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Dr.

Tahani Abualteen

Oral Ulceration
Definition: Ulcer = localized defect in the surface epithelium exposing the underlying connective tissue base leading to inflammation Most common lesion of the oral mucosa May be a manifestation of many disease entities (local and general disorders) Erosion = superficial ulcer (partial loss of epithelial thickness not exposing the connective tissue base) Causes of oral ulceration: Infective (viral, bacterial, fungal) Traumatic (mechanical, chemical, thermal, factitious injury, radiation, eosinophilic ulcer "traumatic granuloma") Idiopathic (recurrent aphthous stomatitis "major, minor, herpetiform") Neoplastic (SCC, other malignant neoplasms) Associated with systemic diseases (GIT diseases, hematological diseases, Behcets disease, HIV infection) Associated with dermatologic diseases (lichen planus, chronic discoid lupus erythematosus, vesiculobullous diseases) ** All these should be kept in mind as differential diagnoses for ulcers Traumatic Ulceration: 1- Mechanical Ulceration: o Three criteria for diagnosis: Define a cause of trauma (e.g. sharp cusps, biting, outstanding teeth, ill-fitting appliances) Cause must fit size, shape and location of ulcer On removal of the cause, ulcer must show signs of healing within 10 days o Mechanical ulcers don't usually present a problem in clinical diagnosis o Problems in diagnosis arise with chronic traumatic ulcers o Chronic Traumatic Ulcers Present for several weeks Present as deep crater-like lesions with rolled everted margins and Induration on palpation (due to surrounding fibrosis) Differentiation of chronic traumatic ulcers from a neoplastic ulcer may be difficult o When is biopsy indicated? If we remove the cause and the presumed chronic traumatic ulcer does NOT show signs of healing within a period of 10-14 days
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Dr. Tahani Abualteen


2- Chemical ulceration: o Wide variety of chemicals may cause oral ulcerations o Highly concentrated or caustic materials used in dental practice (e.g. hydrogen peroxide) that may be accidentally applied to oral mucosa or preparations used by patients in self-treatment of oral complaints (e.g. local use of aspirin to relieve toothache, inadequately diluted mouth washes) o Reaction varies in severity (edema to necrosis), so the concentration and duration of the irritant is important o Recall: Low-grade chronic irritation hyperplasia or hyperkeratosis High-grade or severe acute trauma ulceration or necrosis o Aspirin burn: Caustic action of aspirin is dose and time related Reactions vary in severity from edema of epithelium (resembling Leukoedema) to necrosis of epithelium (presenting as white patches which slough off leaving areas of ulceration) Painful Patients history and location of the lesion are important for clinical diagnosis o Hydrogen peroxide burn: Hydrogen peroxide is an agent used in bleaching or as an antimicrobial irrigant Leakage into soft tissues may induce ulcerations o Anesthetic necrosis: NOT clearly understood! May be due to tissues being stretched or damaged by giving too much solution Or due adrenaline which is a vasoconstrictor in anesthetic solutions o Formocresol burn: Formocresol is an agent used in pulpotomy (extirpation of pulp in deciduous teeth) Leakage into soft tissues may induce ulcerations 3- Thermal ulceration: o E.g. hot foods Pizza burn and hot drinks "coffee, tea burns" o Can occur in any part of the oral mucosa but is most commonly seen in the palate 4- Factitious ulcerations (self-induced): o Self-inflicted ulcers (induced on purpose!)
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Dr. Tahani Abualteen


