Lichen planus

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white lesion of the oral mucosa

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Lichen planus

  1. 1. ORAL LICHEN PLANUS SOYEBO O.A.
  2. 2. OUTLINE •INTRODUCTION •EPIDEMIOLOGY •AETIOLOGY •PATHOGENESIS •CLINICAL FEATURES •DIAGNOSIS & MANAGEMENT •LICHENOID REACTIONS •CONCLUSION
  3. 3. INTRODUCTION • It was Erasmus Wilson who coined the term ‘lichen planus’ in 1869 • He considered it to be the same disease as ‘leichen rubra’ previously described by Hebra Wickham who noted the punctuations & striae atop the lesions that currently bear his name today • Lichen planus is a chronic mucocutaneous disease of unknown cause. • Usually involves the oral mucosa along with or preceded by lesions on skin and genital mucous membrane.
  4. 4. • Oral lichen Planus can be defined as a rather common chronic inflammatory mucocutaneous disease which probably arises due to abnormal immunologic reaction • Usually involves the oral mucosa along with or preceded by lesions on skin and genital mucous membrane • The importance of this disease relates to • its degree of frequency of occurrence, • its occasional similarity to other mucosal diseases, • its occasionally painful nature.
  5. 5. EPIDEMIOLOGY • It is relatively common, affecting between 0.5% and 2% of the entire world’s population. • Commoner in females, with a F:M ratio: 1.4:1 • Predominantly seen in adults over 40 years. • The mean age at the time of diagnosis is approximately 55 years. • Affects all ethnicities
  6. 6. ETIOPATHOGENESIS • The specific etiology is unknown • It is generally considered to be an immunologically mediated process, which could be as a result of interaction/interplay between multiple factors. • There is also no definitive immunogenetic basis yet established for LP and familial cases are rare • Believed to be related to psychological stress, which affects severity.
  7. 7. • Pathologically, there is a local cell-mediated immunological response characterized by a dense T lymphocyte inflammatory cell infiltrate in the upper lamina propria causing cell death (apoptosis) in the basal epithelium. • This is probably caused by the production of cytokines such as • tumor-necrosis factor alpha (TNF∝) • interferon gamma (IFN-γ) • Interleukin -1
  8. 8. • Interleukin-1 produced by Langerhans cells and macrophages stimulates the T lymphocytes to produce interleukin 2 which cause T cell proliferation. • Activated lymphocytes are cytotoxic for basal cells and they secrete gamma interferon, which induces keratinocytes (epithelial cells) to express the class II histocompatibility antigen HLA DR and increase their rate of differentiation.
  9. 9. • This results in thickening of the surface, which is seen clinically as a white lesion. • In this disease process, self-antigen may therefore be recognized as foreign and cause an autoimmune response
  10. 10. • It is characterized by an intense T-cell infiltrate (predominantly CD8+ cells) at the epithelium—connective tissue interface. • Other immunoregulating cells elaborated include macrophages, factor Xllla-positive dendrocytes, Langerhans cells. • A lichen planus-specific antigen is expressed in conjunction with MHC class 1 molecules on keratinocytes at the oral lichen planus lesion site. • The result in the activation of antigen specific CD8+ T cells the area. • Activated antigen-specific CD8+ cytotoxic T lymphocytes trigger keratinocyte apoptosis, possibly by secreted TNF-α. • The activated T lymphocytes undergo intra-lesional clonal expansion and release soluble mediators (cytokines and chemokines).
  11. 11. • These chemokines include vascular adhesion molecules such as ELAM-1, ICAM-1, VCAM-1 on the vascular endothelium and reciprocal receptors L-selectin, LFA-1, and VLA4 on the infiltrating lymphocytes. • The cytokines include tumor necrosis factor (TNF-a), interleukin-1, and interferon-y. • The source of these cytokines is thought to be from resident macrophages, factor XIIIa-positive dendrocytes, Langerhans cells, and the lymphocytes. • Which recruit lymphocytes from the local microvasculature and cause migration toward the epithelium.
  12. 12. • Majority of lymphocytes recruited to the OLP lesion site are not specific for the lichen planus-specific antigen. • However, they may contribute to the pathogenesis of OLP by secreting matrix metallopeptidase-9, which leads to epithelial basement membrane disruption. • Epithelial basement membrane disruption allows for the passage of lymphocytes into the epithelium and denies keratinocytes a cell survival signal, resulting in further keratinocyte apoptosis
  13. 13. • There are also lesions very similar to OLP – termed lichenoid lesions – are sometimes caused by: • Dental restorative materials (mainly amalgam and gold). • Drugs (non-steroidal anti-inflammatory agents, antihypertensive agents antimalarials, and many other drugs). • Chronic graft-versus-host disease seen in bone marrow (haemopoietic stem cell) transplant patients. • Infection with hepatitis C virus (HCV) in some populations such as those from southern Europe and Japan. • A variety of other systemic disorders such as hypertension and diabetes — probably a reaction to the drugs used.
