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DENT 1530 > misc lectures for midterm > Flashcards

misc lectures for midterm Flashcards

1
Q

1-dental caries

A

1-multifactorial—tooth, bacteria, diet. bacteria will accumulate at specific tooth to form plaque (biofilm)

  • can ferment sugars & carbs to form lactic acid—acid generation can result in microscopic dissolution of minerals in tooth enamel & formation of opaque white/brown under enamel
  • frequency of carb consuption, physical characteristic of food, & timing of food intake
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2
Q
A

radiolucent

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3
Q

1-horizontal angulation

2-advantage of bitewing radiograph

3-detection

4-radiographic detection

A

1-adjusted so that line connecting front and back edge of PID is parallel w/ line conecting buccal surfaces of premolar & molars

2-bc of horizontal angulation of bitewings, help assess secondary caries that may not be seen in periapical
-calculus detection in interproximal area

3-30-40% demin is needed for radiographic detection of a lesion

  • thickness of tooth buccolingually masks the carious lesion when small
  • depth of penetration of a lesion is deeper clinically than radiographically

4-visual exam of teeth may not find caries if surface is intact due to remin (not cavitated)…radiographs may be only way to detect caries if surfaces are intact

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4
Q

1-shape of carious lesion

2-factors affecting caries diagnosis

A

1-early lesion in enamel—a triangle w/ braod base at tooth surface spreads along enamel rods

  • notch, dot, band, or thin line are commonly seen
  • when lesion reaches DEJ a second triangle w/ apex projected to pulp chamber

2-buccolingual thickness of tooth
2 dimensional film
xray beam angle
exposure factors

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5
Q
A 
left= E
Right= D1
Bottom= D2
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6
Q

1-E

2-D1

3-D2

4-spread of caries

A

1-lesion penetrates though enamel (incipient)
radiolucent triangle w/ base at enamel surface & point to DEJ

2-lesion penetrates into dentin but is less than 1/2 through thickness of dentin toward pulp
radiolucent triangular lesion in enamel and point less than halfway to dentin

3-lesion extends more than 1/2 of dentinal thickness towards pulp

4-caries spread through dentin more rapidly than enamel because dentin is softer than enamel

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7
Q

1-metallic restorations

2-temporary restorations

3-composite restorations

4-cervical burnout

A

1-metallic restorations are radiopaque, no transmission of xrays—amalgam & gold

2-somewhat radiopaque: IRM, ZOE

3-somewhat radiopaque bc of fillers—some can be radiolucent (older materials)

4-between CEJ & alveolar crest
diffuse radiolucency
ill-defined borders
presence of edge of root
clinical evaluation

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8
Q
A

cervical burnout

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9
Q

1-occlusal caries

2-buccal/lingual caries

3-root caries

4-secondary/recurrent caries

A

1-penetrated into dentin, diagnosed from clinical exam
-sharp explorer may contribute to spread of caries

2-use clinical exam & cant determine depth

3-older patients w. recession or periodontitis
xerostomia may be present

4-occurs adjacent to pre-existing restoration

  • inadequate cavity prep
  • defective margins or incomplete removal of caries before restoration placement
  • high caries incidence, poor oral hygiene
  • –recurrent caries=radiolucent beneath restoration, usually seen beneath interproximal margins of restoration
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10
Q

1-full mouth series

2-types of surveys

3-alveolar bone

4-alveolar bone proper

5-alveolar bone

A

1-look at lamina dura, crown:root ratio, interproximal bone, furcation involvement, periapical path, overhangs, calculus, & resorption

2-periapical, bitewing (horizontal & vertical), panoramic films, CT scans

3-alveolar crest, interproximal bone, & interradicular bone

4-cribriform plate

5-crestal lamina dura, perio ligament space, lamina dura

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11
Q

1-alveolar crest

2- interdental bone/septa

3-crestal bone

4-radiographic signs of periodontitis

A

1- 2 mm from cej & is angular

2-pointed crest & flat crest

3-follows the CEJs

4-early disease may not show changes…look for thinning/absence in crestal lamina dura or cupping

