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Fundamentals of Oral Disease Flashcards

1
Q

Primary factors contributing to oral disease

6

A
  1. Smoking
  2. Etoh (including mouth wash)
  3. Systemic disease
  4. Medications (dexamethasone can be prone to getting candida infections)
  5. Stress/hormonal changes
  6. Genetics (some individuals are more prone to oral lesions/dz)
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2
Q

What systemic diseases can contribute to oral disease?

5

A
  1. Infections
  2. Diabetes (immunocompromised) ~ thrush due to hyperglycemic levels which promote environment for yeast to grow.
  3. Anemia
  4. Bowel disease
  5. Autoimmune Disease (Bechet’s)
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3
Q

What is Oral Frictional Hyperkeratosis?

A 
excessive growth of stubbornly 
attached keratin (a fibrous protein produced by the body)
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4
Q

Causes of Oral Frictional Hyperkeratosis?

4

A

may happen for a number of reasons and
1. may be genetic
(runs in the family),
2. physiological (normal bodily response to
certain stimuli),
3. pre-cancerous and cancerous. The change
may result from
4. chemical, heat or physical irritants.
USUALLY NONINFECTIOUS

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5
Q

Why should we always refer Oral Frictional Hyperkeratosis?

A

You should refer this to R/O malignancy and ensure it is benign.

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6
Q

Oral Disease Groupings

6

A
  1. “Local” infections
  2. Mucosal dermatologic changes
  3. Halitosis
  4. Pharmaceutical-induced changes
  5. Systemic disease manifestations
  6. Dental trauma
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7
Q

“Local” Infections

9

A
  1. Dental caries/acute pulpitis
  2. Gingivitis/periodontitis
  3. Dental abscesses
  4. Necrotizing periodontal disease (Vincent’s angina)
  5. Ludwig’s angina
  6. “Fever blister” or “Cold Sores”
  7. Herpangina
  8. Thrush
  9. Hairy tongue
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8
Q

Dental caries/acute pulpitis

  1. Cause?
  2. Pathophysiology? 2
  3. Symptoms? 2
A
  1. Cause: Streptococcus mutans and other bacteria
  2. Pathophysiology:
    - Destoys hard tissues of teeth
    - Progresses into dental pulp (acute pulpitis)
  3. Sx:
    - Hot/cold sensitivity
    - Continuous throbbing pain (later)
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9
Q

Dental caries/acute pulpitis

  1. Prevention? 5
  2. Tx? 2
  3. High risk populations? 3
A
  1. Prevention:
    - Fluoride,
    - brushing,
    - flossing,
    - mouthwashes
    - routine cleanings
  2. Tx:
    - Simple caries: restoration
    - Pulpitis: antibiotics and NSAIDs; root canal may be necessary
  3. High Risk Populations:
    - Chemotherapy
    - Diabetics
    - Xerostomia secondary to other causes
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10
Q

What is Gingivitis?

2

A
  1. Inflammation of marginal gingiva (gums)

2. Earliest form of periodontal disease

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11
Q

Etiology of Gingivitis?

Clinical presentation of Gingivitis?
3

Treatment?

A

Etiology:
1. Anaerobes (cause of halitosis) most common cause

Clinical:

  1. Usually painless
  2. Increased bleeding with brushing
  3. Soft tissue separation (“pocket” formation)

In a non-allergy pt, penicillin/amoxicillin has great coverage against anaerobes/Clindamycin as alternative

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12
Q

Dental (periodontal) abscess

  1. PP?
  2. Clinical presentation? 4
  3. Treatment? 2
  4. Prevention?
A
  1. Pathophysiology:
    Gingival soft tissue inflammation/infection
  2. Clinical:
    - Edema,
    - erythema,
    - pyorrhea,
    - pain
  3. Treatment:
    - Oral antibiotic (penicillin or clindamycin)
    - NSAID (prn)
  4. Prevention:
    - Good oral hygiene (brushing, flossing, antibacterial mouth rinses, removal of impacted food debris, routine visits to dental hygienist)
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13
Q