  14. 14. CLINICAL FEATURES • OLP may be associated with pain or discomfort, which interferes with function and with quality of life. • Symptoms vary from mucosal sensitivity to continuous debilitating pain • The buccal mucosa is the most commonly affected site. • Other sites include the tongue and the gingivae • OLP lesions usually persist for many years with periods of exacerbation and quiescence.
  15. 15. • Exacerbation of OLP has been linked to periods of psychological stress and anxiety. • Periods of exacerbation characterized • increased erythema or ulceration • increased pain and sensitivity. • Quiescence period is associated with • decrease of erythema or ulceration • decreased pain and sensitivity. • Quiescent OLP typically as faint white striations, papules or plaques which patient may not be aware of.
  16. 16. CLINICAL VARIANTS • Reticular • Erosive • Plaque • Papular • Atrophic • Bullous
  17. 17. RETICULAR OLP • Most common and most readily recognized form. • Characterized by numerous interlacing white keratotic lines or striae – called Wickham's striae that produce an annular or lacy pattern. • The buccal mucosa is the site most commonly involved- bilaterally. • This form generally presents with minimal clinical symptoms and is often an incidental discovery. • It is the baseline presentation found in almost all OLP patients. • They may also be seen on the lateral border of tongue and less often on the gingiva and the lips. • Reticular lichen planus is likely to resolve in 4l % of cases.
  18. 18. EROSIVE OLP • The 2nd most common type after the reticular type. • The lesion consist of mixture of erythematous and ulcerated areas surrounded by radiating keratotic striae. • It has a similar appearance to candidiasis and pemphigus. • Lesions tend to migrate and are often multifocal. • Mostly affect the buccal mucosa and vestibule • It is usually symptomatic, characterized by: • Sore mouth sensitive to heat, cold, spices, and alcohol • Pain and bleeding on touch
  19. 19. PLAQUE OLP • Tends to resemble leukoplakia clinically but has a multifocal distribution. • The plaques generally range from slightly elevated to smooth and flat. • The primary sites for this variant are the • dorsum of the tongue • buccal mucosa. • Resolves in only 7% of cases. • This form is significantly more common among tobacco smokers.
  20. 20. PAPULAR OLP • The papular type of OLP is usually present in the initial phase of the disease • This form presents as small white pinpoint papules about 0.5 mm in site. • It is rarely seen and being small, it is possible to overlook them during a routine oral examination.
  21. 21. BULLOUS OLP • Appear as small bullae or vesicles that tend to rupture easily. • The bullae or vesicles range from a few millimeters to several centimeters in diameter which when ruptured leave an ulcerated, painful surface. • This form is rarer than the other forms of oral lichen planus. • Usually present in combination with reticular or erosive pattern. • The bullous form is commonly seen on the buccal mucosa, particularly in the postero-inferior areas adjacent to the second or third molar teeth. • The next most common site is the lateral margin of the tongue. • The lesions are rarely seen on the gingiva or inner aspect of the lips
  22. 22. ATROPHIC OLP • The atrophic type is diffuse, red and there are usually white striae within the lesion. • Striae that radiate peripherally are usually evident at the margins of the atrophic zones of the lesion. • The attached gingiva is often involved and the condition is commonly referred to as `chronic desquamative gingivitis'. • The lingual gingiva is usually less severely involved. • This condition can cause a burning sensation particularly when in contact with certain foods. • Patients may complain of burning, sensitivity, and generalized discomfort • About 12% of the atrophic lesions will resolve spontaneously.
  23. 23. DIAGNOSIS • Diagnosis is based on: • Clinical Presentation. E.g. Reticular lichen planus with characteristic appearance of Wickham’s striae. • Histological Examination. requires biopsy. • Direct Immunofluorescent Examinations: requires biopsy.
  24. 24. HISTOLOGY • The following histologic features are essential for the diagnosis of lichen planus. • Areas of hyperparakeratosis or hyperorthokeratosis. • The spinous cell layer may be thickened (acanthosis) with shortened and pointed rete pegs. • The thickened areas are seen clinically as Wickham’s striae. • Liquefaction degeneration or necrosis of the basal cell layer- Max Joseph spaces. • Which is often replaced by an eosinophilic band.
