ENDODONTICSPart 1: Pulpal/Periradicular Diseases

Pulp-made of loose, fibrous CT and contains nerves, blood vessels, and lymphatics-almost completely surrounded by dentin, which limits room for expansion and restricts ability to tolerate edema-lacks collateral circulation, which limits ability to cope w/ bacteria, necrosis, and inflammation-possesses unique, hard-tissue secreting cells (odontoblasts) as well as mesenchymal cells that differentiate into osteoblasts to form more dentin to protect pulp from injury

Functions of Pulp1) Dentin formation (primary fxn)2) Induction: forms dentin which induces enamel formation3) Nutrition through dentinal tubules

Zones of Pulp1) Central zone (pulp proper): contains large nerves and blood vessels2) Cell rich zone: innermost layer containing fibroblasts3) Cell free zone (zone of Weil): rich in capillaries and nerves

-plexus of Rashkow located here4) Odontoblastic layer: outermost pulp layer containing odontoblasts

Cells of Pulp1) Fibroblasts (primary pulp cell)2) Odontoblasts3) Histiocytes/macrophages4) Lymphocytes`

Aging of Pulp-as pulp ages, there is:

1) decrease in reticulin fibers2) decrease in pulp size3) increase in collagen fibers and calcifications

Reparative Dentin (Tertiary Dentin)-following injury/irritation, primary odontoblasts die, resulting in formation of secondary odontoblasts that produce reparative dentin as defense at site of irritant

-pulp uses this as defense against most nonmicrobial irritants-if irritant is too great and deposition of reparative dentin insufficient, pulp defenses become overwhelmed and lead to imminent and irreversible pulp necrosis-bacteria from dental caries is main cause of main pulpal injury and pulpitis

Physiology of Pulpal Pain-controlled by A-delta and C-afferent fibers

1) A-delta fibers: responsible for dentinal pain-larger, myelinated nerves that enter root canal and divide into smaller branches coronally in pulp-A-delta fiber pain immediately perceived as quick, sharp, momentary pain that dissipates quickly on removal of stimulus-pulpodentinal complex: association of A-delta fibers w/ odontoblastic cell layer and

dentin2) C-afferent fibers: responsible for pulpitis pain

-smaller, unmyelinated nerves that course centrally in pulp-progression of pulpal inflammation changes pain response from sharp A-delta fiber pain

to dull, throbbing C-afferent fiber pain (w/ increasing inflammation, only C-fiber pain remains) -C-afferent fibers not involved in pulpodentinal complex and not easily

provoked-C-fiber pain occurs w/ pulp injury and mediated by inflammation, blood flow,

and pressure increase-hot liquids can raise intrapulpal pressure to levels that excite C-fibers-when C-fiber pain dominates, it signifies irreversible local tissue damage-pulpitis pain is diffuse and can refer to other sites/teeth-a sustained inflammatory cycle inhibits pulpal recovery and leads to tissue necrosis

Normal Pulpal Response-asymptomatic w/ mild-moderate transient response to thermal/electrical stimuli that subsides almost immediately when stimulus is removed-does not cause painful response on percussion or palpation

Reversible Pulpitis-thermal stimuli cause quick, sharp, hypersensitive response that subsides as soon as stimulus is removed-can be caused by caries, SRP, or deep restorations w/o a base-if irritant is removed, can revert to healthy state but if not, symptoms can lead to irreversible pulpitis-does NOT involve complaint of spontaneous/unprovoked pain-penetration of bacteria into pulp is when crossover to irreversible pulpitis occurs

Irreversible Pulpitis-pulp is damaged beyond repair even w/ removal of irritant-micro-abscesses within pulp begin to form as tiny zones of necrosis within acute inflammatory cells-leads to eventual necrosis of pulp-may be symptomatic or asymptomatic

Symptomatic Irreversible Pulpitis-spontaneous, unprovoked, intermittent or continuous pain-thermal stimuli elicit prolonged pain that lingers after stimulus is removed-may have pain on postural changes-EPT and radiographs of little value in diagnosis (radiograph may show widened PDL in advanced stage)

Asymptomatic Irreversible Pulpitis1) Hyperplastic pulpitis: reddish growth of pulp tissue through/around a carious exposure

-pulp proliferates due to low-grade chronic irritation2) Internal resorption: can eventually perforate the root

-appears as chronic pulpitis w/ chronic inflammatory cells, giant cells, and necrotic pulp cells-only prompt RCT will stop process and prevent further tooth destruction

