post graduate at narayana medical college

1. LICHEN PLANUS
AND
LICHENOID DISORDERS
-Dr M.HIMA VINUTHNA
M.D (DVL) PG

2. LICHEN PLANUS
Idiopathic,Chronic,Inflammatory disease that
affects the Skin,Mucous membranes and
Appendages.

3. MORPHOLOGICAL
• Extremely pruritic
• Flat topped
• Polygonal
• Violaceous papules and plaques

4. • Compact hyperkeratosis
• Wedge shaped hypergranulosis
• Irregular acanthosis
• 'Saw-toothing' of rete ridges
• Vacuolar degenerationof basal epidermalkeratinocytes
• Band like infiltrate that often obscures the DEJ
 HISTOLOGICAL
• Degenerative keratinocytes (colloid bodies) in the lower
epidermis
• Ocassionally,space between epidermis and dermis (Max-
Joseph space) seen due to interface inflammation

5. EPIDEMIOLOGY
 FREQUENCY - 0.1-4%
 DISTRIBUTION – World wide
- High prevalence rate in Indian subcontinent.
 RACE – Not significant.
 SEX – Not significant
- But females are affected earlier than males.
 AGE – Can occur at any age but more in people aged between 30-60 years.
 FAMILY HISTORY – Positive family history in childhood LP cases than adult LP cases.
 INVOLVEMENT –Mucous membrane -30-70%
- Nail-10%

6. ETIOLOGY
Auto immune
Drugs
T-cell theory
Infections &
vaccines

7. o Auto immune theory: increased association between LP & other auto
immune diseases such as -Ulcerative colitis
-Myasthenia gravis
-Lupus erythematosus
-Alopecia areata
-Diabetic mellitus
o Infections & vaccines: Hepatitis C & B
Killed Influenza
MMR
DPT

8. o Drugs:

9. o T-Cell Theory(CD4+,CD8+,Th17): Induces production of chemokines and
other cytokines which upregulate local inflammatory infiltrate.

10. PATHOGENESIS
 Autoimmune
 Familial
 Viruses
 Dental Amalgam
 Miscellaneous

11.  Autoimmune
 T-cells
CD4+
CD8+
Th17
 Cytokines
IFNγ
TNFa
NF-kB
IL-1a,IL-6,IL-8
Fas/2 Apo-1 &
Bcl-2

12.  Familial : HLA-B7(1)
HLA-28
 Viruses : Hepatitis C virus
 Dental Amalgam :
• Dental restorative materials containing silver-Mercury compounds have
known to induce oral lichenoid lesions.
• Allergens that elicit a positive reaction are-
 METALS – Silver,Mercury,gold,nickel,palladium
 CEMENT – Eugenol,potassium dichromate,cobalt chloride
 PERFUME – Balsam of peru
Miscellaneous : Anxiety,Depression,Stress
Radiotherapy

13. CLINICAL FEATURES
 CLASSIC FORM :
• Extremely pruritic,flat topped,
polygonal,violaceous papules
and plaques of size 3-15mm in
diameter
• Delicate radiating white scales
(wickham’s striae)
• Positive koebner’s phenomenon
 SITES INVOLVED :
• Flexor surface of wrist and forearms
• Dorsal surface of hands
• Anterior aspect of lower legs
• Neck and lower back

14. VARIANTS OF LICHEN PLANUS
 MORPHOLOGY
HYPERTROPHIC ATROPHIC
EROSIVE / ULCERATIVE
ERUPTIVE / GUTTATE
FOLLICULAR / LICHEN PLANOPILARISVESICULOBULLOUS
ACTINIC
LP PIGMENTOSUS
 CONFIGURATION
ANNULAR
LINEAR
 DISTRIBUTION
ORAL
OESOPHAGEAL
MUCOSAL
GENITAL
INVERSE
PALMOPLANTAR
NAIL
 SPECIAL
LP- LE OVERLAP SYNDROMELP PEMPHIGOIDES
CONJUNCTIVAL

15. MORPHOLOGY
1. HYPERTROPHIC LP
• Shin and Ankles
• Extremely pruritic
• Thicked and Elevated,Pruritic or reddish brown
• Hyperkeratotic
• Ocassionally,with time they form thick verrucous
plaques & central depigmentation
• SCC in long standing cases.
• Psedoepitheliomatous hyperplasia
• Compact hyperkeratosis
• Irregular acanthosis
• Interface infiltrate less band-like
• Cystic dilatation of hair follicles
DD : Nodular prurigo, LSC, Lichen Amyloidosis,
Warts

