ABE Oral Board Study Guide
Topic List:
1. Tooth Morphology
2. Radiographic Exam
3. Subjective / Objective Exam
4. Medically Compromised
5. NS RCT
6. Procedural Errors
7. Emergency TX / Flare-ups
8 Infections
9. ReTX
10. S RCT
11. Trauma
12. Anesthesia
13. Endo-Perio
14. Endo-Pedo
15. Endo-Ortho
16. Resorption
17. Bleaching
18. Materials
19. Restoration
20. Pulpal Pathosis
21. Periapical Pathosis
22. Anatomy
23. Microbiology
24. Inflammation
25. Immunology
26. Pain
27. Pharmacology
28. Prognosis / Outcomes
29. Regenerative Endodontics
TOOTH CANALS CONFIGURATION AUTHOR
Max. Central Incisor Type I: 100% Vertucci (Dye)
Max. Lateral Incisor Dens in Dente: .04-10%
52% DB dilaceration Hovland
Chohayeb
Max. Canine
Max. 1st Premolar 1 canal - 9%
2 canals – 85%
3 canals – 6%
(2 roots – 57% / 3 roots - 6%) Carns & Skidmore (resin casts)
Max. 2nd Premolar 1 canal – 48%
2 canals – 51%
3 canals – 1% At the Apex:
1 canal - 75%
2 canals – 24%
3 canals – 1% Vertucci (Dye)
Max. Molars MB2 located 1.8mm L MB2:
Hand inst.: 54%
Burs: 31%
Microscope: 10%
Located MB2: 73% 1st molars
51% 2nd Molars
85% >10 deg curvature P root
5% incidence of C shaped (Chinese) MB2:
type I: 5%
type II: 49%
type III: 46% Kulild & Peters
Stropko
Bone & Moule
Yang & Yang
Mand. Incisors 2 canals: 41% type I: 59%
type II: 40%
type III: 1% Benjamin & Dawson (radiographic study)
Mand. Canine 2 canals: 22% type I: 78%
type II: 16%
type III: 6% Vertucci (Dye)
Mand. 1st Premolar type I: 76%
type IV: 24%
(14% C-shaped) Baisden, Kulild & Weller
Mand. 2nd Premolar type I: 97.5%
type IV: 2.5% (2-3X ↑ Af. Americans) Vertucci (Dye)
Trope, Elfenbein & Tronstad
Mand. 1st Molar 2 canals: 7% 3 roots: 2%
3 canals: 64%
4 canals: 29%
Chinese pop. with 3 roots: 15% M root: D root:
type II: 40% 60%
type III: 60% 40% Skidmore & Bjorndal (resin casts)
Walker
Mand. 2nd Molar 1 canal: 1% 1 root: 4%
2 canals: 4%
3 canals: 81%
4 canals: 11%
8% C-shaped M root: D root:
type I: 4% 85%
type II: 52% 9%
type III: 40% 1%
type I – continuous
type II – semicolon
type III – 2 or more distinct canals Weine (radiographic)
Weine / Cooke & Cox
Melton, Krell & Fuller
Morphology Overview
Discuss the types and incidence of lateral / accessory canals?
DeDeus – 27% found most often in the apical area
Lateral – found in the main body of the root canal
Secondary – extends from the main canal to the PDL in the apical region
Accessory – from the secondary canal branching off to the PDL
What is the incidence of furcation canals?
Gutmann – 28%; only 10% extend to the PDL
Discuss canal classification?
Weine: Type I – one canal; Type II – 2 canals, one foramen; Type III – 2 canals, 2 foramina; Type IV – 1 canal, 2 foramina
Who discussed the anatomy of the pulpal floor?
Vigouroux & Bossan – discussed subpulpal grooves & dentinal cornice
Krasner & Rankow –
Law of Centricity: pulpal floor is located in the tooth center at the CEJ level
Law of Concentricity: walls of the pulp chamber are concentric to external suface
Law of CEJ: landmark pulp chamber location
Law of Symmetry: Except Max molars, orifi are equidistant & perpendicular from M-D line drawn through center of pulpal floor;
Law of Color Change: pulpal floor is darker than walls
Law of Orifice Location: orifi are located at the junction of the floor and walls
Discuss the apical constriction?
Stein & Corcoran – Width of the CEJ was avg. .189mm (size 20 file)
Dummer – 4 types of apical constriction: single constriction 46%; tapering 30%; multiconstricted 19%; parallel 5%; 6% were completely blocked
Discuss Abnomalities of the Teeth:
MICRODONTIA
• TEETH SMALLER THAN THEY SHOULD BE
MACRODONTIA
• TEETH LARGER THAN THEY SHOULD BE
GEMINATION
• SINGLE ENAMEL ORGAN ATTEMPTS TO MAKE TWO TEETH
• TWO CROWNS – ONE ROOT
FUSION
• JOINING OF TWO DEVELOPING TOOTH GERMS
• MAY INVOLVE ENTIRE TOOTH OR JUST CEMENTUM AND DENTIN
• ROOT CANALS MAY BE SEPARATE OR SHARED
• MAY BE IMPOSSIBLE TO SEPARATE FUSION OF A NORMAL AND SUPERNUMERY TOOTH FROM GEMENATION
CONCRESCENCE
• FORM OF FUSION IN WHICH ADJACENT TEETH ARE JOINED BY CEMENTUM
• MOST COMMONLY SEEN BETWEEN MAXILLARY 2ND AND 3RD MOLARS
DILACERATION
• EXTRAORDINARY CURVING OR ANGULATGION OF TOOTH ROOTS
• CAUSE RELATED TO TRAUMA DURING TOOTH DEVELOPMENT
DENS INVAGINATUS
• AKA DENS IN DENTE OR TOOTH WITHIN A TOOTH
• EXADURATION OR ACCENTUATION OF THE LINGUAL PIT
• MOST COMMON IN MAX LATERAL INCISSORS
DENS EVAGINATUS
• COMMON DEVELOPMENTAL CONDITION AFFECTING PREDOMINANTLY PREMOLAR TEETH
• ALMOST EXCLUSIVELY OF THE MONGOLOID RACE
• FREQUENTLY BILATERAL
• ANOMALOUS TUBERCLE OR CUSP LOCATED IN THE CENTER OF THE OCCLUSAL SURFACE
TAURODONTISM
• TEETH THAT HAVE ELONGATED CROWNS OR APICALLY DISPLACED FURCATIONS
• PULP CHAMBERS HAVE INCREASED APICAL-OCCLUSAL HEIGHT
• ASSOCIATED WITH SYNDROMES SUCH AS DOWN AND KLINEFELTER’S
• HIGH PREVELANCE IN ESKIMOS AND 11% IN MIDDLE EAST
SUBERNUMERARY ROOTS
• ACCESSORY ROOTS MOST COMMONLY SEEN IN MANDIBULAR CANINES, PREMOLARS AND MOLARS
ENAMEL PEARLS
• DROPLETS OF ECTOPIC ENAMEL
• COMMONLY SEEN IN THE BIFURCATION OR TRIFURCATION AREA OF TEETH
• MAX MOLARS MOR COMMON
ANODONTIA
• ABSENCE OF TEETH
• MOST COMMON ARE 3RD MOLARS THEN MAX LAT INCISSORS AND SECOND PREMOLARS
• COMPLETE ANODONTIA ASSOCIATED WITH ECTODERMAL DYSPLASIA- X-LINKED RECESSIVE DISORDER
SUPERNUMERARY
• EXTRA TEETH
• ASSOCIATED WITH GARDNERS SYNDROME AND CLEIDOCRANIAL DYSPLASIA
• THE ANTERIOR MIDLINE OF THE MAXILLA IS THE MOST COMMON SITE FOLLOWED BY MAXILLARY MOLAR AREA
AMELOGENESIS IMPERFECTA
• HERIDITARY DISORDER OF ENAMEL FORMATION IN BOTH DENTITIONS
1. HYPOPLASTIC – INSUFFICIENT AMOUNT OF ENAMEL
2. HYPOCALCIFIED – QUANTITY OF ENAMEL IS NORMAL BUT SOFT AND FRIABLE
3. HYPOMATURATION
• COLOR RANGE FROM WHITE OPAQUE TO YELLOW TO BROWN
• RADIOGRAPHICALLY DENTIN THIN ROOTS NORMAL
DEFECTS OF DENTIN
DENTINOGENESIS IMPERFECTA (HEREDITARY) OPALESCENT DENTIN
• AUTOSOMAL DOMINANT
1. TYPE 1 – OCCURS IN PATIENTS WITH OSTEOGENESIS IMPERFECTA
2. TYPE 2 – PATIENTS HAVE ONLY DENTAL ABNORMALITIES NO BONE DISEASE
3. TYPE 3 – OR BRANDYWINE TYPE SIMILAR TO TYPE 2 BUT INCLUDE FEATURES SUCH AS MULTIPLE PULP EXPOSURES AND PERIAPICAL RADIOLUCIENCIES
• CLINICALLY ALL THREE TYPES SHARE NUMEROUS FEATURES
1. TEETH EXHIBIT AN UNUSUAL TRANSLUCENT, OPALESCENT APPEARANCE
2. COLOR RANGES FROM YELLOW – BROWN TO GRAY
3. ENAMEL NORMAL BUT FRACTURES EASILY
4. ABNORMAL MORPHOLOGY TEETH TULIP OR BELL SHAPED DUE TO CONSTRICTION OF CEJ
5. ROOTS ARE SHORT AND BLUNTED
• RADIOGRAPHICALLY
1. TYPES 1 AND 2 PULP SPACE OPACIFIED
2. TYPE 3 PULP CHAMBERS AND ROOT CANALS EXTREEMLY LARGE
DENTIN DYSPLASIA
• AUTOSOMAL DOMINANT TRAIT
• TYPE 1 RADICULAR
1. CROWNS NORMAL
2. TEETH SHOW GREATER RESISTANCE TO CARIES
3. ROOTS EXTREMELY SHORT
4. PULPS OBLITERATED
5. PERIAPICAL LEUCENCIES
• TYPE 2 CORONAL
1. CROWNS NORMAL
2. PULPS LARGE (THISLE TUBE)
3. ROOTS EXTREMELY SHORT
Radiographic Exam Overview
Can a PARL be seen with irreversible pulpitis?