Internal Resorption-caused by inflammation from infected coronal pulp

-often caused by trauma-undifferentiated CT cells of pulp activated to form dentinoclasts, which resorb portion of root in contact w/ pulp-absence of predentin (unmineralized dentin) predisposes tooth to internal resorption by pulp cells-usually asymptomatic and detected by radiograph showing increased seize (bulb) of pulp anywhere along length of canal-must be treated w/ RCT to remove pulp tissue, which will stop resorption

Pulp Necrosis-death of pulp resulting from untreated irreversible pulpitis, trauma, or interruption of pulpal blood supply-necrosis may be partial or total

1) Partial necrosis: may occur w/ some symptoms of irreversible pulpitis (multi-canaled teeth)2) Total necrosis: asymptomatic so no response to thermal/electrical tests

-may cause discoloration of crown-protein breakdown products and bacterial toxins will spread beyond apical foramen, causing widened PDL that leads to sensitivity to percussion and palpation-w/ increasing inflammation and necrotic by-products, tissue pressure builds to cause percussion sensitivity-bacteria can penetrate dentinal tubules, making it necessary to remove superficial layers of dentin during cleaning/shaping of canals

Signs of Periradicular Disease-are inflammatory responses to irritants from root canal system-symptoms range from asymptomatic to sensitivity to chewing, swelling, fever, malaise, and intense pain-radiographically, has loss of lamina dura apically

-if radiolucency is assoc. w/ vital pulp, it can’t be of pulpal origin and will either be a normal structure or other type of pathosis

Acute Periradicular/Apical Periodontitis (AAP)-localized inflammation of PDL in periradicular region-caused by extension of pulpal disease into periapical region, overinstrumentation/overfilling of canal, or occlusal trauma/bruxism-can occur around vital and nonvital teeth, so pulp testing is only way to determine need for RCT

-if vital, occlusal adjustment can relieve pain-if nonvital, needs RCT

-tooth may be sensitive to percussion-radiographically, may appear WNL or widened PDL-histologically appears as localized inflammatory infiltrate within PDL

Acute Periradicular/Apical Abscess (AAA)-painful, purulent exudate around apex as result of exacerbation of AAP from necrotic pulp

-can also result from infection from CAP (called a phoenix abscess)-symptoms of AAP and phoenix abscess are same, but phoenix abscess has periapical

radiolucency-may have swelling, pain on percussion and palpation, tooth mobility, and can lead to cellulitis-radiographically, can have normal or widened PDL and normal or widened lamina dura-histologically, is central area of liquefactive necrosis w/ neutrophils, macrophages, and some lymphocytes

-bacteria not always present-can be differentiated from lateral periodontal abscess by pulp testing (won’t be vital) and probing (no pocketing)

Chronic Periradicular/Apical Periodontitis (CAP)-long-standing, asymptomatic or mildly symptomatic lesion

-may have slight tenderness to palpation or percussion-bacteria and endotoxins cascade out of periapical region from necrotic pulp and cause demineralization of bone, leading to radiographically visible apical resorption/radiolucency-diagnosis confirmed by absence of symptoms, periapical radiolucency, and negative pulp test-only way to distinguish from periradicular cyst or periradicular granuloma is by histopathological exam-acute exacerbation of CAP has painful response to biting/percussion w/ periapical radiolucency (necrotic pulp)

Suppurative Periradicular Periodontitis-chronic periapical abscess that has continuously or intermittently drained via sinus tract w/o discomfort

-can also drain through sulcus, mimicking perio lesion-negative pulp tests b/c necrotic pulp-radiographically appears as periapical radiolucency -sinus tracts resolve spontaneously after RCT

Chronic Focal Sclerosing Osteomyelitis (Condensing Osteitis)-excessive bone mineralization around apex of asymptomatic vital tooth-caused by low-grade pulp irritation-is benign and requires no endo therapy

Part 2: Endo Diagnosis, Examination, and TestingOdontogenic vs Nonodontogenic Pain-many orofacial diseases can mimic endodontic pain-signs of nonodontogenic pain include:

1) episodic pain w/ pain free remissions2) trigger points3) pain crosses midline4) pain increases w/ mental stress5) pain is cyclic/seasonal6) paresthesia

Contraindications to Endo Therapy-only systemic conditions that conflict w/ endo therapy are uncontrolled diabetes and myocardial infarction in past 6 months

Referred Pain1) Max. molars: refer pain to zygomatic, parietal, and occipital regions2) Mand. molars: refer pain to ear, angle of mandible, or posterior neck3) Max. incisors: forehead4) Max. canines, PM: nasolabial region5) Max. 2 nd PM: temporal region6) Mand. anteriors and PM: mental region of mandible

Quality of Pain1) Bony origin: dull, drawing, aching2) Vascular: throbbing, pounding, pulsating3) Nerve pathosis: sharp, electric, stabbing4) Pulpal/Periapical pathoses: aching, pulsing, throbbing, dull, radiating, stabbing, jolting

