Lichen planus / dental crown & bridge courses

LICHEN PLANUS
Seminar on
www.indiandentalacademy.com

Introduction
Epidemiology
Clinical features
Types of cutaneous LP
Classification
Types of intra-oral LP
Scoring system
Causes
Treatment

• First described by Erasmus
Wilson in 1869
• Flat fungal infection,
mucocutaneous disorder
mediated by numerous
complex immunologic events.
• Non-contagious inflammatory
papular dermatitis with
chronic or sub acute course.
• Clinical appearance like
lichens growing on rocks.

 Affects 1%-2% of overall population, Approximately 10% of patients
have a positive family history
 Highest (3.7%) in those people with mixed oral habits and lowest
(0.3%) in non- users of tobacco.
 40% of lesions occur on both oral and cutaneous surface, 35%-
Cutaneous & 25%- OMM
 Oral LP follows chronic course.
 Spontaneous remission of cutaneous LP after 1 yr. – 70% cases.
 Spontaneous remission of OLP is less common - < 5%
 Mean duration of OLP is 5 yrs.

Incidence of lichen planus was highest (8.2 per
1000) among men who smoked as well as chewed
tobacco; among women it was highest (4.5 per
1000) in chewers. The relative risk for oral lichen
planus was highest (13.7) among those who smoked
and chewed tobacco.

Actual overall frequency of malignant transformation is
low, varying between 0.3% and 3%.
The forms that more commonly undergo malignant
transformation are the erosive and atrophic forms.
Women – 70 times higher
Men – 14 times higher

Erosive & atrophic form more prone for malignant
transformation
To monitor progression & transformation –
Toluidine blue – biopsy site selection
Exfoliative cytology & biopsy – diagnosis &
assessment of response to treatment
Regular follow up for 3 yrs. (annual- keratotic LP)
When all evidences suggests changes in the lesion,
follow up period should be shortened & additional
biopsy & careful histologic analysis should be
performed.

 Occurs 30-70 years.of age
 Children and adolescent are rarely affected
 Common in females
 Six P's of lichen planus: pruritic, planar (flat-topped), polyangular,
purple papules plaques
 Involves skin, mucosa, scalp & nails.
 Cutaneous lesion – small, pruritic, white to violaceous flat topped
papules, can increase up to 3cm.
 Often bilateral on flexor surface of extremities, inner surface of
knees, thighs, trunk usually lumbar & sacral areas.www.indiandentalacademy.com

Guttate plaques
Linear lichen planus
Hypertrophic plaques

1. Annular – appears as round or ovoid, white outline
with either pink or reddish pink center.
2. Follicular – centered around hair follicle
3. Actinic - face – hyper pigmented patches with
surrounding zone of hypo pigmentation
4. Lichen planus pigmentosus – deeply pigmented
macules on face & extremities.

Linear LP – may follow marks of injury in spontaneous
long linear arrays
Annular LP – central depressed areas with raised
margins
Guttate LP – large number of drop shaped lesions

Reticular
Papular
Plaque
Atrophic
Ulcerative
bullous
Andreasen
1968

 Axell 1987
White forms:
papular, reticular, plaque
 Red forms:
atrophic, ulcerative, bullous
 Silverman 1985
Reticular ( lacy like keratotic)
Atrophic ( reticular, keratotic
and erythema),
Erosive ( ulcerative, & atrophic)

 Silverman 1991
-Reticular,- Atrophic
(reticular keratosis with an
erythematous mucosa),
-Erosive
( reticular & atrophic with
mucosal ulceration)
 Bagan – Sebastian 1992
Grp 1 exclusively white
reticular lesion
Grp 2 atrophic & or
ulcerative lesions with or
without reticular lesions

 Eisen 2002
Reticular ( white lines, plaque & papules)
Atrophic or erythematous
Erosive ( ulceration & bullae)

 Types of OLP
 Reticular
 Papular
 Plaquelike
 Erosive
 Atrophic
 Bullous
 OLP can persists as long as 25 yrs.

Discovers accidently due to lack of subjective complaints.
There can be decreased taste and increased rigidity of
affected area.
Appears whitish, non-removable, stippled-like fine lines
arranged in net forming or branched patterns, sometimes
surrounded by a discrete erythematous border.
Delicate, white, slightly raised lines are called Wickham's
striae – diagnostic of LP.
Reticular LP

Preferred locations – middle & dorsal third of the cheek –
80%, vestibule of posterior teeth, tongue, gingiva, palate
and lips.
Striae & net forming changes rarely affect gingiva & lips
Ring form structures & foci in disk forms appear in the
area of dorsum of tongue as local variations.
Women predilection, after 30 yrs. of age
Best prognosis, as spontaneous remission occurs in
40% cases.