Yes – Yamasaki – Rat study demonstrating PARL prior to pulp necrosis
Jordon, Suzuki & Skinner – PARL with IP; 11/24 healed with IDPC
How much bone loss before a PARL is noted radiographically?
Bender – Avg 7% MBL & at least 12.5% CBL; lesion must penetrate endosteum
Lee & Messer – Lesions in cancellous bone detected if lamina dura is affected
What radiographic features are important when evaluating PA pathology?
Kaffe & Gratt – continuity & shape of lamina dura; width & shape of PDL
How many films should be taken for diagnosis?
Byrnholf – 73% accurate with 1 film; 87% accuracy with 3 films
How accurate is our radiographic assessment?
Goldman, Pearson & Darzenta - 6 examiners agreed 47%; 6-8mo later they agreed approx. 80% with their first interpretation
What is the most accurate technique?
Forsberg – paralleling is more accurate in length determination vs. bisecting angle
What type of conventional film (speed) is the most diagnostic?
Eleazer & Farman – NSD in WL measurements or image preference
Compare conventional radiography to digital:
Evaluating for PARL
Mistak & Loushine – NSD between digital, transmitted digital & conventional radiography for PARL identification
Folk – NSD between shick (cmos) & trophy RVG ui (ccd)
Nair – conv. film displayed the highest % of PARL detection (vs. ccd & storage phos.)
Comparing WL measurements
Lamus & Katz – NSD between shick & conv.
Goodell & McClanahan – Kodak > schick or conv. for size 10 & 15 files
Lozano – Conv. was more precise with any size file (digital ok with size 15 file)
How much radiation reduction is there between digital and conventional radiography?
Soh – Used only 22% of radiation dose compared to conv. film
Ludlow, Platin & Mol – Insight (f speed) required 44% of exposure of Ultra (D speed)
Is 3-D imaging better than conventional radiography?
Low – improved detection of PA lesions and missed canals with Cone-beam Tomography
Subjective / Objective Overview
Can pts. determine which tooth hurts?
Friend & Glenwright - No, only 37% accurate; usually tooth to either side; 3.4% referral to opposite jaw; 1.5% referral across midline
Discuss cold testing?
Trowbridge & Franks – response sooner than temp change @ PDJ – supports Branstom
Walton / Miller – response quicker with endo ice; use with FCC
Jones – use large cotton pellet
Who discussed heat testing?
Cooley – hot water test
Does temp testing harm the tooth?
Peters – CO2 does not harm the enamel
Rickoff & Trowbridge – heated GP or CO2 showed no pulpal injury
Discuss EPT?
Nahri – stimulates A-beta and A-delta fibers; not C-fibers
Abdel Wahab & Kennedy – slow increase in current – 2uA/sec
Mumford – no relationship with value and pulp pathology
Where do you place the probe tip?
Bender – incisal-edge of incisors
Jacobson – occlusal two-thirds of the buccal surfaces of max incisors and premolars
Is EPT safe on pts. with pacemakers?
Yes – Baumgartner
Can you tell the histologic dx from clinical test?
Seltzer & Bender – No, only correlation exists, but not extent of pathology
How reliable are our pulp tests?
Petterson & Soderstrom –
probability the neg.=necrosis: cold – 89%; EPT – 88%; hot – 48%
probability the pos.=vital: cold – 90%; EPT – 84%; hot – 83%
Fulling & Andreasen – cold test are more reliable in kids
Do any other pulp tests have potential?
Ingolfsson & Tronstad – Laser dolpler flowmetry is more accurate than EPT
Wilcox & Johnson – pulse oximetry
What causes pain while flying / diving?
Ferjentsik – Barodontalgia - Navy study found 86% with faulty restorations
American Board of Endodontics Pulpal & Periapical Diagnostic Terminology:
PULPAL:
Normal pulp – A clinical diagnostic category in which the pulp is symptom free and normally responsive to vitality testing.
Reversible pulpitis – A clinical diagnosis based upon subjective and objective findings indicating that the inflammation should resolve and the pulp return to normal.
Irreversible pulpitis – A clinical diagnosis based on subjective and objective findings indicating that the vital inflamed pulp is incapable of healing.
Additional descriptions:
Symptomatic – Lingering thermal pain, spontaneous pain, referred pain
Asymptomatic – No clinical symptoms but inflammation produced by caries,
caries excavation, trauma, etc.
Pulp necrosis – A clinical diagnostic category indicating death of the dental pulp. The pulp is non-responsive to vitality testing.
Previously Treated – A clinical diagnostic category indicating that the tooth has been endodontically treated and the canals are obturated with various filling materials, other that intracanal medicaments.
Previously Initiated Therapy – A clinical diagnostic category indicating that the tooth has been previously treated by partial endodontic therapy (e.g. pulpotomy, pulpectomy).
APICAL (PERIAPICAL):
Normal apical tissues – Teeth with normal periradicular tissues that will not be abnormally sensitive to percussion or palpation testing. The lamina dura surrounding the root is intact and the periodontal ligament space is uniform.
Symptomatic apical periodontitis – Inflammation, usually of the apical periodontium, producing clinical symptoms including painful response to biting and percussion. It may or may not be associated with an apical radiolucent area.
Asymptomatic apical periodontitis – Inflammation and destruction of apical periodontium that is of pulpal origin, appears as an apical radiolucent area and does not produce clinical symptoms.
Acute apical abscess – An inflammatory reaction to pulpal infection and necrosis characterized by rapid onset, spontaneous pain, tenderness of the tooth to pressure, pus formation and swelling of associated tissues.
Chronic apical abscess – An inflammatory reaction to pulpal infection and necrosis characterized by gradual onset, little or no discomfort and the intermittent discharge of pus through an associated sinus tract.
NS RCT Overview
Apex Locators
Who was instrumental in developing the apex locator / Root ZX?
Suzuki – electrical resistance between periodontium & oral mucous membrane was 6500 ohms in dogs
Sunada – found same results in human (basis for resistance type EALs)
Kobayashi – developed the Root ZX base on a ratio of impedance at 8 and .4 kHz frequencies
How accurate is the Root ZX?
Shabahang – 96.2% +/- .5mm of the apical foramen
Ounsi – 84% accurate – use apical foramen (major diameter) as measurement
Does the pulp status affect EAL readings?
Dunlap – NSD between vital and necrotic pulps
Does the irrigant solution affect the reading?
Jenkins – No; NSD in function with 7 irrigants tested
Does apical resorption or an open apex affect the reading?
Goldberg – accurate with resorption
Katz – preferable method to determine WL in primary dentition
Are EALs safe for use in pts with pacemakers?
Garofalo & Dorn – In vitro Root ZX safe – Bingo caused interference
Baumgartner – In vivo study found EALs and EPTs safe in 27 pts
Canal Preparation
Why is the ideal working length .5 – 1mm short of the apex
Burch and Hulen – avg. .59mm from occlusal aspect of maj diameter to apex
Kuttler - .525mm (18-25yr olds) - .659mm (.55yr olds) from major to minor diameter
Discuss historical preparation techniques?
Clem, Mullaney – Step back
Torabinejad – Passive Step back
Marshall – Crown Down Pressureless
Abou Ross – Anticurvature Filing
Roane – Balanced Force
Do you preflare the canal and why?
Stabholz – better tactile sense of the apical constriction
Ibarrola – preflaring allowed more consistent EAL readings (allowed access to apical foramen)
Roland - .04 taper NiTi files were far less likely to separate in preflared canals
Can patency filing cause problems?
Goldberg – cause apical transportation (61% #25, 25% #10) – use small files
Why do you create a guide path?
Peters – No Protaper instrument fractured is guide path was created
What are the advantages of the balanced force technique?
Wu & Wesselink – produced cleaner apical portion of canals vs other hand techn.
McKendry – extruded less debris
Sepic – less apical canal alteration in curved canals vs step back techn.
Why would you choose to use NiTi rotary files over SS hand files?
Baumgartner – NiTi rotaries were faster and stayed more centered
What are the properties of NiTi files?
Haikel – 55% Nickel / 45% Titanium; 2 phases: Austentite & Martensite – cycling between the two phases allows for superelasticity and shape memory; radius of curvature is most important factor for cyclic fatigue, causing failure
Do NiTi files remove more bacteria?
Trope – Not any more effected than SS hand files
Peters – all type of NiTi rotaries left 35% or more of canal surface area unchanged
At what speed should NiTi rotaries be run at?
Gabel & Hoen – Profiles at 333 rpm separated 4x more often as files at 167 rpm
Gambarini – recommended electric low torque or right torque motors
How many times can NiTi files be used
Yared – Up to 10 canals (2-3 cases)
Does sterilization affect NiTi files
Hicks – 10 cycles through heat sterilization did not increase chance of fracture
Irrigation
How large should the apical preparation be for irrigation?
Brilliant – size 30
What makes sodium hypochlorite antibacterial?
Hurst – pH 11; hypochlorus acid is the active antibacterial property of sodium hypochlorite; disrupts oxidative phosphorylation and other membrane activites
Why use full strength sodium hypochlorite?