  • may show signs of uneven buccal/lingual bone loss
  • evidence of furcational bone loss? triangle in upper molars
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12
Q

1-horizontal bone loss

2-vertical bone loss

3-comparison of horizontal & vertical bone loss

4-optimal radiographic technique

5-horizontal bitewings

A

1-crest of bone is parallel to CEJ line between adjoining teeth…remaining bone = horizontal but positioned apically

2-crest of remaining bone isnt parallel to CEJ line between adjoining teeth= oblique angulation to CEJ line

3-use CEJ of adjacent teeth as a guideline for either

4-optimizes assessment of alveolar cortication & bone heights

  • visualizes crown/root ratio & root lengths
  • beam quality/energy= higher kVp= subtle changes better
  • long cone paralleling technique is used bc of its superior diagnostic yield

5-missing the maxillary crestal bone

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13
Q

1-vertical angulation

2-horizontal angulation

3-normal alveolar crest

A

1-correct vertical angulation records crestal bone= no bone loss between mandibular 1st and 2nd molars
-incorrect vertical angulation= radiolucent, cupping out appearance of lamina dura = false indication of bone loss between teeth

2-correct horizontal angulation= doesnt reveal vertical defect on mesial of maxillary first molar
-slightly varied horizontal angulation of same region= vertical bony defect

3- 1-2 mm apical to CEJ, parallel to line joining CEJ of adjoining teeth, smooth, continuation of lamina dura

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14
Q

1-evidence of early periodontitis

2-radiographic examination

A

1-localized erosion of crest of bone
blunting of crest-anterior teeth
loss of sharp angle between lamina dura & crest
widening of PDL near crest

2-continuity of lamina dura (crestal), PDL space,
root proximity
type & percentage of bone loss
furcation involvement
concurrent factors—calculus, caries, defective restorations, periapical path, fractures

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15
Q

1-contributing factors

2-healthy/gingivitis

2-slight chronic periodontits

4-limitations of perio radiographics

A

1-calculus & amalgam overhand are likely to collect bacterial pathogens that can contribute to progression of perio disease

2-radiopaque flat appearance of lamina dura & thin radiolucent line of PDL space

3-slight radiolucent cupping out of lamina dura,
radiopaque calculus is visible on proximal surfaces of teeth, looking at alveolar crest
-blunting of lamina dura & slight radiolucent widening of PDL—radiopaque calculus is visible

4-doesnt show perio pockets
doesnt show morph of defects
misses buccal & lingual deformities
doesnt distinguis between treated & untreated case

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16
Q

1-intial comprehensive oral exam

2-patient interview

3-perio conditions

4-contraindications to treatment

A

1-interview, extraoral exam, intraoral exam, radiograph, consultations, photos, casts

2-demographic, complain, history, social history, dental history & exam

3-bleeding gums, loose teeth, drifting teeth, food stuck, foul taste in mouth, itchy feeling in gums, dull/throbbing pain, receding gums

4-affect symptoms= uncontrolled hypertension
modify treatment= uncontrolled diabetes
need for premedication= anticoagulant therapy

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17
Q

1-gingival enlargement

2-xerostomia

3-social habits

4-gingival inflammation

A

1-interaction of phenytoin, cyclosporine, & Ca channel blockers w/ epithelial keratinocytes, fibroblasts & collagen can lead to an overgrowth of gingival tissue in individuals
-gingival inflammation & plaque= cofactor that induces gingival overgrowth

2-500 drugs reported to cause xerostomia as side effect

  • anticholinergic medications reduce salivary flow
  • sympathomimetic medications make less salivary volume & more viscous saliva

3-smoking, substances, oral habits

4-color, contour, & consistency

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18
Q

1-function of perio probes

2-clinical signs of inflammation

3-UNC Probe

4-Goldman Fox

5-furcation probe

A

1-perio probe is calibrated instrument used to measure the depth of gingival crevice—perioe probe accurate way to assess supporting tissues of dentition