  25. 25. • There is also dense subepithelial band of lymphocytes. • Isolated epithelial cells, shrunken with eosinophilic cytoplasm and one or more pyknotic nuclear fragments-Civatte bodies. • Often scattered within the epithelium and superficial lamina propria. • These represent cells that have undergone apoptosis
  26. 26. DIRECT IMMUNOFLUORESCENCE • Differentiates LP between other autoimmune conditions. • Shows shaggy deposition of fibrinogen along the basement membrane. • DIF section may also multiple IgM-staining cytoid bodies, usually located in the dermal papilla or in the peribasalar area. • Cytoid bodies in large numbers or in clusters - highly suggestive of lichen planus if they are present
  27. 27. LICHENOID REACTIONS • 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. • They can grouped as:
  28. 28. Lichenoid drug reactions (LDR) • Follows the administration of a systemic drug. • These lichenoid drug reactions (LDR) may be unilateral but usually appear as idiopathic OLP. • Drugs that have been implicated in oral LDR include nonsteroidal anti- inflammatory drugs (NSAIDS), angiotensin converting enzyme (ACE) inhibitors and beta-blockers.
  29. 29. LICHENOID DRUG REACTIONS
  30. 30. • Lichenoid Contact Reaction (oral lichenoid 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 amalgam or composite resin dental restoration or a denture component in close proximity to the oral mucosa. • Also following exposure to flavorings, especially cinnamates in toothpaste
  31. 31. • Lichenoid reactions of Graft versus Host disease Oral mucosal lichenoid lesions are also seen within the spectrum of chronic graft-versus-host disease following allogeneic bone marrow transplantation.
  32. 32. Graft versus host disease
  33. 33. OLP AND SYSTEMIC DISEASES • OLP and systemic diseases is relatively common. • It occurs predominantly in older adults. • Many drugs used in the treatment of systemic diseases trigger oral lichenoid lesions as a side effect. • An example is the oral lichenoid lesions in Grinspan’s syndrome
  34. 34. MALIGNANT TRANSFORMATION • Controversy • Increased risk of oral squamous cell carcinoma • Frequency of transformation is low, between 0.3% and 3% • Erosive and atrophic forms commonly undergo transformation
  35. 35. DIFFERENTIAL DIAGNOSIS • Lichenoid reactions • Leukoplakia • Candidiasis • Syphilis • Mucous membrane pemphigus • Erythema multiforme • Recurrent aphthae • Lupus erythematosus • Squamous cell carcinoma
  36. 36. TREATMENT • No treatment for OLP is curative • Goal: • Reduce painful symptoms • Resolution of oral mucosal lesions • Reduce risk of oral squamous cell carcinoma • Improve oral hygiene • Eliminate exacerbating factors • Repair defective restorations or prosthesis • Remove offending material causing allergy • Diet • Eliminate smoking and alcohol consumption • Eat fresh fruit and vegetables (but avoid tomatoes and nuts) • Reduce Stress
  37. 37. • Medication • Topical corticosteroids • 0.05% clobetasol proprionate gel • 0.1% or 0.05% betamethasone valerate gel • 0.05% fluocinonide gel • 0.05% clobetasol butyrate ointment • 0.1% triamcinolone acetonide ointment • Can be applied directly or mixed with Orabase
  38. 38. • Medication • Systemic Steroid Therapy • Prednisone (for 70kg adult) • 10-20mg/day for moderately severe cases • As high as 35 mg/day for severe cases • Should be taken in the morning to avoid insomnia • Should be taken with food to avoid peptic ulceration • Azathioprine (Imuran) – Inhibits synthesis of DNA • 1mg/kg/d for 6-8 weeks • Methylprednisolone (Medrol Dosepak) • to reduce pain and inflammation • Prophylactic use of 0.12% chlorhexidine gluconate may help reduce fungal infection during corticosteroid therapy
  39. 39. COMPLICATIONS • Oral lichen planus can be very painful and ulceration may lead to scarring. Sometimes eating is so uncomfortable that affected person is unable to maintain adequate nutrition. • Oral squamous cell carcinoma (SCC) developed in fewer than 5% of patients with oral lichen planus who did not use tobacco
  40. 40. CONLUSION • Oral Lichen Planus is a common non-infectious cause of oral white lesions, its specific aetiology is unknown and clinical evidence is sufficient for a diagnosis of this condition to be made. • The painful distress and controversial potential for malignant transformation of this lesion makes its fast and accurate diagnosis by the attending clinician important.

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