oral lichen planus and lichenoid reaction

1. Oral Lichen Planus

2. • Lichen planus (LP) is derived from the Greek Leichen
meaning Tree Moss and the Latin Planus meaning flat
• Lichen’s are primitive plants composed of symbiotic algae
and fungi
• Term suggests flat fungal condition

3. Definition
• Lichen planus (LP) is a common disorder in which auto-
cytotoxic T lymphocytes trigger apoptosis of epithelial cells
leading to chronic inflammation. Oral LP (OLP) can be a
source of severe morbidity and has a small potential to be
malignant.
- Crispian Scully 2007

4. • Common skin disorder which affects 0.5 – 1% of world
population (Prevalance in indian population : 1.5%)
• Mucocutaneous Skin Disease: Can affect Skin and Oral
mucous membrane
• Oral lesions are frequent and many times precede the
appearance of lesions on skin and genital mucous membrane

5. Etiology
• The cause of the disease is unknown.
• Current evidence indicates Immunologically Mediated
mucocutaneous disorder
• Inciting factors that have been noted are Psychosomatic
Factors and Lichenoid Drug Reactions

6. PredisposingFactors
1. GENETIC BACKGROUND
2. AUTO IMMUNITY – ASSOCIATED WITH OTHER
AUTO IMMUNE DISEASE
3. IMMUNODEFICIENCY
4. DRUGS
5. DENTAL MATERIALS
6. STRESS
7. ADVERSE HABITS

7. Pathogenesis of Oral Lichen Planus
• The various mechanisms hypothesized to be involved in the
immunopathogenesis are:
1. ANTIGEN SPECIFIC CELL MEDIATED
MECHANISM
2. NON SPECIFIC MECHANISM
3. AUTOIMMUNE RESPONSE
4. HUMORAL IMMUNITY PATHOGENESIS OF OLP

8. NON SPECIFIC MECHANISM
• Epithelial Basement Membrane Interactions
• Matrix Metalloproteninases Mediated
• Chemokine Mediated
• Mast Cells Mediated

9. Immunologic Mechanisms

10. Expression of an Unknown antigen associated with MHC class-I on
basal keratinocytes only at the lesion site
(Self-peptide , Lichen Planus antigen)
Influx of Antigen specific CD8+ T-cell due to either:
(i) Encountering the keratinocyte antigen by chance on routine
surveillance in the epithelium (“Chance Encounter” hypothesis)
OR
(ii) Attracted to the epithelium by keratinocyte-derived chemokines
(“Directed Migration” hypothesis).

11. Activated CD8+ T-cells (and possibly keratinocytes) release
chemokines that attract additional lymphocytes and other
immune cells into the developing OLP lesion
CD8+ cytotoxic T-cells in OLP secrete TNF-α that triggers
keratinocyte apoptosis via TNF-R1.

12. Keratinocyte antigen expression at the developing lesion site
could be induced by:
– Systemic drugs (lichenoid drug reaction),
– Contact allergens in dental restorative materials or
toothpastes (contact hypersensitivity reaction),
– Mechanical trauma (Koebner phenomenon),
– Bacterial or Viral infection, or
– An Unidentified agent.
Subsequently, intra-epithelial CD8+ cytotoxic T-cells
recognize the lichen planus antigen associated with MHC
class-I on lesional keratinocytes and trigger keratinocyte
apoptosis.

13. LichenoidDrug Reaction
Some of the drugs commonly associated with Lichenoid
reactions are:-
1. Anti – malarials
2. NSAIDs
3. Diuretics
4. Antihypertensives
5. Antibiotics
6. Heavy metals.

