misc lectures for midterm Flashcards
1-dental caries
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
radiolucent
1-horizontal angulation
2-advantage of bitewing radiograph
3-detection
4-radiographic detection
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
1-shape of carious lesion
2-factors affecting caries diagnosis
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
left= E Right= D1 Bottom= D2
1-E
2-D1
3-D2
4-spread of caries
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
1-metallic restorations
2-temporary restorations
3-composite restorations
4-cervical burnout
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
cervical burnout
1-occlusal caries
2-buccal/lingual caries
3-root caries
4-secondary/recurrent caries
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
1-full mouth series
2-types of surveys
3-alveolar bone
4-alveolar bone proper
5-alveolar bone
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
1-alveolar crest
2- interdental bone/septa
3-crestal bone
4-radiographic signs of periodontitis
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
1-horizontal bone loss
2-vertical bone loss
3-comparison of horizontal & vertical bone loss
4-optimal radiographic technique
5-horizontal bitewings
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
1-vertical angulation
2-horizontal angulation
3-normal alveolar crest
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
1-evidence of early periodontitis
2-radiographic examination
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
1-contributing factors
2-healthy/gingivitis
2-slight chronic periodontits
4-limitations of perio radiographics
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
1-intial comprehensive oral exam
2-patient interview
3-perio conditions
4-contraindications to treatment
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
1-gingival enlargement
2-xerostomia
3-social habits
4-gingival inflammation
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
1-function of perio probes
2-clinical signs of inflammation
3-UNC Probe
4-Goldman Fox
5-furcation probe
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
1-probing health vs diseased tissue
2-5 mm perio pocket
3-measurement
4-probing essentials
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
1-walking the probe
2-adaptation
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
1-interproximal technique
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
1-width of keratinized gingiva
2-frenum pull
3-gingival recession w/ lack of attached gingiva
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
1-examing furcations
2-furcation probe
3-class 1 furcation
4-class 2 furcation
5-class 3 furcation
6-class 4 furcation
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
1-mandibular molars
2-maxillary molars
3-maxillary 1st premolar
4-tooth mobility
5-local factors
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
1-probe crevicular depth
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
1-Amalgam
2-dental amalgam
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
1-traditional: silver, tin, copper, zinc
2-high copper: silver, tin, copper, zinc
3-silver
4-tin
5-copper
6-zinc
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
1-indium
2-palladium
3-platinum
particles
4-lathe cut
5-spherical
6-ad mix
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
1-spherical amalgam
2- admix amalgam
3-amalgamation
4- gamma
5-gamma 1
6-gamma 2
7-eta
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
1-conventional amalgam
2-high copper amalgam
3-amalgam reaction
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
1-properties of amalgam compressive strength
2-strength
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
1-properties of amalgam tensile strength
2-properties of amalgam dimensional change
3-positive dimensional change
4-negative dimensional change
5- creep
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
1-corrosion
2-tarnish
3-galvanism
4-thermal conductivity
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
Thermal Conductivity
- 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
1-modulus of elasticity
2-polymerization shrinkage
3-co-efficient of thermal expansion
4-thermal conductivity
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
1-amalgam comparison
2-trituration
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
1-condensation
2-carving amalgam
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
1-carving anatomy too deep
2-amalgam advs
3-amalgam disadvs
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
1- resin composite
2-amalgam
3-when to use amalgam
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
1-mercury toxicity
2-metallic mercury
3-methyl mercury
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
1-mercury in the environment
2-mercury w/in dental
3-mercury toxicity
4-composite material
5-amalgam materiam
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
1-dental local anesthesia
2-sensation sequence
4-local anesthetic action
5-issues w/ pH and pKa
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
1-Pharmacokinetics
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
1-amide anesthesia
2-ester anesthesia
3-3 segments of anesthesia
4- Composition of LA
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
1-ester anesthetics
2-topical anesthetics
3- amide local anesthetics
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
1-rates of biotransformation
2-solubility & protein binding
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
1-tachyphylaxis
2-minimal overdose
3-moderate overdose
4-severe overdose
5-management of overdose
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
1-intraligamental local anesthesia
2-inferior alveolar
3-gow gates
4-akinosi
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
1-intraosseuous & PDL
2-Mandibular infiltration
3-local anesthetic techniques
4-gauges
5-handling of cartilages
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
1-silicone rubber plunger
2-aluminum cap
3-diaphragm
4-mylar strip
5-aspirate
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
1-slow deposit anesthetic solution
2-communicate w/ patient
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
1-maxillary injection types
2-posterior superior alveolar PSA
3-middle superior alveolar MSA
4-anterior superior alveolar ASA
5-greater palatine GP
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
1-nasopalatine NP
2-mandibular techniques
3-inferior alveolar nerve block
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
1-long buccal
2-mental nerve block
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
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
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
1-risk
2-risk factors
3-risk determinants
4-risk indicators
5-risk markers/predictors
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
1-risk factors
2-tobacco
3-NEGATIVE effects of tobacco
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
1-diabetes mellitus
2-metabolic syndrome
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
1-diabetes promotes periodontal tissue loss by
2-bacteria
3-dental calculus
4-localized aggressive periodontitis
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
1-papillon lefevre syndrome
2-age
3-race/ethnicity
4-stress
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
1-immunosuppressive drugs/dosages
2-risk marker
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
