3. (Erythema migrans, Benign Migratory Glossitis)
tiology: Exact cause still unknown
a) hypersensitivity to environmental factors
b) hormonal factors
c) emotional stress
d) recently linked to psoriasis genetic predisposition (HLA-Cw6)
athogenesis
atrophy of filiform papillae result in erythematous spots
ncidence:
common benign condition
affect the tongue, lip and palate
1~3% of population
♀2♂1
January 20, 2014
Dr Wael M. Swelam
4. Clinical features
– Usually asymptomatic but occasionally painful
– Usually discovered accidentally
– Affect anterior 2/3 of dorsal tongue mucosa
– White annular lesions with atrophic red centers
– There is no loss of the sense of taste
– There is, a measurable decrease in the tongue's sense of touch.
– Course of disease
• Appear quickly in one area
• Heal within days,
• Then appear in a very different area
January 20, 2014
Dr Wael M. Swelam
5. Histopathology
–
–
–
–
Thinning of the epithelium,
Elongation of the rete ridges,
Focal submucosal accumulation of inflammatory cells,
Leukocytes are often noted within microabscess, {Munro
abscess} near surface
– Surface parakeratosis
January 20, 2014
Dr Wael M. Swelam
6. common non- neoplastic dermatologic condition manifesting as flat, lacy, white, intersecting
lines on the oral mucosa; lichen planus has a distinctive microscopic appearance
Etiopathogenesis:
Exact cause still unknown BUT immunologic mechanisms triggered by poorly
defined antigenic stimulations plays a pivotal role in the disease pathogenesis
a) Chronic stress, as the disease is oftenly affects the educated, the well-to-do, and
high achievers.
b) Cell-mediated immune response because
i) Presence of activated antigen presenting cells (Langerhans' cells, dendritic macrophages) in the
lesion could be demonstrated in the early stage of the disease.
ii) CD4+ cells initiates immune response in which activated keratinocytes also take part.
iii)CD8+ T lymphocytes mediate the damage to the epidermis and leads to the characteristic
reaction.
c) HLA-associated genetic susceptibility in the causation of the disease
d) Hepatitis C virus infection are implicated in the triggering of LP
January 20, 2014
Dr Wael M. Swelam
7. Antigenic stimulation
Langerhans cells
F XIIIa dendrocytes
Endothelium upregulate
Adhesion molecules
Lymphocytes recruited to
retained in submucosa
Basal keratinocytes express
ICAM lymphocytes attach
Attract lymphocytes -attach
Basal cell apoptosis
8. Clinical features
– Middle aged adults
– ♀3♂2
– Skin lesions incidence among population is 1%
– Affect flexor surfaces of extremities
– Skin lesion appear as purple, pruritic, polygonal papules
– Oral lesions prevalence is 0.1~2.2%
January 20, 2014
Dr Wael M. Swelam
10. Lesions are named after their shape
Plaque
Reticular/annular
Wickham’s straia
are diagnostic
January 20, 2014
Dr Wael M. Swelam
Bullous/Erosive
11. Histopathological features
–
–
–
–
–
–
Characteristic but not specific
Varying degree of ortho/para keratosis,
Varied thickness of prickle cell layer,
Rete ridges either absent or hyperplastic=Saw toothed,
Destructed (hydrobic degeneration) basal cells
Intense band of T lymphocytes subjacent to epithelium
Degenerating keratinocytes may be seen around basement membrane
as Civatte, Colloid, Cytoid bodies
January 20, 2014
Dr Wael M. Swelam
13. Genetic factors
B cell reactivity
alter the function of T cells,
antigen-presenting cells
cytokines production
B cells to enhance the
function of other cells
autoantibody
production
Organ damage
January 20, 2014
Dr Wael M. Swelam
14. It is inflammatory disease that target skin and to lesser extent mucosa
Clinical features
– No sex predilection (systemic
♀8~10♂1 )
– Middle age
– Skin lesions affect mainly face scalp
– Skin lesions appear as disk-shaped erythematous
plaques with hyperpigmented margins
– Involvement of hair follicles results in
permanent hair loss (Alopecia)
– Mucous membrane lesions affect 25% of
patients mainly (buccal mucosa, gingiva,
vermilion border)
January 20, 2014
Dr Wael M. Swelam
15. Commonly affect buccal mucosa,
gingiva, and vermillion border
Lesions are either erythematous or
ulcerative with delicate white,
keratotic striae radiate from the
periphery
January 20, 2014
Commonly affect buccal mucosa,
gingiva, and vermillion border
Lesions are generally similar to
DLE; erythematous or ulcerative
with delicate white, keratotic striae
radiate from the periphery
Systemic symptoms include fever,
weight loss, malaise
Involve many organ systems (Joints,
kidneys, heart, and lungs)
Kidney lesion = glomerulonephritis
Glomerulonephritis are mostly
responsible for death
Dr Wael M. Swelam
16. “Anti Nuclear Antibody” ANA test
“Regarded as reliable specific test”
• Anti-single stranded DNA
• Anti-double stranded DNA
• Antinuclear ribonuclear protein
“LE” cell test
“less sensitive less specific”
Anti Small nuclear “Sm” antibodies {very specific}
Ro (SS-A), (SS-B) Antibodies to cytoplasmic antigens
January 20, 2014
Dr Wael M. Swelam
17. – Basal cell destruction
– Thickened basement membrane
– Hyperkeratosis
– Epithelial atrophy
– “perivascular” Lymphocytic infiltration
• DLE more intense less diffuse
• SLE less intense more diffuse
– Vascular dilatation with submucosal edema
Direct Immunoflurescent show:
* Granular-linear deposits of:
IgG, IgM, IgA, C3, fibrinogen
January 20, 2014
Dr Wael M. Swelam
19. Thrush, Angular cheilitis, median rhomboid
glossitis, denture sore mouth, moniliasis
Causative microorganism: Candidal species specially albicans
Acute
Chronic
Mucocutaneous
Erythematous
Pseudo membranous
“Thrush”
Erythematous
Hyperplastic
Familial
Localized
Syndrome
associated
January 20, 2014
Dr Wael M. Swelam
20. Erythematous
Pseudomembranous “thrush”
White, soft plaques grow centrifugally
merge, symptomatic only in sever cases
Composed of :
– Fungal organisms
– Keratotic debris
– Inflammatory cells
– Desquamated epithelial cells
– Bacteria
– Fibrin
Can be wiped away with gauze
Site:
– Buccal mucosa, mucobuccal fold,
– Lateral aspect of tongue
– Oropharynx
January 20, 2014
“Antibiotic stomatitis”
• Develop on the top of persistent
acute pseudomembranous C.