Acute necrotizing ulcerative gingivitis

  1. AKA?
  2. Signs/Sx? 2
  3. Tx? 2
A
  1. Vincent’s angina (Trench mouth)
  2. Signs/Sx:
    - Halitosis
    - Ulcerations of the interdental papillae
  3. Tx:
    - Penicillin (PO) + metronidazole
    - Clindamycin (alone)
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14
Q
  1. Acute necrotizing ulcerative gingivitis is strongly associated with what?
  2. How does it differ from gingivitis?
A
  1. Strongly associated with HIV infection but not pathognomonic
  2. Differs from gingivitis as this is more necrotic and much more serious.
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15
Q

Ludwig’s angina

  1. PP? 2
  2. Signs/Sx? 3
  3. Tx covers what? 2
  4. Tx? 2
A
  1. Pathophysiology
    - Rapidly spreading cellulitis of sublingual (SL) and submandibular spaces
    - Usually begins as infected lower molar
  2. Signs/Sx:
    - Febrile
    - Drooling/trismus
    - Edema in SL area spreading down neck
  3. Tx:
    IV antibiotics covering streptococcus and oral anaerobes
    • Penicillin or ampicillin/sulbactam (unasyn) combination of a beta lactam and a beta lactam inhibitor
    • Plus metronidazole (Flagyl) ~ 500mg PO tid (metallic taste in their mouth)
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16
Q

Herpatic Leisons

  1. Presentation? 2
  2. Etiology? 1
  3. Lesions? 5
  4. Treatments? 3
A
  1. Presentation:
    - Cold sores (“fever blisters”) or
    - painful vesicles on tongue/buccal mucosa
  2. Etiology:
    - HSV-1 (or HSV-2)
  3. Lesions:
    - Vesicles
    - White coated tongue
    - Ulcerative gingivitis
    - Lip lesions
    - Facial lesions
  4. Treatments:
    - Acyclovir (Zovirax) 400mg 5x/d
    - Valacyclovir (Valtrex) 1000tid
    - Valtrex is prophylaxis
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17
Q

Herpangina

  1. Etiology?
  2. Clinical features?
  3. How long does it last?
  4. Tx?
A
  1. Etiology: Picornovirus (not Herpes) called coxsackie virus
  2. Clinical features:
    -PAINFUL, fever, malaise, sore throat
    -Vesicles are present on the soft palate
  3. 7-10 days
  4. Tx:
    Supportive (analgesics)
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18
Q

Herpangina complications can lead to what?

A

dilated cardiomyopathy from the coxsackie virus.

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19
Q

Oral candidiasis (Thrush)

  1. Etiology?
  2. Occurrence? 3
  3. Signs/Sx?
  4. Treatment? 2
A
  1. Etiology: Candida sp.
  2. Occurrence:
    - neonates;
    - prolonged antibiotic use;
    - immunocompromised patients
  3. Signs/Sx:
    - white plaques on tongue/oral mucosa; “burning” tongue; “raw” throat
  4. Treatment:
    - Topical antifungals: clotrimazole (Mycelex) troches or nystatin (swish & spit/swallow)
    - Oral fluconazole (Diflucan) ~ used w/ recurrent candidiasis. 200mg one dose and 100mg for 7 days.
20
Q
  1. What is hairy tongue?

2. What is the coloration?

A
  1. Elongation of filiform papillae of dorsal surface

2. Coloration due to staining (by tobacco or food) or infection with chromogenic organisms (commonly fungi)

21
Q

Mucosal Dermatologic Changes

4

A
  1. Aphthous stomatitis (ulcers) ~ canker sores
  2. Geographic tongue
  3. Oral leukoplakia
  4. Oral cancer
22
Q

Most common oral ulceration, seen in 10-20% of the population

A

Aphthous stomatitis (ulcers)

23
Q

Aphthous stomatitis (ulcers)
1. Etiologies?
5

A
  1. Thought to be an auto-immune process but with numerous etiologies
  2. CMV (cytomegalovirus which is ubiquitous in about 50% of population)
  3. Hormones
  4. Nutritional deficiency (vit B def)
  5. Some studies report predilection for females
    - Hormonal changes
    - Common ages are puberty through age 22
24
Q

