Oral dermatology: Canker sores and aphthous ulcers

Oral dermatology: Canker sores and aphthous ulcers

Introduction 

I. Canker sores: 

1. Definition 
2. Epidemiology
3. Etiopathogenesis
4. Clinic: Mechanisms of occurrence 
5. Differential diagnosis 
6. Treatment
   1. First-line treatments
   2. Non-specific treatments 
   3. Treatments for severe canker sores 
   4. Therapeutic strategies 

II. Aphthous ulcers: 

1. Introduction 
2. Classification 
3. Clinical forms
4. Diagnosis of secondary aphthosis 
5. Diagnosis of Behçet’s disease 
6. Aphthosis and HIV 
7. Treatment of aphthosis
   1. Etiological treatment 
   2. Preventive treatment  
   3. Therapeutic strategy

Conclusion 

Introduction :

Aphthae is the most common lesion of the oral cavity. It is important to know how to recognize and classify it according to its clinical manifestation, isolated, or found in oral aphthosis. 

I. Canker sores 

1. Definition : 

Superficial lesion of the oral mucosa and oropharynx of unknown etiology. 

The word “ Aphte ” comes from the Greek “ aphta ” which means ulcer or burn.

This is the most painful ulceration, causing difficulty in chewing, swallowing and maintaining oral hygiene. Oral ulcers can be isolated or part of an aphthous ulcer affecting other organs (Behçet’s disease). 

They can be sporadic (canker sores) or recurrent (aphthosis), trivial or severe.

2. Epidemiology  :

• Canker sores affect 5 to 25% of the population.
• Begins in adolescence with a tendency to decrease in frequency and severity with age. 
• 80% of canker sores develop before the age of 40.   
• Aphthous ulcers have been reported in 2 to 4% of HIV positive patients.
• There is no geographical distribution  
• A certain predominance seems to exist among women and non-smokers.

3. Etiopathogenesis: 

1. Genetic etiology: concept of familial aphthosis. 
2. Immune pathogenesis: Aphthous ulceration appears to be due to a cytotoxic action of TCD4-CD8 lymphocytes and monocytes.
3. Local predisposing factors: involvement of local traumatic factors (tooth brushing, dental prosthesis, intraoral injection, etc.) 
4. Smoking: appears to have a protective effect on the mucous membranes. 
5. Vitamin deficiencies (vitamin B1-B2-B6-B12), folic acid and iron deficiency.
6. Gastroduodenal disease (celiac disease, Crohn’s disease).
7. Hormonal influence.
8. Drug-induced injury (nicorondil used in the prevention of angina). 
9. Clinic: Mechanisms of occurrence: 

A common mouth ulcer goes through four phases:

1. Prodromal phase  : tingling or burning sensations lasting less than 24 hours; it is often absent in Behçet’s disease.
2.  Pre-ulcerative phase: during which one or more erythematous, macular or papular lesions develop, or perhaps even vesicular ones (ephemeral vesicles that are most often unnoticed), with increasing pain.
3. Ulcerative phase: the ulcer then ulcerates, in a punctiform or lenticular manner, but never bleeds , persists for a few days to a few weeks, with pain that gradually diminishes.

Typically 2 to 10 mm in diameter, with a yellowish necrotic background, 

“Fresh butter”, then grayish. Its edge is clean , cut with a punch, with a bright red inflammatory peripheral border. The base , very slightly edematous, remains flexible and not indurated.

4. Re-epithelialization phase (painless, from a few days to a few weeks).
5. Differential diagnosis: oral aphthae should not be confused with: 

• Traumatic ulceration 
• Syphilis or tuberculosis inoculation chancre 
• Malignant tumor ulceration: squamous cell carcinoma.

Oral dermatology: Canker sores and aphthous ulcers

6. Treatment : 

6.1 First-line treatment: 

• Local anesthetics: short duration of action, the most effective is lidocaine (Xylocaine® viscous 2% oral gel, Dynexan® 2%) applied directly with the finger to the ulcer.

• Sucralfate mouthwash 4 times a day. 

• Topical corticosteroids are the most commonly used treatments. They work by reducing inflammation. (Dermoval®, Diprolène®) in an adhesive paste (Orabase®) in equal quantities and apply them 2 to 4 times a day until the ulcer has healed. 

