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Lichen Planus
- 1. ORAL LICHEN PLANUS Pathogenesis DR. SHYAMALA KARNAM
- 3. SKIN LESIONS Purple, Polygonal, Pruritic Papules with Wickham’s striae and bilaterally symmetrical on flexor surfaces of extremities DR. SHYAMALA KARNAM
- 5. Etiological (triggering) factors Drugs and chemicals Genetics Infection Psychogenic actors Habits Diabetes Mellitus (Grinspan Syndrome) Hypertension Graft vs Host diseases mechanical trauma (koebner phenomenon) Immunodeficiency autoimmunity heat shock proteins Urolithiasis Miscellaneous factors DR. SHYAMALA KARNAM
- 6. Association of OLP DR. SHYAMALA KARNAM OLP HCV, EBV, HPV, HHV OLP+HCV HLA-A3,A11, A26,A28, B3, B5, B7,B8, DR1,and DRW9 AI DISEASES CANDIDIASES
- 8. Max –Joseph Space DR. SHYAMALA KARNAM
- 10. Key Questions Why and how do t-cells accumulate in the superficial lamina propria in OLP? What triggers basal keratinocyte apoptosis in OLP? Why and how do T-cells enter the oral epithelium in OLP? What does CD4 T cell do? Reason for Chronicity of OLP? - Antigen specific mechanism - Non specific mechanism DR. SHYAMALA KARNAM 1 2 3 4 5
- 11. KEY FACTORS • MHC I - present endogenous antigens • MHCII - Present exogenous antigens • HLA team Antigen Presentation • Keratinocytes • Lymphocytes Cytokines DR. SHYAMALA KARNAM
- 13. Lets clear these clouds … Why and how do T-cells accumulate in the superficial lamina propria in OLP? DR. SHYAMALA KARNAM 1
- 14. MHC1 CYTOKINES TNF-α IFN-γ ILI ICAM VCAM MHC -II L 8 Direct Migration ECAM receptors on lymphocytes ECAM L4 L L 8 L 8 +HLA-DR Ag Specific Mechanisms MHC1 Activated cells RANTES MAST cells Degranulation ProteaseChymaseTNF- α MMP9ECAM L L L L L Non Specific Mechanisms Chance Counter Homing of Lymphocytes LLL L L L LLL L L L L 8 LH DR. SHYAMALA KARNAM
- 15. Lets clear these clouds What triggers basal keratinocyte apoptosis in OLP? DR. SHYAMALA KARNAM 2
- 16. A MHC1 CD8TL CD8TL MHC1 Mast cell Chymase TNF-α Proteases TNF-α Granzyme-β L L L L L L L L L L L L L L L L L L TNF-R Ag Specific Mechanisms Non Specific Mechanisms DR. SHYAMALA KARNAM
- 17. Lets clear these clouds Why and how do T-cells enter the oral epithelium in OLP? DR. SHYAMALA KARNAM 3
- 18. Basal keratinocyte Col 4 laminin 5 BM secretion & maintainance Cell survival signal Basal keratinocyte degeneration No BM No survival signal Basal keratinocyte apoptosis No production of BM DR. SHYAMALA KARNAM
- 19. A MHC1 CD8TL Cytokines Apoptosis LLL L L LLL L L L LLL L L L LL L L L L L L L L L MHC1 Activated L RANTES Mast cell degranulation proteases MMP 9 BM disruption LL L L Ag specific Mechanism Non specific Mechanism Lymphocytes migration in to epithelium DR. SHYAMALA KARNAM
- 20. What does CD4 T cell do? DR. SHYAMALA KARNAM 4Lets clear these clouds
- 21. MHC I CD8TL RCA RCA R CD4TL MHC II CD 154 R CD 40 L IFN-𝛾 IL 2 L L L L L L L L L L L L L L L L L L IFN-𝛾 𝑅 DR. SHYAMALA KARNAM
- 22. Reason for Chronicity of OLP DR. SHYAMALA KARNAM 5Lets clear these clouds
- 23. Chronicity of OLP CD4 T CELLS INCREASE IFN-𝛾 DECREASE TGF-𝛽1 REDUCED IMMUNIOSUPPRE SSION PREDISPOSES TO AUTO IMMUNITY DR. SHYAMALA KARNAM
- 24. Malignant potential of OLP Small –sample size/ study design Low percentage of malignant transformation Misdiagnosis Malignant transformation 0.2-0.5% Or predisposes? Intrinsically precancerous Or Lichenoid Dysplasia? Reason for controversy DR. SHYAMALA KARNAM
