2. Definition
• “Stoma” from greek meaning mouth
• “itis” –inflammation
• Inflammation of the mouth and lips plus the oral mucous membranes
with or without ulcerations.
3. Causes of Non infective stomatitis
• Traumatic Ulcers
• Aphthous stomatitis
• Behcets disease
• HIV associated
• Lichen planus
• Lupus erythematosus
• Chronic ulcerative stomatitis
Miscellaneous mucosal ulcers;
• Eosinophilic ulcer (atypical or traumatic eosinophilic
granuloma)
• Wegener's’ granulomatous
• Mucosal drug reactions
4. Traumatic Ulcers
Causes
• A denture often seen in buccal / lingual sulcus
• Biting the cheek after local anaesthesia
Characteristics
• The ulcers have a yellowish floor, red margin and no indurations
• Heal within 7-10 days
NB. Biopsy should be carried out to rule out other causes
5. Factitious Ulcerations (Self Inflicted ulcers)
• A factitious disorder is a mental disturbance where person inflicts pain
to themselves to deceive that they are sick.
• This is a form of traumatic ulcers.
• Less common and the most common type “self tooth extraction”
Features suggestive of factitious oral lesions.
• Clinical features inconsistent with history
• Usually in otherwise in healthy individuals
• Lack of correspondence with recognizable disease
• Bizarre configuration with sharp outlines
PERSON NEEDS PSYCHIASTRIC ASSESSEMENT
6. Aphthous Stomatitis (Canker sores)
• An illness that causes small ulcers to appear in the mouth, usually inside the
lips, on the cheeks, or on the tongue
• Round or ovoid painful ulcers recur on the oral mucosa
Aetiology
1. Genetic factors e.g. in Behcets disease there is a strong
2. Trauma –exaggerated response to trauma in already existing disorder
e.g. from tooth brush bristle
3. Infections- No clear evidence but streptococcus is implicated
4. Immunological Disorders
5. Haematological Disorders- Vitamin B12 folate and iron deficiency
6. Stress – only that it is not quantifiable
7. HIV infection
8. Non-smoking.
7. Clinical features of Aphthous Stomatitis
• More in males, rare in the elderly especially edentulous
but may be effected by haematological deficiencies
• Onset is frequently in childhood but peaks in
adolescence
• Affects the clerical, professional workers and non-
smokers
• Mostly affects the non keratinised mucosa (buccal
mucosa, sulcuses, lateral borders of the tongue)
• Major aphthae can affect masticatory mucosa
• Usually self-limiting occurring in health individuals.
9. Minor Aphthae
• Most common
• Affects nonkeratinsed mucosa
• Ulcers swallow (5-7mm with an erythematous margin, yellow floor
10. Major Aphthae
• Less common
• Ulcers are several centimetres
• Ulcers persist for several months
• Masticatory mucosa e.g. dorsum of the tongue or gingiva may be may
be affected
• Scarring may follow healing
11. Herpetiform Aphthae
• Not common ulcers (1-2mm)
• Many Ulcers may be present
• May coalesce to form irregular ulcers
• Wide spread bright erythema around the ulcers
12. Diagnosis of Aphthous Stomatitis
• History of recurrent self healing ulcers at regular intervals
(only condition with this history is Behcets disease)
• Haematological investigation especially in elderly people-
Most common finding is abnormal MCV
13. Treatment of Aphthous Stomatitis
• Usually empirical and palliative only
• No Medication gives complete relief but we can give
Corticosteroids (orally e.g. Hydrocortisone Hemisuccinate pellets)
Triamcinolone Dental Paste- also corticosteroid
Tetracycline mouth wash
Antifungal to those susceptible to super infection e.g. Candida
Chlorhexidine
Major aphthae may be persistent to usual treatment so we use
Azathioprine, Cyclosporine, Colchicine, Dapsone, Thalidomide(most
effective but should be given under special supervision)
14. Behcets disease
• Aetiology is unknown but is thought o be immunological to infectious
agent but has a genetic predisposition.
• It is a multisystem disorder that manifest as:
1.Mucocuteanous lesion (oral and genital ulcerations)
2.Arthritic (Joint inflammation)
3.Neurological
4.Ocular lesions
NB. Oral aphthae of Behcet is not distinguishable from common
aphthae so when diagnosing Aphathe stomatitis consider Behcets.