Recognised by its considerable epithelial thickening
Distinguished by heavy, flat plaques from of reticular LP
Resembles homogenous leukoplakia with striae in border
zone
Locations – buccal mucosa, tongue
Can be derived from irritation of already existing LP
Frequently seen in smokers
Resolves in only 7% of cases

Sometimes referred as acute LP
Multiple, minute, white papules(0.5mm)
Highest chances of remission
Can transform to reticular type
Rarely diagnosed, as lesions are very small and
asymptomatic

Not common as reticular
Symptomatic
Erosions can be small and scattered over large areas
Floor of ulcer – yellow with a layer of fibrin covering base
Edge of ulcer – may have sunken margins due to fibrosis
& an erythematous border.
Periphery shows basic form

Sometimes atrophy & ulcerations are confined to the
gingival mucosa – desquamative gingivitis
Can persists for 15-20 yrs.
If erosive component is severe, epithelial separation may
occur, resulting in rare presentation of bullous lichen
planus
It is demonstrated that there is a high prevalence of HPV in
erosive LP

Erosive form
reticular form

Annular and linear forms:
Annular and linear forms consist of striae that
occur in a circular and linear fashion.
Linear form
Annular form

Results from greater amount of inflammatory exudate in
connective tissue, which leads to a circumscribed lifting of
the epithelial surface with colliquation of the basal cell layer
& consequent blister formation.
Blister can be few mm to several mm
It ruptures easily giving appearance of erosive or fibrin
covered shallow ulcerations.
Commonly seen on buccal mucosa, in the posterio-inferior
areas adjacent to second & third molar

• Lateral margins of tongue
• Rarely seen on gingiva or inner aspect of lips.

Can be seen in combination with erosive LP
May continue for decades
Well limited, slightly depressed smooth areas, bordered by
Wickham's striae
Rarely melanin pigmentation in the center of the lesion
Areas get easily traumatized showing poor healing
Attached gingiva is often involved
Can display patchy distribution over all 4 quadrants
Atrophic LP

•Should be evaluated at regular intervals
•12% spontaneous resolution

 In about 11% of cases, oral lichen planus may be associated with
pigmentation . It may begin either with pigmentation, or the
pigmentation may appear subsequently.
 The appearance of pigmentation in cutaneous lichen planus
indicates the resolution of the condition, no such conclusions can be
made in regard to its oral counter part.
Annular form associated
with pigmentationReticular forms with
pigmentation

Kaliakatsou 2002
0- no lesion
1- white striae only
2- white striae & erosion < 1 cm2
3- white striae & erosion >1 cm2
4- white striae & ulceration < 1 cm2
5- white striae & ulceration > 1 cm2


Unknown
 Importance of psychological factors in OLP – though
patients with OLP had greater psychological alterations like
depression/anxiety, there is no direct cause & effect
relationship with it.
 OLP was found in cases who had amalgam restoration
older than 5 yrs (poorly contoured). After replacement of
amalgam with GIC , resolution of OLP seen in 20% cases.
Cause

Genetic predisposition
Immunologically mediated process that resembles a
hypersensitivity reactions. Characterized by intense t cell
infiltrate(cd4, cd8) localized to epithelium connective tissue
interface.

 First described by Dubeuill in 1906 followed by Shklar 1972.
 Basic features are; liquefactive degeneration of basal epithelial
cells
 Dense, band like inflammatory infiltrate consisting of
lymphocytes
 Saw tooth rete pegs
 Civatte bodies (present in initial stages of disease.)
 Hyperkeratosis

Focal areas of epithelial hyperplasia with surface showing
ortho or parakeratosis.
Spinous cell layer thickened with shortened & pointed
rete pegs. (saw tooth)
Thickened areas clinically seen as wick ham's striae.
Adjacent connective tissue is narrow, with dense
accumulation of T lymphocytes that transgreeses
basement membrane which is observed in basilar and
parabasilar cell layer.
Within epithelium civatte bodies are seen
Occasionally lymphoid follicles will be found deeper in the
connective tissue in long term diseases.

Exhibits an extensively thinned epithelium with areas of
complete loss of rete pegs & dense infiltrate of T
lymphocytes obscuring basement membrane.(narrow
zone in upper layers of connective tissue)
Liquifaction of basement membrane & vacuolization &
destruction of basal cells in most areas
Occasionally subepithelial separation
Often epithelium loss exposing connective tissue
Ulcerated surface which is covered by fibrinous exudate
having neutrophil predominance, sometimes bulges
upward above epithelial surface.

 Resembles histology of striae of reticular LP but without intermittent
atrophic areas of the epithelium
 Generalised hyerortho or hyperparakeratosis combined with
acanthosis.
 Loss of rete pegs or saw tooth pattern.
 Basement membrane is thickened
 Band of T lymphocyte less dense than reticular
( juxtaepithelial inflammatory infiltrate)
 Civatte bodies are seen in lower layers of epithelium or within upper
layers of connective tissue.

Epithelium is thin with flattened lower junction in
which there is similar dense & band like
inflammatory infiltrate is seen.

Keratosis extensive & stratum corneum may show
considerable increase in width
Parakeratosis common than hyperkeratosis
Acanthosis not usually seen
Epithelium shows moderate hyperplasia
Saw tooth rete pegs

Hydropic degenaration of basal cell layer
Leads to collection of oedema at epithlium connective
tissue interface forming bulla.
Bulla contain clear fluid or blood
Broad band of lymphocyte seen.