Hand, Smith & Harrison – dilution of 5.25% significantly decreases the ability to dissolve necrotic tissue
Siqueira – Increased concentration (4%) most effective against gram – anaerobes and facultative anaerobes
Baumgartner – 5.25% is safe for clinical use and does not increase postop pain
When should chlorhexidine be considered as an irrigant?
Jeansonne – 2% chlorhexidine & 5.25% NaOCl showed NSD in antibacterial activity; CHX does not dissolve tissue; Consider with NaOCl allergies, perfs and open apicies
Haapasalo – CHX activity is reduced by dentine
What about MTAD?
Torabinejad – Doxycycline, citric acid & Tween-80; use with NaOCl and recommended for smear layer removal – did not cause dentinal erosion seen with EDTA; kills E. faecalis more effectively than NaOCl
Who discussed smear layer removal?
McComb & Smith – 1st to describe; used NaOCl & REDTA
Sen – made up of organic & inorganic debris (pulp, bacteria and byproducts)
Baumgartner – 2 layers: 1-2 microns thin layer on canal wall; up to 40 microns in tubules
Should the smear layer be removed?
Torabinejad – Yes - in infected cases it allows more thorough disinfection of canal & tubules; allows better adaptation of obturation material
Jeansonne – less coronal leakage with smear layer removal (AH 26)
Walton & Drake – No – blocks bacterial entry into tubules
How do you remove the smear layer?
Calt - > 1min EDTA caused excessive peritubular and intertubular erosin
Crumpton & McClanahan – 1mL 17 % EDTA for 1 min, followed by 3mL NaOCl
What is EDTA & how does it work?
Ethylendiamine tetraacetic acid – Chelating agent – collects Ca ions in dentin making it softer
Schilder – self limiting after 7hrs
Ultrasonics
How do ultrasonics work?
Ahmad, Pitt Ford & Crum – acoustic streaming & not cavitation
Do ultrasonic remove more bacteria?
Sjogren & Sundqvist – ultrasonics were better than hand instrumentation
Are ultrasonics effective in cleaning canals?
Jensen & Hutter – 3min passive sonic or ultrasonic following hand instrumentation produced cleaner canals
Intracanal Medicaments
Discuss Calcium hydroxide and how it works?
Hermann – introduced
Siqueira – · Hydroxyl ions create free radicals destroying components of bacteria cell membranes.
· Free radicals (hydroxyl ions) react with bacterial DNA inhibiting DNA replication and cell activity.
· Increased pH (12.5) alters enzyme activity disrupting cellular metabolism and structural proteins.
· Ca(OH)2 effective when in direct contact with bacteria which may not always be possible such as bacteria located in dentinal tubules or in the center of bacterial colonies. pH in tubules is increased, but only up to 8-11 (Tronstad).
· Certain bacteria such as enterococci tolerate high pH levels of 9-11.
· Vehicle used to deliver Ca(OH)2 must not alter the pH significantly.
Safavi & Nichols – inactivates LPS in vitro
How long do you keep Ca(OH)2 in the canal?
Sjogren & Sundqvist – 7 day dressing eliminated bacteria that survived instrumentation
Nerwich, Figdor & Messer – 2-3wks before increase in outer root dentin pH (9.3)
Andreasen – use < 1mo
How do you place Ca(OH)2 in the canal?
Sigurdsson & Madison – lentulo>injection>K-file
How do you remove Ca(OH)2 from the canal?
Kenee – use rotary or ultrasonics over irrigation alone (none completely removed)
Obturation
Discuss the hollow tube theory?
Richert & Dixon – introduced; canal must filled to the end to prevent outward diffusion of circulatory elements which cause inflammation
Torneck – sterile empty polyethylene tubes healed in rat ct – disputes HTT
Goldman – no evidence of inflammation at the open ends of Teflon rods implanted in guinea pigs – disputes HTT
Wenger – Polyethylene tubes sealed 1mm short with GP/Grossman’s cement elicited little or no inflammation in rat bone – disputes HTT
What is gutta percha made of and what are its properties?
Friedman – 65% Zinc oxide; 20% GP; 10 metal sulfates (radiopacity); 5% waxes and resins
Schilder – GP exists in beta-semicrystalline state; undergoes change to alpha phase upon heating (42-29 C); compactable not compressable
Is latex allergy a concern for gutta percha? Is it biocompatible?
Costa & Johnson – no cross reactivity but slight concern with gutta balata additive
Nair – large pieces were encapsulated and free of inflammation; fine particles evoked inflammatory reponse (macrophages and multi-nucleated giant cells)
How do you sterilize gutta percha points?
Senia – 1min immersion in 5.25% sodium hypochlorite
How do you place sealer?
Wilcox – NSD found between file, lentulo, ultrasonics or coated MC
Does extrude material cause problems?
Augsburger & Peters – did not prevent healing; removed over 6 yr period
Baumgartner - extruded GP or sealer was associated with postop pain
What type of spreader should be used for lateral compaction? How far should it penetrate?
Joyce – NiTi induce less stress and decrease risk of VRF
Walton – less leakage with deep spreader penetration (within 1-2mm)
Discuss the custom cone technique?
Keane – 1 sec dip gave best adaptation and less leakage
Compare lateral compaction and warm vertical technique?
Baumgartner – NSD in bacterial leakage (continuous wave vs cold lat)
Reader – NSD in fill quality; more lateral canals obturated with warm techniques
Can warm techniques damage the periodontium?
Eriksson & Albrektsson - > 10 deg C is threshold level for bony necrosis
Sweatman & Baumgartner – System B, obtura and ultrasonic delivery of GP < 10 deg change at external root surface
Does the Thermafil system work well?
Walton – Thermafil leaked most possibly due to stripping of GP off carrier
Is Resilon a better obturation material?
Trope – teeth were more resistant to fx
Pashley – NSD in leakage compared to GP/AH plus
Is there a problem with Sargenti Paste?
Newton – demonstrated 6m & 1 yr cytotoxicity
Procedural Errors Overview
How are perforations classified?
Trope & Fuss – Old or Fresh (better prognosis; Large or small (<size 20=good prognosis); Cervical (unfavorable), Coronal/middle (fair), Apical (favorable)
How can they be detected?
Fuss – apex locators
Also: radiographs, blood on paper points, microscope, perio probings
What criteria are important for successful management?
Time, size & location
Beavers – monkey study showed best repair when immediate; acute inflammation, then formation of new PDL
Benenati – delay ok if aseptic
How would you manage a perforation?
If larger, consider an internal matrix as proposed by Lemon:
Rosenberg – Collacote
Alhadainey – Calcium sulfate (Capset)
Frank – Ca(OH)2
Also: hydroxyapatite, DFDBA, Gelfoam, Calcium phosphate
Repair with MTA as proposed by Torabinejad (no matrix required) – 16/16 success X1 yr; Biocompatible and caused cementum formation; less leakage than amal & IRM
Baumgartner – less bacterial leakage than amal
Daoudi – less dye leakage than Vitrebond
What’s the prognosis of perforation repairs?
Kvinnsland – 92% using ortho grade and surgical repair
What’s the incidence of separated instruments & does it affect prognosis?
Messer – 3% prevalence of retained fractured instruments; NSD in healing - 92% with fx inst & 95% without; lower success (87% & 93%) with preop PARL
Crump & Natkin– NSD in failure rate
How would you manage a separated instrument?
Attempt removal, bypass or obturate to fx
Ruddle – staging platform with modified gates; ultrasonic with DOM; IRS
Other methods: Endo extractor tubs with cyanoacrylate; braiding headstroms; wire loop and tube
How do you manage a sodium hypochlorite accident?
Gluskin – long acting anesthetics, irrigation with saline to dilute, Amoxicillin, analgesics, steroids, cold compresses & recalls
Kleier – diplomate survey – did not affect prognosis; more women than men, necrotic with PARL more common
Emergency / Flare-up Overview
What is the incidence of a Flare-up and are there any predictable indicators?
Walton – 3%; Female 2X more than males; Pre-op pain or swelling before initial appt are at greater risk
Torabinejad – Pre-op pain was an excellent predictor; Females age 40-59; no or small PA lesions increased the frequency of interappointment emergency
What causes flare-ups?
Seltzer & Naidorf – Overinstrumentation, overmedication, extruded debris, incomplete pulp removal, over-irrigation, hyperocclusion, root fx, or another tooth
Is it ok to close a tooth previously left open?
August – only minimal flare-ups seen – 5%
Do prophylactic antibiotics help decrease flare-up rate?
Reader – Pen VK did not decrease flare-ups with IP
Amox did not help decrease flare-ups with necrotic, asymptomatic teeth
Pen VK did not decrease flare-ups with necrotic, symptomatic teeth
When are Antibiotics indicated?
Pathways – Antibiotics are recommended in conjunction with appropriate endo tx for progressive infections with systemic signs and symptoms such as fever (100 deg F), malaise, cellulits, unexplained trismus, and progressive or persistent swelling. I & D is indicated for any infection marked by cellulites (fluctuant or indurated).
What are other tx considerations for a flare-up?
