Download Oral ulcers Mutaz Ali Hassan Faculty of Dentistry University of

Oral ulcers
Mutaz Ali Hassan
Faculty of Dentistry
University of Khartoum
Definitions
An ulcer is the loss of continuity of the mucous membrane or skin.
An erosion is the partial loss of the superficial layer of oral epithelium.
Primary ulcer: are ulcers that present from the intial stage of the lesion.
Secondary ulcer: are ulcer following or secondary to vesiculo-bullous
lesions.
Vesicle: A superficial blister filled usually with clear fluid, less than 5mm in
diameter.
Bulla: A large blister filled usually with clear fluid, greater than 5mm in
diameter.
Classification
A) Primary ulcers:
Traumatic ulcers.
Infectious causes of oral ulcers.
Idiopathic ulcers.
Oral ulcers related to systemic diseases.
Neoplastic ulcers.
A) ٍٍSecondary ulcers:
According to histopathology classified into:
1) Intra-epithelial vesiculo-bullous lesions.
2) Sub-epithelial vesiculo-bullous lesions.
Traumatic ulcers.
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Mechanical: denture clasps, sharp teeth.etc.
Physical: thermal, electrical and radiation.
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Chemical: acids and basic.
Single painful ulcers related to the cause (physical cause) with yellow
base and red margins.
Infectious causes of oral ulcers:
Viral: infectious mononucleeosis.
Bacterial: ANUG, cancrum oris, TB, syphilis, gonorrhea.
Fungal: candidiasis, aspergillosis, Paracoccidiodomycosis, Histoplasmosis
and Mucormycosis.
Protozoal: leishmaniasis.
Infectious mononucleosis
Caused by EB virus.
Spread by direct contact.
Children >4 yrs: fever, lymphadenopathy, pharyngitis, hepatosplenomegaly.
Young adult: fever, lymphadenopathy, pharyngitis, & tonsilitis.
Acute necrotizing ulcerative gingivitis
Etiology
Fusobacterium nucleatum, Borrelia vincentii, and other bacterial species
including Prevotella and oral treponemes
Infection requires modification of local or systemic factors including
immunosuppression, local hygiene, nutritional deficiencies, intense
smoking, and psychological stress.
Clinical Presentation
Engorged, enlarged, and blunted interdental papillae with punch-out
necrosis.
Symptoms include pain, regional lymphadenitis, fetid breath, fever, and
malaise.
Ulcerated areas covered with grayish pseudomembrane.
Often accompanied by dental plaque and calculus.
Bleeding noted spontaneously or with minimal tissue manipulation.
Extension of disease process into adjacent soft tissues noted on occasion.
Acute necrotizing ulcerative gingivitis
Cancrum oris
Rapidly progressive infection caused by spirochaetes predisposed by
poverty, malnutrition, poor oral hygiene, immunodeficiency.
Children.
Starts as ANUG to involve adjacent soft tissues.
Idiopathic ulcers: Recurrent aphthous stomatitis:
Etiology
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Unknown—probably represents a focal immunodysfunction; no viral or
other infectious agent identified
Triggers vary from case to case (e.g., increased stress/anxiety, hormonal
changes, dietary factors, trauma).
Alterations in barrier permeability may be a factor, as occur with human
immunodeficiency virus/acquired immunodeficiency syndrome
(HIV/AIDS), bone marrow suppression, neutropenia, gluten sensitivity,
Crohn’s disease, ulcerative colitis, food allergy, Behçet’s disease, and
dietary deficiencies (iron, folate, vitamin B12, zinc).
Although likely immunologic in nature, the specific mechanism is
undetermined.
Human leukocyte antigen (HLA) subtype susceptibility a factor in some
cases (-B12, -B51, and others)
Clinical Presentation
Affects 18 to 27% of the population; prevalence is approximately 20%.
Recurrent, self-limiting, painful ulcers usually restricted to nonkeratinized
oral and pharyngeal mucosa (not hard palate or attached gingiva).
Well-demarcated ulcers with yellow fibrinous base and erythematous halo.
Three clinical forms: minor ulcers, major ulcers, herpetiform lesions.
Minor variant (most common subtype):
Occasional
Single but more often multiple
Less than 1 cm in diameter
Oval to round shape
Healing within 7 to 14 days.
Minor RAS
Major variant (Sutton’s ulcers):
1 cm or greater in diameter
Single or less commonly several
Deep
Ragged edges with elevated edematous margins.
May persist for several weeks to months
Often heal with scarring.
Major RAS
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Herpetiform variant (least common variant):
Grouped superficial ulcers 1 to 2 mm in diameter; crops of 10 to 100 lesions.
In nonkeratinized and keratinized tissues
Healing within 7 to 14 days
No etiologic role for herpes simplex virus
Herpetiform variant
Oral ulcers related to malignancy
Oral squamous cell carcinoma.
Non-Hodgkin’s lymphoma.
Kaposi’s sarcoma.
Salivary gland malignancy (e.g. mucoepidermoid ca, adenoid cystic ca).
Metastatic deposits (uncommon).
Oral ulcers related to systemic diseases:
Haematological: anemia, agranulocytosis, Lymphoproliferative disease,
Leukaemia.
Gastroenterological: Crohn’s disease, celiac disease, ulcerative colitis.
Immunological: lupus erythematosus, Behcet syndrome, Reiter’s syndrome,
allergic reactions.