  • measure crevice, CAL, width of keratinized gingiva, bleeding & size of lesions
  • mini rules
  • blunt, rod shaped working end may be ciruclar or rectangular in cross section

2-redness, glossy, loss of stippling, bleeding on probing & suppuration

3-1-12 mm markings

4-1-10 mm

5-furcation probes have curved, blunt tipped working ends that allow easy access to furcation ends—double ended—NABERS 2N

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19
Q

1-probing health vs diseased tissue

2-5 mm perio pocket

3-measurement

4-probing essentials

A

1-pressure exerted w/ probe tip to base of gingival crevice between 10-20 g

2-healthy crevice will have depth of 1-3 mm
measurement at 6 sites

3-at 6 sites

4-modified pen grasp, stable fulcrum= finger rest

  • exploratory/light pressure
  • short walking strokes
  • side of probe remains in contact w/ tooth surface
  • slight angulation under contact
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20
Q

1-walking the probe

2-adaptation

A

1-walking stroke is movement of calibrated probe around perimeter of base of crevice

  • cover entire circumference of crevice base
  • probe is inserted into crevice while keeping probe tip against tooth surface
  • press apically until tip encounters resistance of base of crevice
  • base of crevice feels soft & resilient when touched by probe
  • record deepest measurement

2-side of probe tip should be kept in contact w/ tooth surface

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21
Q

1-interproximal technique

A

1-slant probe slightly so tip reaches under contact area while upper portion touches contact area

  • with probe in position gently probe apically to reach base of crevice
  • be careful not to overangle probe
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22
Q

1-width of keratinized gingiva

2-frenum pull

3-gingival recession w/ lack of attached gingiva

A

1-mucogingival condition
-lack of keratinized gingiva is a risk factor for attachment loss

-gingival recession= reduced gingival width

2-frenum pull w/ retraction of gingival margin is a risk factor for attachment loss

3-width of attached gingiva= gingival width minus probing depth
keratinized ginigva doesnt mean attached gingiva
-measure recession from gingival margin to NCCL

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23
Q

1-examing furcations

2-furcation probe

3-class 1 furcation

4-class 2 furcation

5-class 3 furcation

6-class 4 furcation

A

1-assessing attachment loss in furcations = comprehensive perio exam

2-insert tip of probe under gingival margin as a straight probe and rotate the tip towards root surface
-use walking motion along root surface and probe for entrance of furcation

3-incipient furcal involcement

4-patent furcal involvement

5-communicating furcal involvement

6-clinically visible furcation

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24
Q

1-mandibular molars

2-maxillary molars

3-maxillary 1st premolar

4-tooth mobility

5-local factors

A

1-facial/buccal and a lingual furcation

2-facial/buccal furcation is accessed from facial
mesial & distal furcations are accessed from mesiolingual & distolingual

3-mesial furcation is accessed from mesial
distal furcation is accessed from distal

4-class 1\< 1 mm
class 2 up to 2 mm
class 3 greater than or equal to 2 mm

5-sharp tip of explorer
gently feel root surface for accretions, root surface irregularities, & fit of restorations

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25
Q

1-probe crevicular depth

A

1-insert probe at proximal (distal mesial) line angle

  • assess area beneath contact area by bringing probe into contact area & then slightly tilting the probe & extending the tip beneath contact area
  • press probe down gently to probe the base of crevice
  • position probe as parallel as possible to long axis of tooth surface being probed
  • adapt tip of probe to surface as up and down strokes w/in crevice
  • walk probe around circumference of crevice using strokes—light stroke pressure
  • 6 measurements per tooth
  • use furcation probe to assess attachment in root furcations
  • use explorer to assess for root accretions & irregularities and marginal integrity of restorations
26
Q

1-Amalgam

2-dental amalgam

A

1-1st used in erope
GV Black used dental amalgam formula
-since its inception there have been controversy about dental amalgam bc of the mercury component

2-amalgam is a solution of any metallic element in mercury
-mercury, silver, tin, copper, zinc