Occlusal Adjustment – Rosenberg – works for IP pre-op pain (perc. sens)
Re-enter for complete debridement
Establish Drainage – I & D; Trephination is ineffective (Moos, Reader)
Evaluate for Analgesics – Hargreaves – 3D pain control (diagnosis, definitive tx, drugs )
Flexible prescription plan – 1) max nonnarcotic (aceto or NSAID) or 2) add aceto (w or w/out opiod) to NSAID –
Match the pts needs
Evaluate for Antibiotics – systemic involvement or immunocompromised
Evaluate for Steroids – Reader – Oral (48mg methylprednisilone) or IO
Marshall & Walton – IM dexamethasone
Infections Overview
Discuss the infections of the Mandibular area:
Fascial Space Source Borders
Buccal Vestibule Any Mand tooth – exudates breaks through B cort. plate and apicies lie above attachment of Buccinator or Mentalis muscle • Buccal cortical plate
• Alveolar mucosa
• Buccinator (post)
• Mentalis (ant)
Body of the Mandible Any Mand tooth – exudate has not perforated the periosteum • Buccal or lingual cortical plate
• Periosteum
Mental Space Mand anterior tooth – exudate breaks through the B cort. plate and apex lies below attachment of Mentalis • Mentalis (superiorly)
• Platysma (inferiorly)
Submental Space Mand anterior tooth – exudate breaks through L cort. plate and apex lies below attachment of Mylohyoid • Mylohyoid (superiorly)
• Platysma (inferiorly)
Sublingual Space Any Mand tooth – exudates breaks through L cort. plate and apex lies above attachment of Mylohyoid • Mucosa of floor of the mouth (superiorly)
• Mylohyoid (inferiorly)
• Mandible (lateral)
Submandibular Space Mand posterior tooth – exudates breaks through the L cort. plate and apicies lie below attachment of the Mylohyoid • Mylohyoid (superiorly)
• Platysma (inferiorly)
• Mandible (lateral)
Pterygomandibular Space Mand second or third Molars – exudates drains directly into the space or contaminated IAN block • Medial Pterygoid (medial)
• Ramus (lateral)
• Lateral Pterygoid (superior)
What 3 spaces are involved in Ludwigs angina?
Submental, Submandibular & Sublingual - life threatening cellulites which can advance to the pharyngeal and cervical spaces, resulting in airway obstruction
Discuss the infections of the lateral face and cheek:
Fascial Space Source Borders
Buccal Vestibule Max posterior tooth – exudates breaks through the B cort plate and apicies lie below attachment of the Buccinator • Buccal cortical plate
• Alveolar mucosa
• Buccinator (superiorly)
Buccal Space Any Mand or Max posterior tooth – exudates breaks through B cort plate and apicies lie above/below the attachment of the Buccinator respectively • Buccinator (medial)
• Skin of Cheek (lateral)
• Zygomatic arch/Buccinator attachment (superiorly)
• Mandible/Masseter attachment (inferiorly)
Submasseteric Space Impacted 3rd Molar • Ramus (medial)
• Masseter (lateral)
Temporal Space Involved indirectly if an infection spreads superiorly from the inferior pterygomandibular or submasseteric spaces Deep Temporal:
• Skull (medial)
• Temporalis (lateral)
Superficial Temporal:
• Temporalis (medial)
• Fascia
Discuss the infections of the midface:
Fascial Space Source Borders
Palate Any Maxillary tooth with apex near palate • Palate (superiorly)
• Periosteum (inferior)
Base of the Upper Lip Maxillary Central Incisor with apex close to B cort plate & above attachment of Obicularis Oris • Mucosa of the Base of the Upper Lip
• Obicularis Oris (inferior)
Canine Space (Infraorbital) Maxillary Canine or 1st Premolar – exudates breaks through B cort plate and apex lies above the attachment of the Levator Anguli Oris • Levator Anguli Oris (inferior)
• Levator Labii Superioris (superiorly)
Periorbital Space Spread of infection from the Canine or Buccal Spaces • Lies deep to the Orbicularis Oculi
Why are infections of the midface dangerous?
Cavernous sinus thrombosis – life threatening infection in which a thrombus formed in the cavernous sinus breaks free, resulting in a blockage of an artery or the spread of infection. Infections in the midface initiate an inflammatory response. Increased pressure can reverse the direction of venous blood flow (due to lace of valves) causing stasis in the cavernous sinus – this may initiate thrombus formation.
Retreatment Overview
Are Silver points a concern?
Seltzer – corrosion products of silver sulfides, silver sulfates, silver carbonates, and silver amine sulfate amide hydrates which are cytotoxic
What are some techniques to remove Silver points?
Krell – ultrasonics with hedstroms
Ruddle – ultrasonics with IRS
How do you remove posts?
Johnson – 16 min ultrasonic vibration
Baumgartner – Gonan produced less cracks than ultrasonics and was quicker
Can ultrasonic post removal cause any problems?
Eleazer - > 15 sec caused high root surface temps
Huttula & McClanahan – irrigate with ultrasonics reduced temps
What solvent is most effective at gutta percha removal?
Kaplowitz – tested 5 solvents; only chloroform dissolved GP completely
Is chloroform safe for the patient and the dental staff?
Chutich – no health risk to the pt; .32mg extruded – 49mg is permissible toxic dose
McDondald – safe for staff; air vapors well below OSHA standards
How are Thermafil carriers removed?
Bertrand – chloroform and endo files
Baratto – Profiles at 300 rpm
Wolcott & Hicks – System B 225 deg & hand instruments
What is Red Russian paste and how do you remove it?
Gound – Resorcinol-formaldehyde resin; 10% sodium hydroxide causes polymerization
Krell – use ultrasonics
Hartwell – no solvent works; NaOCl works best
Surgery Overview
What are the anatomical concerns during periapical surgery?
Maxillary:
Eberhardt & Torabinejad – MB root of 2nd molar is closest to the sinus (2mm) and furthest from buccal cort plate (4.5mm); buccall root of 1st premolar is closest to buccal cort plate (1.6mm) and furthest from sinus (7mm); 5% of roots protrude into the sinus
Mandibular:
Phillips & Weller – mental foramen located 60% the distance from the buccal cusp tip of the 2nd premolar to the inferior border of the mandible; exits posterior-superiorly; radiographically 3mm below and slightly mesial of apex of 2nd premolar
Torabinejad – IAN S shaped – buccal to the D root of 2nd molar; crosses to L below the M root of 2nd molar; L to 1st molar; crosses to buccal below 2nd premolar
How would you manage a sinus exposure?
Lin & Langeland – prescribe decongestants (.5% neosynephrine); antibiotic only if sinusitis develops
How do you avoid the mental foramen and nerve?
Moiseiwitsch – take vertical PA radiograph; triangular incision w/ D vert release; notch bone superiorly for retractor
Discuss hemostasis during surgery?
Kim – Recommends racellet epi pellets; other hemostasis measures include:
Bone wax – may act as foreign body if any remains
Chemical vasoconstrictors – epi pellets placed 2-4min – little systemic absorption
Ferric sulfate – must be completely curetted or healing will be delayed (Jeansonne)
Calcium sulfate – acts via tamponade effect; biocompatible and resorbs
Collagen – causes platelet aggregation
Are epi pellets a concern systemically?
Baumgartner – epi pellets produce no significant cardiovascular effects
How much blood is typically lost during endodontic surgery?
Messer – Avg 9.5mL; similar to tooth extraction; time is biggest factor
Buckley – use 1:50,000 epi – ½ the blood loss
How much of the root end should be resected? Bevel?
Kim – 3mm resection = 98% of apical ramifications and 93% of lateral canals removed
Niemczk & Kim – 4mm root resection of MB root of Max 1st molar will expose a complete or partial isthmus 100% of the time
Gilheany & Figdor – aim for 0 deg bevel for decreased leakage
Why use ultrasonics for the retro-prep? Do ultrasonics cause cracks?
Baumgartner – 3mm prep with diamond coated ultrasonics; no crack seen and minimal bony crypt required
Does the entire lesion need to be curetted and removed for healing to occur?
Lin & Langland – No, but must remove all foreign objects
Is it necessary to remove the apical smear layer?
Jeansonne – no difference in healing noted (used tetracyc. & citric acid)
Is a retro-fill required? What do you use and why?
Altonen – teeth with retrofills had greater success
Dorn – Super EBA (best) showed better success rates 95% compared to IRM or amal
Jeansonne – Washout noted with MTA
Discuss MTA as a retro-fill material?
Torabinejad – biocompatible; demonstrates the least leakage; ok with blood contamination; substrate for osseous and cementum growth
Would you consider guided tissue regeneration?
Pecora & Kim – If > 10mm; through & through; endo-perio defect
Suda – Calcium sulfate was effective in bone regeneration
What type of sutures do you use and why?
Becker – Vicryl (polyglactin) produced little inflammatory response compared to polypropylene, silk or gut
Discuss incision and wound healing following endodontic surgery?
Harrison & Jurosky –
Healing of the incisional wound:
24 h – thin epithelial seal
24-48 h – multilayered epithelial seal
48-72 h – epithelial barrier; collegen fiber synthesis
Preserve root attached tissue; submarginal & intrasulcular flaps performed equally
Healing of the osseous wound:
Day 1-3 – fibrin clot
Day 4 – granulation tissue replaces clot
Day 14 – new periosteum forms; osteoblastic activity; new woven bone trabeculae occupy 80%
Day 28 – maturing new trabecular bone
Periosteum does not survive flap reflection; don’t curette cortical retained tissue; crestal bone levels will reduce following sx
When should sutures be removed?
Kim – 2-3 days
When would decompression be considered and discuss different approaches?
Large lesions in order to avoid: divitalizing adjacent teeth, damage anatomical structures, parasthesia or risky sx (elderly)
Freedland – used polyvinyl tubing and daily irrigation
Hoen – Aspiration & irrigation
Trauma Overview
How do you classify crown fractures?
Andreasen: Crown infraction (craze line); Uncomplicated crown fx (enamel and/or dentin with no pulp exposure); Complicated crown fx (pulp exposed)
What is the probability of pulp necrosis following crown fx?
Ravn – 6% with uncomplicated crown fx; if concussion & mobility, then 30%;
80% success with DPC and uninflammed pulps
Cvek – 96% success cvek pulpotomy ( remove 2mm pulp up to 7days after fx)
What is the tx for a crown fx?