16. 2. ATROPHIC LP
• Lower limbs
• Occurs after resolution of typical LP
• They start as violaceous papules &
coalesce to form large plaque with
depressed atrophied centre
• Thinning of epidermis upto granular layer
• Fibrosis of papillary dermis
• Effacement of rete ridges
• Fewer colloid bodies
DD : Lichen sclerosus et atrophicus, Morphea

17. 3.EROSIVE/ULCERATIVE LP
• Mucosal surfaces of oral cavity and
genatalis. Rarely- Palms and Soles
• Aggressive form of LP & may end to SCC
• Presence of erosions on surface of
papular lesions
• Epidermal ulceration with typical changes of LP at
margin of the ulcer

18. 4.ERUPTIVE/GUTTATE LP
• Trunk, inner aspect of wrist, dorsum
of feet.
• Acute or Exanthemous LP
• Widely distributed & Disseminated
lesions
DD:Guttate psoriasis
Pityriasis lichenoides chronica
papulosquamous secondary syphilis

19. 5.FOLLICULAR LP/LPP
• Frontocentral scalp and Crown
• Women
• Lesions are multifocal and eventually may
coalesce to produce large area of hairloss;
underlying skin is hypopigmented and devoid
of follicular ostia
• Perifollicular erythema and perifollicular scales
are typically present at the periphery of active
lesions.
• Disease activity is greater at periphery of
alopecia patch.
• LPP usually presents as irregular patchy
haiross, with loss of follicular ostia, a hallmark
of cicatricial alopecia
• Moderate to severe scalp pruiritis and
dysesthesia are common.
RARE VARIANTS OF LPP:
• Graham-Little-Piccardi-Lassueur Syndrome
• Frontal Fibrosing Alopecia

20. • Compact orthokeratosis.
• Dilated follicular infundibula filled
with hyperkeratosis.
• Slight hypergranulosis.
• Atrophic follicular epithelia with
perifollicular fibrosis and new
collagen formation.
• Dense lichenoid infiltrate of
lymphocytes and histiocytes at DEJ of
the upper portion hair follicles.
• Prominent vacuolar degeneration &
keratinocytic necriosis of basal layer
DD : SKIN - lichen nitidus,lichen spinulosus
SCALP - DLE, cicatricial
pemphigoid,PIF,alopecia areata

21. 6.VESICULOBULLOUS LP
• Shin,upper limbs and thighs
• Development of bristles within the
papules of LP due to severe
liquefactive degeneration of basal
layer of epidermis
• Typical histopathological changes of LP with
subepidermal bulla.
• There is a heavy dermal infiltrate with
numerous colloid bodies.

22. 7.ACTINIC LP
• Forehead and Face followed by dorsal
surface of Hands and Neck.
• Young adults and children
• Summer
• Lesions are blue,brown plaques that show
annular configuration with atrophied
centre and hypopigmented raised border
• Epidermis is atrophic at centre of lesion
• Focal parakeratosis.
• Melanophages are more abundant
• Pigment incontinence more intense
DD: PMLE
HISTOLOGY

23. 8.LP PIGMENTOSUS
• Sun exposed areas and flexural folds
• Seen in skin types 3 & 4
• Slate grey to brownish-black macules
• Diffuse pattern of pigmentation is more
common
• Prominent pigment incontinence extending to the
reticular dermis
• Inflammatory infiltrate less prominent
DD:Erythema dyschromicum perstans

24. CONFIGURATION
• Glans penis or trunk
• Typical violaceous papules arranged
in ring like fashion or a single large
plaque showing central clearing.
• Most unusual variant- ANNULAR
ATROPHIC LP
1.ANNULAR LP (Ring-like lesion)
DD : Granuloma annulare

25. 2.LINEAR LP
• Limbs, Trunk
• Lesions are in linear pattern along
the Lines of Blaschko.
• Not to be confused with koebner
phenomenon
DD: Lichen spinulosus
linear verrucous epidermal naevus

