, where the College is considered to be one of
the main referral centers for oral diseases. Other patients were referred from
different parts of the Kingdom
of Saudi Arabia. Another
group of patients was referred from oral diagnosis clinic in the same College
where their lesions were discovered during a routine dental examination.
Age, gender, site of lesion,
presence of dental restorations and/or
appliances were recorded and analyzed. Classification of cases was based on the
scheme of Scully and El-Kom.6 The diagnosis, especially for the
reticular or plaque type of LP, was based on the history and clinical
examination. Cases presenting atrophic, erosive or bullous type were biopsied
whenever the diagnosis was questionable [Figs. 1-2].
Age-range of patients was 16 to
80 years, with the highest prevalence
among the 41-50 years old. There was a slight preponderance of females (53%) in
comparison to the males (47%). Females were
affected almost equally between the ages of 31-40 (16%) and 41-50 (17%) years. Males showed a significantly higher
prevalence at the age of 41-50 years (19%) compared to other age ranges. Distribution of age and gender
is presented in Table 1.
Two-hundred and forty clinical lesions were seen in 150
patients (Table 2). In both males and
females, the reticular form predominated
followed by the erosives, the plaque and the atrophic forms, respectively. Bullous type was rare and
seen in only one female patient.
The distribution of lesions in the oral cavity is
shown in Table 3. The right and left buccal mucosa were affected almost equally
with 123 and 124 lesions, respectively.
Similarly, the upper and lower
gingiva were almost equal with 31 and 29 patients affected, respectively. The
least commonly affected site was the
dorsum of the tongue (5%).
The presence of dental restorations and/or appliances
is summarized in Table
4. One hundred and two patients (68%) had amalgam restorations, 21(14%) had fixed metal
prostheses, while those wearing partial or complete dentures were
27(18%) and 19 (13%),
respectively.
Table 5 presents the relationship
of local factors to the site of lesions. Amalgam restorations were found to be associated with a significantly high percentage of
oral LP lesions on the right buccal mucosa
(55%), left buccal mucosa (56%), lateral border and dorsum of tongue (63%), ventrum of tongue (41%) and
palate (65%). On the other hand, lesions
of the upper and lower gingivae were
associated with fixed metal prostheses, 78% and 73%, respectively.
Systemic findings showed that
diabetes mellitus was the most common condition among the studied cases (19%) followed by skin lesions
(16%), allergy (13%), hypertension (9%), and history of stress (9%). In fifty one
patients (34%) no medical condition were
detected or reported (Table 6).
The current study of 150 cases of
oral LP is the largest report to date from
a single center in Saudi
Arabia. In 1985, Mani10 reported four cases among 674 dental patients. Salem" reported 72 cases in 1989 among a Saudi population of 4,277
individuals.
Findings of the present
study in regard to age and gender of patients and the site distribution of oral LP lesions are in agreement with previously reported studies from
different parts of the world.12"15
Among the clinical forms of oral LP in this study, the reticular type was the most common, followed
by the erosive, plaque and atrophic
types, respectively. One study, however, reported that the erosive type was the most common.16 This
could be explained by the fact that the erosive type presents with associated
clinical symptoms, thus, patients are more likely to report for treatment. In our institution the initial examination of all patients seeking any type of dental treatment is
usually carried out by a trained oral diagnosis specialist, thus, the reticular
type of oral LP is
recognized and referred to the oral medicine clinic.
Several reports linked LP with
some systemic conditions, like diabetes, hypertension, stress, liver diseases and others.17"20 In this study, the
general percentage of patients with diabetes mellitus (19%) was found to be higher than
the reported incidence of 6.5% and 4.3.% among normal individuals.'1" The association
of LP in this regard
could not be determined due to shortage of information on the prevalence of other systemic
conditions among the general population of
Saudi Arabia.
