|Traumatic ulcer :
-Most common cause of oral ulcerations.2nd most common is RAS.
-Present for the first time or of recent onset.
-Source of injury is identified.
-single, superficial ulcer (yellowish ulcer surrounded by erythema).
-Location: according to the aetiology( most common in hard palate and lower lip ).
-if it get infected with oral flora (Staph.aureus and candida albican ) there will be small degree of ipsilateral cervical lymph node enlargement , so you should palpate submental and submandibular areas to exclude any infection .
-chronic irritation may cause hyperplasia or hyperkeratosis of the adjacent mucosa.
-Physical ,chemical (aspirin burn: aspirin cause slaving of all mucosa that why it’s appear white).
-Electrical (when there’s gold restoration opposed to silver one ).
-Thermal ( impression materials )
-Fractured, carious, malposed or malformed teeth as well as premature eruption of teeth.
-poorly maintained and ill-fitting dental prosthetic appliances.
-Accidentally biting oneself while talking, sleeping or secondary to mastication.
Removal of the irritant or cause.
Consumption of soft bland diet.
Use of antiseptic and analgesic mouth washes.
Application of topical corticosteroid oral gel.
If the ulceration is accompanied with secondary infection, lymphadenitis and fever, then oral antibiotic therapy is recommended( amoxicillin usually )
Biopsy is needed if there is any suspicion of malignancy, or if the ulcer does not heal within 2 weeks of removal of the cause .
Small lesion :excisional biopsy , large lesion: incisional biopsy.
-Uncommon benign ulcer, develops suddenly.
-it affects middle-aged to elderly adults.
-slight female predominance.
-60% of reported cases in the lateral and dorsal surface of the tongue, followed by lower lip.
-present as: solitary, painful nonhealing deep ulcer ( may cause trauma to muscle and mucosa ).
-Size ranges from few mm to several cm.
- it should be differentiated from neoplastic ulcer.
-with chronic irritation, a reactive hyperplasia of the surrounding epithelium occurs , which appear as a keratosis (raised white border).
*** this keratosis is not present in a neoplastic ulcer which appear as a crater-like defect with raised rolled border and indurated base.
-The cause is unknown in most of the cases.
-sometimes due to sharp teeth or orthodontic appliances ( seen in lateral border of the tongue ).
-or due to crush injury ( seen in the dorsal surface of the tongue ).
- or anesthesia ( seen in lower lip ).
The lesion is self-limiting.
It has a characteristic appearance under the microscope ( certain histopathological features ).
If left untreated, most heal spontaneously within 1 month or more , and this may be accelerated by excisional biopsy.
The source of chronic irritation must be eliminated when an eosinophilic ulcer is due to obvious trauma.
NSAIDs and topical anaesthetic oral rinses (eg lidocaine or dyclonine) may be used to provide temporary relief and comfort when the patient eats.
Topical corticosteroid (eg triamcinolone oral gel or dexamethasone elixir) is often effective.
As a rule, if the lesion does not resolve or if it continues to appear after 2 weeks of treatment, excisional biopsy is warranted.
After biopsy, rapid healing of the ulcer is often typical, and no further treatment is necessary.
-it is a form of eosinophilic ulcer ( in histo-pathologyical finding) that develops in infants, and typically is seen in children aged 1 week to 1 year.
- It usually occurs on the anterior ventral surface of the tongue.
It develops as a result of chronic mucosal trauma from adjacent lower anterior primary teeth, and it usually occurs in association with breastfeeding.
The distinctive, self-limiting ulceration heals spontaneously upon removal of the trauma.
Although extraction of the anterior primary teeth is not recommended, this may resolve the ulceration.
If the teeth are stable, they should be retained and breastfeeding should be discontinued, or a protective shield should be constructed to prevent any further trauma.
These measures are usually sufficient to resolve the condition
Psychiatric ulcer :
- Rarely, oral ulceration may be self-induced (stomatitis artefacta) in the same way that some patients deliberately cause skin lesions in dermatitis artefacta.
- It is sometimes difficult to diagnose, and it is uncommon in children.
- It varies and depends on mode of production.
- Aetiology :
Lesions are produced or perpetuated by the patient’s own action.
External causes include fingernails, sharp instruments, and chemicals.
Location in anterior buccal mucosa and lower lip.
A vague history with frequent recurrence of ulcerations in the same area, which is accessible to the patient, delayed healing, non-specific histological features, and healing without scarring usually leads to diagnosis.
Patients with repeated self-induced ulcerations may be considered for referral to a psychiatrist or psychologist.
