This document summarizes various skin diseases and their oral manifestations. It describes different skin lesions such as macules, papules, nodules, plaques, vesicles, bullae, pustules, and vascular changes. It then discusses specific diseases including ectodermal dysplasia, white sponge nevus, hereditary benign intraepithelial dyskeratosis, pemphigus, cicatrial pemphigoid, bullous pemphigoid, erythema multiforme, lupus erythematosus, and systemic sclerosis; and their oral signs and symptoms, histopathological features, and treatments.

1. SKIN DISEASES

3. Introduction
• Few basic principles – critical in understanding
the interpretation of physical signs
• These principles arise from the morphological &
functional diff of the 3 main levels of the skin
Epidermis
Dermis
S/C fat

4. Discrete flat lesion, not raised above the adjacent
normal skin
Large macule – patch
Size limit at which a macule becomes a patch
varies in diff texts – 1.5-2cms
Usually darker red or brown than normal skin,

5. Papules & nodules –
Discrete lesions – usually visibly raised above the
skin surface
Nodules – may also lie deep to the dermis –
lipoma
Size at which the a papule should be called a
nodule – varies 5-10mm
All nodules starts as papules but not all papules
will grow into nodules

6. Plaques –
Raised lesion with a flat top
Scaling frequently present
E.G – lesions of psoriasis

7. Vesicles & bullae –
Both terms – describe diff sizes of blister
Discrete accumulation of fluid – components run out when top is incised
Occur within or just below the epidermis
Vesicle is small & blister is large – cut off –
5-10mm
Useful to note the size range

8. Pustules –
Epidermal or upper dermal accumulation of pus – breakdown product of PMNL
Clinically – yellow or green
Deeper collection of pus –abscess – but the
content not visible through the skin
Some pustules – infiltration of PMNL
few – start as vesicle & gradually accumulat
pus cells

9. Erythema, telangiectasia, purpura, petechiae & ecchymosis
Terms – describe vascular changes
Erythema – diffuse redness due to increased
Visibility of I/V blood – due to vasodilatation
Telangiectasia – individually visible dilated
vessels
Purpura – visible extravascular blood
If this occurs – tiny pinpoint spots – petechiae
Large area of extravasated blood – ecchymosis

10. Dermatological diseases with oral
manifestations
 Ectodermal dysplasia
 White sponge naevus
 Heriditary benign intraepithelial dyskeratosis
 Pachyonychia congenita
 Dyskeratosis congenita
 Xeroderma pigmentosum
 Darier’s disease
 Wrty dyskeratoma
 Peutz zegher’s syndrome
 Heriditary hemorrhagic telengiectasia
 Ehler’s danlos syndrome
 Epidermolysis bullosa

11. Immune mediated skin diseases –
 Pemphigus
 Cicatrial pemphigoid
 Bullous pemphigoid
 Erythema multiforme
 Erythema migrans
 Rieter’s syndrome
 Lichen planus
 Psoriasis
 Lupus erythematosus
 Systemic sclerosis
 CREST syndrome
 Acanthosis nigricans
 Graft versus host disease

12. Ectodermal dysplasia
 Relatively rare
 X linked recessive inheritance pattern
c/f –
 Soft, smooth dry skin – partial or total loss of sweat glands
 Cannot perspire – unexplained high temp
 Sebaceous glands & hair follicles – absent
 Hair of the scalp & eyebrows – fine, scanty
 Bridge of the nose is depressed
 Frontal bossing
 Lips become protruberant

14. Oral manifestations
 Anodontia or Oligodontia
 Malformation of both deciduous & permanent teeth
 Truncated or cone shape
 Jaws will be normal but the alveolar process will not develop in the absence
of teeth – reduced vertical dimension – protuberant lips
 High palatal arch & cleft palate may be present
 Salivary glands – hypoplastic – xerostomia
 Hypolasia of nasal & pharyngeal mucous glands – pharyngitis/ rhinitis

16. Treatment & prognosis
 No treatment
 For dental problems – prosthetic replacement of dentition

17. White sponge nevus / Cannon’s
disease
 Genodermatologic disease
 Autosomal dominant trait
Etiology –
 Due to defective normal keratinisation of oral mucosa
 Keratins 4 & 14 specifically expressed in spinous layers

18. c/f –
 Appears at birth or in early childhood’
 Symmetric thickened, white corrugated or velvety, diffuse plaque
 Affects BM –b/l
 Other sites – ventral tongue, labial mucosa, soft palate & alveolar mucosa

19. Prominent hyperparakeratosis
Acanthosis with clearing of cytoplasm of spinous cell layers
Eosinophilic condensation in perinuclear region of cells

20. Treatment & prognosis
 Completely a benign condition
 No treatment required
 Good prognosis

21. Hereditary benign intraepithelial
dyskeratosis / Witkop’s disease
 Rare autosomal dominant genodermatologic disease
c/f –
 Childhood
 Oral lesions similar to white sponge nevus
 Milder cases – similar to leukodema
 Ocular lesions develop early in life
 Bulbar conjunctivitis

23. Prominent hyperkeratosis & acanthosis
Involves upper spinous layers of the epithelium

24. Treatment & prognosis
 Benign condition – no treatment
 If superinfected with candidal infection – antifungal therapy