Uncomplicated – Restore with GI or composite resin; attempt bonding fx’d segment
Complicated – Cvek pulpotomy with Ca(OH)2 or RCT
What is the tx for a root fx?
3 radiographs; Reposition coronal segment & physiologic splint X3 wks; relieve occl
-if fx is coronal, remove coronal segment; consider gingivectomy or ortho extrusion
What is probability of pulp necrosis with root fxs?
Andreasen – 25% of the coronal segment
What are the methods of healing for a root fx?
Andreasen – Calcified tissue; connective tissue; interproximat bone & ct; inflammatory tissue w/out healing
What is the tx for a luxation injury?
Take multiple angled radiographs to discern root fx or not;
Reposition tooth in normal position (consider ortho reposition with intrusion); physiologic splint X3 wks; relieve occlusion; monitor for pulpal necrosis/pathology
-If intrusion of fully formed root apex, initiate RCT in 2wks
What is the probability of pulp necrosis following luxation injuries?
Andreasen – Concussion 3%; Subluxation 6%; Extrusion 26%; Lateral Luxation 58%; Intrusion 85%
How do you manage an avulsed tooth with an open apex (<1 hr dry)?
Clean root and socket with saline; Soak tooth in doxycycline 1mg/20mL for 5 min (Cvek- less ankylosis or inflammation); examine for alveolar fx & replant; physiologic splint X1 wk; monitor for necrosis/PA pathology
How do you manage an avulsed tooth with an open apex (>1 hr dry)?
Replantation is not indicated
How do you manage an avulsed tooth with a closed apex (<1 hr dry)?
Clean root and socket with saline; examine for alveolar fx & replant; physiologic splint X1 wk; initiate RCT X7-10 days
How do you manage an avulsed tooth with a closed apex (>1 hr dry)?
Clean root surface and soak in 2% stannous fl- X5min; clean socket with saline; examine for alveolar fx and replant; physiologic splint X1 wk; initiate RCT X7 days
What type of healing can you expect with an avulsed tooth?
Andreasen – normal, replacement resorption, surface resorption & inflammatory resorption; <30min before replanted, 90% no resorption; >90min = resorption
Discuss storage media for avulsed teeth?
Trope: Best to worst: HBSS > Milk > Saline > Saliva > Water
Blomlof – Milk gives you 6 extra hrs
Discuss splinting of avulsed teeth?
Castilli – splinting X7 days recovered uneventfully; 30 days induced resorption & ankylosis
What are some general adjuncts for trauma tx?
Tetanus booster; chlorhexidine rinses; analgesics
Antibiotics – Pen VK or doxyclycline (Trope – anti-resorptive) X1wk for avulsions
What is the role of Ca(OH)2 in replanted teeth?
Trope – decrease incidence of inflammatory resorption; 1wk = 8wks
Dumsha – NSD in inflammatory resorption with GP or 5mo tx with Ca(OH)2; recommends obturating immediately
What is the role of fluorides in replanted teeth?
Klinge – SnF2 delays replacement resorption
Coccia – delays resorption; 2X survival time
What is the recommended follow-up for traumatic dental injuries?
Pathways – after tx 3, 6, 12 mo and yearly thereafter
Anesthesia Overview
What properties of local anesthetics determine the onset of action, potency, and duration of action?
Malmed
pKa determines the onset of action – the lower the pKa the more rapid the onset
Lipid solubility determines the potency – permits anesthetic to penetrate the membrane more easily
Protein binding is responsible for the duration of action. Duration also increased with vasoconstrictor which decreases blood flow and systemic absorption
Amide LAs are metabolized in the Liver
What is the mechanism of action for local anesthetics?
Blockage of sodium channels by partitioning into 2 types, the charged acid (RNH+) and the uncharged basic form (RN), which penetrates the nerve membrane, ionizes and blocks the influx of sodium ions preventing depolarization (-70 mV → 40 mV)
What are some explanations for anesthetic failure?
Hargreaves - 1) lower pH of inflamed tissue → reduces the amount of base form of anesthetic that penetrates the nerve membrane
2) Unsuccessful technique
3) Inflamed nerves have altered resting potentials and decreased excitability thresholds
4) TTX-R sodium channel which are resistant to LAs (increased expression in IP cases)
5) Apprehensive pts have decreased pain thresholds
Fouad – 6 fold increase in TTX-resistant sodium channels in IP cases
Does accessory nerve innervation affect anesthesia?
Frommer – mylohyoid nerve may supply accessory innervation
Pogrel – cross innervation of Mand incisors
What are some supplemental anesthesia techniques and how do they work?
PDL – IO anesthesia (Walton) – 92% effective
Stabident / X-tip – IO anesthesia
Intrapulpal – pressure anesthesia (Birchfield)
What are alternative injection techniques to the IAN block? Are they more successful?
Gow-Gates & Vazirani-Akinosi
Malmed – Gow-Gates is superior to IAN block
Reader, Petrovic – failed to show either GG or V-A is better than IAN block
Compare the efficacy of different anesthetics?
Reader – NSD in 4% prilocaine, 3% mepivicaine & 2% lidocaine with IAN block
Is Articaine the solution?
Reader – NSD between 4% articaine & 2% lidocaine with IAN block & IP
Aritcaine did show increased success if given as a buccal infiltration injection following IAN block (88% vs 71% success rate)
Haas – Articaine has a 5 fold higher incidence of paresthesias compared to lidocaine
Discuss Intraosseous anesthesia success and side effects?
Reader – 67% had an increase in heart rate – ok with healthy pts; consider mepivicaine
- Stabident with 2% lidocaine – 88% effective for IP
- Stabident with 3% mepivicaine for IP– 80% successful x1 injection; 98% x2
What are the anesthetic and epinephrine concentrations in common anesthetics?
2% lidocaine w/ 1:100,000 epi = 36mg lido w/ .018mg epi
3% mepivacaine (Cabocaine, Polocaine) = 54mg mepivacaine
4% articaine w/ 1:100,000 epi = 72mg articaine w/ .018mg epi
0.5% bupivacaine (Marcaine) w/ 1:200,000 epi = 9mg bupivacaine w/ .009mg epi
What drug interactions are a concern with epinephrine?
Tricyclic antidepressants – amitriptyline, doxepin
Nonselective beta blockers – nadolol, propranolol
Recreational drugs - cocaine
Nonselective alpha adrenergic blockers – chropromazine, clozapine, haloperidol
Digitalis - Digoxin
Thyroid hormones – Levothyroxine
MAO inhibitors
What is the max dosage of anesthetic?
Moore – rule of 25 = 1 carp for every 25 pounds of pt weight
Adults 4.4mg /kg
ENDO-PERIO Overview
Can Endo pathosis create perio pathology?
Sinai & Soltanoff – rat study showed pulpal disease affects the periodontium quickly with inflammation; perio disease affects the pulp slowly with degenerative changes
Does perio disease cause endo pathosis?
Yes: Seltzer – disease caused through lateral/accessory canals and vice-versa
Langeland, Rodregues & Dowden – if all main apical foramina are involved
Kipioti & Kobayashi (2 sep. studies) – caries free teeth with endo path showed similar microorganisms in perio pockets and root canals
No: Mazur & Massler / Czarneck & Schilder – histo studies showed no correlation
Who discussed endo-perio terminology?
Simon – Primary endo; Primary endo with 2nd perio; Primary perio; Primary perio wth 2nd endo; true combined lesions (ie root fx)
Does perio tx affect the pulp?
Wong & Hirsch – pulpitis was noted adjacent to areas of root planning/scaling
Does endo tx affect future perio tx?
Dunlap – in vitro study found RCT does not interfere with growth of fibroblasts on planed dentin surfaces
What is the biologic width?
Gargiulo, Wentz & Orban – sulcus depth - .7mm
epithelial attachment - 1mm
CT attachment – 1.1mm
What are common perio pathogens?
Red complex Bacteria: P. gingivalis, T. forsythensis & T. denticola
Other bacteria linked to perio disease: Actinobacillus actinomycetemcomitans, B. forsythus & P. intermedia.
Trope – spirochetes common in perio abscesses but less likely in endo abscesses
ENDO-PEDO Overview
Discuss Primary tooth anatomy:
Hibbard: Mand incisors – 2 canals 10%
Max 1st molar – 2 MB canals – 75%
Max 2nd molar – 2MB canals – 85-95%
Mand 1st molar – 2 mesial canals – 75%; 2 distal canals – 25%
Mand 2nd molar – 2 mesial canals – 85%
Discuss formocresol pulpotomies: technique, formulation & concerns?
Technique – remove coronal pulp, moist cotton pellet until heme control, place formocresol X5 min, ZOE cement & SSC
Fuks – recommends 1/5 concentration
Pashley – found formocresol systemically (spleen, liver & kidney) after placing in dogs teeth
Are there any other options & compare success rates?
Vargas – NaOCl- & FeSO4 – 100% clinical success; 91% & 64% success radiographically
Fuks – Formocresol success - 84%; Glutaraldehyde - 72%; FeSO4 - 93%; MTA - 97%
How would you obturate primary teeth?
ZOE or Ca(OH)2 paste
Coll – 78% success with ZOE pulpectomies
Who decribed Apexification & what types of repair are seen?
Frank – long term tx with Ca(OH)2
4 types of repair/closure: recession of the root canal
obliterated apex w/out change of canal space
no radiographic evidence of closure / apparent clinically
calcified bridge coronal to the apex
How long does this take?
Kleirer – 1yr +/- 7months
Cvek – Avg 18 months; check q 3-6 months
Are there concerns about long term use of Ca(OH)2?