o May be a manifestation of stress, anxiety, or more severe emotional disturbance o Appearances and distribution vary considerably depending on how they are induced o Common causes are: biting/chewing of lips, cheeks, or tongue, and damage to the gingiva from sharp finger-nails 5- Radiation ulceration: o In patients undergoing radiotherapy for head and neck cancer, the oral mucosa may suffer from: Damage to the epithelium (resulting in Erythema, radiation mucositis, and ulceration) Damage to blood vessels (resulting in epithelial atrophy) Damage to lymphatics (resulting in edema) o Thin atrophic epithelium is prone to traumatic ulcers o Differentiation of radiation ulcers form neoplastic ulcers may be difficult but radiation ulcers (mucositis) are generally painful while pain is not a common feature of early malignant disease 6- Eosinophilic ulcer (traumatic ulcerative granuloma): o Unusual type of ulceration o Etiology: chronic trauma and crush injury to skeletal muscles o Pathogenesis is still unclear but probably injury causes certain proteins or antigens to leak resulting in inflammatory or allergic response o Occurs most commonly in the tongue o Clinical appearance: chronic, well-demarcated ulcer which may mimic Sequamous cells carcinoma ulcer (indurated and fixed due to histiocytes infiltration) o Histopathological features Ulcer covered with a thick layer of fibrinous exudate Dense chronic inflammatory cell infiltrate in the base of the ulcer involving underlying damaged muscle Deeper parts of the lesion are characterized by an infiltrate rich in histiocytes & Eosinophils ** Called eosinophilic ulcer because it is microscopically infiltrated with Eosinophils o True granulomas aren't present and the condition has no relation to eosinophilic granuloma of bone o Treatment: remove the cause and follow-up to see signs of healing Idiopathic ulceration: Recurrent aphthous stomatitis (RAS): o Idiopathic or immune mediated ulcers
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Dr. Tahani Abualteen


o Natural history is characterized by frequent recurrences ** Ulcers associated with mechanical trauma & dermatological diseases may recur too o 3 types of ulcers are recognized based on their clinical features: minor major and herpetiform ** Any of the 3 types may be associated with Behcet's diseases (syndrome) o Clinical features of RAS: Prodromal symptoms at the sites of future ulcers are recognized by many patients 1-2 days before the onset of ulceration - Soreness, tingling or burning sensations - Red macule Minor aphthous ulceration: Accounts for 80% of RAS 1-5 ulcers (that are shallow, round or oval, with grey/yellow base and an erythematous margin) Affect non keratinized mucosa Less than 10 mm in diameter Heal without scarring within 10 days Recur in 1-4 month intervals 1-10 ulcers Affect any area in the mouth (keratinized & non-keratinized mucosa) ** Common sites: lips, soft palate, tonsils, oropharynx Greater than 10 mm in diameter Heal with scarring within 4-6 weeks Recur in less than 1 month (in severe cases, ulceration of the oral cavity is continuous and may be associated with severe discomfort and with difficulty in eating & speaking) Extends deeper than the shallow minor aphthae and may present as crater-like ulcer with rolled everted margins an Induration on palpation ** Differentiation of isolated major aphthous ulcer from a neoplastic ulcer may be difficult ** History of recurrence guide the diagnosis Herpetiform Ulceration: The least common Affects older age group Hundreds of small pin point ulcers resembling herpetic ulcers Affect any area in the mouth (keratinized & non-keratinized mucosa)
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Major aphthous ulceration:

Dr. Tahani Abualteen


1-2 mm in diameter When several ulcers are clustered together, coalescence can result in larger areas of ulceration of irregular outline Heal in 2-3 weeks (large coalesced ulcers may take longer time to heal and may heal with scarring) Recur in less than 1 month (in severe cases, ulceration of the oral cavity is continuous and may be associated with severe discomfort and with difficulty in eating & speaking) ** Major Aphthous ulcers are usually associated with more severe symptoms ** Differential diagnosis between the three types is based entirely on clinical features

o Etiology of RAS: Most likely immune mediated (there is increasing evidence that damaging immune responses are involved) A number of Co factors (local and general factors) may play a contributory role in a proportion of cases Pathogenesis of RAS: Epithelial destruction is most likely the result of T-cell mediated cytotoxicity Epithelial antigen(s) which are responsible for triggering the immune response leading to the Cytotoxic damage remain unknown However, it is suggested that immune mediated damage may be due to cross-reactivity between streptococcal protein antigens and epithelial plasma membrane proteins ** Cross-reactivity between bacterial and epithelial heat shock proteins (HSP) has been demonstrated ** In susceptible individuals, the host's immune response to streptococcal antigens may also damage the oral epithelium T cell mediated cytotoxicity: CD4 + T cells predominate in the pre-ulcerative phase CD8+ Cytotoxic T cells predominate ulcerative phase CD4 + T cells predominate in the healing phase Hereditary predisposition 45% of patients have family history Mode and pattern of inheritance hasn't been established Trauma May precipitate and influence the site of some ulcers Doesn't play an essential role in the etiology of RAS Emotional stress Precipitating factor Unlikely to be the direct cause of ulceration Stress may be associated with pernicious habits, such as: check biting, which may precipitate and influence the pattern of ulceration