Palpation Testing-periapical inflammation from pulp necrosis burrows into facial cortical bone and affects mucoperiosteum-before swelling is evident, sensitivity to finger pressure will be evident

Percussion Testing-inflammation of apical PDL causes sensitivity of proprioceptive fibers-indicates not only presence of inflammation of PDL, but extent of inflammation-other conditions that periapical infection cause percussion sensitivity: ortho, high restoration, and lateral periodontal abscess

Thermal Testing1) Cold test: cold water bath, ice stick, ethyl chloride, dichloromethane (EndoIce), CO2 ice sticks

-apply cold test to middle third of facial surface 2) Heat test: warmed temporary filling/gutta percha, dry prophy cup, or hot water bath w/ rubber dam (most accurate test)-responses to thermal testing:

1) No response: nonvital pulp or negative response of vital pulp from calcified canal, trauma, previous pulpotomy, premedication, partially necrotic pulp or immature apex2) Mild/Moderate response that subsides in 1-2 seconds: normal, vital pulp3) Strong, momentary response that subsides in 1-2 seconds: reversible pulpitis4) Moderate-strong response that lingers: irreversible pulpitis

-pulp vitality/thermal testing contraindicated in recently traumatized teeth b/c trauma usually causes temporary paresthesia and gives false reading

Electric Pulp Testing-uses electric current to stimulate sensory nerves of pulp

-stimulates A-delta fibers-doesn’t indicate health of pulp, just that pulp has vital sensory fibers (must be combined w/ other tests)

-EPT reading of 1-79 is vital, EPT reading of 80 is necrotic-doesn’t provide any info about vascular supply to pulp, which is true determinant of vitality

-has high incidence of false positives and false negatives-don’t use gloves w/ EPT b/c impedes response

-technique:1) isolate and dry tooth2) coat electrode w/ conductor (toothpaste)3) apply electrode to middle third of facial surface and increase current flow slowly

-electrode should not be applied to restorations (false reading)-thicker enamel will cause delayed response

-if patient has cardiac pacemaker, then EPT is contraindicated

Responses to EPT1) Chronic pulpitis: elicits response at higher than normal current2) Acute pulpitis: elicits response at lower than normal current3) Hyperemia: elicits response at lower than normal current, but current higher than acute pulpitis4) Pulp necrosis/abscess: no response elicited at any current

Causes of False Readings on EPT1) False positive

a) electrode contacts metal restoration or gingivab) patient anxiety/nervous ptc) liquefactive necrosis (pus)d) failure to isolate/dry teeth

2) False negativea) premedicated w/ analgesics, narcotics, alcohol, or tranquilizersb) inadequate contact btw electrode and enamelc) recent trauma to toothd) excessive calcification of canale) immature apexf) partial necrosisg) insulating restoration

Pulpal Diagnosis ChartComplaint Radiograph EPT Cold

Reversible pulpitis cold sensitivity

normal or widened PDL responds exaggerated w/o lingering

Irreversible pulpitis

hot/cold sensitivity w/ lingering pain

normal or widened PDL, apical radiolucency responds exaggerated w/ lingering

Necrotic variable

normal or widened PDL, apical radiolucency no response no response

Perio Exam-if significant isolated pocket is found in absence of perio dx, likely a vertical root fracture-to distinguish from perio and pulpal origin, must vitality test and probe

Other Pulpal Tests1) Selective anesthesia: only done when no other test has yielded determinative results; anesthetic diffuses to numb adjacent teeth so not very reliable2) Test cavity: only in cases where strong suspicion of necrotic pulp; not a definitive test

Buccal Object Rule (SLOB Rule)-used to decipher place of superimposed images on radiograph-moving x-ray cone to one direction will cause object to move to same side if lingual and opposite side if buccal

Radiographic Differential Diagnosis of Periapical Radiolucencies1) Vertical root fracture2) Lateral periodontal cyst: lamina dura visible and normal vitality tests3) Osteomyelitis4) Developmental cysts: ex. Nasopalatine/incisive canal cyst; use vitality tests to differentiate5) Traumatic bone cyst: vitality testing usually WNL6) Ameloblastoma: usually multilocular and can resorb roots7) Cemental dysplasia: mixed radiolucent/radiopaque; teeth are vital (mandibular anteriors)8) Cementoblastoma: radiopaque, well-circumscribed9) Normal anatomy: mental foramen, submand. fossa, max. sinus, incisive foramen, marrow spaces

Periapical Diagnosis ChartComplaint Radiograph Percussion

AAP biting sensitivity normal or widened PDL mild-mod sensitivity

AAA pain w/ swellingnormal or widened PDL,apical radiolucency mild-mod sensitivity