14. Alternate Immunologic Mechanism

15. Langerhan’s Cells or basal keratinocytes may present antigen
associated with MHC class-II to CD4+ helper T-cells that are
stimulated to secrete the Th1 cytokines IL-2 and IFN-γ
Activation of CD8+ cytotoxic T-cells
Trigger basal keratinocyte apoptosis
(Local production of IFN- γ maintains keratinocyte MHC class-II
expression, thereby contributing to disease chronicity)

16. Psychosomatic Factor
• Stress, anxiety and emotional changes may trigger Lichen
planus
• Proven fact that patients with erosive and atrophic lesions
exhibits greater anxiety and other psychologic disorders.
• Difficult to determine cause and effect relation between
psychologic disorders and oral Lichen planus.
(Psychologic disorders could be a consequence of oral
Lichen planus and its lesions)

17. General Clinical features
• AGE- middle aged or elderly people
• MEAN AGE OF ONSET- 5 th decade of life
• Rarely in young adults and children
• Female : Male = 3 : 2
• Lichen planus commonly affects 1-2% of the general
population , prevalence rate being 0.5to 2.2%
• 40% lesions occur on both oral and cutaneous surfaces,
35% occur on cutaneous surfaces alone, and 25% occur
on oral mucosa alone

18. • The skin lesions are small, angular, flat topped papules only
a few millimeters in diameter bilaterally distributed on
Flexor Surfaces
• Discrete lesions which gradually coalesce into large
plaques. The centre of the papule/plaque may be slightly
umblicated with a glistening scale covering it.
• Characteristic, very fine, grayish–white radiating lines
called “Wickham’s striae” seen. Also called “Honiton Lace”
• The primary symptom of Lichen planus is “Severe
Pruritis”.

19. • Self limiting disease with periods of regression and
recurrence
• Initially Red --> Purple or Violaceous hue --> a dirty
Brownish color
• Grinspan Syndrome = Lichen Planus + Hypertension +
Diabetes Mellitus
• “Koebner’s phenomenon”- skin lesions extend along the
areas of injury or irritation (ISOMORPHIC RESPONSE)

24. Oral Manifestations
Patient Commonly Presents with Burning sensation of oral
mucosa when he has food. Sometimes Pain may be felt
Types of Oral Lichen Planus:
1. Reticular
2. Papular
3. Plaque like
4. Atrophic
5. Erosive
6. Bullous
7. Ulcerative

25. Distribution of Oral Lesions
1. Buccal mucosa = 80%
2. Tongue = 65%
3. Lips = 20%
4. Gingiva, Floor or mouth & Palate = 10%

26. Reticular Lichen Planus
• Most common type
generally seen bilaterally on
posterior Buccal mucosa
• Outer radiating Wickham
striae seen which often
displays a peripheral
erythematous zone ,which
reflects the subepithelial
inflammation

27. PapularType
• Usually present in the
initial phase of the disease.
• Characterized by small
white dots, which usually
intermingle with the
reticular form.
• Size approx. 0.5mm

28. Plaque Type
• Shows a homogenous well
demarcated white plaque
with Wickham striae
• Plaque type lesions may
clinically be very similar to
homogenous leukoplakia
• Common in tobacco users

29. Atrophic Type
• Characterized by a
homogenous red area which is
smooth, poorly defined with
peripheral striae
• Usually associated with
Desquamative gingivitis
• Pain & Burning sensation
• Histopathologic examination
mandatory to confirm
diagnosis

31. Erosive Type
• Symptomatic Lesions = Pain,
Burning sensation, bleeding,
desquamative gingivitis
• Atrophic areas with central
ulceration of varying degree
• Periphery shows striae
• Pseudo membrane covered
ulcerations with keratosis and
erythema

32. Bullous Type
• Vesciculobullous presentation combined with reticular or
erosive pattern
• Rare form characterized by large vesicles or bullae (4mm
to 2cm)
• Lesions usually develop within an erythematus base,
rupture immediately leaving painful ulcers
• Usually have peripheral radiating striae and seen on
posterior part of buccal mucosa

35. Ulcerative Type WHO 1972
• They are the most disabling form of oral lichen planus
• Clinically the fibrin coated ulcers are surrounded by an
erythematous zone frequently displaying radiating white
striae.
• This appearance may reflect a gradient of the intensity of
sub epithelial inflammation that is most prominent at the
centre of the lesion.