Degenerative changes in the basal keratinocyte
frequently lead to pigmentation.
The melanin pigment is ingested by macrophages can
result in an area of brownish pigmentation in the mucosa
which persists long after the LP has resolved.

Immunofluorescense technique

The tissue diagnosis of lichen planus is difficult but
aided by immunofluorescense.
All forms of LP will negative for IgG, IgM, IgA A but
positive for fibrinogen.

Grinspan syndrome
Graham little syndrome

Leukoplakia
Cheek bite
Electrogalvanic allergy
Graft versus host disease
 Atrophic candidiasis
Pemphigus
Mucous membrane pemphigoid
Lupus erythematosus
Lichenoid drug reaction.
Secondary syphilis
Erythema multiforme

One can treat this challenging abnormality only
after….;
Proper history Elimination of irritants
Drug /medical history Alcohol, tobacco
Clinical evaluation Fracture tooth
histopathology Ill fitting denture
Liver function test Oral hygiene
Amalgam restoration
Drugs

Local/ systemic therapy -
- topical antifungal/ topical steroid(0.05%, 0.1% &
0.18% 2-4 times /day)
- topical immunosuppressive
* azathioprine (1mg/kg/day 2-3 months)
* cyclosporine(500mg rinse 1-3 times/ day)
(1% paste for local application)
* tacrolimus (0.1% for local application)
- systemic immunosuppressive
* steroids 25mg/3 times day for 4-12 weeks
* combination therapy [steroid + azathioprine(50-
100mg 3 months)]

 Local application of tretinion 0.05% (metabolite of vitamin A)
 Betamethasone dipropionate 0.05% local application
 Hydroxychloroquine – 200-400 mg daily 15 days.
 Betamethasone sodium phosphate 0.5mg/ 10ml water held in mouth
for 3 minutes 4 times daily for 1 month for refractory lichen planus.
 Fluticasone propionate 50 µ g aqueous solution 4 times daily in
areas difficult to apply ointment.

Topical steroids in a conventional cream base do not
adhere to the oral mucosa for a sufficiently long time to
cause therapeutic action. Use of intralesional
corticosteroids, though effective, has the drawback of
pain at injection sites and risk of secondary infection.
Other therapeutic modalities include oral vitamin A,
topical cyclosporine (100 mg/ ml) in the form of an oral
rinse .Orabase(a gel of carboxymethylcellulose, pectin
and gelatin), available commercially, is an ideal vehicle
for topical corticosteroids (triamcinolone acetonide )for
oral mucosa. This was prepared by adding Vi syneral
syrup (30 ml) and Moisol (hydroxypropyl cellulose) eye
drops (10 ml). Triamcinolone acetonide (40 mg/ml) was
added in this base. The preparation adheres to the oral
mucosa for a long time and can be applied twice daily

Although the precancerous nature of oral lichen
planus is still not settled, patients with this
condition must be carefully evaluated and
observed.
The fact that a vast majority of oral lichen planus
patients in India use tobacco, which is a known
etiologic factor for oral cancer, highlights the
need to educate all patients with this condition to
discontinue their tobacco use.

1. Regezi : oral path : clinical pathologic correlation 3 & 4
ed.
2. Cowson Binnie : oral disease; clinical & pathologic
correlation second ed.
3. R. A. Cowson : Cowson’s essential of oral pathology &
oral medicine seventh ed.
4. Neville : oral & maxillofacial pathology second ed.
5. Sonis Fazio : principles & practice of oral medicine
second d.
6. Warren Birnhaum : oral diagnosis ( clinician’s guide)
7. Burket oral medicine diagnosis & treatment: 10 ed.

10 Epstein et al : OLP progress in understanding its malignant
potential & the implications for clinical management;
OOO;2003;96;32-7
11 Molloaglu : oral lichen planus : a review Br. J OMFS 2000;38;370-7
12 Villaroel : OLP ;immunohistology of oral lesions; J OP MED.
2002;31;189-95
13 Buajeeb : efficacy of fluocinolone acetonide in OLP ; OOO2000;
89;42-5.

18. Martin S.- controversies in OLP; OOO
2005,100,40-51
19. Siribang P. – scoring for OLP; OOO 2005,99,696-
703.
20. R Rajendran. Oral lichen planus. Journal of Oral
and Maxillofacial Pathology. 2005 :(9)1; 3-5
21. Vijay Gandhi, RK Pandhi. Tropical triamcinolone
acetonide in an indigenous orabase in oral lichen
planus. Indian j dermatology, venereology and
leprology ; 1996(62 )2 : 128-129

 HK Kar, D Prasad, RK Gautam, RK Jain, PK Sharma.
Comparison of topical tretinoin and betamethasone in
oral lichen planus. . Indian j dermatology, venereology
and leprology. 1996; (62) 5: 304-305
 Juan Seoane; María Amparo Romero; Pablo Varela-
Centelles. Oral lichen planus: a clinical and
morphometric study of oral lesions in relation to clinical
presentation. Brazilian Dental Journal : 2004 (15) 1
 Ibtisam Al-Hashimi. Oral lichen planus and oral
lichenoid lesions: diagnostic and therapeutic
considerations. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod 2007;103(1):S25.e1-S25.e12.

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