Predisposing Factors
1.GENETIC BACKGROUND
2.AUTO IMMUNITY –ASSOCIATED WITH OTHER
AUTO IMMUNE DISEASE
3.IMMUNODEFICIENCY
4.DRUGS
5.DENTAL MATERIALS
6.STRESS
7.ADVERSE HABITS
Pathogenesis of Oral Lichen Planus
•Thevariousmechanismshypothesizedtobeinvolvedinthe
immunopathogenesisare:
1.ANTIGEN SPECIFIC CELL MEDIATED
MECHANISM
2.NONSPECIFICMECHANISM
3.AUTOIMMUNE RESPONSE
4.HUMORAL IMMUNITYPATHOGENESISOFOLP
NON SPECIFIC MECHANISM
•EpithelialBasementMembraneInteractions
•MatrixMetalloproteninasesMediated
•ChemokineMediated
•MastCellsMediated
Immunologic Mechanisms
Expression of an Unknown antigen associated with MHC class-I on
basal keratinocytesonly at the lesion site
(Self-peptide , Lichen Planusantigen)
Influx of Antigen specific CD8+ T-cell due to either:
(i)Encountering the keratinocyteantigen by chance on routine
surveillance in the epithelium (“Chance Encounter” hypothesis)
OR
(ii)Attracted to the epithelium by keratinocyte-derived chemokines
(“Directed Migration” hypothesis).
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-αthat triggers
keratinocyte apoptosis via TNF-R1.
Lichenoid Drug 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.
Alternate Immunologic Mechanism
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-γmaintains keratinocyte MHC class-II
expression, thereby contributing to disease chronicity)
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
Distribution of Oral Lesions
1.Buccal mucosa = 80%
2.Tongue = 65%
3.Lips = 20%
4.Gingiva, Floor or mouth & Palate = 10%
Reticular Lichen Planus
•Most common type
generallyseenbilaterallyon
posteriorBuccalmucosa
•OuterradiatingWickham
striaeseenwhichoften
displaysaperipheral
erythematouszone,which
reflectsthesubepithelial
inflammation
Papular Type
•Usuallypresentinthe
initialphaseofthedisease.
•Characterizedbysmall
whitedots,whichusually
interminglewiththe
reticularform.
•Sizeapprox.0.5mm
Plaque Type
•Showsahomogenouswell
demarcatedwhiteplaque
withWickhamstriae
•Plaquetypelesionsmay
clinicallybeverysimilarto
homogenousleukoplakia
•Commonintobaccousers
Atrophic Type
•Characterized by a
homogenousredareawhichis
smooth,poorlydefinedwith
peripheralstriae
•Usuallyassociatedwith
Desquamativegingivitis
•Pain&Burningsensation
•Histopathologicexamination
mandatory toconfirm
diagnosis
Lichenoid Reactions of Graft Vs Host disease
•Oralmucosallichenoidlesionsarealsoseenwithinthe
spectrumofchronicgraft-versus-hostdiseasefollowing
allogenicbonemarrowtransplantation.