25. Darier’s disease (keratosis follicularis)
 Rare genodermatosis – striking skin involvement
 Autosomal dominant trait
 Lack of cohesion among the surface epith cells –
characteristic
 Mutation in genes coding intracellular pump –
identified as the cause for abnormal desmosomal
organization in affected epith cells

26. C/F –
Erythematous, often pruritic, papules – skin of trunk & scalp
•Accumulation of keratin – rough texture
•Gen becomes worse during summer – due to
sensitivity of patient to UV light
•Palms & soles exhibits pits & keratoses – nails
show longitudinal line

27. Oral lesions –
Consists of multiple, normal colored or white, flat topped papules – cobble stone
appearance
t
h
e
s
e
Lesions affect – hard palate, alveolar mucosa
Primarily others b. mucosa & tongue

28. H/P –
Shows dyskeratotic process characterized by
Central keratin plug that overlay epith
exhibiting a suprabasilar cleft
Intraepithelial clefting phenomenon –
acantholysis
Rete ridges – narrow, elongated & test tube
Shaped
2 types of dyskeratotic cells –
Corps ronds – dyskeratotic basophilic mass
surrounded by eosinophilic cytoplasm
grains – elongated parakeratotic cells

29. Treatment
 Depends on the severity of the disease
 For mild cases – keratolytic agents
 Severe cases – systemic retinoids
 Condition is nor premalignant nor life
threatening

30. Pemphigus
 Autoimmune mucocutaneous disease characterized by
intraepithelial blister formation
 Due to loss of intercellular adhesion known as acantholysis
 4 types of pemphigus –
 P. vulgaris
 P.vegetans
 P. erytematosus
 P. foliaceous
Affects whole epith & involves oral mucosa
Affects only prickle cell layer

31. Pemphigus vulgaris
Initiating factors –
genetic background
diet – garlic
drugs – penicillamine, phenol durgs
viruses – herpes
other factors –
smokers
female patients

32. c/f –
Pts – erosions & ulcerations covered by white or blood tinged
exudate
•Usually affects – palate, L. mucosa, B. mucosa
ventral tongue & gingivae
• pts rarely complains of vesicles or bullae
severe pain, ↑ salivation
•Most of the pts will have oral lesions before the
onset of cutaneous lesions

36. Cicatrial pemphigoid / benign mucous
membrane pemphigoid
 Term pemphigoid – clinically appears like pemphigus
 Cicatrix – scar (scarring of conjunctivitis)
 Group of chronic blistering, mucocutaneous autoimmune
disease in which autoantibodies are directed against any 1 or
more components of basement membrane

37. Antigenic targets – laminin 5 & 180 KD protein –
Bullous pemphigoid antigen
IgG & C3 – along with IgA, IgM – deposited along
the basement memb

38. c/f –
Age – older pts
Sex – F:M – 2:1
Site – oral lesions, involvement of conjunctiva, nasal,
Esophagus, laryngeal & vaginal mucosa
Becoz the blisters are subepith – produces a thick strong
Roof
Later – blisters rupture leaving large, superficial ulcerations,
& denuded areas of mucosa
Ulcerations – painful & persists for weeks

42. Epidermolysis bullosa
Immunologically mediated disease in which antibodies are directed against type VII
Collagen- principle component of anchoring fibrils
Anchoring fibrils – play imp role in bonding the
Epith to underlying conn tissue

46. Erythema Multiforme
 Blistering, ulcerative, mucocutaneous condition of uncertain etiology
 Probably a immunologically mediated disease – Ag – Ab complexes targeted
against small vessels in skin & mucosa
 In few cases – preceding infection – herpes simplex, mycoplasma
pneumoniae

49. c/f –
Skin lesions – target eye or iris lesions

52. h/p –
Mucosa – intraepithelial or subepith
vesiculation Due to intra & inter cellular
edema
Edema results in pooling of eosinophilic
Coagulum within epith
Necrosis of basal keratinocytes

54. Lupus erythematous
 Immunologically mediated condition
 Etiology -
 Both humoral or cell mediated arms of immune systems are
involved
 Genetic factors are known to play an imp role
 Autoab against cellular antigens in both nucleus & cytoplasm

55. c/f –
Age – middle aged
Sex – f >m
General symptoms – fever, wt loss, fatigue
Characteristic – butterfly rash – develops over malar
Area and nose

56. Oral manifestations –
An ulcerated or atrophic, erythematous central zone surrounded by white, fine, radiating
Striae
Atrophic lesions – may be painful

57. H/P –
 Hyperkeratosis
 Alternating atrophy & thickening spinous layer
 Degeneration of basal layer
 Subepithelial lymphocytic infiltration
Lab diagnosis –
 LE test – LE bodies
 ANA

58. Systemic sclerosis
 Rare immunologically mediated condition
 Characterized by deposition of dense collagen in tissues in the body
c/f –
 Age – middle age
 Sex – F:M=3:1
 First sign of the disease – Raynaud’s phenomenon – a vasoconstrictive event
triggered by emotional stress or exposure to cold
 CREST syndrome

59. Oral manifestations
 Microstomia
 Dysphagia
Rad /f –
 Diffuse widening of PDL space throughout the dentition
 Varying degree of resorption – post ramus, coronoid process,
chin and condylar area

60. h/p –
 Shows diffuse deposition of dense collagen within and around
the normal structure
 Replaces almost all the normal structure of conn tissue
Treatment –
 Systemic medication – D-penicillamine inhibits collagen
production