CAP no symptoms apical radiolucency no responseSAP sinus tract apical radiolucency no responseFocal sclerosing osteitis asymptomatic apical radiopacity no or mild response

Cracked Tooth Syndrome1) Clinical features

-pain on biting (only upon release of biting)-occasional, momentary, sharp, diffuse pain that is hard to reproduce-thermal sensitivity, as well as sensitivity to sweet or acidic foods

2) Radiograph-mesiodistal crack is impossible to see on radiograph

3) Incidence: most in lower molars w/ slight preference for 1st molar over 2nd molar4) Diagnosis

a) transilluminationb) Tooth Slooth (test each cusp tip separately)c) Stain (methylene blue)d) Stream of air if dentin is exposede) wedging tooth and taking x-ray

5) Treatmenta) Healthy pulp/reversible pulpitis: splint w/ ortho band and observe or place crown (place temp. crown and observe before placing permt. crown)b) Irreversible pulpitis/necrosis w/ AAP: RCT, restoration, and crown

6) Prognosisa) Presence of deep pocket: guarded prognosisb) Crack extends to floor of pulp chamber: guarded prognosisc) Fracture extends entire mesiodistal surface: poor prognosis

Vertical Root Fracture1) Clinical Findings

-starts apically and extends coronally, usually in buccal-lingual plane-endo treated teeth most susceptible-isolated probing defect -J-shaped/tear-shaped radiolucency from apical to middle 1/3 of root

2) Etiologya) heavy enlargement of canal during RCTb) stress from obturation (most common cause)c) unfavorable post placement

3) Diagnosis-only by surgical exploration by flap surgery

4) Treatmenta) Single-rooted teeth: extractionb) Multi-rooted teeth: hemisection w/ removal of affected root or extraction

5) Prognosis: hopeless

Endo-Perio Relationships-pulp and periodontium communicate via:

a) tubules c) furcation canalsb) accessory/lateral canals d) apical foramen

-endo dx can cause perio dx, but perio dx usually doesn’t cause endo dx (unless it reaches apex of tooth)-perio txt can cause endo problems b/c it can force bacteria into exposed dentin tubules

Primary Endo vs Primary Perio Lesions1) Primary endo lesion: tooth is nonvital

-treated by RCT or extraction2) Primary perio lesion: pocket formation and vital teeth

-treated by perio therapy

Primary Perio Lesion w/ Secondary Endo Involvement-deep pocketing w/ hx of extensive perio dx or possible past txt of perio dx-treated by endo therapy and then perio txt

True Combined Perio-Endo Lesion-once perio and endo lesions coalesce, it may be impossible to distinguish the two-txt requires correction of both endo and perio problems

-endo txt should occur before perio txt

Part 3: Nonsurgical EndodonticsAccess Preparation-represents the most important phase of technical aspect of RCT, b/c proper access prep maximizes cleaning, shaping, and obturation-objectives:

1) straight line access2) conservation of tooth structure3) unroofing of chamber to expose orifices and pulp horns

Working Length Determination-select a reference point that is stable and easily visualized-techniques: 1) Estimate WL w/ diagnostic film using paralleling technique and 10 or 15 K-file; correct for

WL by measuring discrepancy btw tip of file and apex (adjust 1mm short of radiographic apex)

2) use apex locator (operates on principles of resistance, frequency, or impedance) 3) feel for apical constriction (may be unreliable)

Cleaning and Shaping-best indicator of clean walls is level of smoothness obtained-best to precurve files in shaping b/c nearly all canals are curved-taper of canal should be adequate to prepare canal for obturation and allow insertion of spreader-most acceptable method to achieve adequate root canal debridement is to achieve glassy smooth walls of canal

-not by obtaining clean shavings or clean irrigant solution

Apical Preparation-apical stops help confine instruments, materials, and chemicals to canal space and create barrier against which gutta percha can be condensed

File Dimensions1) D0: file size at tip of file (.08mm for #8 file; .15mm for #15 file, etc.)2) D16: diameter of file where cutting flutes end (usually 16mm for hand files)3) Taper: amount the file diameter increases each mm from tip toward handle

-ex. For .02 taper file, the diameter at D16 is D0+(16x.02)

Sodium Hypochlorite (NaClO)-used to disinfect root canal by hypochlorite ion (ClO-)-proteolytic material dissolves organic matter-does not remove smear layer-is irrigating solution of choice in RCT

-alternative is chlorhexidine b/c it is less toxic, but lacks solvent action-other alternatives: urea peroxide (Gly-Oxide) and 3% hydrogen peroxide