- 25. Recent studies in pathogenesis Markers to distinguish between OLP and LD Diagnostic criterion Treatment aspect explanation based on pathogenesis Scope DR. SHYAMALA KARNAM
- 26. Oral Lichenoid Reaction The controversy DR. SHYAMALA KARNAM
- 27. Lichenoid Reaction DR. SHYAMALA KARNAM
- 30. Factors Dental restorative materials Drugs and medications Graft-versus-host disease (GVHD) Other factors DR. SHYAMALA KARNAM
- 31. Dental restorative materials - Pathogenesis Byproducts Toxic reaction Primary contact Local inflammation Not lymphocyte mediated Allergic reaction Previous sensitisation Lymphocyte mediated delayed type hypersensitivity reaction DR. SHYAMALA KARNAM
- 32. Drugs and medications NSAIDS ACE inhibitors antimalarials Antihypertensive Oral hypoglycemic Gold salts Penicillamine Diuretics Beta blockers DR. SHYAMALA KARNAM
- 33. Drugs - Pathogenesis Precipitate immune response to epithelial Ags Change enzyme system Different routes of Ag presentation Change the surface Ag or sulfhydryl groups OLL DR. SHYAMALA KARNAM
- 34. Graft-versus-host disease (GVHD) - Pathogenesis Donor’s immune cells react to patient’s cells donor-derived, antigen presenting cells (APCs) initiate GVHD Impaired function Increased susceptibility to infection DR. SHYAMALA KARNAM
- 35. GVHD types aGVHD (<3 months ) skin Liver Oral mucosa GIT bGVHD (>3 months ) Liver Lung fibrosis Sclerodermatosis OM &GIT skin DR. SHYAMALA KARNAM
- 36. Other factors Dental tartar/ plaque Tooth paste Cinnamon Etcetera DR. SHYAMALA KARNAM
- 37. Clinical differences Features OLP OLL Types All clinical forms are seen Mostly plaque corrosive patches Ocurence Bilateral Unilateral Cause No causative agent Topographical association Site All sites involved Rare on tongue and palate
- 38. Histopathological differences Features OLP OLL Inflammation location Limited to lamina propria Diffuse and penetrating Type of inflammation Lymphohistiocytic Mixed variety Perivascular congregation of inflammation Not seen Seen Keratosis Diffuse Focal with focal interruption of granular layer Cytoid bodies Basal and sub basal layers Granular and keratin layers Mast cells Increased and degranulated Subdued Vascularity Increased with increased PAS material on BM Not seen
- 39. Markers DR. SHYAMALA KARNAM OLP Not seen Not seen LH cells express more HLA DR OLL Increased cox 2 Basal cell cytoplasmic auto Abs LH cells express more of T6 receptor
- 40. Malignant transformation DR. SHYAMALA KARNAM OLP 0.2- 0.5% OLL 2.1% ( Van der meiji et al)
- 41. WHO diagnostic criteria (1978) of oral lichen planus Clinical criteria • Presence of white papule, reticular, annular, plaque-type lesions, gray-white lines radiating from the papules • Presence of a lace-like network of slightly raised gray-white lines (reticular pattern) • Presence of atrophic lesions with or without erosion, may also bullae Histopathologic criteria • Presence of thickened ortho or para keratinized layer in sites with normally keratinized, and if site normally non keratinized this layer may be very thin • Presence of Civatte bodies in basal layer, epithelium and superficial part of the connective tissue • Presence of a well-defined band like zone of cellular infiltration that is confined to the superficial part of the connective tissue, consisting mainly of lymphocytes • Signs of ‘liquefaction degeneration’ in the basal cell layer DR. SHYAMALA KARNAM