Andreasen – >30 day use will weaken dentin; ½ strength in 1 yr
Are there other options to manage an open apex?
Apical Bariers: Dentin Chips - Holland
Ca(OH)2 – Weisenseel, Hicks & Pelleu
MTA – Torabinejad
ENDO–ORTHO Overview
Can orthodontics cause pulp necrosis?
Butcher – extreme ortho forces can cause circulatory interruptions leading to necrosis
Can ortho cause resorption?
Reitan – ortho movement too quickly = resorption
Can you orthodontically move an endo treated tooth?
Wickwire – ok to move endo teeth – no signs of pathologic changes
Who first discussed ortho extrusion?
Heithersay – indicated for transverse root fx 1-4mm subcreastal; 6 wk stabilization
How long should you stabilize an extruded tooth?
Lemon – 1 mo stabilization for every 1mm of movement
Can anything else be done to prevent a relapse?
Malmgren – fiberotomy may help
Resorption Overview
How is resorption classified?
Tronstad – transient inflammatory (surface), progressive inflammatory, internal & external (progressive external, cervical, and replacement)
How do you differentiate internal from external resorption?
Gartner & Mack – radiographic differences: internal – symmetrical, cannot trace canal through lesion, stays centered in shift shots; external – irregular, can trace the canal through the lesion, moves on shift shots
What causes resorption?
Trope – Two things must happen: 1) the loss or alteration of the protective layer (pre-cementum or pre-dentin); 2) inflammation must occur to the unprotected root surface
Osteoclasts will not adhere to or resorb unmineralized matrix; if the cemental layer is lost or damaged, the inflammatory stimulators can pass from an infected pulp space through the dentinal tubules into the PDL resulting in both bone resorption and root resorption
Discuss internal resorption and tx approach?
Wedenberg – normal pulp is replaced with periodontal-like connective tissue
Turkun - >90% success with non-perforating using 1 wk CaOH2 and warm GP; 25% success with perforating defect
Stamos – ultrasonics & warm GP
Discuss external inflammatory resorption and tx approach?
Johnson – Necrotic teeth with AP had more apical resorption than those with a normal periapex or IP
Trope – Long term (12 wk) CaOH2 tx may be more effective than 1wk for established inflammatory root resorption
Discuss external cervical resorption an tx approach?
Heithersay – strong association with ortho, trauma & bleaching; distinguished class 1-4 defects; recommended topical 90% trichloracetic acid, curettage & GI restoration (endo tx)
Frank – Tx and prognosis based on complete debridement of the defect
Can ortho tx cause resorption?
Reitan – ortho movement too quickly = resorption
Bleaching Overview
Who described internal bleaching?
Spasser – described Na perborate walking bleach
Nutting & Poe – recommended Super oxol + Na Perborate for greater efficacy; change every week
Can bleaching cause resorption?
Madison & Walton – bleaching factors associated with resorption were heat with 30% hydrogen peroxide
Papadopoulos – gaps at the CEJ lead to increased leakage of hydrogen peroxide
What can you do to prevent resorption?
Rotstein – use a 2mm base material at the CEJ; also recommends water instead of super oxol
Can tetracycline stained teeth be bleached?
Walton – only internal bleaching is effective
Does bleaching affect bonding of composite restorations?
Titley & Torneck – H2O2 may inhibit resin polymerization
Demarco – short term use of Ca(OH)2 restores bonding capabilities
Is internal bleaching effective?
Glockner - 5 yrs later; pts are 98% satisfied; 80% subjective success for dentists
Is vital tooth bleaching effective?
Haywood – 92% experience some lightening; 66% experienced transient side effects
Ritter – safe for the pulp up to 10 yrs post-op; bleaching effectiveness may decline
Endodontic Materials Overview
RC Prep: EDTA, Urea Peroxide, Cetyl Alcohol
Gutta Percha: 65% Zinc Oxide; 20% GP; 10% metal sulfites; 5% waxes and resins
AH Plus: epoxy-amine resin (Bisphenol paste A / Amine paste B)
Roth 801 Sealer: ZOE
Cavit: Zinc oxide; calcium sulfate, barium sulfate, talc, ethylene diacetate, zinc sulfate, polyvinyl acetate
MTA: 75% Portland Cement, 20% bismuth oxide, 5% gypsum
Super EBA: Powder – 60% Zinc Oxide, 34% Silicate dioxide, 6% resins
Liquid – 65% Ethylene Benzoic Acid, 35% Eugenol
Restorative Overview
Are endodontically treated teeth more brittle?
Sedgley – Vital dentin 3.5% harder; biomechanical properties are not significantly altered
Messer – NSD in moisture content
Reeh, Messer & Douglas – RCT reduces cuspal stiffness by 5%; Occl cavity prep. 20%; MOD 63%
Is the seal of the coronal restoration important?
Swanson & Madison – loss of coronal seal = bacterial contamination in as little as 3d
Ray & Trope – Quality of coronal seal more important than quality of endo tx
Berganholtz – GP exposed for up to 3 yrs showed lesions did not worsen
What type of temporary restorations do you use?
Cavit, IRM & Glass ionomer:
Weber – use 3.5mm thickness of Cavit
Beach & Hutter – 3 wk bacterial leakage test: no leakage w/ Cavit<IRM (1 samp)<Term
Pashley – Cavit, Term & GI provided leakproof seals for 8wks
Is cuspal coverage important for endodontically treated teeth?
Aquilino – teeth without crown lost at 6X higher rate
When should post space be made? What technique and dimensions?
Immediately due to familiarity to canal anatomy & setting of sealer
Lemon – NSD with immediate or delay
Todd – NSD with heat or rotary removal of GP
Sorensen & Martinoff – post = crown length
Madison – leave at least 4mm GP
Johnson – max post width is 1/3 root width
Does Eugenol affect post cementation?
Yes – Nemetz – with panavia (resin) cement
No - Boone
Can posts cause root fractures?
Akin – Stress patterns are a result of post insertion
Randow – pts detect pressure earlier in vital teeth
Pulpal Histology/Pathology Overview
What the cellular elements of the pulp?
TenCate – Odontoblasts, fibroblasts, undifferentiated mesenchymal cells, macrophages, Lymphocytes & Dendritic cells
Farnoush – found mast cells in both inflamed and normal pulps
Reader – mylenated A-delta fibers 28%; unmylenated C fibers 72% of total
How far do the odontoblastic processes extend into the tubules?
Pashley – 1/3 the length of the tubule
What types of collagen are found in the dental tissues & what cells synthesize collegen?
Pulp – type I & III; Dentin – type I (90% of organic component)
Synthesized by mainly fibroblasts, but also odontoblasts, osteoblasts & cementoblasts
Are lymphatics found in the pulp?
Bernick – demonstrated lymphatics in the pulp
Discuss the pulp vasculature and regulation of blood flow?
Takahashi & Kim – SEM showed AV anastomosis, VVanastomosis, U-shaped arterioles
Kim – PBF increased with C-fiber activation (A-delta insignificant); C-fibers release substance P which increases PBF; the increase in tissue pressure excites both A-delta & C fibers
Describe the ‘strangulation theory’ & does it occur?
As pulpal inflammation ↑, pulpal pressure ↑. With this increased pressure, veins and lymphatics collapse at the apex and strangle the pulp – necrosis results
Tonder – cat study disproved this theory; localized increase in pressure with no strangulation
Discuss calcific metamorphosis? Is RCT indicated?
Pathways - Pulp canal obliteration due to trauma – resembles cememtum or bone
Andreasen – 22% of traumatized teeth undergo CM; only 8.5% developed pulp necrosis
Walton – canal present histologically, although absent radiographically
Holcomb & Gregory – RCT if PARL develops; only 7% require RCT
Discuss the pulpal rxn to caries?
Reeves & Stanley – if caries is < .5mm from the pulp or if it invades reparative dentin, there is irreversible damage; if >1.1mm then little pathosis is seen
Trowbridge – chronic inflammation occurs long before bacteria penetrates the pulp
What is the effect of restorative dentistry on the pulp?
Stanley, White & McCray – tertiary dentin begins to form @ 19 days at 1.49 um/day
Abou-Rass – consider RCT for teeth with stressed pulps
Zach – heat is capable of causing pulp necrosis
Felton & Madison – 13% incidence of pulp necrosis following FCC
How does age affect the pulp?
Bernick – decreased vascularity, nerves & pulp chamber size; increased calcifications
Describe the hydrodynamic theory of dentinal hypersensitivity. Any solutions?
Brannstrom – heat causes inward fluid movement; cold – outward; distortion of odontoblastic processes stimulates nerve response
Pashley – occlude tubules with unfilled resins or oxalate salts
Kim – K+ ions desensitize nerve ending
How does vital bleaching affect the pulp?
Ritter – safe for the pulp up to 10 yrs post-op; bleaching effectiveness may decline
Periapical Pathology Overview
Define:
Granulation tissue: healing tissue with fibroblasts, collagen, proliferating capillaries and leukocytes
Granuloma: chronic inflammatory tissue primarily infiltrated with lymphocytes, plasma cells & macrophages
True cyst (bay cyst – Simon): inflammatory lesion with a distinct pathological cavity completely enclosed in an epithelial lining
Pocket cyst: lined with epithelium, but communicates with the root canal
Abscess: acute inflammation consisting primarily of PMNs
Is it possible to differentiate between a granuloma or cyst?
Priebe – No, can’t determine from a radiograph
What is the incidence of a granuloma, cyst & abscess?
Nair – 50% granuloma; 35% abscess; 15% cyst (distinguishes 9%pocket / 6% true)
Rubenstein & Kim – 85% granuloma; 15% cyst
What are the theories of cyst formation?