-no single conc. best suited and ones used are 1%, 2.6%, 5, 25% (5.25% provides excellent germicidal action and dilute enough to not be severely irritating)-always use rubber dam as it is toxic to tissues

Sodium Hypochlorite Accident1) Signs

a) instant, extreme painb) excessive bleeding from toothc) rapid swellingd) rapid spread of erythemae) later on, have bruising and sensory/motor nerve deficits

2) Treatmenta) long-lasting local anestheticb) encourage drainagec) steroids, analgesics, and antibioticsd) cold compressese) daily follow-up

Ethylenediaminetetraacetic acid (EDTA)-aqueous solution of 17% EDTA

-active ingredient in RC-Prep-removes inorganic material and smear layer-is chelating agent that removes Ca+2 to demineralize and soften dentin (facilitates negotiating calcified canals)

-only works on calcified tissues and little effect on periapical tissues-poor irrigant solution-remains active in canal for 5 days if not inactivated by sodium hypochlorite at end of procedure

Variants of EDTA1) EDTAC: EDTA plus cetavlon, a quaternary ammonium compound

-has greater antimicrobial action than EDTA alone2) RC-Prep: EDTA plus urea peroxide to provide both chelation and irrigation

Calcium Hydroxide-is best intracanal medicament available-high pH (12.5) causes antibacterial effect

-also encourages calcification and inhibits resorption-inactivates lipopolysaccharide (LPS) and has tissue-dissolving capacity

Purposes of Obturation1) Eliminate all avenues of leakage from oral cavity or periradicular tissues into root canal system2) To seal within the system any irritants that can’t be fully removed during cleaning and shaping

Gutta Percha-is pliable at room temp and becomes plastic at 140 degrees F-can be dissolved in chloroform, xylol, and eucalyptol1) Advantages

a) plasticity (adapts w/ compaction to irregularities) d) easy to removeb) easy to manage e) self-sterilizing (doesn’t support bacterialc) low toxicity growth)

2) Disadvantagesa) does not seal w/o sealer d) shrinkage after coolingb) lack of dentin adhesionc) elasticity causes rebound from dentin

Sealers-used to fill discrepancies btw canal walls and gutta percha-4 groups based on constituents

a) ZOE b) CaOH c) resin d) glass ionomer-characteristics of ideal sealers:

1) nonirritating 4) hermetic sealing 7) good adhesion to canal walls2) insoluble 5) radiopaque 8) nonstaining to dentin3) dimensionally stable 6) bacteriostatic 9) readily removable if needed

-fxn of sealer:1) act as lubricant for gutta percha2) form bond btw gutta percha and canal wall3) exert antimicrobial activity

Solvent-Softened Custom Cones-to be used in following situations:

1) lack of apical stop2) abnormally large apical portion of canal3) irregular apical portion of canal4) after apexification procedure

-not to be used if tugback within 1mm of apex achieved-is more time-consuming and does not provide better apical seal-common solvents used to soften gutta percha:

1) chloroform 3) halothane 5) eucalyptol2) methylchloroformate 4) white turpentine

Root Canal Therapy in Primary Teeth-if a permt. successor tooth is present, the canal is obturated w/ a resorbable material such as ZOE-if no permt. successor is present, an acceptable nonresorbable material can be used (gutta percha)

Endodontic Re-Treats-chloroform is best reagent to dissolve gutta percha-crown down sequence (large-to-small) of instrumentation used from coronal to apical-rotary instruments faster and improve access better than heated instruments

-very light apical pressure used w/ rotary files-over-extended gutta percha cones can be removed by extending file periapically

Part 4: Surgical EndodonticsIncision and Drainage-objectives are to evacuate exudates, purulence, and toxic irritants

-removal speeds healing and reduces discomfort from irritants and pressure-best treatment for swelling from AAA is to establish drainage and to clean/shape canal

-incision and drainage indicated when:a) pathway is needed in soft tissue w/ localized fluctuant swelling to establish drainageb) pain is caused by accumulation of exudates in tissuesc) needed to obtain samples for bacteriologic analysis

-trephination of hard tissues indicated when:a) pathway is needed from hard tissue to obtain drainageb) pain is caused by accumulation of exudate within alveolar bonec) to obtain samples for bacteriologic analysis

-procedure:1) incision and drainage is surgical opening created in soft tissue for purpose of releasing exudates or decompressing an area of swelling2) trephination is surgical perforation of alveolar cortical bone to release accumulated tissue exudates3) profound anesthesia is difficult to achieve in presence of infection due to acidic pH of abscess and hyperalgesia4) incision should be made firmly through periosteum to bone

-vertical incisions are parallel w/ major blood vessels and nerves and leave little scarring5) may include placement of a drain6) antibiotics may be indicated if there is diffuse swelling (cellulitis), systemic symptoms, or immunocompromised

