Oral Lichen Planus.pptx

Lichen planus (LP) is a chronic mucocutaneous disorder
of the stratified squamous epithelium that affects oral
and genital mucous membranes, skin, nails, and scalp

1. Oral Lichen Planus Presented by Dr. Rahul Srivastava Professor Rama Dental College Hospital & Research Centre Kanpur

2. Lichen planus (LP) is a chronic mucocutaneous disorder of the stratified squamous epithelium that affects oral and genital mucous membranes, skin, nails and scalp. Word lichen planus derived from the Greek word “ leichen ” means tree moss and Latin word “ planus ” means flat.

3. The designation and description of the pathology were first presented by the English physician Erasmus Wilson in 1866. He considered this to be the same disease as “lichen ruber ,” previously described by Hebra and characterized the disease as “an eruption of pimples remarkable for their color, their figure, their structure, their habits of isolated and aggregated development.”

4. In 1892, Kaposi reported the first clinical variant of the disease, lichen ruber pemphigoides . In 1895, Wickham noted the characteristic reticulate white lines on the surface of LP papules, today recognized as Wickham striae . Darier is credited with the first formal description of the histopathological changes associated with LP.

5. Etiology of oral lichen planus Exact etiology is still unknown, but some factors are associated with it. These are as follows: 1- Genetic background Familial cases are rare. An association observed with HLA‑A3, A11, A26, A28, B3, B5, B7, B8, DR1, and DRW9.

6. 2- Dental materials Silver amalgam, gold, cobalt, palladium, chromium and even non ‑ metals such as epoxy resins (composite) and prolonged use of denture wear.

7. 3- Drugs Oral lichenoid drug reactions triggered by systemic drugs like: NSAIDs, beta blockers, sulfonylureas , some angiotensin‑converting enzyme (ACE) inhibitors, antimalarials , contact allergens including toothpaste flavorings, especially cinnamates .

8. 4- Infectious agents A- Hepatitis C virus (HCV) B- Epstein Barr virus (EBV). C- Human herpes virus 6 (HHV‑6). D- Human immunodeficiency virus (HIV). 5- Autoimmunity. 6- Stress. 7- Diabetes and hypertension.

9. Pathophysiology Cellular-mediated immunity, initiated by predisposing factors results in the production of Tumor Necrosis Factor-alpha (TNF-a), Interferon- cytokine (IFN-c), and keratinocyte , T cell or antigen- presenting cell associations.

10. The increased production of T-helper 1 (Th1) cytokines occurs in the early event in OLP, genetic polymorphism of cytokines and IFN-gamma will lead to the development of oral mucosal lesions, increase in the frequency of 308A TNF-alpha allele will lead to the development of skin lesions.

11. A hypothesis of the pathogenesis of OLP was introduced by Sugerman et al. and is based on a theoretical interaction between CD8+ T cells and CD4+ T cells through a “request cytotoxic activity” (RCA) cell surface molecule. The activated CD8+T cells can trigger keratinocytes apoptosis through TNF-alpha or a Fas–Fas Ligand mechanism.

12. The role of metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) are proven to initiate pro‑ inflammatory cytokines which will lead to inflammation.

13. RANTES (regulated on activation, normal T cell expressed and secreted) a chemokine family also plays a role in pathogenesis by activating the number of cells like lymphocytes, monocytes , natural killer cells, eosinophils , basophils , and mast cells in oral lichen planus and the cell surface receptors are also increased.

14. Clinical features of lichen planus : The lesions show white striations, which are slightly elevated, fine, whitish lines known as Wickham’s striae ( Honiton lace). Usually affect buccal mucosa, ventral and lateral borders of tongue, gingiva and floor of the mouth. Lingual papillae become atrophied in the areas of involvement and the resulting smooth surface accentuates the white striae .

15. Gingival lesions present as fiery red areas affecting the entire width of attached gingiva called desquamative gingivitis. It is associated with intense sensitivity of gums to hot or spicy food or brushing of teeth with intense burning sensation to pain. Skin lesions described by the six p's : Planar, plaque, pruritic , purple, polygonal, and papular .

16. They may be discrete and gradually coalesce in to large plaques each covered with fine glistening scale. Early in onset of disease they appear red, soon they take on reddish purple or violaceous colour . Skin lesions commonly involve flexor surface of legs and arms, especially the wrists, forearms, inner aspect of thighs, trunk especially in sacral areas.

17. Nail beds may also be affected with resultant ridging, thinning and subungual hyperkeratosis. Scalp involvement, if untreated can lead to scarring and permanent hair loss. Patients are often unaware of quiescent OLP, which may be present only with faint white striations, papules or plaques.

18. Exacerbations of OLP have been linked to periods of psychological stress, anxiety or mechanical trauma. This phenomenon is referred as Koebner’s phenomenon.

19. Vulvovaginal -gingival syndrome Association of LP of vulva, vagina and gingiva is recognized as vulvovaginal -gingival syndrome. Graham-Little syndrome The combination of follicular LP with scarring alopecia of scalp and non-scarring alopecia of axilla and pubis or other areas is known as Graham-Little syndrome.

20. Greenspan syndrome Triad of Diabetes mellitus, hypertension and oral lichen planus .

21. Clinical Presentation of Oral Lichen Planus

22. Reticular It is the most common clinical form of this disease and presents with fine, asymptomatic intertwined lace-like pattern called “Wickham striae ” in a bilateral symmetrical form and involves the posterior mucosa of the cheek in most cases.

23. Erosive This is the most significant form of the disease because it shows symptomatic lesions often surrounded by fine radiant keratinized striae with a network appearance.

