Aphthous Stomatitis Flashcards

1
Q

Aphthous Ulcers

A

Most common oral mucosal disorder.
• Polygenic mode of inheritance
• >40% of RAS sufferers have 1st degree relatives with RAS.
• Acute and extremely painful recurring mouth ulcers
usually involving non-keratinized oral mucosal sites.
• May interfere with eating, drinking, or swallowing.
• They may be classified as minor, major or herpetiform.

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2
Q

Minor RAS

A
• “Canker sores”
• High prevalence: 5-25%
• 75-85% of all RAS cases
• <10mm in diameter
• Ulcer is shallow, round/oval, a yellow
pseudomembrane with slightly raised
margin and erythematous halo.
• Resolve without treatment in 7-14
days
• No scarring
• Recurrence rates vary
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3
Q

Major RAS

A
  • 10-15% all RAS cases
  • > 10mm in diameter
  • Ulcer is deeper, often with irregular border
  • Healing can take weeks or months
  • May be associated with fever or malaise
  • Predilection for the throat
  • Often leaves scarring
  • Recurrence rates vary
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4
Q

Herpetiform RAS

A
• 5-10% all RAS cases
• Crops of ulcers <5mm in diameter which
may fuse.
• Resolve without treatment in 7-14 days
• No scarring
• Recurrence rates vary
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5
Q

Etiology of RAS

A

vast and unknown!

  • local/oral factors
  • microbial
  • nutritional/allergic
  • systemic conditions/factors
  • genetic/immunologic

Most likely mucosa damage sets the stage and (???) and then triggers a cytotoxic cascade

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6
Q

Ulcer Formation

A

T-helper cells initially predominate and affect a Th1 immune response
• Adjacent keratinocytes express HLA-DR (MHC-class II) and ICAM-1
molecules
• Local blood vessels express E-selectin and VCAM-1 molecules
• Release of pro-inflammatory cytokines eg IL-1, IL-6, TNF-a, IFN-g
• Cytotoxic T-cells mediate keratinolysis
• Neutrophils, macrophages & NK cells also seen

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7
Q

Histopathology of Ulcer

A

Ulcer filled with inflammatory cells and fibrin pseudomembrane

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8
Q

Classification

A

• Simple
- minor, major, herpetiform

• Complex
- diagnosis almost constant presence of greater than 3 oral aphthae or recurrent oral/genital aphthae and exclusion of Behcet’s disease
- forms of complex include
1. primary, idiopathic complex aphthosis
2. secondary complex aphthosis
a. Inflammatory Bowel Disease
b. HIV
c. cyclic neutropenia
d. FAPA (fever, aphthous stomatitis, pharyngitis,
adenitis)
e. Hematinic deficiency (iron, zinc, folate,
vitamins, B1, B2, B6, B12)
f. Gluten sensitivity enteropathy
g. Ulcus vulvae acutum
• Behcet’s
• Magic Syndrome
- NB Magic syndrome may be a systemic
manifestation of BD. Polychondritis affects ears,
nose, throat and ribcage.

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9
Q

HIV-Associated Aphthous

A

CD4 counts <100 cells/mm³ are predisposed
to major RAS
• Other sites may be affected: esophagus,
genitals, anus/rectum
• We see this less frequently since ART
• Diagnosis is important, particularly if no
prior history

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10
Q

Periodic fever, aphthosis, pharyngitis, adenitis syndrome (PFAPA)

A

Marshall’s syndrome
•Unknown cause: bacterial ?
• Affects young children (mean age <5 yrs)
• Periodicity of episodes q3-4 weeks
•High fevers lasting 4-6 days (up to 40ºC)
• Perfect health between episodes

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11
Q

Hematinic Deficiencies

A
  • Equivocal associations with iron, Vit B1, B2, B6, B12, and folate.
  • Blood tests are not recommended routinely in all patients with RAS.
  • Indications for blood work:
  • Older patient with recent RAS history
  • Suspicious medical history/review of systems
  • Strict vegetarian patients
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12
Q

Celiac Disease

A
Celiac sprue or gluten-sensitive enteropathy
• Small intestinal malabsorption
• 4% of patients presenting with RAS
• Gluten-rich foods: cereals eg wheat, rye, barley
• European descent, 7:1 female:male
• Associated clinical findings:
• chronic diarrhea or flatulence
• Laboratory findings
• é IgG and IgA antigliadin &amp; IgA anti-endomysial levels
• Malabsorption tests
• Treatment
• strict gluten-free diet
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13
Q

Reiter’s Syndrome

A

• Reactive arthritis usually following dysentery or a sexually transmitted
infection
• HLA-B27-positive
• Oligoarthritis (knee/ankle), conjunctivitis, urethritis, and mouth ulcers
most common features

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14
Q

Smoking & RAS

A

• Cigarette smoking prevents RAS
• Increase keratinization &/or effects of nicotene ?
• Use of smokeless tobacco & nicotine therapy may have a beneficial
effect on RAS.

