Chronic Inflammatory dermatoses: -Psoriasis -Lichen Planus -PEMPHIGUS VULGARIS -BULLOUS PEMPHIGOID -Dermatitis Herpetiformis

1. Chronic Inflammatory dermatoses

2. Psoriasis
• A chronic disorder characterized by scaly,
erythematous plaques
• Presents as salmon color plaques with silver
color scales
• When the scale is picked off-see pinpoint
bleeding sites (Auspitz sign)
• Site: scalp, pressure areas
• Koebner’s phenomenon – Psoriasis can be induced in
susceptible individuals by local trauma
• Nail changes (50% of cases)

3. Psoriasis

4. Pitting of the Nails in Psoriasis
Pitting is a result of the loss of parakeratotic cells from the surface of the nail plate.

5. Psoriasis
• Characteristic histologic features
– Hyperkeratosis & Acanthosis
– Absence of the stratum granulosum cells
– Parakeratosis
– Regular, club-shaped elongation of the rete pegs
with vessel proliferation in the papillary dermis
(reason for Auspitz sign)
– subcorneal collection of neutrophils called a
Munro’s microabscess (diapedesis from vessels in
papillary dermis)

6. Psoriasis
• Note the parakeratotic scale. Psoriasis and
similar lesions are characterized by uniform
elongation of the rete ridges as seen here.

7. Psoriasis
• Note parakeratotic scale, elongate rete ridges, and
prominent thin-walled vessels in the papillary dermis.

8. Psoriasis
• Munro’s abscess

9. Pathogenesis
• genetic and immune
• Hypersensitivity to stratum corneum antigens
and complement mediated reaction
• Sensitized T cells infiltrate the skin and secrete
cytokines and growth factors
– Increased cell turnover
– Inflammatory infiltrate
– Vascular proliferation

10. Lichen Planus
• Self-limited chronic disorder
• Characterized by intensely pruritic, scaly, violaceous,
flat-topped papules on the wrists, lower back, legs
and scalp (3 P’s)
• Lichen planus may occur in the oral mucosa (50%)
• Papules are highlighted with white dots or lines
(wickham striae)
• Like psoriasis, koebner phenomenon can also be
observed in LP

11. Lichen Planus
• 3 P’s – Purple, Polygonal, Pruritic Papules

12. Lichen Planus
• Micro:
• hyperkeratosis,
• prominent granular layer (Hypergranulosis),
interface
• lichenoid dermatitis (band like infiltrate of
lymphocytes), and typical basal “saw tooth”
pattern of the rete ridges

13. Lichen Planus
• Hypergranulosis
• “Saw tooth” rete
• Band like
infiltrate of
Lymphocytes

14. Lichen Planus
• Note prominent granular layer, interface dermatitis, and
typical basal “saw tooth” pattern. In addition, note
necrotic keratinocytes in the basal layer.

15. LP - Pathogenesis
– ?immunologic – release of antigens in basal layer
and dermo-epidermal region eliciting a cell
mediated immune response

16. Inflammatory Blistering (Bullous)
Diseases

17. BLISTERING DISEASES
• Subcorneal
• Suprabasal
• Subepidermal

18. Blister Formation

19. PEMPHIGUS VULGARIS
• Chronic Auto-immune blistering disorder
• Pathogenesis : Auto-antibodies against
desmosomes (Acantholysis of Sq cells)

20. PV

21. Deposition of Igs & Complements

22. Pemphigis Vulgaris
• 40-60 yrs
• Clinical : Large blisters
in skin and mucus
membranes
• Nicholsky sign: After
rubbing the skin of patients with
pemphigus, which caused a
blistering or denudation of the
epidermis with a glistening,
moist surface underneath.

23. Pemphigis Vulgaris - SUPRA Basal blister
• Acantholysis
• Tombstone
like Basal
cells

24. Pemphigus vulgaris

25. Pemphigus vulgaris
• Fishnet pattern
immuno-
flourescence

26. BULLOUS PEMPHIGOID
• Chronic Auto-immune blistering disease clinically
similar to PV.
• Pathogenesis:
• No Acantholysis
• Auto-antibodies target Hemidesmosomes
(against Bullous Pemphigoid antigen)
• Results in SUB EPIDERMAL blister
• Eosinophils are often prominent in the superficial
dermal infiltrate.

28. Bullous Pemphigoid
• Older Pts
• Multiple Bullae
• (Nikolsky’s sign)
is negative***
because there
is no
acantholysis.

29. Bullous Pemphigoid
• Higher power of sub-epidermal bulla with serum and
degenerating eosinophils. Note bulla is non-
acantholytic

30. Bullous Pemphigoid

31. Bullous Pemphigoid
• Linear deposition of IgG & C3 in the basement
membrane as seen in this immunoflourescent
image is typical of bullous pemphigoid.

32. Dermatitis Herpetiformis
• Grouped papules and vesicles
• Intensely pruritic
• May be associated with a
gluten-sensitive enteropathy
• Immune mediated disease
characterized by a granular
deposition of IgA along the
basement membrane zone of
the epidermis (anchoring
fibrils).
• These patients often respond
to gluten free diet

33. Dermatitis Herpetiformis

34. Dermatitis Herpetiformis
• Histology: Subepidermal vesicle with aggregates of
neutrophils at the tips of dermal papillae
(Microabscesses). With immunofluoresence IgA can be
demonstrated in these areas.

35. Infections

36. Cutaneous Warts
• Common wart (verruca
vulgaris): typically occur
on hands flat-topped
papules on hands and
face
• Caused by infection with
various strains of the
human papillomavirus
(HPV)

37. Veruca Palmaris

38. Warts
• Note the prominent granular layer and
presence of perinuclear halos.

39. Fungal Infections - Dermatophytes
• Scaly patches and plaques, often annular in
configuration
• Sites include scalp (tinea capitis), body (tinea corporis),
groin (tinea cruris), feet (tinea pedis), hand (tinea
manuum), face (tinea faciei), nails (onychomycosis).

40. Impetigo