27
Q

1-traditional: silver, tin, copper, zinc

2-high copper: silver, tin, copper, zinc

3-silver

4-tin

5-copper

6-zinc

A

1-60%, 29%, <6%, <2%

2-40-70%, 12-30%, 12-30%, 0-1%

3-inc strength

4-controls expansion, lengthens setting time

5-inc strength, reduces corrosion, reduces creep & marginal breakdown

6-prevents oxidation

  • when contaminated w/ mositure during placememnt, Zn amalgam exhibited delayed expansion
  • Zn free amalgam is used
28
Q

1-indium

2-palladium

3-platinum

particles

4-lathe cut

5-spherical

6-ad mix

A

1-permite SDI= reduces creep, inc strength

2-valian phD- reduces corrosion & tarnish

3-logic+ = inc compressive & tensile strength

4- irregular shapes cut from a mold by lathe

5-molten material is sprayed into cold room, material forms spehres since a sphere is most stable shape w/ lowest surface energy

6-combination of spherical & lathe cut particles

29
Q

1-spherical amalgam

2- admix amalgam

3-amalgamation

4- gamma

5-gamma 1

6-gamma 2

7-eta

A

1-needs less mercury, less condensation forces, develops compressive strength earlier than lathe cut
smooth surface texture

2-higher condensation forces required
easier to produce proximal contact areas in proximal restorations

3-physically distincy, homogenous & mechanically separable portion of alloy in microscopic structure

4-unreacted alloy powder is gamma

5-silver mercury

6-tin mercury —low copper alloy

7-copper tin—high copper alloy

30
Q

1-conventional amalgam

2-high copper amalgam

3-amalgam reaction

A

1-low copper: gamma + Hg= gamma + gamma 1 + gamma 2
gamma 2= weakest

2-12% copper: gamma + Hg= gamma + gamma 1 +eta
high copper allows eliminate gamma 2
elimination of weak gamma 2 phase improves properties of high copper amalgam

3-set amalgam has unreacted allow (gamma) 50%- imp for corrosion, resistance & strength
-little or no mercury remains unreacted

31
Q

1-properties of amalgam compressive strength

2-strength

A

1-resist forces of mastication w/o fracture

  • 1 hr gets 40-60% of its compressive strength- so patients cant chew right after placement
  • spherical high copper amalgams develop strength earlier
  • all amalgams reach final strength after 7 days

2-improper trituration will affect strength (mix too long to too short)
-inadequate condensation will result in voids in restoration= weak restoration

32
Q

1-properties of amalgam tensile strength

2-properties of amalgam dimensional change

3-positive dimensional change

4-negative dimensional change

5- creep

A

1-resistance to elongation or stretching

  • weakest attribute of amalgam
  • amalgam is brittle/weak when thin
  • cavity prep for amalgam must allow for a large bulk of amalgam and to avoid thin marginal areas—1.5-2 mm deep

2-dimensional change= % shrinakge or expansion of material

  • dissolution of gamma= contraction
  • formation of gamma 1 and eta= expansion
  • dimensional change is the sum of the 2

3-is expansion= post placement pain

4-is negative= leave gaps at the margins

—most amalgams = little expansion or contraction
improper manipulation of amalgam alters ratio of gamma, gamma 1 & eta= dimensional change

5-permanent deformation under load (chewing)

  • –marginal breakdown and fracture
  • –high copper alloys exhibit reduced creep
33
Q

1-corrosion

2-tarnish

3-galvanism

4-thermal conductivity

A

1-result of chemical reactions= w/in body of restoration

  • reduce strength of amalgam over time
  • corrosion reduces marginal leakage
  • high copper amalgams exhibit less corrsion than traditional amalgams

2-occurs at surface of restoration

  • occurs due to food & saliva
  • smooth amalgam resotrations exhibit less tarnish

3-result of 2 dissimilar metals in mouth
-2 metals touching in oral fluis= electrical cell= metallic taste

4-measure of heat transferred…enamel & dentin= poor thermal conductors
metallic restorations are good thermal conductors