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15
Q

Others for Complex

A

• Sweet’s Syndrome
- Acute febrile neutrophilic dermatosis
- May occur in conjunction with leukemia
• Cyclic Neutropenia
• Medication-induced RAS

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16
Q

Behçet’s Disease

A

Recurrent inflammatory disorder of unknown cause:
bacterial ?
• Affects Middle Eastern Males & Asian Females
• Onset 3rd-4th decade
• HLA-B51 association
• Recurrent aphthous ulcers generally precede other signs:
genital/skin/eye lesions & others (arthritis, GI lesions, CNS
symptoms, vascular lesions)
• Diagnosis based upon criteria: no laboratory tests

17
Q

Steps in managing RAS patients

A
History of RAS
• Medical History
• Medications
• Review of Systems
• Social History
• Dental History
• Diet/Nutritional History
• Physical Examination
• Laboratory Tests
18
Q

History of RAS Outbreaks

A
Onset (childhood vs adult)
• Level of pain &amp; quality of life
• Dysphagia
• Weight loss ?
• Recurrence rate
• Healing time
• Possible precipitating factors
• Extra-oral ulcers (eg genitals)
• Prodrome ?
• Associated signs &amp; symptoms during episodes
19
Q

Medical History

A
• Associated medical conditions
• Review of systems
• Skin, GI, throat, eyes, joints, genitals, neurological system, immune system,
hematological
• Medications
• NSAIDs, nicorandil (UK)
20
Q

Social History

A
  • Tobacco history
  • Recrudescence since tobacco cessation ?
  • Alcoho
21
Q

Oral/Dental History

A
  • Oral hygiene practices/products

* Dry mouth

22
Q

Diet/Nutritional History

A
  • Able to eat ?
  • Foods
  • Gluten ?
  • Citrus
  • Vegetarian ?
23
Q

Physical Examination

A
  • Extra-oral
  • Lymphadenoapathy ?
  • Skin ?
  • Intra-oral
  • Number, location, size
24
Q

RAS Treatment Plan

A
Treatment dictated by:
• Associated symptoms &amp; ability to function
• Number &amp; location of ulcers
• Recurrence history
• Possible underlying cause
Consider 4 options (can combine):
• No treatment
• Prevention/treatment of/for possible causes
• Topical therapy
• Systemic therapy
• Referral for severe disease
25
Q

Infrequent Minor RAS TXT

A

Treatment to reduce pain

OR NO TXT

26
Q

Frequent Minor RAS or Major RAS TXT

A

Treatment to reduce pain v.
Treatment to reduce healing time v. Treatment to prevent recurrences

• Repair sharp
teeth/restorations
• Remove plaque
•Optimize lubrication

27
Q

Topical Therapy Categories

A

• Topical anesthetic agents
• Surface protective agents/bioadhesives
• Anti-inflammatory/immunomodulatory agents
• Anti-microbials
• Chemical/physical cautery
• Lasers
Over-the-counter (OTC) versus prescription (Rx)

28
Q

Rx Topical Treatments: Cautery

A

• Debacterol (Sulfonated phenolics; sulfuric acid
solution)
• Chemical cautery
• Label: one time application for 5-10 seconds

29
Q

Rx Topical Treatments: Corticosteroids

A

Triamcinolone acetonide in Orabase 0.1% (intermediate)
• Disp: 5g tube
• Label: apply a thin film over ulcer after meals and bedtime
• Do not use for more than 2 weeks
• Fluocinonide gel or ointment 0.05% (Potent)
• Disp: 15g tube
• Label: apply a thin film over ulcer after meals and bedtime
• Do not use for more than 2 weeks
• Clobetasol ointment 0.05% (Ultra potent)
• Disp: 15g tube
• Label: apply a thin film over ulcer bid
• Do not use for more than 2 weeks

30
Q

Rx Topical Treatments: Corticosteroid Rinse

A

Dexamethasone elixir 0.5mg/5ml (ETOH base) or
solution (H2O base) Indicated for multiple or
difficult to reach lesions
• Disp: 600ml
• Label: swish with 5-10 ml for 5 minutes up to
4x/day and expectorate
• May be used as preventive therapy in selected
patients with close surveillance

31
Q

Problems with Topical Treatments

A

Drug is easily washed away or rubbed off
• Topical anesthetics have a short-lived effect
• Often difficult to apply due to location
• Cost may be a disincentive to buy OTC/Rx

32
Q

Prednisone

A

• Glucocorticoid & immunosuppressant
• Decreases inflammation by suppressing chemotaxis of polymorphonuclear
neutrophil leukocytes, reduces capillary permeability lymphocytic activity.
• Used to gain initial control of severe disease
• Dose: initially give 0.5-1.0 mg/kg a day for 1 to 2 weeks and monitor the patient’s
response
• If there is no response, dosage should be increased in 0.25 mg/kg increments a
day until the lesions respond, complications arise, or a maximum dose of 2.0 to
2.5 mg/kg is reached
• Multiple adverse effects with long-term use