Breakdown theory – (Toller): Osmotic pressure buildup due to semi-permeable membrane (remnants of cellular debris inside lumen leads to increased osmotic pressure due to Starling’s law)
Cavitational Breakdown theory – (Ten Cate): Continuous growth of epithelial cells (rests of Malassez) removes central cells from their nutrition; innermost cells die & cyst cavity forms
Epithelial Proliferation theory – (Seltzer): epithelial cells proliferate to line the abscess cavity
Immunologic theory – (Torabinejad): Immune rxn (to antigens-bacteria in infected RC) responsible for proliferation of epithelium
Do cysts heal following RCT?
Nair – pocket cysts should heal; true cysts, particularly large ones with cholesterol crystals are less likely to resolve following RCT
What are the histologic features of a sinus tract?
Baumgartner – lined with either epithelium or granulomatous tissue; 67% lined with epithelium to level of rete ridges; 33% were completely lined with epithelium to the PA lesion
Is condensing osteitis a LEO?
Eliasson, Halvarsson & Ljungheimer – tx successfully and resolved with RCT 85%
Provide a differential diagnosis for the following:
Unilocular Periradicular Radiolucency:
PA Granuloma
PA Cyst
PA Abscess
PA Fibrous Scar – more frequent with thru & thru lesions or S RCT
Nasopalatine Duct Cyst – max midline; > 6mm between central incisor roots
Traumatic Bone Cyst – not a true cyst; trauma etiology; mand teeth
Benign Fibro-osseous lesions (early stages) – periapical cemental dysplasia
Lateral Periodontal Cyst – mand and max canine & premolar area
Mutiloculary Periapical Radiolucency:
Myxoma
Ameloblastoma – aggressive neoplasm; any tooth-bearing area, but mand most common; peak age 30-40
Central Giant Cell Granuloma – multinucleated giant cells; rule out hyperparathyroidism
Hemangioma
Odontogenic Keratocyst – post mand most common but may occur in any tooth bearing area; multiple OKCs associated with Basal cell nevus syndrome
Periradicular Radiopacities
Condensing Osteitis - LEO
Idiopathic Osteosclerosis – idiopathic dense bone; vital pulps
Benign Fibro-osseous lensions – mixed radiolucent/radiopue; ossifying fibroma, cemento-osseous dysplasia, PCD; vital pulps
Cementoblastoma – attached to root with radiolucent rim; neoplasm of cementoblasts
Osteoblastoma – neoplasm of osteoblasts; may occur in any bone; not attached to root
Odontoma - compound (tooth like) or complex
Anatomy Overview
Describe the Nerve supply to the teeth?
The Anatomic Basis of Dentistry
Brain stem → Trigeminal nerve (cranial nerve V) → 3 Divisions (I – Opthalmic; II – Maxillary; III – Mandibular)
Nerve supply to the Maxillary teeth:
Trigeminal nerve → 2nd Div Maxillary nerve (foramen rotundum) →
PSA → Maxillary Molars
MSA → Maxillary Premolars (MB root Max. Molar)
ASA → Maxillary Anteriors
Nerve supply to the Mandibular teeth:
Trigeminal nerve → 3rd Div Mandibular branch (foramen ovale) →
IAN → Mandibular Molars / Premolars → Incisive branches → Canines / Incisors
Describe the blood supply to the teeth?
The Anatomic Basis of Dentistry
Arterial supply:
R atrium/R ventricle → Pulmonary artery → Lungs → Pulmonary vein → L atrium/L ventricle → Aorta → Common Carotid artery → External Carotid artery → Maxillary artery →
Maxillary Posterior teeth: Pterypopalatine artery → PSA artery
Maxillary Anterior teeth: Pterypopalatine artery → PSA artery → ASA artery
Mandibular Posterior teeth: Mandibular artery → Inferior Alveolar artery
Mandibular Anterior teeth: Mandibular artery → Inferior Alveolar artery → Incisive artery
Venous supply:
Veins from the Mandibular teeth → Inferior Alveolar vein →
Veins from the Maxillary anterior teeth→ Infraorbital vein →
Veins from the Maxillary posterior teeth →
Maxillary Vein → Pterygoid venous plexus → retromandibular vein → Internal Jugular vein → Brachiocephalic vein → Superior vena cava → Heart (r. atrium)
Microbiology Overview
What causes periapical pathology?
Bacteria: Kakahashi – lesions developed with exposed pulp in conv. rats & not
germ-free
Moller – lesions only developed in infected devitalized pulps in monkeys
Sundqvist – bacteria were necessary to cause lesions in human teeth
*Host immune response mediates tissue and bone destruction in response to bacteria (see inflammation section)
What is the general distribution of bacteria within the tooth?
Crown = Aerobes associated with careis: Strep mutans
Mid-root = Facultative species (Gram + rods/cocci): Staph aureus, Actinomyces,
Lactobacillus
Apex = Anaerobes (Gram – rods/Gram + cocci): Bacteroides, Fusobacterium
What specific bacteria are involved the pathogenesis of a primary root canal infection?
Siqueira – mixed flora (avg. 5 species), predominately gram – anaerobic rods (Porphyromonas endodontalis most common)
Baumgartner – Prevotella nigrescens most common BPB isolated
Fabricius - # of obligate anaerobes increase with time & nearer the apex
Gram - Anaerobic rods: Porphyromonas, Prevotella, Fusobacterium, Bacteroides
Also Candida (Waltimo) & HIV (Trope) found
What bacteria are more likely to infect a previously treated case?
Usually 1 or a few species, generally treatment resistant gram + facultative cocci
Sundqvist – Avg. 1.3 species; E. faecalis frequently isolate 38%
Nair – Yeast / Candida involve in treatment failures
Gram + facultative cocci: Enterococcus, Streptococcus, Staphylococcus
Why are Enterococcus species resistant?
Love- able to invade dentinal tubules and adhere to collegen in the presense of serum
Distal – forms biofilm resistant to defense cells and antibiotics
Evans – proton pump resists high pH of calcium hydroxide
Are any bacteria associated with symptoms?
No: Baumgartner – No relationship between BPB and symptoms & signs
Yes: Gomes – Association between Prevotella & Peptostreptococcus and pain
Sundqvist – BPB associated with purulent infections
Discuss the bacterial flora found in acute PA abscesses?
Siqueira – Polymicrobial – similar to primary infections – BPB
Sundqvist – BPB associated with purulent infections
Are bacteria found in PA lesions? Controversy?
Yes: Tronstad – found extraradicular (anaerobes) in 8 refractory lesions
Siqueira – SEM study; only 1/24 cases or 4%
No: Walton – histo study; confined to canal space
Nair – histo study; criticized Tronstad for contamination
Does RCT cause bacteriemia?
Baumgartner – very low incidence if confined to RC system – 3.3%
Are bacteria present in traumatized teeth with intact crowns?
Bergenholtz – Yes – 64% mixed flora with necrotic pulp; remaining had aseptic necrosis; proposed bacterial entry through tubules and cracks
Does anachoresis occur?
Yes: Robinson & Boling – cat study; inflammation & bacteria required
Gier – bacteria attracted to inflamed pulps (IV injection of bacteria)
No: Doyle – not demonstrated through IV injection of bacteria; cat study
Moller – non-infected pulp did not induce PA inflammation; monkeys
Inflammation Overview
Discuss the focal Infection theory.
A localized or generalized infection resulting from a dissemination of bacteria or toxic products from a “foci of infection” (necrotic pulp or dental abscess).
WD Miller(1890) – introduced “focal infection”
William Hunter (1900) – ignited the theory; multitude of diseases attributed to focal infection
Frank Billings(1912) – introduced focal infection to American physicians (started era)
Reimann & Havens (1940) – critique of theory – unproven
Torabinejad - chronic periapical lesions cannot act as a focus to cause systemic diseases via immune complexes.
Siqueira (2002) – no clear evidence that microorganisms from the RC can cause disease in remote sites of the body
Describe the Zones of Fish.
Necrosis / Infection – bacteria, PMNs
Contamination – bacterial toxins, lymphocytes, macrophages
Irritation – osteoclasts, lymphocytes, macrophages
Stimulation – osteoblasts, fibroblasts
What is the role of neuropeptides?
Cause neurogenic inflammation
Byers – demonstrated “sprouting” of CGRP nerve fibers after dental injury
Wakisaka – neurpeptides found in pulp – regulate PBF and precipitate pain; neuropeptides include SP, CGRP, NKA, NPY(sympathetic/vasoconstrictive) & VIP (parasympathetic/vasodilation)
Who studied LPS and what is its role in PA pathology?
Schein & Schilder – pulpless teeth ↑endotoxin (LPS) than vital pulps; symptomatic teeth and those with PARL have ↑LPS than asymptomatic teeth
What are cytokines and which are involved in bone resorption? Any other factors involved?
Polypeptide products of immune cells. They modify behavior of other cells, produce systemic effects & act as growth factors
Stashenko (rat studies) – bone resorbing activity is due to cytokines rather than LPS
Cytokine involved in bone resorption alone or in synergistic combination: IL-1beta, TNF alpha & PGE2
Torabinejad - arachidonic metabolites and the complement system play an important role in bone resorption
Immunology Overview
Discuss the 4 types of immune rxns?
Type I – Anaphylactic Rxn – IgE mediated; binds to basophils & mast cells which release inflammatory mediators (allergic rhinitis & asthma)
Type II – Cytotoxic Rxn – IgG & IgM mediated; triggers complement or phagocytosis (autoimmune hemolytic anemia, some organ rejection & idiopathic thrombocytopenic purpura)
Type III – Immune Complex (Ag-Ab) Rxn – Ag-Ab complexes activate complement; (Arthus type – large complexes within blood vessel; serum sickness-type – small & soluble complexes which pass into the tissues)
Type IV – Delayed-Type Hypersensitivity – no Ab required; cell mediated immunity; macrophages and Killer T cells recognize Ag bearing cells; Involves memory T cells; 4 types: 1) chronic infection of intracellular bacteria, viruses & fungi
2) contact dermatitis
3) graft rejections
4) autoimmune diseases
Torabinejad – Ag-Ab complexes & IgE mediated rxns can initiate changes in PA tissues; type IV rxns may be involved in PA lesion progression
Discuss the complement cascade.