34
Q

Thermal Conductivity

A
  • patients experience sensitivity to heat/cold after placement of metallic (amalgam) restorations
  • glass ionomer materials similar to dentin w/ respect to thermal conductivity…so glass ionomer liners are used under deep restorations to dec thermal sensitivity
35
Q

1-modulus of elasticity

2-polymerization shrinkage

3-co-efficient of thermal expansion

4-thermal conductivity

A

1-measure of stiffness: amalgam has greater modulus of elasticity than composite

2-composite shrinks upon polymerization, amalgam doesnt polymerize the dimensional change for amalgam is little to none

3-tooth= 8-15, composite= 25-68, amalgam=22-28

4-measure of heat transferred, related to rate of heat flow

  • tooth structure is poor conductor
  • composite is poor conductor
  • amalgam & metallic restoration are good conductors
36
Q

1-amalgam comparison

2-trituration

A

1-corrosion, tarnish, galvanism, & creep
-metallic materials which are not exhibity by resin composite

2-speed, time & force of trituration has effect upon amalgam…
triturated amalgam= dry & crumbly
—insufficient matrix to hold amalgam mass together
—difficult to properly condense
—poor corrosion resistance
over triturated amalgam= wet & soupy
—excessive expansion
—reduced strenght

37
Q

1-condensation

2-carving amalgam

A

1-adapt amalgam to cavity prep walls & margins

  • produce restoration w/o voids
  • reduce & minimize mercury in restoration
  • mercury rich layer at surface is removed during carving
  • done in 3.5 min—8-10 lbs of pressure: use smaller condenser to get higher pressure and then larger condenser towards the end

2-carving time, amalgam should provide resistance to carver

  • carvers should be on both tooth structures & amalgams—prevents ditching
  • carving along margins—anatomy guide
  • 70-90 degree angle of metal at margin
38
Q

1-carving anatomy too deep

2-amalgam advs

3-amalgam disadvs

A

1-thin amalgam, margins less than 70-90
thin margins may fracture

2-inexpensive, not technique sensitive
no shrinkage upon setting
longevity of restorations

3-unesthetic

  • prep may require sound tooth structure removal to provide for resistance & retention
  • mercury
39
Q

1- resin composite

2-amalgam

3-when to use amalgam

A 
1-conservative, esthetic, bonds to tooth
technique sensitive (multiple), polymerization shrinkage (gap formation at margins)

2-not conservative for initial small lesions, not esthetic, doesnt bond to tooth, easy to condense/carve, no poly shrinkage (seals margins over time)

3-esthetics not essential, moderate to large lesions
-moisture control isnt possible, where margins are on dentin

40
Q

1-mercury toxicity

2-metallic mercury

3-methyl mercury

A

1-based on form of mercury, dose, duration of exposure, age of person, route of exposure, & health
—tremors, insomnia, emotional disturbance, headache, lack of cognitive function

2-poorly absorbed from gut, ingested= mildly toxic

  • primary portal into body is inhalation
  • ability to penetrate CNS where it is ionized, trapped, & toxic

3-more toxic than elemental mercury

  • efficiently absorbed from gut
  • accumulate through food chain
  • accumulated in body—long half life
  • fetuses, infants, childrens= neuro development
  • impairment of peripheral vision
  • disturbance in sensation
  • lack of coordination + muscle weakness
41
Q

1-mercury in the environment

2-mercury w/in dental

3-mercury toxicity

4-composite material

5-amalgam materiam

A

1-through chemical industries—cement, metal refining, & combustion of fossil fuel
-pollution—travels long distance, like via water

2- exposure by direct contact or vapor
inorganic level of exposure= high
organic level of exposure= the same

3-hundred surfaces of dental amalgam would be necessary to expose an individual to mercury conc w/ minimum effect

4-conservative, moisture control needed
technique sensitive & takes longer time to place for same type of prep

5-not conservative (amalgam requires bulk), mositure control is desirable but not needed
technique tolerant, takes less time
less expensive