15. Diagnosis of Behcets disease
• Oral aphthae are always present
Then any other two manifestations are adequate only that they are variable
in appearance.
Vasculitis is the main pathological finding and anti-endothelial antibodies
can be found
Pathergy Test: is positive. This involves an exaggerated skin response on
injury by sterile needle
Complications of the disease life-threatening Thrombosis, Risk of blindness
Brain damage
-
16. Treatment of Behects Disease
• Its difficult to treat
• Oral ulcerations can be treated in the same way as aphthae stomatitis
(corticosteroids……)
• Thalidomide and Colchine are highly effective.
Ulcer in Behects
Disease
17. HIV Associated oral Ulcerations
• They are indistinguishable from common aphthae
• Unknown aetiology
• Biopsies may help exclude opportunistic infections
Treatment
• Thalidomide
• In case CMV co infection add Ganciclovir
18. Lichen Planus
• Lichen (primitive plants algae and fungi)
Planus means flat so the scientist Erasmus Wilson identified the lesions as
lichens growing on rocks hence the name.
• Common inflammatory disease of the skin and mucous membranes.
Aetiology.
• Auto immune disease mediated by T lymphocyte in which there is
immunological damage to epithelium.
19. Clinical features of Lichen Planus
Oral lichen Planus manifests as
1. Reticular type
2. Atrophic/ erythematous
3. Erosive/ ulcerative
4. Plaque/ hypertrophic
20. Reticular type of Lichen Planus
• Most common type manifests in the buccal mucosa
• Bilateral and symmetrical
• Other sites that may be affected; Lips, gingiva, tongue (either edges or
lateral margins)
• There may be striae (white lines) also called Wickham's striae
21. Atrophic/ erythematous type of Lichen Planus.
• Red patch surrounded by white striae
• Sometimes occurs with erosive variant.
• Patients may complain of burning sensation in the mouth
• There may be desquamative gingivitis.(This can also be seen in
pemphigus vulgaris, cicatricial pemphigoid and linear IgA disease.
• Frequently occurs in buccal mucosa.
22. Erosive/ Ulcerative type of Lichen Planus
• Presents as an ulcer(shallow irregular area of epithelium) surrounded by
striae, ulcers may be covered by pseudomembrane(smooth slightly raised
layer of yellow fibrin)
• There are red patches, sore mouth making mastication difficult
23. Plaque/ hypertrophic type of Lichen Planus
• Raised or flat plaques, may be seen in the early stage of the disease
particularly on the dorsum of the tongue
• Occurs with white striae
• They resembles leukoplakia
24. Diagnosis of Lichen Planus
• Made basing on history and appearance of lesions
• Take biopsy if plaques are present.
• OLP is a common skin disease and purplish papules (2-3mm)on the flexor
surface of forearms hence can be used to confirm diagnosis
NB. Dysplastic leukoplakia occasionally have whitish appearances and should
be distinguished.
Management.
Reassure the patient that the disease is non-infectious.
Anti-inflammatory -Beclomethasone
Triamcinolone dental paste
When Gingivitis lichen planus occurs, treatment becomes hard and we must.
Systemic corticosteroids may be used in severe cases.
25. Lichenoid like Reactions
• Lichen planus reactions in which the histological picture of the is not
completely diagnostic of “true Lichen Planus”
• Can be distinguished since they contain only white striae which are
UNILATERAL.
Causes of the reactions.
1. Drugs e.g. antimalarial
2. Amalgam restorations
3. Graft versus host diseases (e.g. bone marrow transplantation)
4. Some foods e.g. Arecanut and Betel quid (pepper)
These reaction take years to manifest.
26. Pathogenesis of Lichenoid reactions.
• Using amalgam as a model,
• Amalgam contains several metals that act as haptens
• Corroded amalgam restorations can also trigger reactions
• The air turbine removes tiny particles of the restoration
and deposits them in the mucosa.
• Dendritic cells pick the antigen and present it to CD4+
cells that release cytokines to activate CD8+ cells that
attack and induce apoptosis of the epithelial cell through
release of granzymes and perforins.
27. Management
• Withdrawal the drug
• Remove the restoration (if healing occurs then metal causation is
confirmed) Decision to remove amalgam is trial and error.
Metal sensitivity testing is not useful since the skin may be sensitive to
metals that the oral mucosa doesn’t.
