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20 Cards in this Set

  • Front
  • Back
1. what is the single most numerous bacteria genus in the oral cavity?
2. term for a biofilm w/ bacteria, salivary polymers & EC bacterial products
1. alpha hemolytica streptococci (salivarius is 1st)
2. plaque
Phases: colonization then outgrowth then 2ndary colonization and finaly a climax community
Bacterial disease of mouth: CHRONIC, result of MIXED INFECTIOn, usu caused by NORMAL FLORA, NOT SELF LIMITING - need Rx

Bacteria release things that can damage enamel
plaque and tartar precede caries (tooth decay) - Dx by probing and radiographs
1. where is the periapical portion fo the tooth?
2. presence of what in diet predisposes to caries?
3. bacteria product leading to plaque formation
4. product that causes demineralization of enamel
1. area embeded in the gum
2. sucrose
3. glucans - ECM components
3. lactic acid
1. bacteria in healthy pulp?
2. approach of caries starts what response in pulp (rvrsbl?)

if bacteria breath thru have acute inflam., small abscess formaton & pulp necrosis
1. nope
2. chronic inflammatory response (yes)
1. a painful infection following caries/cavities; traumatic blow to teeth, or entry thru apical foramen of bacteria colonizing peridontal pockets
2. infection of structure surrounding the teeth all the way up to alveolar bone
1. pulp infection; Dx made by clinical sign & radiographs... Rx w/ root canal therapy, open tooth, drill out pulp cavity
2. periodontal teeth
1. relative asymptomatic, mild or intermittent pain; radiolucency in periapical region of nonvital tooth; host defense vs bacteria/degradation products seeping in from necrotic pulp canal
--rarely see bacteria
1. chronic apical osteitis - dying tooth
requires extraction
Acute inflammation and swelling; very painful; large #s of bacteria from necrotic pulp to periapical region; occasional spreads to alveolar bone; **swelling can cause airway obstruction**
1. acute apical abxcess
dx made on clinical signs, pain + swelling as well as radiographic imaging
Rx w/ pulp extirpation, tooth extraction, incision/drainage & antibiotics
1. due to build up of plaque on teeth, a milder reversible form of gum infection that can lead to periodontal disease
2. how 1 rx?
1. gingivitis - inflammation of superficial margin due to plaque bacteria;
**no loss of CT or alveolar bones**
2. removal of plaque and bacteria
1. infection of deeper gingival tissues; plaque derived, chronic progressive loss of CT, exposes root cementum, resorption of alveolar bone, loosing/loss of teeth
1. periodontal disease
healthy gums -> plaque buildup irritates gums, become inflamed then pull away from tooth creating a pocket --> pocket gets deeper, plaque hardens to tartar then + more plaque -> event kills bone supporting the tooth
1. what is the color of root cementum?
2. if it is seen what does this indicate?
3. most common cause of gastric and duodenal ulcers
1. gray
2. periodontal disease due to excessive plaque/tartar
3. h. pylori
Stomach: ph = 2.0; aerobic has pepsin, lipase proteolytic enzymes, transit time = 15-20 min

sparse flora usu streptococcus or lactobacillus sometimes helicobacter
est to be in 80% of pop by age 10 but only 5-10% see disease; more comon in underdeveloped countries/ low socioeco status

person-person; fecal oral or oral-oral
1 a gram (-) microaerophilic, spiral shaped, motile multiple flagella at one pole bug?
2. where does it attach itself
3. what does urease produce for H pylori
1. H. Pylori
2. mucosal wall of stomach or in mucous layer
3. Ammonium that helps to raise pH arround it
5 day infection or weeks H pylori infection
1. rise in gastric pH (near neutral), hypochlorhydria; intense bacterial proliferation & gastric inflam
2. persistent gastritis, acute, severe upper GI Sx, normal gastric pH, inflam. of gastric antrum
1. weeks
2. 5 days
Urease - 10-15% of protein by wt; needed for gastric acidity resistance, ; has a unique structure that allows it to work in acid environment;
1. what are 3 virulence factors of H pylori

Humoral response is ineffective at eliminating H pylori & inflammatory response at low level for life
most infected ppl assymptomatic for yrs
1. Urease, Cag pathogenicity island - secretion sys., Vac A - vacuolating cytotoxin
1. region in bacterial genome where many genes r encoded that allow virulence of the organism?
2. e.g. of this in h pylori
CagA -tyrosin phosphorylation -> SHP-2 kinases -> morpho changes & cell proliferatoin
1. pathogenicity island
2. CagA

peptidoglycan -> NOD 1-> NF-kappa B -> proinflammatory response
1. is Cag more common in gram + or -
2. what does H. Pylori secrete through this mech?

body has the wrong response to H Pylori uses TH1 although not intracellular
1.it is a pump to get proteins out of bacteria needed b/c of the double membrane in gram - bacteria
2. CagA (causes morpho changs and cell proliferation) & Peptidoglycan (proinflammatory response)
1. effects of H. Pylori Vac A?

years - decades w/ H pylor: PUD; chronic superficial gastritis, lymphoproliferative disease, gastric adenocarcinoma
1. proinflammatory, apoptosis, vacuolization, forms membrane channels

chronic irritation caused by infection leads to cancer
H Pylori Path mech:
- prolonged existence in host: evasion of immuno clearance & less potent endotoxin
- ulcer formation through cont. inflam.; mucosal breakdown, erosive gastritis
Adenocarcinoma - takes 15-20 yrs post infection; enhanced cell prolif. 2ndary to chronic infection may increase potential for DNA damage from environmental mutagens
H Pylori Dx: test ppl w/ upper GI Sx;
Rx if PUD & H . pylori or dyspepsia & H. Pylori

Dx - invasive requires a BX, use urease test or histo w/ giemsa / culture
Dx non invasive - seroogy of serum (Ab to it)
Dx - urea breath test w/ labelled C14 urea and see how much is exhaled due to urease breakdown of urea
1. H. Pylori Rx?
1. triple therapy - amoxicillin, clarithromycin + PPI (omeprazole)