42
Q

1-dental local anesthesia

2-sensation sequence

4-local anesthetic action

5-issues w/ pH and pKa

A

1-loss of sensation in circumscribed area of body caused by depression of excitation in nerve ending/ inhibition of conduction process in peripheral nerve

2-pain—>cold—>warmth

3-alters basic resting potential of nerve membrane
alter threshold potential (firing level)
dec rate of depolarization
prolongs rate of repolarization
primary action=dec permeability of ion channels to Na

4-Normal= 7.4
pKa= pH at which drug is 1/2 base & salt
Salt= solid, H20 soluble, stable, acidic, charged cation,a ctive form
Base= viscous liquid, fat soluble, unstable, alkaline, uncharged, penetrates nerve tissue, present in tissue pH
Basic form= Active form

43
Q

1-Pharmacokinetics

A

1-ADME
-Absorption= depends on vascularity, depends on LA type, pH of tissue
dec absorption= dec toxicity
-Distribution= throughout body
-Metabolism= esters—plama & liver & amides—liver/lungs
-Excretion= Kidney
—-inc distribution & dec absorption

44
Q

1-amide anesthesia

2-ester anesthesia

3-3 segments of anesthesia

4- Composition of LA

A

1-principle injection & low allergy factor

2-highly allergenic, rarely used as injectable, mostly topical

3-aromatic nucleus, linkage by amide/ester, amino group

4-vasoconstrictor (if added)= retards absorption, reduces toxicity, & prolongs action

  • antioxidant= prolongs shelf life
  • Sodium Hydroxide= adjusts pH
  • Sodium Chloride= isotonic
45
Q

1-ester anesthetics

2-topical anesthetics

3- amide local anesthetics

A

1-hydrolyzed in plasma via enzyme pseudocholinesterase
esters= higher rate of allergic reactions not related to procaine but to PABA
-1/2800 people have inability to hydrolyze ester LA

2-placed on mucous membrane before needle penetration—-ester classification, poor solubility in H20, poor absorption, penetration 2-3 mm

3-metabolism more complex—primary site= liver
esp for=Lidocain, mepivacaine, articaine, etidocaine, & bupivacaine
-prilocacin in liver & lungs

46
Q

1-rates of biotransformation

2-solubility & protein binding

A

1-prilocaine is most rapid biotransformation, done in 2 locations
-liver function influences rate of biotransformation of AMIDE LA’s

2-lipid solubility of amide anesthesia= more soluble the anesthetic in lipids the longer anesthetic effect
marcaine=higher lipid solubility than lidocaine
-protein binding= cation to be attached to proteins at receptor—-inc protein binding> duration of anesthetic action greater
marcaine>mepivacaine>lidocaine

47
Q

1-tachyphylaxis

2-minimal overdose

3-moderate overdose

4-severe overdose

5-management of overdose

A

1-dec in effectiveness of drug adminstered repeatedly

  • develops if nerve function is allowed to return prior to reinjection
  • edema, local hemorrhage, clot formation, & dec pH of tissue= factors

2-talkativeness, apprehension, sweating, vomiting, & disorientation

3-metallic taste, dizziness, visual/auditory disturbance

4-depressed BP, HR, & resp
CNS depression
loss of consciences

5-mostly mild & transitory—very little treatment (O2)
-most local anesthetic overdose reactions= self limiting, since blood level in tissues (brain & heart) dec as reaction progresses while transformation of anesthesia takes place

48
Q

1-intraligamental local anesthesia

2-inferior alveolar

3-gow gates

4-akinosi

A

1-use of 2% lidocaine w/ 1:100,000 epinephrine for PDL injection is better in acheiving pulpal anesthesia than using local anesthesia w/o vasoconstrictor
-reinjection of PDL inc the success rate of achieving pulpal anesthesia from 74-96% on teeth w/ pretreatment pulpal diagnosis of irreversible pulpitis

2-intratragic notch (ear) & corner of mouth

  • 10-15% aspiration
  • IAN, incisve, mental, & lingual
  • 3-5 min onset

3-wide open mouth, 2% aspiration
buccal, mylohyoid, auriculotemporal
-5-10 min onset