26. DISTRIBUTION
• Buccal mucosa,lateral margins of
tongue,Gingiva,Lips & Hard Palate
• MORPHOLOGICAL TYPES:
A) ORAL LP:
1.MUCOSAL LP
o Reticular
o Plaque- like
o Bullous
o Atrophic
o Erosive
o Papular
• Reticular oral LP-
Assymtomatic,irregular,atrophic plaques
with white streaks in a lacy pattern
involving posterior buccal mucosa
bilaterally
• Dental amalgam materials cause oral LP
• Stress,spicy and acid foods flare-up the
disease.
DD: leuloplakia, oral pemphigus

27. B) GENITAL LP:
• Males- Glans
penis,shaft,prepuce,srotum
• Females- Vulva,vagina
• Annular lesions more common in men
• Vulval introital erosions surrounded by
white,lacy,reticulate borders extending
onto vagina.
DD: Males-psoriasis,lichen sclerosus et
atrophicus
Females- leukoplakia,lichen sclerosus
et atrophicus

28. • Rarely involves esophagus
• Middle aged women
• Dysphagia, Odynophagia or both
• Esophageal stricture & SCC
• Endoscopy to be done
C) OESOPHAGEAL LP:
D) CONJUNCTIVAL LP :
• May manifest as cicatricial conjuctivitis

29. 2.NAIL LP
• Most common in
adults(50-60years)
• Usually affect several or
most nails with a chronic
course
• Finger nails nails more
commonly affected than
toe nails.
• PUP- TENT Sign

31. • Unusual changes of LP
• Granular layer is present
• Colloid bodies are rare
DD: Onychomycosis,nail psoriasis
HISTOLOGY

32. 3.PALMOPLANTAR LP
• Internal plantar arch and palms with
sparing of finger tips
• Young Men aged between 20-40yrs.
• Highly Pruirigenous, Erythematous,Scaly
Plaques with or without Palmoplantar
Keratoderma.
DD: Callosities,Warts,Secondary Syphillis

33. 4.INVERSE LP
• Axillae,groin,cubital and popliteal
fossa.
• Reddish brown,discrete papules and
nodules

34. SPECIAL FORMS
1. LP PEMPHIGOIDES
• Distal limbs
• Tense blisters occurs both on LP lesions
and unaffected skin
• DIF shows linear deposition of IgG & C3
along the BMZ
• On uninvolved skin :
o Sub epidermal bullae
o Dermal infiltrate not band like
o Plenty of eosinophils
• On LP:
o Features same as LP
o Few neutrophils and eosinophils.
DD: Bullous LP

35. 2.LP-LE OVERLAP SYNDROME
• Patients have overlapping clinical,
histological & immunological
features of LP-LE.

37. DIAGNOSIS
 Based on the characteristic clinical and histological features.
 DIF reveals ragged or shaggy fibrin BMZ band.
 Globular deposition of colloid bodies staining with IgM mainly & lesser extent
with IgA, IgG, C3 is seen in upper dermis.

38. TREATMENT
 1ST LINE THERAPY – TOPICAL CORTICOSTEROIDS
-1ST GENERATION ANTI-HISTAMINES (Hydroxyzine&Chlorphenaramine)
-INTRALESIONAL STEROIDS (Hypertrophic,NLP,Erosive LP)
-IMMUNOMODULATOR (Tacrolimus&Pimicrolimus)
-TOPICAL MINOXIDIL (LPP)
 2ND LINE THERAPY – SYSTEMIC CORTICOSTEROIDS
ORAL- Oral prednisolone(0.5-1mg/kg/day) for 4-6weeks
or
-Oral minipulse therapy with Betamethasone
IM- Triamcinolone (40-80mg) every 6-8 weeks
- ORAL RETINOIDS – Acitretin 30mg daily for 8 weeks
- PHOTOTHERAPY – NVUVB/PUVA
CUTANEOUS LP

39.  3rd LINE THERAPY – IMMUNOSUPPRESSIVE AGENTS
Methotrexate-10-15mg/week (Severe Erosive & Generalized LP)
Cyclosporine- 5mg OD for 4-6 wks (LPP)
Others-Azathioprine, Cyclophosphamide, Myophenolate mofetil
MUCOSAL LP:
 1st LINE THERAPY – TOPICAL STEROIDS-Clobetasol propionate (Oral LP)
ILS (Localised chronic ulcerative LP)
TOPICAL TACROLIMUS&PIMICROLIMUS (ulcerative cases)
 2nd LINE THERAPY – Hydroxychloroquine(Oral LP)
- Local phototherapy-NVUVB,PUVA(Oral LP)