• Antiseptics: mouthwashes, chlorhexidine and triclosan 

• Cyclines: 4 times a day.

• Physical treatments: cauterization of the canker sore (trichloroacetic acid)

         6.2 Non-specific treatments

• Paracetamol: systemically 
• acetylsalicylic acid in mouthwashes (3 to 4 g diluted).
• Injection after local anesthesia with viscous Xylocaine®, a few drops of Kenacort® retard at 40 mg/ml intralesionally 

3. Treatments for severe mouth ulcers: systemic treatment 

• Prednisone (1 mg/kg/day) for 1 week 
• Thalidomide has demonstrated its efficacy in the treatment of severe forms of mouth ulcers in HIV-positive patients, at a dosage of 200 mg/day for 4 weeks. 

       6.4 Therapeutic strategies: 

Minor flare-ups: a local analgesic is sometimes sufficient, preferably lidocaine gel.

Common canker sore outbreaks: combine local analgesics with very strong local corticosteroids, possibly in an adhesive paste (Diprolène ® ointment and Orabase®).

More extensive attacks with posterior involvement: combine local corticosteroids with sucralfate mouthwashes 3 to 4 times a day.

Severe forms with very disabling giant mouth ulcers preventing eating: Thalidomide combined with local corticosteroids and sucralfate.

Oral dermatology: Canker sores and aphthous ulcers

II. Aphthous ulcers: 

1. Definition : 

Multiple canker sores developing in flare-ups lasting 3 to 10 days, recurring at least twice a year. Canker sores pose two problems: diagnostic and therapeutic. 

2. Classification  : aphthous ulcers are classified according to six clinical and evolutionary criteria (Table)

Criteria	Common aphthosis	Multiple aphthosis	Miliary aphthosis	Giant aphthosis	Recurrent aphthosis
Number	1 3	3 10	10 100	Unique++
Size	< 1 cm	< 1 cm	< 0.3 cm	> 1 cm
Frequency of thrusts	Less than 4 per year				More than 4 per year
Duration of thrusts	7 – 14 days		7 – 14 days	15 – 60 days

3. Clinical forms: We distinguish: Common aphthosis, Multiple aphthosis, Miliary aphthosis, Giant aphthosis, Aphtosis and AIDS, Extraoral forms, Oral aphthosis 

3.2 Common aphthosis (banal-vulgar-simple):

The flare consists of 1 to 3 elements, measuring 3 to 10 mm in diameter. Evolving spontaneously in 8 days towards healing without leaving a scar. Triggering circumstances are sometimes mentioned:

• Food (nuts, gruyere, strawberry, chocolate, tomato, fruit skin)
• Dental care (scaling, saliva cotton)
• Stress, fatigue.

Outbreaks are rare with latency periods of several months; it can begin in early childhood.

3.3 Multiple aphthosis: Rarer, made up of 4 to 10 clearly individualized elements.

Sometimes confluent, they take on a “herpetiform” appearance evoking an outbreak of recurrent herpes. This form heals in about ten days.

Treatment is symptomatic as for common aphthosis.

The differential diagnosis is discussed with:

• Herpes
• Erosive lichen planus, 
• More rarely bullous stomatitis-erythema multiforme

            3.4 Miliary aphthosis: The lesions are very numerous, with 10 to 100 punctiform elements, rarely confluent. Miliary aphthosis must be differentiated from primary infection herpetic stomatitis, the clinical diagnosis of which is sometimes difficult, but certain elements can point towards viral infection, namely:

• Confluence of elements creating ulcerations with polycyclic contours,
• General malaise, fever and ADP,
• Perioral lesions.

5. Giant aphthosis: 

Characterized by the significant size of the ulcers, greater than 1 cm, which can reach 3 cm. The ulceration is sometimes infiltrated with edema, sometimes necrotic and evolves over several weeks, sometimes several months. The evolution towards healing is at the cost of retractile scars

4. Diagnosis of secondary aphthosis:

Aphthae or aphthous ulcers are observed in several general diseases that they can reveal. Also, the interview must specify the medication taken, the existence of digestive signs and look for malnutrition.