Complications of Oral Lichen Planus
Malignant transformation to oral cancer after about 10 years.
Only 1-4% develop the complication yet OLP is a common disease.
hence the complication could be former cases of dysplastic lesions
since a higher %age would be expected
28. Lupus Erythematosus
• Multifactorial, autoimmune multisystem disease.
Aetiology
1.Genetic – since certain genes enhance the formation of immune
complexes.
-genes that impair clearance of immune complexes or
apoptotic bodies
2.Environment- UV light, viruses (EBV) Drugs (Hydralazine,
procainamide, penicillamine)
3.Immunological- through self reacting B and T cells
30. Oral manifestations of Lupus Erythematosus
• Disease has two forms namely : Discoid and systemic forms but the
former is typically a skin disease with mucocutenous lesions.
• Both affect the oral mucosa
• They occur on the vault of the palate, buccal mucosa, and gingiva
• Appear as erythematous patches, ulcers,white plaques often
unilateral
• There is crusting and bleeding on the lower lip
• Sjogrens syndrome develops(explain the lower lip bleeding)
• Oral lesion resemble lichen planus and leukoplakia
31. Other manifestations of lupus Erythematosus
• Rarely cervical lymphadenopathy is the first sign
• Butterfly rush
• Arthralgia
• Vasculitis in SLE not Discoid
• Histologically , there is more irregular patterns of acanthosis (thickening
of skin)
32. Diagnosis of lupus Erythematosus
• Detection of antinuclear antibodies
• Haematological findings like increased ESR, Leukopenia and
thrombocytopenia
• Oral lesions in Discoid form respond to topical corticosteroids
• Oral lesions in systemic form don't respond to doses adequate to
control systemic effects
So what's the plan??
Palliative treatment (to relieve symptoms until disease resolves)
Treatment
33. Chronic Ulcerative Stomatitis
• Uncommon mucosal disease associated with IgG antibodies that
attack the squamous epithelium .
Clinically,
• Affects females over 40 years, skin involvement is rare
• Lesions are erosions lichen planus like and often confused with lichen
planus
• It is more common than it is appreciated
Diagnosed by Immunofluorescence that shows antinuclear IgG
antibodies in the perilesional mucosa and shaggy deposits of fibrin in
basement membrane zone
34. Treatment of Chronic Ulcerative Stomatitis
• Chloroquine
• Hydroxychloroquine
NB. Give recommended doses of these drugs to minimise risk of ocular
damage
• May add prednisolone
35. Pemphigus (Blister disease)
• Autoimmune mucocutenous condition where autoantibodies attack
epithelial cells with desmosomes leading to split epithelium (blister
formation)
Types of Pemphigus
• Pemphigus vulgaris (most common)
• Pemphigus vegetans
• Pemphigus Erythematosus
• Pemphigus Herpetiform
• Pemphigus foliaceus
36. Pathogenesis
• At the cellular junctions, we have desmosomes (macular adherens) composed of
three proteins that is
I. transmembrane proteins(desmoglein 3 and desmocollin)
II. Cytoplasmic adapter proteins
III. Cytoskeleton filaments
Pemphigus is a type II hypersensitivity reaction in which antibodies attack
desmoglein 3 and ICAM interrupting the intercellular junction. IgG4 is the most
predominant
Also antibodies may stimulate epithelial cells to synthesize proteases that destroy
the intercellular attachments
Epithelial cells lose their attachments and become rounded in shape (tzanck cells),
cytoplasm contracts
This leads to a split in the supra basal mucosa (acantholysis)around the spinosum
layer and clefts are formed superficial to the basal cells
. Desmoglein 1 is found in the skin and later these changes in occur in the
granulosum layer leading to superficial split
37. Pemphigus Vegetans
• Variant of vulgaris
• Has two subtypes that is :
Neumann type (characterised by erosion and ulcers)
Hallopean type (characterised by pastules)
Both types lead to developmet of plaques and there is also a
cerebriform tongue characterised by sulci and gyri.
38. •In Pemphigus vesicles are infrequently seen in the
mouth because they rupture leading to painful ragged
erosions
•Pemphigus is characterised by a positive Nikolsky’s sign
in which a gentle stroke to mucosa causes vesicles and
bullae to appear.