- 42. Modified WHO diagnostic criteria of OLP and OLL (2003) Clinical criteria • PRESENCE of bilateral, more or less symmetrical lesions • Presence of a lacelike network of slightly raised gray-white lines (reticular pattern) • Erosive, atrophic, bullous and plaque-type lesions are accepted only as a subtype in the presence of reticular lesions elsewhere in the oral mucosa. • In all other lesions that resemble OLP but do not complete the aforementioned criteria, the term “clinically compatible with” should be used Hisopathologic criteria • Presence of a well-defined band like zone of cellular infiltration that is confined to the superficial part of the connective tissue, consisting mainly of lymphocytes • Signs of liquefaction degeneration in the basal cell layer • Absence of epithelial dysplasia • When the histopathologic features are less obvious, the term “histopathologically compatible with” should be used DR. SHYAMALA KARNAM
- 43. Final diagnosis Histopathological criteria +Clinical criteria OLP Clinically typical of OLP histopathologically only compatible with OLP OLL Histopathologically typical of OLP clinically only compatible with OLP OLL Clinically compatible with OLP histopathologically compatible with OLP OLL
- 44. Scenario 1 DR. SHYAMALA KARNAM Diagnosis OLL Clinically compatible with OLP HP OLP Apply 2003 Criteria Symptom Radiating striae on buccal mucosa Unilateral
- 45. Scenario 2 DR. SHYAMALA KARNAM Diagnosis OLL HP compatible with OLP Clinically OLP Apply 2003 Criteria Symptom Bilateral OLP HP though typical shows dysplasia
- 46. Scenario 3 DR. SHYAMALA KARNAM Diagnosis OLL HP compatible with OLP Apply 2003 Criteria Symptom Pt with the History of OLP Consults another pathologist Now there is dysplasia in epithelium
- 47. Are all these diagnoses justified? This line has considerable relevance if we consider the above example DR. SHYAMALA KARNAM “We do realize that application of these criteria will exclude a number of patients who actually may have the disease but do not meet the strict criteria.” Van der Meiji and Van der Waal (2003)
- 48. What should we know ? DR. SHYAMALA KARNAM Probably not all patients with OLP manifest with the classical bilateral white striae. Consider other clinical manifestations like: Manifestation in cancer-prone areas, Skin manifestations, Association with etiology Clinicians and pathologists must be cautious in blindly branding the lesion as OLL by strict adherence to the 2003 modified criteria.
- 49. Key take away Differentiating between OLP and OLL is very significant as both the lesions are potentially malignant and management is different
- 50. References • Kamath VV, Setlur K, yerlagudda K, Oral Lichenoid Lesions - A Review and Update. Indian J Deramtol. 2015. Jan-Feb; 60(1): 102. • Sugerman PB, Savage NW, Walsh LJ, Zhao ZZ, Zhou XJ, Khan A, et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med. 2002;13:350–65. • Scully C, Beyli M, Ferreiro MC, Ficarra G, Gill Y, Griffiths M, et al. Update on oral lichen planus:etiopathogenesis and management. Crit Rev Oral Biol Med. 1998;9:86–122. • Shankargouda Patil, Roopa S. Rao, D. S. Sanketh, Sachin C. Sarode, Gargi S. Sarode, “A universal diagnostic criteria for oral lichen planus: An exigency!,” Int J Contemp Dent Med Rev, vol. 2014, Article ID 041214, 2014. DR. SHYAMALA KARNAM
- 51. Thank you
Notes de l'éditeur
- HCV, EBV, HPV, HHV infections OLP+HCV- consider as precancerous lesion HLA-A3,A11, A26,A28, B3, B5, B7,B8, DR1,and DRW9 AI diseases- primary biliary cirrhosis, chronic active hepatitis, ulcerative colitis, myasthenia gravis and thymoma Candidiasis (37% to 50% of OLP) synergistic oscc