Associated factors: -

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Dr. Tahani Abualteen


Cigarette smoking Reverse relation (protect against RAS) Cessation of smoking onset of RAS Protective effect is maybe due to increased keratinization or systemic mechanism Infective agents? Various microorganisms have been isolated from recurrent oral ulcers but attempts to incriminate them as causal factors have been largely unsuccessful Suggestions: Hypersensitivity to Streptococcus sanguis antigens has been implicated in the pathogenesis of RAS but studies have produced conflicting results Cross-reacting antigens between streptococcus sanguis and oral mucosa has some evidence and there is a possibility that these could be involved in the immune-pathogenesis of RAS Adenoviruses have been isolated from RAS but there's no evidence that they are causal. Their presence may be purely incidental, as so called passenger viruses A rise in IgM antibody titers to Varicella-zoster and CMV at times of recurrences has also been reported but the significance of this is unknown Allergic disorders: Food allergy Some patients with RAS associate the onset of ulceration with certain foods and this, together with the raised IgE found in some patients, has led to the claim that food allergies play a role in the etiology of RAS Results from controlled studies in which patients were challenged with specific foods are inconclusive Hematological disorders Hematological abnormalities associated with deficiencies of hematinics may be found in 20% of patients with RAS Iron (ferritin) deficiency occurs most frequently Deficiencies in folic acid and/or vitamin B12 are also associated with RAS, but much less frequently that Iron The role of hematological deficiency states in the etiology of RAS is unclear, although it is known that deficiencies in Iron, folic acid and vitamin B12 can produce atrophic changes in the oral mucosa Ulceration in some patients improves when the deficiency is corrected, suggesting a causal role Gastrointestinal diseases RAS has been reported in patients with a variety of gastrointestinal diseases, some of which are associated with secondary hematological abnormalities as a result of malabsorption or chronic blood loss Association between RAS and Celiac disease (idiopathic gluten hypersensitivity) is well recognized Incidence of celiac disease in patients with RAS is low (about 2-4%) Minor aphthous type is a common symptom amongst patients with celiac disease
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Dr. Tahani Abualteen


Ras may also be seen in patients with Ulcerative colitis & Crohn`s disease Hormonal disturbance: In small number of female patients a relationship between RAS and the menstrual cycle has been reported Hormonal association in some patients has also been suggested by observations that the onset of ulceration may coincide with puberty and that remissions may occur in pregnancy No consistent association between RAS and the menstruation, pregnancy, or the menopause has been established

o Histopathology of RAS: In the pre-ulcerative stage, there is infiltration of the lamina propria by lymphocytes Small number of lymphocytes also infiltrate the epithelium As the ulcerative stage approaches, there's increased infiltration of the tissues by lymphocytes (especially the epithelium) associated with damage to epithelial cells leading eventually to their death and the formation of an ulcer In the healing phase, the number of lymphocytes decreases ** The fluctuations in lymphocytic infiltration throughout the ulcerative cycle suggests that immune mechanisms are involved in the pathogenesis of RAS ** As the ulcerative phase begins, the population of T lymphocytes capable of inducing Cytotoxic effects (CD8+) in epithelial cells increases within the epithelial infiltrate ** Current evidence suggests that RAS is due to immune-mediated Cytotoxic damage to oral epithelial cells through the activity of T lymphocytes o Diagnosis: Clinical features (site, number, history of recurrence, family history) Histopathological features (non-specific to RAS)

Behcet's disease (syndrome): o Characterized by RAS and at least 2 of the following: Genital ulcers Eye lesions Skin lesions Positive Pathergy test (rapid acute inflammation of skin in response to minor trauma) ** Cutaneous Pathergy test = development of sterile papule of the skin 1 day after injection of saline
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Dr. Tahani Abualteen


o Rare disorder in western countries, and is seen mainly in countries from eastern Mediterranean are to the far east corresponding to the route of the ancient silk traders o Pathogenesis: Genetic predisposition - Strong genetic link with the histo-biocompatibility antigen HLA- B51 Immune mediated mucosal damage (as discussed for RAS) Vasculitis - Associated with the hyper reactivity of polymorph-neutrophils

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