*Sideropenic or latent anemia : Hb is normal , ferritin is low( at early stage of the disease ).
* we called a patient anemic ,if Hb level is lower than 12g/dl in female and lower than 14 g/dl in male.
- It is the most common haematological deficiency, and can result in oral ulceration that resemble apthous ulcer.
- Patients usually present complaining of a red sore tip of tongue, especially when eating hot or spicy food, which is an early sign of iron deficiency.
- Clinical examination may not reveal any obvious abnormality; although in long standing cases, loss of the fungiform and filiform papillae ( in the dorsum of the tongue ) produce a smooth surface and a patchy atrophy with thinning of the mucosa which make it more susceptible to superficial ulcers due to trauma. As the deficiency advances, the epithelium becomes eroded , , leaving shallow ulcers resembling aphthae. *** circumvallate papillae and foliate papillae in the back of the tongue
- Occasionally, in severe cases, large chronic ulcers are seen surrounded by areas of hyperkeratosis, which may resemble carcinoma.
- Angular cheilitis( or angular stomatitis ) is common in iron deficiency, and pallor is unreliable, but may occur with low haemoglobin
Poor absorption of iron by the body ( malabsorption , as in celiac disease )
Inadequate daily intake of iron.
Blood loss due to heavy menstruation or internal bleeding.
Growth spurt ( age 10-14 ).
- Diagnosis :
CBC , serum vit.B12 level , WBC total and differential level,serum and red cell folate level and serum ferritin level should be routinely performed. In iron deficiency anaemia the blood picture is of hypochromic microcytic.
Glossitis due to iron deficiency can occur even before the condition has progressed to anaemia, as measured by the haemoglobin level (sideropenic or latent anaemia).
* note : red cell folate level is more accurate than serum folate level because red cell folate gives results about the folate level for months and does not depend on daily consumption .
Analgesic mouth washes for oral ulcers.
Ferrous sulphate or gluconate iron supplement for 3-6 months ( but ferrous gluconate is more tolerable by stomach than ferrous sulphate )
Taking vitamin-C aides iron absorption.
Referral to a haematologist is indicated.
Also called Paterson-Brown-Kelly syndrome or sideropenic dysphagia.
-present as : dysphagia ( due to esophageal web ), glossitis and iron deficiency anaemia.
-the patient complain of burning sensation of the tongue and oral mucosa, and atrophy of lingual papillae produces a smooth shiny red tongue dorsum.
-women at a high risk than men , middle age.
-esophageal squamous cell carcinoma risk is increased.
-genetic factors and nutritional deficiencies.
-serial contrasted gastrointestinal radiography or upper gastrointestinal endoscopy may reveal the web in the esophagus .Biopsy taken of suspicious lesions may show epithelial atypia ( loss of differentiation in single cell ) or dysplasia ( loss of differentiation in large area).
- Blood test show a hypochromic microcytic anaemia .
-primialy aimed at correcting the iron deficiency anaemia.
-patients with PVS should receive iron supplementation in their diet, which may improve dysphagia and pain.
-if no improvement, then the web can be dilated during upper endoscopy to allow normal swallowing and passage of food.
Vitamin B12 deficiency;
Clinical presentation is similar to that iron deficiency anaemia , the initial and most differential sign is red raw beefy tongue which later regresses as the filiform,fungiform and circumvallate papillae atrophy.
Angular chelitis is un common.
- secondary to gastric surgery( because of intrinsic factor that help in absorption if vitamin B12) , autoimmune, due to disease of terminal ileum.
CBC,serum vitamin B12 level ,and antiparietal cell antibodies APCA ( autoantibodies against the intrinsic factor in pernicious anaemia ).
-vitamin B12 deficiency results in Megaloblastic macrocyctic anaemia.
-Schilling test may be helpful .
-Vitamin B12 IM injection of cyanocobalamin 500mg.
-oral vitamin B12 1-2mg daily .
Folic acid deficiency:
-oral mucosal atrophy is un common,angular chelitis always occur.
-cause slow growth rate in children.
-large and prolonged doses of folic acid can lower the blood concentration of vitamin B12,
-Folic acid never be given alone due to the risk of precipitating subacute combined degeneration of the spinal cord.
-result in megaloblastic macrocytic anaemia.
-Malabsorption syndrome like celiac disease ( sensitivity to gluten)
-inadequate dietary intake, pregnancy,cytotoxic drugs and anticonvulsants.
CBC,low serum folate and red cell folate level.
Folic acid tablets , gluten free diet in case of celiac disease.