• Site: Dorsum of the tongue
• Etiology: follow prolonged usage
of narrow spectrum antibiotic
• Symptomatic
Dr Wael M. Swelam
21. Erythematous/ Atrophic
“Denture sore mouth”
Hyperplastic
“Candidal leukoplakia”
Similar to speckled leukoplakia
Age: adults
Site: Dorsum of tongue,
Usually asymptomatic
Can't be wiped away with gauze
Histopathologically:
• Develop under Dentures specially
ill-fitting ones + poor oral hygiene.
• Site: Palatal mucosa
• shape: bright red, velvety surfaces
“Angular cheilitis”
– Evident epithelial hyperplasia
– Bulbous rete process
– Candidal hyphae seen in upper epithelium
Considered as premalignant lesion
“Papillary hyperplasia”
Site: Under palatal dentures
Shape: ovoid or spherical nodules on
erythematous background
January 20, 2014
• Site: oral commeasures
• Affect individuals with deep folds
at oral commeasures secondary to
over closure
• Subsequently colonized with yeasts
staphylococcus aureus
• Moderately painful
Dr Wael M. Swelam
23. Long standing, persistent candidiasis
Site: Oral mucosa, nails, skin vaginal mucosa
Age: Often resistant to treatment
Usually start as pseudomembranous and soon is
followed by nail and cutaneous candidiasis
Familial
Hereditary
Auto-immune
associated
• Autosomal recessive
Triad consisting of :
a. Myositis
b.Mucocutaneous C
c. Thymoma = deficiency of
T cell mediated
immunologic function
•Associated with
autoimmune
disease
• Etiopathogenesis:
depleted cellmediated arm of
immune system
• 50% associated with
endocrinopathy
• 50% associated with defects in iron metabolism
January 20, 2014
Dr Wael M. Swelam
24. Acute forms
– Fungal hyphae penetrate the upper layers of epithelium at
acute angles
– Neutrophilic infiltration = superficial micro-abscess
Chronic forms
– Epithelial Hyperplasia is characteristic
No clear evidence that chronic candidiasis is precancerous
January 20, 2014
Dr Wael M. Swelam
27. Etiopathogenesis
– Habitual chewing of areca nut
– Nutritional vitamin deficiency specially
• prolonged deficiency of Vit B complex
• Folic acid
– Hypersensitivity to various dietary constituents
Increase cellular sensitivity to many potential irritants
Areca nut (alkaloids)
Impaired degradation of collagen by fibroblasts
rather than excessive deposition
January 20, 2014
Dr Wael M. Swelam
28. Clinical features
– Age: 20~40
– Site:
• soft palate,
• buccal mucosa
– Shape: Whitish yellow, chronic,
– Geographic incidence:
• Southeast Asia,
• India neighboring countries
– Insidious course might be preceded with vesicle formation
– Symptoms: affected mucosa loose its resilience and elasticity
January 20, 2014
Dr Wael M. Swelam
29. Atrophic epithelium
Subjacent fibrosis
mild, moderate, and sever
Poorly vascularized lamina propria hyalinized
Diffuse mild to moderate inflammatory cell infiltrate
January 20, 2014
Dr Wael M. Swelam
30. Ectopic sebaceous glands (developmental condition)
Multiple, in aggregates
Site: Buccal mucosa vermilion border of upper lip
January 20, 2014
Dr Wael M. Swelam
31. Lingual tonsil:
–
–
–
–
At posterolateral surface of tongue
Consist of aggregates of lymphoid tissue
Appear white-yellow, dome-shaped elevations
Crypts of these structures when obstructed lymphoepithelial cyst
January 20, 2014
Dr Wael M. Swelam
32. Etiopathogenesis:
• In infants (Bohn’s nodules, Epstein’s pearls): Epithelial entrapment within
midline of palatal fusion
• In adults:
– Proliferation of rests of Serres (remnants of dental lamina)
– Traumatic implantation of surface epithelium into gingival CT.
– Age: 10~12 weeks of age
– Site: along palatine shelves
– Painless growth in attached gingiva often within interdental papilla
January 20, 2014
Dr Wael M. Swelam
33. Gum boil
– Gingival abscess appear either
• The base of gingival pocket
• Apex of non vital tooth
– Yellowish-white gingival swelling
– Painful
January 20, 2014
Dr Wael M. Swelam