24. Atrophic It exhibits diffuse red lesions and it may resemble the combination of two clinical forms, such as the presence of white striae characteristic of the reticular type surrounded by an erythematous area. Atrophic type lichen planus −sometimes representing as desquamative gingivitis

25. Plaque‑ like This type shows whitish homogeneous irregularities similar to leukoplakia ; it mainly involves the dorsum of the tongue and the mucosa of the cheek.

26. Papular This form is rarely observed and is normally followed by some other type of variant described. It presents with small white papules with fine striae in its periphery.

27. Bullous It is the most unusual clinical form, exhibiting blisters that increase in size and tend to rupture, leaving the surface ulcerated and painful. Nikolsky’s sign may be positive.

28. Gingival Involvement The gingival lesions in LP fall into one or more of the following categories: Keratotic lesions are usually present on the attached gingiva as small raised round white papules of pinhead size with a flattened surface.

29. Vesiculo‑bullous lesions are other mucocutaneous disorders especially pemphigoid , dermatitis herpetiformis or linear IgA disease. Atrophic and Erosive: Produce the desquamative gingivitis.

30. Pigmentation is frequently associated with OLP? Degenerative changes in basal keratinocytes frequently led to pigmentary incontinence. Gamma- aminobutyric acid (GABA) imbalance occurs in anxiety disorders and might be passed through the cranial nerve, stimulating production of melanocytes , resulting in excessive deposition in OLP.

31. Investigations for lichen planus Direct Immunofluorescence Fibrinogen and fibrin are deposited in a linear pattern in the BM zone. Colloid bodies contain fibrin, IgM , C3, C4 and keratin. Laminin and fibronectin staining may be absent in areas of heavy fibrin deposition and colloid body formation. This finding suggests BM damage in these areas.

32. Immunohistochemical ( Ihc ) Studies Immunohistochemical staining using the antibody to the S-100 protein indicates an increase in langerhan cells in mid layer of the epithelium. Serology There are no consistent serological changes associated with OLP but some patients do present an elevated antinuclear antibody (ANA) titer.

33. Biopsy Histopathology Liquefactive degeneration of the basal cell accompanied by apoptosis of the keratinocytes , a dense band-like lymphocytic infiltrate at the interface between the epithelium and the connective tissue. Focal areas of hyperkeratinized epithelium (which give rise to the clinically apparent Wickham’s striae ).

34. Occasional areas of atrophic epithelium where the rete pegs may be shortened and pointed (saw tooth rete pegs). Eosinophilic colloid bodies ( Civatte bodies).

35. Treatment of lichen planus A- Topical agents 1- Corticosteroids 0.05% clobetasol propionate gel, 0.1% or 0.05% betamethasone valerate gel, 0.05% flucinonide gel, 0.05% clobetasol butyrate ointment or cream and 0.1% triamcinolone acetonide ointment.

36. 2- Retinoids Isotretinoin gel 0.1%, topically administered Vitamin A, beta-all-trans retinoic acid all are effective. 3- Topical Tacrolimus Tacrolimus ointment is available in two strengths: 0.1% and 0.03%. The 0.1% formulation twice daily is more effective in erosive lichen planus .

37. 4- Intralesional injection Intralesional steroids such as triamcinolone acetonide (10– 20 mg/ml) injections can be effective and repeated every 2–4 weeks. B- Systemic Steroid Therapy The oral dose of prednisone for 70-kg adult ranges from 10-20 mg/day for moderately severe cases to as high as 35 mg/day (0.5 mg/kg daily) for severe cases.

38. C- Griseofulvin It is administered systemically in doses of 500mg/day to 1 gm/day. D- Azathioprine Azathioprine in doses of 50 to 100mg/day in combination with systemic steroids shows positive response. E- Efalizumab Efalizumab therapy with initial dose of 0.7mg/kg followed by dose of 1.0 mg/kg per week for 5 week provide good results.

39. F- Surgical excision, cryotherapy , CO2 laser, and ND:YAG laser have all been used in the treatment of OLP. G- Photo chemotherapy, uses ultraviolet A (UVA) with wavelengths ranging from the 320 to 400 nm, after the injection of psoralen (8-Methoxypsoralen, 0.4-0.6 mg/kg) is also used.

40. References 1- Serrano‑ Sanchez P, Bagan JV, Jimenez‑ Soriano , Sarrion G. Drug induced oral lichenoid reactions. A literature review. J Clin Exp Dent 2010;2:e71‑5. 2- Scully C, Carrozzo M. Oral mucosal disease: Lichen planus . Br J Oral Maxillofac Surg 2008;46:15‑21. 3- 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.

41. 4- Issa Y, Brunton PA, Glenny AM, Duxbury AJ. Healing of oral lichenoid lesions after replacing amalgam restorations: A systematic review. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2004;98:553‑65. 5- Wray D, Rees SR, Gibson J, Forsyth A. The role of allergy in oral mucosal leisons . QJM 2000;93:507‑11. 6- Moravvej H, Hoseini H, Barikbin B, Malekzadeh R, Razavi GM. Association of Helicobacter pylori with lichen planus . Indian J Dermatol 2007;52:138‑40.

42. 7- Vainio E, Huovinen S, Liutu M, Uksila J, Leino R. Peptic ulcer and Helicobacter pylori in patients with lichen planus . Acta Derm Venereol 2000;80:427‑9. 8- Hulimavu SR, Mohanty L, V Tondikulam N, Shenoy S, Jamadar S, Bhadranna A. No evidence for Helicobacter pylori in oral lichen planus . J Oral Pathol Med 2014;43:576‑8. 9- Ertugrul AS, Arslan U, Dursun R, Hakki SS. Periodontopathogen profile of healthy and oral lichen planus patients with gingivitis or periodontitis . Int J Oral Sci 2013;5:92‑7.