Root End Resection (Apicoectomy)- is preparation of a flat surface by excision of apical portion of root and any subsequent removal of attached soft tissues1) Procedure

a) a mucoperiosteal flap is elevated and, if needed, bone removed to allow direct visualization and access to affected areab) diseased root tip is removedc) traditional 45 degree bevel has been replaced w/ lesser bevels (0-20 degrees)

-use of ultrasonics has allowed for less beveld) remove 3mm of root tip if possible and leave 3mm for root end cavity prep and fillinge) increasing depth of root end filling significantly decreases apical leakagef) after retrofilling of canal w/ biologically acceptable material (MTA), primary closure of site obtained

2) Indicationsa) persistent or enlarging periapical pathosis following nonsurgical RCTb) nonsurgical endo txt unfeasible

-overextension of obturating materials interfering w/ healing-biopsy necessary-access for root-end preparation and root end filling needed-apical portion of root canal can’t be cleaned, shaper, and obturated

3) Contraindicationsa) anatomic factorsb) medical complicationsc) nonrestorable toothd) poor crown/root ratio

Hemisection-is surgical division of a multi-rooted tooth into equal halves by making vertical cut through crown into furcation and defective half of tooth is extracted

-usually in mandibular molars- requires RCT on all retained root segments-when possible, preferable to complete RCT and place permanent restoration into canal orifices prior to hemisection-indications:

1) class III or IV perio furcation defect2) infrabony defect of one root of multi-rooted tooth that can’t be treated periodontally3) coronal fracture extending into furcation4) vertical root fracture confined to root to be extracted5) carious, resorptive root or perforation defects that are inoperable or can’t be corrected w/o root removal6) persistent periapical pathosis where nonsurgical txt isn’t possible and problem confined to one root

Bicuspidization-is surgical division of multi-rooted tooth (usually mand. molar), but unlike hemisection, the crown and root of both halves are retained-procedure results in complete separation of roots and creation of two separate crowns

Root Resection (Root Amputation)-is removal of one or more roots of multi-rooted tooth

-entire root(s) removed, leaving crown of tooth intact-requires RCT on all retained root fragments

-when possible, is preferable to complete RCT and place permt. restoration into canal orifices-indications:

1) class III or IV perio furcation defect2) infrabony defect of one root of multi-rooted tooth that can’t be treated periodontally3) existing fixed prosthesis4) vertical root fracture confined to root to be resected5) carious, resorptive root or perforation defects that are inoperable 6) persistent periapical pathosis where nonsurgical endo not possible7) at least one root is structurally sound

Intentional Replantation-is insertion of a tooth into its alveolus after it has been extracted for purpose of root-end filling procedure-stabilization of replanted tooth may or may not be needed-when possible, RCT performed prior to replantation-indications:

1) persistent periapical pathosis following RCT2) nonsurgical txt not possible or unfavorable prognosis3) periapical surgery not possible or high risk of violating anatomic structures4) tooth has reasonable chance of removal w/o fracture5) tooth has acceptable perio status

Surgical Removal of Apical Segment of Fractured Root-is surgical removal of apical segment of fractured root when coronal segment is restorable and functional

-root fracture must be only in apical portion of root and pulp is necrotic in apical segment

Root Submersion-involves resection of root 3mm below alveolar crest and covering w/ mucoperiosteal flap-prevents bone resorption in area

Transplantation-transfer of tooth from one socket to another-can be in same person or btw ppl-works better when roots are partially developed, rather than fully developed

Part 5: Endodontic Emergencies/MicrobiologyEndo Emergencies-usually associated w/ pain and/or swelling and require immediate diagnosis and txt-can include luxation, avulsion, or fractures as well-a true emergency is one in which only one tooth is causing pain and identified-for txt, relieving pressure is most effective way of reducing pain

-complete cleaning/shaping of canal is preferred, but pulpotomy can be effective in absence of percussion sensitivity-chemical medicaments sealed in chambers don’t help control or prevent pain-antibiotics not indicated-reducing occlusion shown to aid in relief of symptoms if AAP exists

-if localized swelling exists, abscess has invaded soft tissues and requires complete debridement of canal, drainage, but no antibiotics b/c rarely have systemic signs or elevated temps-if diffuse swelling exists, the abscess has dissected into fascial spaces and requires canal debridement or extraction of tooth, incision and drainage w/ drain insertion for 1-2 days, and systemic antibiotics-for interappointment flare-ups, treatment generally involves complete cleaning of canals, placement of intracanal medicament, and prescribing analgesic (antibiotics not indicated except if systemic symptoms/cellulitis exist)