4-closed mouth

  • bending of needle
  • MCG of max molar
  • o bony landmarks
49
Q

1-intraosseuous & PDL

2-Mandibular infiltration

3-local anesthetic techniques

4-gauges

5-handling of cartilages

A

1-Pain, cardiac & pressure

2-best w/ 4% articaine, no diff w/ epi, split buccal & lingual dose

3-stay at height of vestible to distal 2nd or 3rd molar & out of infratemporal fossa
-armamentarium, basic technique, maxillary, & mandibular

4-smaller the number, the bigger the lumen
25=red
27=yellow
30=blue

5-never use on more than 1 patient
change after 3-4 injection
cover needle in sheath
SCOOP

50
Q

1-silicone rubber plunger

2-aluminum cap

3-diaphragm

4-mylar strip

5-aspirate

A

1-seals glass tube, provides way for harpoon to engage aiding in aspiration

2-opposite end of plunger, holds thin diaphragm in position

3-semipermeable membrane

4-provides protection if glass breaks

5-be done at any site where large deposit will be performed

  • create a neg pressure to see if in BV
  • pull on thumb ring
  • any sign of blood= positive aspiration & LA shouldnt be deposited at site—aspirate twice at each site
  • rotate barrel of syringe 45 degrees doing second aspiration and try using 25 guage
51
Q

1-slow deposit anesthetic solution

2-communicate w/ patient

A

1-reasons to deposit slow: watch for emergencies & slow technique reduces tearing tissue & postop pain

  • full 1.8 cc cartridge= 2 min
  • most clinicians deposit in 20 s, but wait at least 60 s

2-alleviate & distract patients fears

  • explain you are depositing slowly so it will be comfortable
  • dont leave the patient alone—most adverse happens w/in 5-10 min
52
Q

1-maxillary injection types

2-posterior superior alveolar PSA

3-middle superior alveolar MSA

4-anterior superior alveolar ASA

5-greater palatine GP

A

1-posterior superior alveolar nerve block (PSA)
middle superior alveolar nerve block (MSA)
anterior superior alveolar nerve block (ASA)
greater palatine nerve block (GP)
nasopalatine nerve block (NP)

2-maxillary molars, not MB root of max 1st molar
-dont enter infratemporal fossa

3-pulp & buccal periodontal tissues
bone of max 1st & 2nd premolar

4-maxillary incisor, canine pulp, bone & perio tissues…sometimes lower eyelid

5-posterior portion of hard palate, up to premolar
change in tissue color

53
Q

1-nasopalatine NP

2-mandibular techniques

3-inferior alveolar nerve block

A

1-anterior portion of hard palate from left to right 1st premolars

2-inferior alveolar, lingual, long buccal, & mental

3-mandibular teeth to midline, body of mandible, inferior portion of ramus, buccal mucoperiosteum, mucous membrane anterior to mandibular 1st molar (mental) anterior 2/3 of tongue, floor or oral cavity (lingual) & soft tissues
-palpate coronoid notch, draw an imaginary line to pterygomandibular raphe to get height of injection

54
Q

1-long buccal

2-mental nerve block

A

1-soft tissue & periosteum buccal to mandibular molar teeth

  • left 10 & right 8
  • insert needle in soft tissue distal & buccal of most distal molar
  • needle should be parallel w/ occlusal plane

2-buccal mucosal membrane anterior to mental foramen—2nd premolar to midline

  • lower lip, skin of chin, pulpal nerve fibers to premolars, canine & incisors
  • thumb + ifnger in mucobuccal fold against body of mandible in M1 area and go anterior until feel bone & between 2 premolars into the area between canine/1st premolar
55
Q

1-inferior alveolar

2-long buccal

3-mental nerve block

4-maxillary

5-PSA, MSA, & ASA

6-palatal= greater palatine/nasopalatine

7- how much LA did you use

8-how much vasoconstrictor

A

1-pterygomandibular raphe
opposite premolar
parallel to occlusal plane & aspirate