40. COURSE
 Skin lesions subside in about 24months in majority of patients, but in 20% of
patients they relapse
 Eruptive LP for short course with remission in 3-9 months
 Oral,Hypertrophic, LPP- protracted course

41. LICHENOID DISORDERS
 Conditions which simulate lesions of LP clinically are called Lichenoid Disorders. They
include
1. Lichenoid Drug Eruptions
2. Lichenoid Contact Dermatitis
3. Lichen Striatus
4. Lichen Nitidus
5. Lichen Spinulosus
6. Benign Lichenoid Keratosis
7. Nekam’s Disease
8. Frictional Lichenoid Eruption
9. Graft Vs Host Disease

42. LICHENOID DRUG ERUPTIONS
• Many drugs may induce lichenoid dermatitis and lesions develop over weeks to months after
starting the therapy.
• Resembles LP on clinical & Histological basis

43. LICHENOID CONTACT DERMATITIS & MUCOSITIS
 Chemicals which induce LCD are- Methacrylic Acid,nickel,silver,gold,musk Ambrette,dental Restorative
Materials,developers used in processing color films.
 Lesions start at site of contact and may spread subsequently
 Intra oral metal contact allergy occur due to contact with Dental Amalgam materials result in Mucositis
 Resolution after removal of Dental Amalgum
 SITES- Buccal Mucosa and Tongue adjacent to amalgum
Histopathology That Distinguish Amalgum Associated Oral Lichenoid Reaction From Oral LP Are :
1. Inflammatory infiltrate locater deeper in interface infiltrate on some or all areas.
2. A focal perivascular infiltrate
3. Plasma cells & neutrophils in connective tissue

44. LICHEN STRIATUS
• Uncommon,benign,self limiting,linear,inflammatory
dermatoses of unknown etiology
• They are shiny,flat topped,erythematous papules-cluster in
a continuous or interrupted linear pattern of width 1-3cm
• Along the lines of Blaschko’s.
• Unilateral & solitary
• Common site-Legs.
• Sudden in onset and progress to clinical picture in days to
weeks.
• Symptoms – Intense pruiritis
• Nail involvement-
o Onychodystrophy and sub ungual hyperkerstosis.
o Restricted to single lane and limited to medial or lateral
portion.
• Hair involvement- transient focal hairloss

45. ETIOPATHOGENESIS
• Combination of genetic and
environmental factors
• Viral infection or immunization
may trigger onset of LS.
• Strong association of atopy
• Happle proposed a theory of
epigenetic mosaicism • Epidermal hyperkeratosis
• Focal parakeratosis
• Band like lymphohistiocytic infiltration of dermis-
this surrounds eccrine sweat glands and duct
DIF: Civatte body staining with IgM,IgG
C3-negative in LS

46. TREATMENT
• Spontaneous resolution
• Topical corticosteroids to hasten
resolution
• Topical Tacrolimus for no risk of
skin atrophy that is seen with
steroids.

47. LICHEN NITIDUS
• Benign inflammatory skin disorder of
unknown etiology
• Children
• Numerous,pin point to pin head cells
sized,flesh to pink colored papules with
flat and shiny surface and localized
• Exhibit Koebner phenomenon.
• Abdomen,chest,penis&flexural surface of
extremities

48. • Mucosal involvement- rare.
but if present-
discrete,grouped,yellowish papules
of 1mm on hard palate and gum.
• Nail involvement- longitudinal
beaded ridges,terminal splitting &
irregular pittings
Clinical variants :
 Confluent
 Vesicular
 Haemorrhagic
 Palmoplantar
 Spinous
 Follicular
 Perforating
 Actinic- summertime actinic lichenoid
eruption
 linear
• ‘Claw clutching a ball’
• Ball represents-well circumscribed area
of lymphohistiocytic infiltrate in
papillary dermis close to DEJ.
• Claw represents- elongated rete ridges
near the margins.
• Epidermis often thinned out.