37. Oral Lichen Planus
Investigations

38. • Histopathology
• Immunoflourescent studies
• Immunoglobulin Assay
• PAS staining
• Skin Patch testing

39. • Hyper orthokeratinisation or hyper parakeratinisation
• Thickening of granular layer
• Acanthosis of spinous layer
• Intercellular oedema in spinous layer
• “ Saw-tooth” rete pegs
• Liquefaction necrosis of basal layer- Max Joseph spaces
Histopathology

40. • Civatte ( hyaline or cytoid) bodies
• An eosinophilic band may be seen just beneath the basement
membrane and represent fibrin covering lamina propria
• Juxta-epithelial well-defined band like zone of cellular
infiltration that is confined to the superficial part of the
connective tissue, consisting mainly of lymphocytes

42. Max Joseph spaces: Sub-epithelial clefts formed by acantholysis or
hydropic degeneration of basal cells.

43. Civatte bodies:
( Hyaline / Cytoid / Colloid / Sabouraud/ Keratin)
– Seen in Basal layer & upper Papillary dermis,
individually or in clumps
– Apoptotic keratinocytes
– Contains of intracellular filaments of dead
keratinocytes, and may entrap immunoglobulin or
fibrin
– Slightly smaller than basal keratinocytes, Rounded,
Eosinophilic, Hyaline, Anucleate structures

46. • Direct immunofluorescence is useful in distinguishing OLP
from other lesions and demonstrates a SHAGGY BAND OF
FIBRINOGEN in the basement membrane zone in 90 to 100
% cases
• Multiple IgM staining cytoid bodies in dermal papilla or
peribasalar area can also be seen. Highly suggestive of
lichen planus if present in clusters
• Indirect immunofluorescence not useful in the diagnosis of
OLP
Immunoflourescence studies

48. • Periodic acid-Schiff (PAS) staining of biopsy specimens and
candidal cultures or smears may be performed.
• Skin patch testing may be helpful in identifying Contact
Allergy in patients to differentiate oral lichen planus and
lichenoid reaction

49. Malignant Transformation
• OLP is considered a pre-malignant condition
• The reported transformation rates vary from 0.4 to 5.3%.
Over a period of 5 years
1. Increased risk of Oral Squamous Cell Carcinoma in
OLP patients who also show Tobacco Abuse
2. EROSIVE and ATROPHIC forms commonly
undergo transformation

50. Microbes in Oral Lichen Planus
• Increased prevalence of Candida species in both
mycological and histological studies of oral lichen planus
• LP more prevalent In HIV + ve patients
• Hepatitis C Virus infection and concomitant occurrence of
oral lichen planus has been observed

51. Syndromes Associated with Oral Lichen Planus
• GRINSPAN SYNDROME is the association of OLP with Diabetes
and Hypertension
• GRAHAM LITTLE SYNDROME and VULVO-VAGINO-
GINGIVAL SYNDROME are other syndromes associated with
OLP in which there is mucosal involvement of gingival and genital
region, usually of erosive type

52. Oral Lichenoid Reaction
• Lichenoid reactions and lichen planus are of different
etiology yet exhibit similar clinical and histopathologic
features
• Lichenoid reactions differs from lichen planus as they occur
following exposure to specific agents
• Such agents are believe to expose the lichen specific antigen
on keratinocytes.

53. • Oral Lichenoid reactions can be grouped as:
1. Lichenoid Drug Reactions
2. Lichenoid contact Reactions
3. Lichenoid reactions of Graft versus host disease

54. LichenoidDrug Reaction
• First reported in military personnel in World War II who
had been prescribed anti-malarial drugs and since then a
wide variety of drugs have been associated with
precipitating Lichenoid Drug Reactions
• Drugs that have been implicated include NSAIDS, ACE-
inhibitors and beta-blockers.

55. • Lichenoid lesions may be unilateral, asymmetric and occur
in uncommon sites and tend to be erosive.
• Histological examination may show a more diffuse
lymphocytic infiltrate and more colloid bodies than in classic
Lichen planus

57. LichenoidContact Reaction
• Following the placement of a dental restoration or provision of a
denture
• These lichenoid reactions are usually the result of a contact
sensitivity or irritation to any restoration or a denture component
in close proximity to the oral mucosa
• Also following exposure to flavorings, especially cinnamates in
toothpaste

59. LichenoidReactions of Graft Vs Host disease
• Oral mucosal lichenoid lesions are also seen within the
spectrum of chronic graft-versus-host disease following
allogenic bone marrow transplantation.