2-external oblique ridge distal to retromolar area

3-infiltrate around—dont enter. bleeds easily

4-dont enter infratemporal fossa

5-PSA= height of vestiuble of most distal molars
MSA= height of vestibule between premolars
ASA= height of vestibule between canine & lateral

6-painful—papilla approach possible if restorative & localized
-dont enter foramen—inject near site of care

7- 1.7 mL of 2% lidocaine (3 mg/lb= max 300 mg no epi/ 500 mg w/ epi)
1.7 mL= 17 * 2= 34

8- 1.7 mL of 1:200000 = 0.0085

56
Q

1-risk

2-risk factors

3-risk determinants

4-risk indicators

5-risk markers/predictors

A

1-probability that individual will develop specific disease in a time period. risk of developing the disease will vary from individual to individual

  • risk factors
  • risk determinant/background characteristic
  • risk indicator
  • risk markers/predictors

2-environmental, behavioral, biological—diabetes, smoking, etc

3-factors that cant be modified—genetic, age, gender, stress, age, gender, genetics

4-probable cause, only w/ cros sectional studies—HIV, AIDS, osteoporosis

5-inc risk but dont cause disease—previous history, bleeding w/ probing

57
Q

1-risk factors

2-tobacco

3-NEGATIVE effects of tobacco

A

1-when present= inc likelihood that individual will develop disease

2-strongest risk factor for periodontitis
-dose effect relationship, temporal relationship, suppressess gingival microcirculation
impress immune system
inhibition of growth & attachment of fibroblasts in PDL ligament of smoekrs

3-locally= vasoconstriction, ischemia, and inc pathogenic organisms
systemically= dec immunity, specific IgG & IgA & nonspecific= dec PMN action chemotaxis/phago activation of catabolic cascade
58
Q

1-diabetes mellitus

2-metabolic syndrome

A

1-higher prevalence & severtiy of perio than non diabetics

  • controlled diabetics= 2x’s likely uncontrolled= 5x’s
  • elevated blood sugar levels (hyperglycemia)=suppress host immune response=poor wound healing & infections such as abscesses

2-abdominal obesity, triglyceride level, high density lipoprotein cholesterol level, BP, & fasting blood sugar level===inc risk of periodontitis

59
Q

1-diabetes promotes periodontal tissue loss by

2-bacteria

3-dental calculus

4-localized aggressive periodontitis

A

1-forming advanced glycation end products AGP

  • stimulating exaggerated inflam response
  • reducing ability of fibroblasts to form collagen & reduce response to growth factors

2-anaerobes & facultattive—Aa, Pg, Tf, plaque serves as reservoir for these microflora
-porphyromonas gingivalis, tannerella forsythia, & aggregatibacter actinomycetemcomitans

3-consists of mineralized bacterial plaque that forms on surfaces of teeth & dental prostheses

4-circumpertal onset, robust serum Ab response to agents, 1st molar & incisors w/ interproximal attachment loss on at least 2 permanent teeth

60
Q

1-papillon lefevre syndrome

2-age

3-race/ethnicity

4-stress

A

1-autosomal recessive trait
hyperkeratosis of palms & soles
keratosis of other skin surfaces
calcification in falx cerebri
exfoliation of teeth + destruction in alveolar bone

2-as age inc, prevalence, extent & severity of chronic perio also increases

3-blacks+ mexicans more
native american, asians & pacific islanders
more plaque + calc = higher in blacks

4-down regulates cell immune response, promoting perio breakdown
-patients w/ high stress/low coping = less oral health motivation

61
Q

1-immunosuppressive drugs/dosages

2-risk marker

A

1-cyclosporine A 5 mg, Tacrolimus 0.1 mg, Mycophenolate mofetil 2 mg

2-previous perio treatment, previous perio surgery, compliance—maitenance & hygiene, historical radiographs
—bleeding on probing= inflammation
no bleeding= health

DENT 1530 (7 decks)

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