| What is Lichen Planus? | Mucocutaneous inflammatory disease of unknown origin, skin and oral mucosa most frequently involved, or other mucus membranes (genital/esophagus) and skin appendages (scalp, hair, nails).
May be one or several areas involved, among men 0.3% cutaneous LP, 1.5% oral LP, women 0.1% and 2.3%. |
| How is LP epidemiology? | Women 60-75% of pt of oral LP, and 50% of cutaneous LP, mean age 50-60 for oral and 40-45 cutaneous.
LP is uncommmon for children <5% |
| What is cutaneous LP? | Widespread eruption of violaceious shiny, isolated flat topped papule and plaques, most profuse on the ankles and lumbar region.
Legs and neck also involved.
Polygonal, violaceious papules w/lacelike white line network most frequently in inner wrist |
| What is oral LP? | Bilateral symmetric lesions associated with a network of white-lined plaques and erosive lesions in posterior oral mucosa and top of tongue.
Areas affected usually posterior cheek (74% male, 91% female), gingiva (33% 57%) and tongue (44%, 54%)
Considered a premalignant condition, 1% cause squamous cell carcinoma, risk factors include alcohol and smoking |
| What is male LP? | • A white-line network within a papule or plaque on the glans penis. In men with skin damage
• Annular papules of the glans
• Rarely linear white streaks |
| What is female genital LP? | • Vulva: reticulate papules or severe erosion
• Dyspareunia, Burns, itching, vulvar, urethral stenosis
• 50% of the women with oral LP have not screened genital impairment!
• The vagina is involved in about 50% of cases and the perianal area in about 20% of cases
• Case reports have also described squamous-cell carcinomas arising from chronic anogenital, esophageal, or hypertrophic cutaneous lichen planus lesions. |
| What is nail LP? | • Present in 10% of the LP
• Thinning of the ungual blade causing grooves and dystrophiy
• Hyperpigmentation
• Onycholysis
• Melanonychia
• Subungual Hyperkeratosis
• Rarely matrix destruction with pterigium
• Children: idiopathic onychoatrophy affecting
10 nails
• Nail thinning, with longitudinal ridging and distal splitting linked to matrix involvement in these two fingernails
• Fingernails are involved more frequently than toenails |
| What is trachyonychia? | • Nail LP-induced TND is typically seen inchildhood
• It has also been described in adults inassociation with gold allergy
• It is characterized by brittle, thin nails, withexcessive longitudinal ridging, pitting, and onychoschizia
• It can be of two types, namely severe, opaquetype trachyonychia, seen as diffusely ridged,thickened nails with lack of luster and asandpaper-like surface, or a milder, shiny typewith numerous, small superficial pitsimparting a shiny nail plate surface |
| What is yellow nail syndrome? | • YNS) was first described by London physicians Peter Samman and William White in 1964
• Marked thickening and yellow to yellowish green nail discoloration which is often associated with systemic disease, most commonly lymphedema (80%) and lung disease
• The nails are typically over curved in both transverse and longitudinal directions and grow very slowly
• There is often onycholysis. There is loss of the lunula and cuticles |
| What is scalp LP? | AKA Lichen Planopilaris.
• Follicular, violaceous erythema and acuminate keratotic plugs surrounding the zone of alopecia
• The plaques are multifocal and occur most frequently on the vertex; other hairy areas can also be involved
• Follicular and perifollicular, purple, scaly pruritic papules
• Atrophic scarring alopecia can appear several weeks after the disappearance of the papules!
• Pseudopelade |
| How is histopathology of LP? | • Thickening of the stratum corneum
• Orthokeratosis and parakeratosis
• Accentuation of the granular-cell layer liquefactive degeneration of the basal-cell layer
• Bandlike inflammatory-cell infiltrate, lmyphocytic and lichenoid infiltrate (hematoxylin and eosin) |
| Why is LP a burden disease? | • Lichen planus has adverse effects on both quality of life and psychological status
• Factors that contribute to these detrimental effects include pruritus, pain and difficulties with eating and with sexual function in association with mucosal disease |
| How is pathophysiology of LP? | • The pathogenesis of lichen planus remains unclear, it appears to be an autoimmune disease
• The basal keratinocyte degeneration observed in LP is attributed to cytotoxic CD8+ T lymphocytes, which are the major component of the infiltrates located within the epithelium and adjacent to damaged keratinocytes
• The triggering antigen is not known
• The existence of rare cases of familial lichen planus and the over representation of certain HLA haplotypes (HLA-DR1 in cutaneous LP) suggest that genetic factors have a role in susceptibility to this disease
• Several autoimmune disorders, particularly alopecia areata and ulcerative colitis have been reported to occur more frequently in patients with lichen planus than in control populations
• There is a significant association between LP and infection with hepatitis C virus (HCV) |
| What are outcomes of LP? | • Body: pruritus. Spontaneous healing, usually within 1 year. Long-lasting residual pigmentation
• Oral LP: Soreness, pain, burning, swelling, irritation, bleeding; isolated reticular form usually asymptomatic. Poor tendency to heal spontaneously in about 2.5%. Periods of exacerbation
• Genital LP: Burning, itching, pain, dyspareunia, impaired sexual function. Vulvar scarring in erosive forms (95% frequency), synechiae with vaginal stenosis and labia minora agglutination in females, phimosis in males
• Scalp LP: Chronic and progressive; atrophic, scarring alopecia with absence of follicular units
• Nails LP: Recovery with treatment, but with frequent relapses; in rare cases, nail loss or pterygium unguis (permanent advancement of medial skin over the nail plate, bisecting the nail) |
| How is tx of LP? | • Cutaneous LP: Potent topical corticosteroids. If ineffective, oral glucocorticoid (GC) for 18 weeks (20-30 mg/day). Phototherapy using narrow-band ultraviolet B therapy had a complete response within a mean of 11 weeks
• Oral LP: Reticular oral LP is usually asymptomatic and does not require treatment. For erosive oral LP: topical GC are the 1st line therapy; topical retinoids, cyclosporine. if resistance, oral GC 0,1 to 0,5mg/kg/d for 4 to 6 weeks
• Anogenital LP: Topical potent corticosteroids
• Nail LP: intralesional injection. Oral GC
• Scalp LP: Topical GC. Topical, intralesional GC |