•There is also a bulla spread sign( asboe Hansen sign) in
which stroking the bulla leads to extension of the blister
to adjacent normal skin.
However this sign may be seen in other vesicullo-bullous
lesions
•Pemphigus may progress to other sites like the skin
39. Diagnosis
• Immunofluorescenve microscopy to view the supra-basal split
• High titre off circulating desmoglein 3 aantibodies
Immunosuppressive treatment including
Systemic corticosteroids
Azioothioprine / mycophenolate mofeit
Topical steroids
But always start with dose of systemic corticosteroids.
Treatment
40. Cicatricial Pemphigoid
• Renamed Mucous Membrane Pemphigoid
• Type II hypersensitivity reaction affecting the oral cavity, conjunctiva,
oropharynx and skin
• Antibodies attack the transmebrane proteins interfereing with the
hemidesmosomal junction.
• Loss of attachement and separation of full thickness of the epithelium
fro the connective tissue leading to a subepithelial split and blister
formation
illustration
Histopathology
41. Manifestations
• Desqumatitive gingivitivs
• Nikolsky’s sign in the positive
• Bleeding into the bulla may occur forming blood blisters
• Lesions may remain localised in the mouth for a long period of time
42. Clinical features
• Affects older adults between 50-60 years
• Oral lesions are the initial signs of the disease
• Blisters are sub epithelial with a strong roof and can be seen unlike
the pemphigus where the blisters rupture because they are weak
• Rupture creates an ulceration and excessive pain
• Other mucous membranes may be affected e,g the eyes, larynx, anus,
vulva, penis and anus
Signicant Complication of ocular region that lead blindness
43. • Maintain goo oral hygiene
• Eat soft foods
• Consult an oculist
• Topical corticosteroids
Diagnosis
Management
• Direct immunofluorescence that revealves IgG and C3 complement.
• Indirect immunofluorescence
• Presence of a sub epithelial split
44. • Mucocutaneous disease with oral manifestation.It is acute and self-
limiting, usually resolving without complications.
• It can be divided in minor and major forms
Erythema Multiforme
Aetiology and pathology
• May be a reaction to a variety of causes e.g infections (HSV) or drugs
like sulphonamides and barbiturates
• It is a hypersensitivity reaction
• Affects oral mucosa, lips, tongue but less commoly affects mouth,
palate and gums
• Skin lesion which red or pink with flat macules.
• Erythema multiforme most commonly affects young adults (20–40
years of age), however all age groups and races can be affected. There
is a male predominance.
46. Management.
• Patients should be warned about recurrences which are severe
• There is no specific treatment but you can use sysyemic
corticosteroids, antiobiotics, lemivasole and aciclovir.
47. Allergic stomatitis
• Contact allergy in the mouth is a type IV hypersensitivity reaction as a
result of sensitization to substance with which one has previously
come in contact with
• Oral mucosa is less affected by contact allergy than the skin because:
1. Brevity of contact with potential allergen
2. Dilution of the allergen by saliva
3. Dense vascularization in which the allergen is rapidly resolved
48. Causes of contact/allergic stomatitis
• Dental products (dentures)
• Local anesthetics
• Oral medication
• Dental fillings ( amalgam restorations)
Amalgam restorations do not cause trouble in patients with skin
sensitivity to mercury
49. Miscellaneous Mucosal Ulcers
Eosinophilic Ulcers:
Tumor-like ulcerated lesions with a microscopic picture
resembling that of Langherns cell histiocytes.
May occur due to trauma that then induces a proliferative
response with tissue eosinophilia.
Occur in the oral soft tissues especially tongue but also
gingiva
Affects any age and clinically may be confused with a
carcinoma are differentiated by absence of Langerhans cell
markers.
Lesions heal spontaneously within 3-8 weeks.
51. Wegener's granulomatosis
• Disorder that causes inflammation of the blood vessels, nose, sinuses
and throat and an oral mucosal ulceration is an occasional feature.
• Oral lesions present as solitary or multiple irregular ulcers surrounded
by an inflammatory zone. May affect the tongue, palate, gingiva and
buccal mucosa
52. Oral reactions to drugs
• Xerostomia and swelling
The dry mouth can cause ulcers on movements.
Drugs may include :Antidepressants, anticholinergic, antihistamines
Swelling can be caused by penicillin, aspirin sulfa drugs and ACE
inhibitors.