The pathogenesis of LP is not
fully understood, but recent investigations at both cellular and molecular levels indicate that cell mediated immunity plays a
major role in the histopathological changes
of LP lesions. Jontell and co-workers reported an increase in mast cells in the subepithelial infiltrate similar to that seen in classic reactions of delayed
hypersensitivity. Walsh et al24 noted changes in the number of
Langerhans and mast cells and suggested
that oral LP may be initiated by degranulation of mast cells, which induces
adhesion of molecules on the endothelium and, subsequently, facilitates lymphocytic infiltrate to the involved tissues. Hypersensitivity reactions to dental
materials, such as mercury, ammonium
chloride, and nickel sulfate, were noted in a significant number of
patients with lichenoid oral mucosal lesions.25"29
In this study, the distribution of
local factors in relation to the site of
LP lesions (Table 5) showed that 78% of the gingival lesions were associated with fixed bridges whereas no cases of palatal lesions were seen in patients with
complete dentures. This might give some indication about the importance of
local factors in the development of LP lesions, an observation for
further investigation.
The malignant potential of lichen
planus is still controversial. In an extensive study involving 722 Indian patients, Murti et al30
observed malignant change in only 0.4% after, a follow-up period ranging between three and ten
years. This observation was not significantly different from the estimated number in the general Indian
population. Holmstrup31 and co-workers reported a 50-fold increase
in malignant development in oral lichen planus cases compared to the general Danish
population. Krutchkoff and Eisenberg32 coined the term lichenoid
dysplasia to describe conditions diagnosed clinically as lichen planus but
which, histologically,
showed some features of epithelial dysplasia. The lichenoid dysplasia concept
was supported by Lovas et al who suggested that the apparent malignant transformation of
oral lichen planus
might likely represent erythroplakia or leukoplakia, which were dysplastic ab initio. In
the present study, there was no malignant transformation in oral lichen planus in contrast to the study conducted in Gizan region of
Saudi Arabia by Salem1' who reported such malignant transformation in 4 cases of 72
patients after a
follow-up period of 3.2 years. Moreover, Gizan region is noted for a relatively high prevalence of oral cancer
due to 'Shama' usage. This explains the
significant difference between our observation and those reported by Salem.
-
Pindborg JJ, Mehta FS, Daftary DK, Gupta PC, Bhonsle RB. Prevalence of
oral lichen planus among 7639 Indian villagers in Kerala, South
India. Acta Derm Venereol (Stockh) 1972;52:216-20.
-
T. Rundquist L. Oral lichen planus - a demographic study. Community Dent
Oral Epidemiol 1987;15:52-6.
-
T. A prevalence study of oral mucosal lesions in an
adult Swedish population. Odontol Revy
1976;27:101-03.
-
Bottomley WK, Brown RS,
Lavigne GJ. A retrospective survey of the oral conditions of 981 patients
referred to an oral medicine private practice. J Am Dent Assoc 1990;120:529-33.
-
Bouquot JE, Gorlin RJ. Leukoplakia, lichen planus, and other oral keratoses in 23,616 white Americans over the age
of 35 years. Oral Surg Oral Med Oral Pathol 1986;61:373-81.
-
Scully C, El-Kom M. Lichen planus: Review and update on pathogenesis. J
Oral Pathol 1985;14:431-58.
-
Silverman S Jr. Lichen planus.
CurrOpin Dent 1991;1:769-72.
-
Bricker SL. Oral lichen planus: A review. Semin Dermatol 1994;13:87-90.
-
Jungell P. Oral lichen planus. A review. Int J Oral Maxillofac Surg 1991;20:129TM35.
-
Mani NJ. Preliminary report on prevalence of oral cancer and precancerous
lesions among dental patients in Saudi Arabia. Community Dent Oral
Epidemiol 1985; 13: 247-48.
-
Salem G. Prevalence of oral lichen planus in
Gizan, Saudi Arabia. Community Dent Oral
Epidemiol 1989;17:322-24.
-
Brown RS, Bottomley WK, Puerte E, Lavigne GL. A retrospective evaluation
of 193 patients with oral lichen planus. J Oral Pathol Med 1993;22:69-72..
-
Thorn JJ, Holmstrup P, Rindum J, Pindborg JJ. Course of various clinical forms of oral lichen planus: a
prospective follow-up study of 611 patients. J Oral Pathol
1988;17:213-18.
