Oral Cavity And Helicobacter

Front 1

What are the normal oral cavity flora? When do they colonize?

Back 1

Strep salivarius- less than 6-9 months
Strep mutans and strep sanfuis- over 6-9 months

Front 2

What characterizes bacterial diseases of the mouth?

Back 2

Chronic
Mixed infections of normal flora.
Not self limiting

Front 3

What is plaque? How does it form?

Back 3

Biofilm of bacteria, salivary polymers, extracellular bacterial products.
Pioneer species colonizes--> outgrowth--> secondary colonization--> climax community

Front 4

How do bacteria contribute to production of caries?

Back 4

Dietary sucrose is fermented by bacteria to produce glucans that contribute to plaque and lactic acid that demineralizes enamel.

Front 5

How do infections of the pulp occur?

Back 5

Caries initiates chronic inflammation.
When bacteria break through the pulp, acute inflammation, abscess and necrosis begins.

Front 6

What are features of pulp infections?

Back 6

Very painful
Follow caries, trauma, or entry of bacteria through the tooth apex.

Front 7

What is chronic apical osteitis? Does it involve bacteria?

Back 7

Asymptomatic infection of periapical tissue.
Radiolucency in the periapical region.
Does not involve bacteria.

Front 8

What is acute apical abscess? Does it involve bacteria? What is a potential complication?

Back 8

Acute inflammation of the periapical tissue.
Very painful
Due to bacteria from necrotic pulp or from dental alveolar infection.
Swelling can obstruct airway.

Front 9

What are treatments for acute apical abscess?

Back 9

Pulp extraction
Tooth extration
Incision/drainage
Antibiotics

Front 10

What is ginigivitis? Does it involve loss of tissue?

Back 10

Inflammation of superficial marge of the gums, caused by plaque bacteria.
NO loss of connective tissue or bone.

Front 11

What is periodontitis? Does it involve loss of tissue?

Back 11

Infection of deep gingival tissues, caused by chronic plaque.
Involves loss of connective tissue and alveolar bone, leading to loss of teeth.

Front 12

What are features of the helicobacter pylori organism?

Back 12

Gram negative
Microaerophilic
Spiral shpaed
Motile, flagellated
Embeds within the mucosal layer of the stomach

Front 13

What is the pathogenesis of H. pylori infection from an acute to chronic infection?

Back 13

Acute- severe upper GI symptoms with gastritis and intense inflammation. Normal pH.
Within a few weeks- rise in gastric pH, hypochlorhydria, bacterial proliferation and gastric inflammation.

Front 14

How does urease contribute the pathogenecity of H. pylori?

Back 14

Urease catalyzes the hydrolysis of urea to ammonia and carbon dioxide.
Ammonia creates a neutral microenvironment around the organism to resist stomach acidity.

Front 15

How does the CagA secreting system contribute to the pathogenecitiy of H. pylori?

Back 15

CagA system allows the passage of CagA protein, which causes morphologic changes and inhibits cell proliferation.
Also allows passage of peptidoglycans to create an inflammatory response.

Front 16

How does VacA contribute to the pathogenecity of H. pylori?

Back 16

Cytotoxin that causes vacuolization and perforates membranes of epithelial cells.
Creates urease for use by the bacteria.

Front 17

What are the outcomes of H. pylori chronic infection?

Back 17

Peptic ulcer disease
Chronic gastritis
Lymphoproliferative disease
Gastric adenocarcinoma

Front 18

How does H. pylori contribute to the development of gastric adenocarcinoma?

Back 18

H. pylori infection incites chronic gastritis. Immune responses and other factors lead to gastric atrophy. Hypochlohydria and carcinogens lead to intestinal metaplasia, which produces dysplasia and eventually cancer.

Front 19

How is H. pylori diagnosed?

Back 19

Invasive- urease test of biopsy, culture and histology of biopsy.
Noninvasive- serology of serum, urea breath test.