Oral lichen planus


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Oral lichen planus

  1. 1. Oral Lichen Planus Dr . Gaurav S. Salunkhe 2ND MDS
  2. 2. Introduction  Oral Lichen Planus  A chronic inflammatory disease that causes bilateral papules, striations or plaques  May cause erythema, erosions and blisters  Found on buccal mucosa, tongue and gingiva  Female:Male ratio: 1.4:1  Predominantly seen in adults over 40 years.  0.5% to 2% of general population  Affects all ethnicities
  3. 3. Picture 1: Plaque-like OLP Picture 2: Reticular OLP Picture 3: Erosive OLP Picture 4: Reticular OLP
  4. 4. Pathogenesis of Reticular LP  Oral Lichen planus is a purely T cell mediated inflammatory response.There are no B cells, plasma cells and no deposits of immunoglobulin or complement.  The trigger for keratinocyte apoptosis in OLP is, for the most part, unknown. However, the lymphocytic infiltrate in OLP is composed almost exclusively of T cells, and the majority of T cells within the epithelium and adjacent to damaged basal keratinocytes are activated CD8+ lymphocytes. Therefore, it is very probable that cytotoxic T cells trigger keratinocyte apoptosis in OLP.
  5. 5. Proposed Immunopathogenesis of OLP  A lichen planus-specific antigen is expressed in conjunction with MHC class 1 molecules on keratiocytes at the OLP lesion site.  Antigen specific CD8+ T cells are activated in 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), which recruit lymphocytes from the local microvasculature and cause migration toward the epithelium.
  6. 6.  This hypothesis predicts that the 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 MMP-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.  This hypothesis predicts that the earliest events in OLP lesion formation are confined to the epithelium and that basement membrane and connective tissue changes occur secondarily.
  7. 7. Clinical Presentation  Oral lesions-more persistant and resistant to treatment than skin lesions 30-50% of pts also have cutaneous lesions Three common types  Reticular  Erosive  Plaque Variants of Plaque and Erosive types Atrophic Bullous
  8. 8. Clinical Presentation  Reticular lesions Most common type Interlacing white kerototic lines w/ erythematous borders (Wickham’s striae) Typically bilaterally on buccal mucosa, mucobuccal fold and gingiva Less common on tongue, palate and lips Assymptomatic
  9. 9. Clinical Presentation  Erosive lesions  2nd most common type  Mix of erythematous and ulcerated areas sorrounded by radiating keratotic striae  Similar appearance to candidiasis, pemphigus and lupus  Lesions tend to migrate and often multifocal  Mostly buccal mucosa and vestibule  Symptomatic:  Sore mouth sensitive to heat, cold, spices, and alcohol  Pain and bleeding on touch  Plaque lesions - Resemble focal leukoplakias - Vary from smooth flat areas to raised irregular plaques - Often multifocal - Dorsum of tongue and buccal mucosa
  10. 10. Clinical Presentation  Variants of Erosive and Plaque lesions Atrophic  Diffuse, erythematous patches  Causes significant discomfort  Gingiva and buccal mucosa Bullous  Intraoral bullae on buccal mucosa and lateral surface of tongue  Rupture soon after appearance resulting in classic appearance of erosive lesions
  11. 11. Diagnostic tests  Clinical exam: for reticular LP with characteristic appearance of Wickham’s striae or annular pattern on erythematous background  Histological and Direct Immunofluorescent examinations: for plaque and erosive LP because they can resemble other mucosal lesions including malignancy
  12. 12. Diagnostic tests  Histological exam  Requires biopsy  Varies based on the type of lesion  Typically: epithelial hyperplasia, orto and para keratosis, acanthosis, atrophic areas w/ loss of rete pegs, dense accumulation of T-lymphocytes in the basilar cell layer  Direct Immunofluorescent examination  Requires biopsy  Differentiates between other autoimmune conditions  Detects shaggy deposition of fibrinogen along the basement membrane
  13. 13. Histology: Reticular Lichen Planus  Consists of local areas of epithelial hyperplasia in which the surface contains a thick layer of orthokeratin or parakeratin.  The spinous cell layer may be thickened (acanthosis) with shortened and pointed rete pegs. The thickened areas are seen clinically as Wickham’s striae.  Between these areas the epithelium is thinned (atrophic), with loss of rete peg formation.  The adjacent underlying c.t. contains a thin, dense accumulation of T lymphocytes that move through the basement membrane and are observed in the basilar and parabasilar cell layers of the epithelium.
  14. 14. Histology: Erosive Lichen Planus  Exhibit an extensively thinned epithelium with areas of complete loss of rete peg formation and a dense infiltrate of T lymphocytes.  This T lymphocyte infiltrate obscures the basement membrane and extends well into the middle and upper levels of the epithelium.  Liquefaction of the basement membrane and destruction of the basal cells is present in most areas.  Occasionally, subepithelial separation will be present. Often, the epithelium is lost, exposing the underlying connective tissue.  The lymphocytes are confined to a narrow zone in the upper layers of the connective tissue.
  15. 15. Histology: Plaque Lichen Planus  Plaque LP resembles the histology of reticular LP because of the striae pattern but it lacks the intermittent atrophic areas of the epithelium.  It consists of generalized hyperorthokeratosis or hyperparakeratosis combined with acanthosis.  There may be loss of rete pegs at the epithelial and connective tissue interface or alteration of their shape into a “saw-tooth” pattern.  The basement membrane is noticeably thickened.  The band of T lymphocytes present in the superficial connective tissue is more sparse than In reticular LP, with only occasional cells found in the lower levels of the epithelium.
  16. 16. Treatment of OLP  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
  17. 17. Treatment of OLP  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
  18. 18. Treatment of OLP  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% dhlorhexidine gluconate may help reduce fungal infection during corticosteroid therapy
  19. 19. Alternative Treatment of OLP  0.1% topical tacrolimus ointment 2x/day  Tacrolimus: immunosuppresive macrolide Suppresses T-cell activation  Intraoral ulceration resolved after 3 months of daily application  Remission for 1 year without maintenance