Aphthous stomatitis (ulcers)

  1. Lasts how long?
  2. Management? 7
A
  1. Last 7-10 days.
  2. Management
    - Sucralfate (Carafate)
    - Acidophilus
    - Folate
    - Vitamin B12
    - Stress relief
    - Licorice
    - Corticosteroids (dexamethasone or temovate or lidex)
25
Q

What is Geographic tongue? 2

A
  1. Asymptomatic inflammatory condition

2. Rapid loss and regrowth of filiform papillae causes denuded red patches to “wander” across the surface of the tongue

26
Q

Oral leukoplakia

  1. PP? 2
  2. Clinical presentation?
  3. Treatment?
A
  1. Pathophysiology:
    - Benign epithelial hyperplasia
    - Strongly associated with HIV infection
  2. Clinical:
    Asymptomatic lesions usually lateral surfaces of tongue (rarely elsewhere)
  3. Treatment:
    Responds to high dose acyclovir (Zovirax)
27
Q

Oral cancer

  1. Etiologies? 2
  2. Detection?
A
  1. Etiology:
    - TOBACCO / ETOH USE
    - HPV
  2. Detection:
    - All ulcerative oral lesions which fail to heal within 2 weeks should be biopsied
28
Q

Drug-Induced Oral Pathology
-Most pharmaceuticals have oral side effects
4

A
  1. Xerostomia (antihistamines)
  2. Pigmentation changes
  3. Hyperplasia
  4. Mucositis
29
Q

Causes of Halitosis?

7

A
  1. Bronchiectasis
  2. Smokers/alcoholics
  3. Fetor hepatis: fishy odor
  4. Azotemia
  5. Diabetes
  6. H. Pylori
  7. metal poisoning
30
Q

Xerostomia

  1. Pharmacologic causes? 2
  2. Clinical presentation?
  3. Treatment? 2
A
  1. -Diuretics
    -Drugs with anticholinergic effect
    (Antihistamines)
    (Tricyclic antidepressants (not often used for antidepressants. Now used more for neuropathy (neuropathic pain) and sleep)
  2. C/O oral dryness, burning of the tissues, difficulty eating and swallowing, tongue irritation, painful ulcerations, progressively increasing caries and periodontal disease
    • Saliva substitutes
    • Salivary stimulation with sugarless hard candies
31
Q

Describe the pigment changes that each of the following cause:

  1. Tetracycline?
  2. Sedatives, OCP, Antimalarials?
  3. Amalgam tattoo?
  4. Heavy metal pigmentation (bismuth, mercury, lead)?
A
  1. Causes permanent discoloration of teeth and enemel hypoplasia if given during 2nd half of pregnancy or to children from infancy thru age 8
  2. Brown, black or gray areas of oral mucosa pigmentation (disappears following drug cessation)
  3. Blue-black pigmentation in the gingival and mucobuccal fold area
  4. Thin blue-black pigmented line along gingival margin
32
Q

What medications can cause gingival hyperplasia?
3

Treatment?

A
  1. Phenytoin (Dilantin) (~40% of those treated)
  2. Calcium channel blockers (nifedipine)
  3. Cyclosporin

Surgical removal of tissue is effective but hyperplasia recurs if drug is discontinued

33
Q

Mucositis

  1. Etiology? 2
  2. Clinical presentation? 2
A
  1. Etiology
    - NUMEROUS chemotherapeutic agents
    - Radiation therapy to head and neck cancers
  2. Clinical:
    - Edema
    - painful chewing/swallowing of food
34
Q

Systemic disease manifestations

7

A
  1. Diabetes
  2. Anemia
  3. Vitamin deficiency
  4. Mononucleosis
  5. HIV/AIDS
  6. Cancer
  7. Bechet’s Disease
35
Q

Oral problems with diabetes?
7

Treatment and prevention?

A
  1. Acute gingival (periodontal) abscesses
  2. Gingival proliferations/red-gingival hypertrophy
  3. Dry burning mouth
  4. Gingival tenderness/spontaneous bleeding
  5. Lip dryness
  6. Tooth mobility
  7. Periodontal disease

Tight glycemic control

36
Q

Pernicious anemia (vitamin B12 deficiency) can cause what?