Oro-facial granulomatous: Wegener’s granulomatosis, sarcoidosis.
Drug induced:
Drug induced oral ulcers
Lichenoid drug reactions (e.g. b-blockers, antimalarials, NSAIDs,
interferon)
Erythema multiforme (e.g. barbiturates, carbamazepine, sulphonamides)
Pemphigus (e.g. penicillamine, ACE inhibitors, rifampicin)
Lupus (e.g. minocycline, statins, terbinafine)
Pemphigoid (e.g. clonidine, psoralens)
Drug-induced neutropenia/anaemia (e.g. azathioprine, carbamazepine)
Drug-induced mucositis (e.g. cyclophosphamide, methotrexate)
Others (e.g. nicorandil).
Drug-induced ulcer
Secondary ulcers:
1) Intra-epithelial vesiculo-bullous lesions:
A) Non-acantholytic VB lesions:
Human herpes simplex 1 and 2.
Varicella zoster virus
Coxsackie viruses (e.g. herpangina, hand foot and mouth disease)
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B) Acantholytic VBS lesions: pemphigus vulgaris.
2) Sub-epithelial VBS lesions: erythema multiforme, benign mucous
membrane pemphigoid, bullous pemphigoid, bullous & erosive lichen
planus, epidermolysis bullosa, dermatitis herpetiformis.
Herpes simplex
2 types (1&2).
Primary infection: acute herpetic gingivo-stomatitis.
Age:6months-5 years.
Cervical lymphadenopathy, chills, fever, nausea, and sore mouth lesions.
Sore mouth lesions: numerous vesicles that coalesce and show central
ulceration, affect gingiva, adjacent mucosa, vermilion of the lip.
Resolve within 5-7days.
Secondary infection:
Reactivation of the virus.
Herpes labialis.
Herpetic whitlow.
Primary herpetic gingivostomatitis
Recurrent herpes simplex
Herpes labialis
Pemphigus vulgaris
Pemphigus is a group of potentially life-threatening autoimmune diseases
characterized by cutaneous and/or mucosal blistering.
Pemphigus vulgaris (PV), the most common variant, is characterized by
circulating IgG antibodies directed against desmoglein 3 (Dsg3), with about
half the patients also having Dsg1 autoantibodies.
There is a fairly strong genetic background to pemphigus with linkage to
HLA class II alleles and ethnic groups such as Ashkenazi Jews and those of
Mediterranean and Indian origin, are especially liable.
Oral lesions are initially vesiculobullous but readily rupture, new bullae
developing as the older ones rupture and ulcerate.
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Diagnosis
Biopsy of perilesional tissue, with histological and immunostaining
examination are essential to the diagnosis.
Serum autoantibodies to either Dsg1 or Dsg3 are best detected using both
normal human skin and monkey oesophagus or by enzyme-linked
immunosorbent assay.
Treatment
Before the introduction of corticosteroids, PV was typically fatal mainly
from dehydration or secondary systemic infections.
Current treatment is largely based on systemic immunosuppression using
corticosteroids, with azathioprine or other adjuvants or alternatives but
newer therapies with potentially fewer adverse effects, also appear
promising.
Erythema multiforme
Etiology
Many cases preceded by infection with herpes simplex; less often with
Mycoplasma pneumoniae or other organisms
May be related to drug consumption, including sulfonamides, other
antibiotics, analgesics, phenolphthalein-containing laxatives, barbiturates
Another trigger may be radiation therapy.
Essentially an immunologically mediated reactive process, possibly related
to circulating immune complexes.
Clinical Presentation
Classified into EM minor, EM major, & toxic epidermal necrolysis.
Acute onset of multiple, painful, shallow ulcers and erosions with irregular
margins.
Early mucosal lesions are macular, erythematous, and occasionally bullous.
May affect oral mucosa and skin synchronously or metachronously
Lips most commonly affected with eroded, crusted, and hemorrhagic lesions
(serosanguinous exudate) known as Stevens-Johnson syndrome when
severe.
Benign mucous membrane pemphigoid
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Mucous membrane pemphigoid (MMP) is a sub-epithelial vesiculobullous
disorder.
It is now quite evident that a number of sub-epithelial vesiculobullous
disorders may produce similar clinical pictures, and also that a range of
variants of MMP exist, with antibodies directed against various
hemidesmosomal components or components of the epithelial basement
membrane.
The term immunemediated sub-epithelial blistering diseases (IMSEBD) has
therefore been used.
Immunological differences may account for the significant differences in
their clinical presentation and responses to therapy, but unfortunately data on
this are few.
Diagnosis
The diagnosis and management of IMSEBD on clinical grounds alone is
impossible and a full history, general, and oral examination, and biopsy with
immunostaining are now invariably required, sometimes supplemented with
other investigations.
Treatment
No single treatment regimen reliably controls all these disorders, and it is not
known if the specific subsets of MMP will respond to different drugs.
Currently, apart from improving oral hygiene, immunomodulatory—
especially immunosuppressive—therapy is typically used to control oral
lesions.
Benign mucous membrane pemphigoid
Herpangina
Necrotic ulcer in HIV
Syphilitic chancre
Mucus patch (syphilis)
Mucus patch (syphilis)
Condyloma lata
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Histoplasmosis
Behcet’s disease
Behcet’s disease
Crohn’s disease
Orofacial granulomatosis
Pyostomatitis vegetans with ulcerative colitis.
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