C’ consists of some 20 interactive plasma and cell membrane proteins. Once activated:
1. Mediate vascular responses (histamine release via C3a and C5a anaphylatoxins)
2. Recruiting phagocytic leukocytes
3. Opsonizing targets of phagocytic cells (C3b)
4. Directly damaging target cells (C5-9 MAC)
Most important step is cleavage of C3.
Classical pathway is activated by Ab coated targets or Ag-Ab complexes (IgM, IgG)
Alternate pathway is activated by LPS, aggregated IgM or IgG, Ag-IgA complexes, plasmin
Which immune components are found in the dental pulp?
Jontell – T & B lymphocytes; Plasma cells; Macrophages; Dentritic cells; Cytokines & Prostaglandins
Are antibodies found in the pulp?
Nakanishi – levels of IgG, IgA, IgM, elastase & PGE2 were higher in inflamed pulps than in normal pulps
Which immune components are found in the periapical tissues?
Nilsen – Lymphocytes, Macrophages, plasma cells Mast cells, NK cells
Pulver – Igs (see below)
Stashenko – cytokines
Which antibodies predominate in a periapical lesion?
Pulver – IgG>A>E>M for cysts and granulomas; IgE cells had degranulated mast cells nearby
Pain Overview
Trace the pain perception originating from a tooth?
Narhi - A-fibers are responsible for sharp pain (direct dentin stimulation, osmotic, temperature changes). C-fibers are activated only if the external stimuli reach the pulp proper and may be responsible for dull, diffuse pain (intrapulpal pressure, increase in pulpal temperature, inflammatory mediators). Prepain sensations induced by electrical stimulation result from activation of the lowest threshold A-fibers
Noxious stimuli → A-delta / C-fibers (primary afferent fibers with cell bodies located in the trigeminal ganglion) → subnucleus caudalis (medullary dorsal horn) → second order projection neuron → cross midline to the thalamus via the trigeminothalamic tract → third order neuron → cerebral cortex via the thalamocortical tract (pain perception)
Define Allodynia & Hyperalgesia:
Hargreaves -
Allodynia – reduction in pain threshold so that non-noxious stimuli are painful (cold sensitivity & chewing discomfort)
Hyperalgesia – the response to noxious stimuli produces more pain than it would normally (exaggerated response to endo ice)
What is neural sprouting?
Byers - Changes in neural structures occur after most dental injuries. Analysis of the progressive stages of pulpal abscess and necrosis showed sprouting CGRP nerve fibers (a) at the retreating interface between abscess and vital pulp; (b) in periapical areas during onset of lesions; and (c) around chronic abscesses in granulomatous periodontal tissues.
Discuss referred pain:
Sessle
Convergence Referred pain caused by afferent input from cutaneous and visceral nociceptors onto the same projection N (i.e., nociceptors from the max sinus and max molar projecting to the same projector N in nucleus caudalis).
Travell - Myofascial pain & Trigger zones:
• Superior belly of masseter referred to maxillary posterior teeth.
• Inferior border of masseter referred to mandibular posterior teeth.
Pharmacology Overview
Discuss the mechanisms of commonly prescribed antibiotics:
Cell wall inhibitors:
Penicillins – bactericidal; inhibits bacterial cell wall synthesis
Augmentin (Amox + Clavulanic acid): clavulanic acid binds and inhibits beta-lactamases (produced by some bacteria) that inactivates amox resulting in expanded spectrum of activity
Cephalosporins – may have cross reactivity with Pen allergic pts
Anti-ribosomal – Inhibit protein synthesis:
Clindamycin – bacteristatic/cidal (based on dosage); inhibits protein synthesis by binding to 50S ribosomal subunit; strong bone penetration (Vacek)
Azithromycin, Erythromycin - inhibits protein synthesis by binding to 50S ribosomal subunit
Tetracyclines – inhibits protein synthesis by binding to 30S ribosomal subunit
Inhibitors of Nucleic Acid Synthesis:
Metronidazole – inhibits nucleic acid synthesis; ineffective against facultative anaerobes; added to penicillins if ineffective
Discuss antibiotic susceptibility:
Baumgartner – susceptibility from isolated endo infections (98 bacterial species):
Pen V – 85%; Amox – 91%; Augmentin – 100%;
Metronidazole – 45%; Pen + Metro – 93%; Amox + Metro – 99%
Clindamycin – 96%
Are antibiotics a concern with birth control pills?
Hersch – Rifampin is only known antibiotic to inihibit bcp; discuss possibility with pt
Discuss non-opiod analgesics:
NSAIDS – Non-selective COX inhibitors – inhibits synthesis of prostaglandins
Acetominophen – COX 3 inhibitor centrally; peripherally blocks pain impulse; produces antipyresis by inhibition of hypothalamic heat-regulating center
Discuss opiod analgesics:
Potency: Codiene < Hydrocodone < Oxycodone
Activate opiate receptors in the CNS & inhibit release of excitatory pain transmitters
Side effects: nausea, dizziness, drowsiness, respiratory depression & constipation
Discuss anxiolytic therapy:
Hargreaves & Dionne – Triazolam safe & effective for dental outpatients
Lundgren & Hutter - .25mg Triazolam better than 5mg Diazepam
Prognosis / Outcomes Overview
When should pts be recalled?
Orstavik – 1 yr; peak incidence of healing / CAP occurred @ 1 yr; may take 4 yrs
Andreasen – 1 yr; wait 4 yrs for uncertain healing cases
How long doe it take a lesion to heal?
Murphy – Avg. rate is 3.2mm/mo.; >70% require >12mo
What factors may be detrimental to a successful outcome?
Crump – (POOR PAST): Perforation, Obturation; Overfill, Root canal missed, Perio disease, Another tooth, Split tooth, Trauma
Friedman – Toronto study: NSRCT – Pre-op lesion
RETX – Pre-op lesion, perforation, fill quality, restoration
S RCT – lesion > 5mm quadrupled risk
Do the radiographic healing correlate to histologic healing?
Byrnolf – No; only 7% demonstrated no inflammation
Walton – Yes; 74%
Is bacterial culturing indicated? Does it influence healing?
Sjogren & Sundqvist – 94% success w/ -culture; 68% w/ +culture; regardless, they state modern anaerobic culturing techniques are not readily available, nor are they required
Peters & Wesselink – found NSD between 1 or 2 visit, or between + and – cultures
What are reasons for failure of NS RCT?
Intraradicular infection – Nair – main reason for failure is microbes persist in canals
Extraradicular infection – Siqueira –rare / Nair – Actinomycosis
Foreign body rxn – Nair – root filling materials
Cysts – Nair – possibly with cholesterol crystals
Does the level of root canal fill influence success/failure?
Seltzer & Bender – Overfill decreased success; underfill had no influence
Ng – meta-anaylsis shows w/in 2mm of apex improved success
Is 1 or 2-visit treatment more successful?
Peters & Wesselink – NSD
Weiger, Rosendahl & Lost – NSD for teeth with AP treated in 1 visit or with 1 wk Ca(OH)2
OUTCOME STUDIES
TX STUDY FAVORABLE PROGNOSIS RATE
NSRCT Toronto (Friedman) 85% healed; 95% functional
Washington Study (Ingle) 92%
Perforation Repair Kvinnsland 92%
RE-TX Toronto (Friedman) 81% healed; 93% functional (with Perforation - 42%)
Allen, Newton , Brown 73%
2nd RE-TX Allen, Newton , Brown 47%
S RCT Toronto (Friedman) 74% healed; 91% functional
Rubinstein, Kim 97% (3-12 mo.); 92% (5-7yrs.)
Allen, Newton , Brown 60%
2nd S RCT Peterson & Gutmann 36% healed; 26% uncertain
Root AMP Blomlof 68%
Int Replant Bender & Rossman 81%
IPC Jordan, Suzuki & Skinner <50% (11/24 cases)
DPC Ravn 80% (uninflammed pulps)
Tronstad <50% (carious exposure - consider IP)
Cvek Pulpotomy Cvek 96% (young incisors)
Mass 91% (young molars)
Apexification Cvek 96% -Ca(OH)2 long term
Whitherspoon 91-94% -MTA
Pulpotomy (primary teeth) Fuks Formo -84%; FeSO4 -93%; MTA -97%
Implants vs. RCT Doyle NSD - 94%
Kim Meta analysis - NSD
Internal Bleaching Glockner 98% -pt. subjective success
Regenerative Endodontics Overview
What cells are potentially utilized for endo regeneration?
Huang – stem cells located in the apical papilla are viable following necrosis
Discuss how regenerative endo may be achieved?
Hargreaves –
1. Achieved most predictably in teeth with open apices
2. Instrumentation with NaOCl irrigation is not sufficient to reliably create the conditions necessary for revascularization of the necrotic tooth
3. Ca(OH)2 placement prevents revascularization coronal to paste
4. The use of (3 mix-MP” triple antibiotic paste, developed by Hoshino (consisting of cipro, metronidazole & minocycline) is effective for disinfection of the necrotic tooth, setting the conditions for subsequent revascularization
3 major components of tissue engineering:
1. Cell source – i.e. apical papilla
2. Physical scaffold – i.e. blood clot or PRP
3. Signaling molecules