49. DD: Keratosis pilaris,lichen
spinulosus,verruca plana
TREATMENT
• Spontaneous resolution in 1year
without scarring or pigmentary
changes
• Therapeutic mordalities-
PUVA,NBUVB,Systemic
steroids,itraconazole,isoniazid.

50. LICHEN SPINOSUS
• Idiopathic disorder
• Children and adolescents
• Males
• Skin colored and asymptomatic,scattered
2-6cm patches of keratotic follicular
papules.individual papules have hair like
horny spine that gives NUT MEG GRATER
feel on palpation.
• Etiology-Atopy and genetic factors.
• Treatment- emollients,midpotency topical
corticosteroids,salicylic acid,12%lactic
acid,tretinoin gel(0.04%

51. BENIGN LICHENOID KERATOSIS
• LP-Like keratosis
• 5th and 6th Decade
• Women
• Upper Trunk and Extremities
• Single,slightly raised, grayish brown or red-
brown papule or plaque with 3-19mm
diameter
• Histopathology: similar to LP
ocassionally reminiscent
of seborrheic keratosis or solar lentigen seen
at periphery of lesion.

52. KERATOSIS LICHENOID
CHRONICA (NEKAM’S
DISEASE)
• Adults btw age 20-40 yrs.children occasionally
• Violaceous,papular & nodular lesions arranged in
linear and reticulate pattern
• Extremities,buttocks,face
• Extensive disease-antecubital fossae,externsor
aspect of forearms forearms,lumbosacral
area,buttocks,posterior aspect of thigh,popliteal
fossae
• Oral manifestations-recurrent aphthous
ulcers,large chronic ulcers,erythrokeratotic papules
• Nail manifestations-thickened,longitudinal
ridging,prone to paronychia

53. HISTIOPATHOLOGY-Diffuse
from LP by presence of
TREATMENT
• Focal parakeratosis
• Alternating areas of acanthosis
and epidermal thinning
• Heavier upper dermal infiltrate
• Presence of plasma cells
• PUVA alone or in combination
with retinoides
• Topical calcipotriol,oral isotretin
and combination of tacalcitol &
acitretin are benefited

54. FRICTIONAL LICHENOID
ERUPTION
• Children between 2 & 12 yrs of age
• Male:female-3:1
• Flat,lichenoid,reddish to skin colored papules,1-
2mm in diameter that often coalesce
• Elbows,knees,dorsum of hands and fingers
rarely-cheeks and buttocks.
• H/O Atopy
• Pathogenesis- Contact with an abrasive material
• Histology- Slight hyperkeratosis,Acanthosis & a
perivascular,peri adnexal,lymphocytic infiltrate in
upper epidermis that does not reach DEJ.

55. GRAFT VERSUS
HOST DISEASE
• Frequent complication of allogenic bone
marrow transplantation,heart or liver
transplantation and after blood
transfusion
• DIFFERENT FORMS:
1.Acute GVHD
2.Chronic GVHD

56. 1.ACUTE GVHD
• Occurs during the first 3 months
following bone marrow
transplantation
• Target organs-skin,GIT,liver
• Cutaneous eruptions-mild,morbilli
form rash with acral accentuation or
rarely a severe toxic epidermal
necrosis
• They develop spontaneously or
triggered by UV radiation,physical
trauma or infections

57. 2.CHRONIC GVHD
• Develop after 3rd month following
transplantation
• TH2 cytokine play a predominant role in
pathogenesis
• Cutaneous eruptions may appear in
continuity of previous acute GVHD
• Skin and mouth are involved
• Cutaneous manifestations- 1.Lichenoid
2.sclerodermoid

58. 1.LICHENOID GVHD
• Violaceous papules and plaques that
resemble idiopathic LP
• Sites-Periorbital region,ears,palms and soles.
• Nails and oral lesions similar to that of
idiopathic LP.
• Genital mucosa may be affected with
development of phimosis and vaginal
strictures.
• Treatment-combination of corticosteroids
and immuno-suppressants like
azathioprine,cyclosporine,methotrexate.
High dose Thalidomide( 200-
800mg/day)
PUVA THERAPY,NVUVB are tried in
management of chronic GVHD

59. REFERENCES
 IADVL
 Rook’s text book of dermatology
 Fitzpatrick Dermatology in GM
 Articles-ijdvl,aad