A

Glossitis: Smooth, beefy-red and sore (tender) tongue

37
Q

Iron deficiency anemia can cause what?

2

A
  1. Glossitis: Reddened, edematous, smooth, shiny and tender tongue
  2. Angular cheilitis/stomatitis: Erosion, tenderness and edema at corners of the mouth
38
Q

Vitamin Deficiency can cause what?

6

A
  1. Oral mucositis
  2. Ulcers
  3. Glossitis and burning sensations in the tongue (glossodynia) (common with B group deficiencies)
  4. Petechiae
  5. Gingival swelling and bleeding
  6. Teeth loosening and ulcerations (common in vitamin C deficiencies)
39
Q

Mononucleosis oral manifestations?

4

A
  1. Palatal (hard palate) petechiae
  2. Pharyngitis (with or without exudate)
  3. Lethargy
  4. Sore throat
40
Q

AIDS/HIV Infections
HIV immunosuppression predisposes patients to what?
5

A
  1. Oral candidiasis
  2. Necrotizing ulcerative periodontal disease (Vincent’s angina)
  3. Stomatitis (enterics)
  4. Hairy leukoplakia
  5. AIDS pathognomonic oral lesions
    - Oral Kaposi’s sarcoma
    - Oral lymphoma
41
Q

Cancer: Acute Leukemias (especially monocytic) will present how?
5

A
  1. Gingival bleeding,
  2. necrotic ulcers,
  3. gingival enlargement/hyperplasia due to massive infiltration of leukemic cells
  4. Bluish gingival appearance
  5. Oral infections and marked discomfort
42
Q

Radiation therapy for head and neck cancer can cause what oral manifestations?4

Labs? 2

A
  1. Severe oral mucositis with ulcers,
  2. candidiasis,
  3. bacterial infections and
  4. xerostomia

check platelets and coags to R/O cancer as it can be associated with leukemias.

43
Q
  1. Cheilosis (cheilitis) is what?
  2. Presentation?
  3. Etiology? 4
  4. Management
A
  1. Inflammation and small cracks in one or both corners of the mouth.
  2. Presentation
    - Inflammation and/or fissuring of the lips
  3. Etiology
    - Environmental irritation (chapping)
    - Metabolic/Nutritional (diabetes, anemia, thyroid disease, vitamin deficiencies)
    - Poor fitting dentures
    - Infection
  4. Management
    Eliminate cause
44
Q
  1. Sialoadenitis is what?
  2. Usually occur where?
  3. Often seen in what kind of pts? 3
  4. Obstruction results in what?
A
  1. Infections of salivary glands may be viral (mumps) or bacterial (usually secondary to obstruction)
  2. Salivary stones (sialolithiasis) usually occur in the major duct of the salivary gland
  3. Often seen in
    - elderly,
    - debilitated or
    - post-op patients who become dehydrated
  4. Obstruction results in inflammation/infections of salivary glands (sialoadenitis)
45
Q

Clinical presentation of sialoadenitis?

3

A
  1. Edema,
  2. pain (worse with eating, especially tart foods like lemons)
  3. Purulent drainage may be obtained from duct orifice
46
Q

TMJ Dysfunction

  1. What gender?
  2. Describe the pain? 6
  3. Difficulty with what?
  4. What kind of sensation on the tongue?
  5. Complications? 3
  6. Pain/tenderness where?
A
  1. Usually adult female patients
    • Unilateral pain
    • dull, aching,
    • worsening throughout the day
    • in region of jaw,
    • joint “popping” or crepitus,
    • acute otalgia
  3. Difficulty chewing or opening mouth widely
  4. Burning sensation of tongue or palate
  5. -Bruxism (teeth grinding),
    -tinnitus,
    -vertigo
    leads to chgs in bite, height of teeth, etc.
  6. Acute tenderness over TMJ
47
Q

TMJ management?

3

A
  1. Physiotherapy: warm moist compresses 15 min qid for 7-10 days
  2. Pureed diet 1-2 weeks
  3. Analgesics and muscle relaxants

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