Cause	Disease
Inflammatory enterocolopathies	– Crohn’s disease, UC (ulcerative colitis) – Celiac disease
Vitamin deficiencies	– Iron, folate, vitamin B12 deficiency and Biermer’s disease – Zinc deficiency
Hematological causes	– Idiopathic cyclic neutropenia – Agranulocytosis (iatrogenic, leukemia, etc.)
Drug causes	-b-blockers- Non-steroidal anti-inflammatory drugs- Nicorandil
Systemic diseases	– Behçet’s disease, vasculitis, lupus.- GVH (graft versus host disease), Sweet’s syndrome
Infectious	– HIV

5. Diagnosis of Behçet’s disease: 

Behçet’s disease is a relapsing, chronic, inflammatory multisystem disease of unknown cause. 

Diagnostic criteria for Behçet’s disease:

Criteria	Comment
1. Recurrent mouth ulceration	Common, giant or miliary aphthae, observed by the doctor or the patient, with a recurrence of at least 3 times in 12 months  Diagnosis: plus 2 of the following 4 criteria  :
2. Recurrent genital ulcers	Aphthous ulcer or scar, observed by the physician or patient
3. Eye injuries	Anterior or posterior uveitis diagnosed by the ophthalmologist
4. Skin lesions	Erythema nodosum, pseudofolliculitis, papulopustular lesions, acne nodules
5.Pathergy- positive  test hypersensitivity at the injection site	Read by the doctor after 24-48 hours

6. Aphtosis and HIV: Giant necrotic aphthae are frequently encountered during AIDS with a probable correlation to a low CD4 count. Ulcerative necrotic gingivitis is often observed.
7. Treatment of aphthous ulcers 

Oral dermatology: Canker sores and aphthous ulcers

7. Etiological treatment: 

Secondary aphthosis: treatment of the cause, if possible. This is particularly the case for aphthae caused by medication.

Idiopathic oral aphthosis Behçet’s disease aphthosis: curative treatment is often insufficient, preventive treatment of flare-ups is therefore necessary.

          8.2 Preventive treatment: 

The therapeutic methods are the same for all aphthosis.

Drugs used: Thalidomide, Colchicine, Etanercept, Azathioprine, Cyclosporine, Sucralfate, Pentoxifylline Interferon

Note: The first-line treatment for recurrent oral aphthosis is colchicine. 

8.3 Therapeutic strategy: 

• First-line treatment: colchicine, at a dose of 1 to 2 mg/day in one or two doses. 
• After 2 to 6 months of effectiveness, the dosage is reduced to 0.5 or 1 mg/day every 2 days. 
• If colchicine fails, Disulone® at a dosage of 100 mg/day. 
• It can be combined with or replaced by sucralfate mouthwashes.
• In severe recurrent oral aphthosis resistant to these two treatments, it is permissible to offer thalidomide at a dosage of 50 mg/day, which can be increased to 100 or 200 mg as an attack treatment.

III. Additional examinations: in general the clinical picture is characteristic. However, the following may be requested:

• A biological assessment for the purpose of etiological diagnosis (FNS looking for anemia, neutropenia) dosage of vitamin B12 and folate
• Serological examination (HIV, BW for syphilis)
• Biopsy: if ulceration persists. 
• Investigations in case of suspected Behçet’s disease 
• Gastro advice. 

Conclusion :

Knowledge of the clinical manifestations as well as the clinical aspect of oral aphthosis is essential, in order to establish a diagnosis , it is necessary to know how to classify and identify isolated attacks and those which can be part of a more complex clinical picture, namely AIDS and Behcet’s disease, the complete clinical examination must be methodical based on a good interview allows the pathology to be labeled.

Oral dermatology: Canker sores and aphthous ulcers

  Wisdom teeth can cause infections if not removed.
Dental crowns restore the function and appearance of damaged teeth.
Swollen gums are often a sign of periodontal disease.
Orthodontic treatments can be performed at any age.
Composite fillings are discreet and durable.
Composite fillings are discreet and durable.
Interdental brushes effectively clean tight spaces.
Visiting the dentist every six months prevents dental problems.
 

Oral dermatology: Canker sores and aphthous ulcers