-
Silverman S Jr, Gorsky M, Lozada-Nur F, Giannotti K. A prospective study of findings and management in
214 patients with oral lichen planus. Oral Surg Oral Med Oral Pathol 1991;72:665-70.
-
Bagan-Sebstian JV, Milian-Masanet MA, Pe_arrocha-Diago M, Jimenez Y. A
clinical study of 205 patients with oral lichen planus. J Oral Maxillofac Surg
1992;50:116-18
-
Tyldesley WR. Oral lichen
planus. Br J Oral Surgy 1974;11:187-89.
-
Bagan JV, Aguirre JM, del Olmo JA, et al. Oral lichen planus and chronic
liver diesease: A clinical and morphometric study of the oral lesions in
relation to transaminase elevation. Oral Surg Oral Med Oral Pathol
1994;78:337-42.
-
Strauss RA, Fattore L, Soltani K. The association of mucocutaneous lichen planus and chronic liver
disease. Oral Surg Oral Med Oral Pathol 1989;68:406-10.
-
Bagan
JV, Donat JS, Pearrocha M, Milian MA, Sanchis JM. Oral lichen planus and
diabetes mellitus. A clinico-pathological study. Bull Group Int Rech Sci
Stomatol Odontol 1993;36:3-6.
-
Albrecht M, Banoczy J, Dinya E et al. Occurrence of oral leukoplakia and
lichen planus in diabetes mellitus. J Oral Pathol Med 1992;21:364-66.
-
Bacchus RA, Bell JL, Madkour M, Kilshaw B. The
prevalence of diabetes mellitus in male
Saudi Arabs. Diabetologia 1982;23:330-32.
-
Fatani
HH, Mira SA, El-Zubier AG. Prevalence of diabetes mellitus in rural Saudi
Arabia. Diabetes Care 1987;10:180-83.
-
Jontell M, Hansson HA, Nygren H. Mast cells in oral lichen planus. J
Oral Pathol 1986;15:273-75.
-
Walsh
LJ, Savage NW, Ishii T, Seymour GJ. Immunopathogenesis of oral lichen planus. J
Oral Pathol Med 1990;19:389-96.
-
Laine J, Kalimo K, Forsell H, Happonen RP. Resolution of oral lichenoid
lesions after replacement of amalgam restorations in patients allergic to
mercury compounds. Br J Dermatol 1992;126:10-5.
-
Skoglund A, Egelrud T. Hypersensitivity reactions to dental materials in
patients with lichenoid oral mucosal lesions and in patients with burning mouth
syndrome. Scand J Dent Res 1991;99:320-28.
-
Jameson MW, Kardus TB, Kirk EE, Ferguson MM. Mucosal reactions to amalgam restorations. J Oral Rehabil
1990;17:293-301.
-
Bolewska
J, Hansen HJ, Holmstrup P, Pindborg JJ, Stangerup M. Oral mucosal lesions related
to silver amalgam restorations. Oral Surg Oral Med Oral Path 1990;70:55-8.
-
Ostman
P, Anneroth G, Skoglund A. Amalgam-associated oral lichenoid reactions.
Clinical and histologic changes after removal of amalgam fillings. Oral Surg
Oral Med Oral Pathol 1996;81:459-65.
-
Murti
PR, Daftary DK, Bhonsle RB, Gupta PC, Mehta FS, Pindborg JJ. Malignant potential of oral lichen planus:
observations in 722 patients from India. J Oral Pathol 1986;15:71-7.
-
Holmstrup P, Thorn JJ, Rindum J, Pindborg JJ. Malignant development of lichen planus affected oral mucosa.
J Oral Pathol 1988;17:219-25.
-
Krutchkoff
DJ, Eisenberg E. Lichenoid dysplasia: a distinct histopathologic entity. Oral
Surg Oral Med Oral Pathol 1985;60:308-15.
-
Lovas
JG, Harsanyi BB, ElGeneidy AK. Oral lichenoid dysplasia: a clinico-pathologic
analysis. Oral Surg Oral Med Oral Pathol 1989;68:57-63

|