-no relationship exists between flare-ups and number of visits

Portals of Entry of Bacteria into Pulp1) Caries2) Permeable tubules

a) cavity prepb) dentin exposedc) leaking restorationsd) in necrotic pulps, there are no more odontoblastic processes or dentinal fluid

3) Cracks/trauma4) Pulp exposure

Nature and Dynamics of Root Canal Infection1) Polymicrobial2) Positive correlation btw number of bacteria in infected canal and size of periapical radiolucency3) Difference btw primary infection and infection resulting from unsuccessful RCT

a) Primary infection: strict anaerobesi) Gram- anaerobes: Porphyromonas and Bacteroides melaninogenica most commonii) Gram+ anaerobes: Actinomyces (root caries)

b) Failed RCT: Enterococcus faecalis and facultative anaerobes

Lipopolysaccharides (LPS)-found on surface of gram- bacteria-when released from cell wall, are known as endotoxins

-endotoxins capable of diffusing across dentin-relationship established btw presence of endotoxins and periapical inflammation

Antibiotics in Endodontics1) Pen VK (first choice)

-effective against most strict anaerobes and facultative anaerobes (Strep, Enterococci)2) Clindamycin

-effective against gram- and gram+ bacteria (strict and facultative anaerobes)3) Metronidazole

-effective against strict anaerobes (not for facultative anaerobes and aerobes)

Part 6: Sterilization Glutaraldehyde-cold or heat-labile instruments (rubber dam frame) may be immersed for period of 24 hours for cold sterilization-immersion may disinfect, but will not kill all organisms-is least desirable sterilization procedure in office and reserved for instruments that can’t tolerate heat

Pressure Sterilization-instruments autoclaved for 121 degrees C and 15 psi-kills all bacteria, viruses, and spores-can use steam or chemicals (chemicals will cause less rusting that water/steam)-both steam and chemical autoclaving will dull edges of cutting instruments caused by expansion from heat then contraction w/ cooling

Dry Heat Sterilization-superior for sharp-edged instruments to preserve cutting edges-cycle is temperature dependent

-temp. should be at 160 C for 60 minutes (if temp. falls below this before 60 minutes, cycle must be repeated)

-disadvantage is long time required

Disinfection-surface disinfection of hand files during canal instrumentation is done by using 70% isopropyl alcohol or quaternary ammonium on gauze-this cleans but doesn’t disinfect the files

Part 7: Radiographic TechniquesAngulation Techniques1) Paralleling technique: most accurate method; film is parallel to tooth

-less distortion, more clarity, and better reproducibility2) Modified paralleling technique: next best technique; used if can’t use paralleling technique due to low palatal vault, maxillary tori, longer roots, etc.

-film isn’t parallel to tooth but central beam oriented at right angles to film 3) Bisecting angle technique: least accurate technique

Working Films1) Working length: distance from reference point to point where canal prep and obturation will end2) Master cone/point: largest gutta percha point that can be placed to full WL prior to obturation

Types of Film1) D film (Ultraspeed): better contrast than E film, but requires higher radiation exposure2) E film (Ektaspeed): adequate clarity compared to D film, but requires only half radiation exposure3) F film: requires 20-25% less exposure than E film-optimal setting for E speed film for max contrast btw radiolucent and radiopaque structures is 70 kV

Cone Image Shifting-reveals 3rd dimension of structures-indications:

1) separation/identification of superimposed canals2) movement/identification of superimposed structures (zygoma overlying root apex)3) determining WL4) determining curvatures of roots (facial or lingual by using SLOB rule)5) determining facio-lingual location6) identification of undiscovered canals (if root contains only one canal, it should be closer to center of root than if there is more than one canal); must take x-ray at mesial or distal angle7) Location of calcified canals

Characteristics of Radiolucent Endodontic Lesions1) Apical lamina dura is absent2) Most often radiolucency is circular around apex3) Radiolucency stays a apex regardless of angulation4) Cause of pulpal necrosis usually evident

Characteristics of Radiopaque Endodontic Lesions (Condensing osteitis/Focal Sclerosing Osteomyelitis)1) Opaque, diffuse appearance2) Represent an increase in trabecular bone3) Have diffuse borders and concentric arrangement around apex4) Pulp often vital and inflamed5) Often appears together w/ apical periodontitis

Part 8: Procedural ComplicationsLedge Formation-a ledge is an artificial irregularity created in surface on root canal that impedes placement of instruments to apex-WL can’t be achieved and instrumentation and obturation will be short of apex and no longer follows true curvature of root-causes:

1) Lack of straight line access (improper access prep)2) Length of canal (longer canals have higher potential for ledging; should recapitulate longer canals to check patency)3) Canal diameter (smaller diameter canals have higher chance of ledging)4) Degree of curvature (as curvature increases, chance of ledging increases)5) Inadequate irrigation/lubrication (lubricants allow for ease of file insertion, decrease stress on instruments, and ease of debris removal)

-NaClO is good irrigant, but additional lubricant is needed6) Excessive enlargement of curved canals w/ files

-files have tendency to straighten out and cut straight ahead instead of bending w/ canal-files cut dentin toward outside of root at apex and create new “canal”, called transportation

-can be avoided by using each successive file in order (don’t jump file sizes)-correction of ledge:

1) relocate canal and renegotiate 2) use precurved small file to re-establish WL w/ plenty of lubricant and a “picking” motion3) once locate original canal, use reaming motion and occasionally an up-down movement to debride canal4) going back and flaring your access prep can also help improve access to apical 1/3 of canal5) if unable to correct ledge, just clean and shape at new ledged WL

-prognosis better if ledge formation occurs after most of debris has been cleaned

Instrument Separation1) Causes

a) limited strength and flexibility of instrumentsb) overuse or excessive force applied to instrumentc) manufacturing defects (rare)

2) How to Avoida) recognize stress limitations on instrumentsb) use copious lubrication and irrigationc) examine instruments before placing into canal

-steel instruments show fluting distortions, but Ni-Ti files don’t and should be discarded before visual signs are seen

d) replace files oftene) don’t proceed to larger files until smaller ones ft loosely within the canal

3) How to Treata) try to bypass the instrument (just like bypassing a ledge)b) remove instrument (often unsuccessful and need to refer to endodontist)c) prepare and obdurate to point of separated instrumentd) if push separated instrument past apex, must raise flap and remove instrument surgically

4) Prognosis-depends on extent of debris remaining in region apical to separated instrument (prognosis improves if separation occurred during later stages of cleaning

-if in apical 1/3 and no radiolucency present, then fill remaining canal space and have on 3-6 month recalls

-poorer prognosis in teeth where smaller size instruments have separated-easier to remove if it is wedged coronal to curvature or at curvature

-if below curvature it is very difficult to remove-overall, as long as managed properly, it has a favorable prognosis-if patient ends up having residual symptoms, must treat tooth surgically (root end resection)

Perforation-is iatrogenic communication of tooth pulp chamber w/ outside environment1) Types

a) Coronal perforation: caused by failure to direct bur toward long axis of tooth during access prep-prevent by using magnification, transillumination, or radiographs

b) Furcal perforation: occurs during search for canal orifices and must be immediately repairedc) Strip perforation: involves furcation side of coronal root surface

-caused by excessive flaring of coronal 2/3 of canald) Root perforation: can occur at apex (transportation) or midroot (from ledge formation)

2) Recognizing perforationa) hemorrhage (from PDL or bone)-doesn’t always occurb) sudden pain (can have burning pain from NaClO seeping out)c) radiographic evidenced) apex locator readings well short of known WLe) file deviates from previous pathf) severe post-op pain

3) Prognosisa) Perforation into PDL causes questionable prognosisb) If located above crestal bone, has favorable prognosis; if below crest of bone, has poor prognosis (causes recession of attachment and permt. perio pocket formation)c) perforation smaller than 1mm are easier to repair and cause less tissue destructiond) perforations occurring after most of canal debridement is completed have better prognosise) sooner the repair is made, better prognosis due to less damage to periodontal tissuesf) good isolation of tooth at time of perforation leads to better prognosisg) good accessibility, good pt oral hygiene, and good dentist capability improve prognosish) using restorative material w/ good sealing capability increases prognosis

i) coronal perforations have good prognosis, furcal perforations are good if repaired immediately, root perforation prognosis depends on size/shape and may need surgical txt, strip perforations are hard to access and have worst prognosis

4) How to Repair (avoid using NaClO b/c it can be extruded and inflame periodontium)a) Surgical repair: try to position apical portion of defect above crestal bone through:

-ortho extrusion -root amputation-crown lengthening -intentional replantation-hemisection

b) nonsurgical internal repair w/ MTA (is very biocompatible and promotes cementum-like material deposition)

Vertical Root Fractures-is fracture along long axis of root; often assoc. w/ isolated severe perio pocket and lateral root radiolucency-can occur after post cementation or excessive condensation forces-can only be confirmed by visualizing fracture through surgery-treated by removing involved root in multi-rooted teeth or extraction

Part 9: Traumatic InjuriesExamination of Teeth w/ Trauma-teeth are sensitive to percussion-apical displacement causing injury to blood vessels entering apical foramen can cause pulpal necrosis-pulp testing often leads to false negative responses and may be unreliable for 6-12 months

-vitality is actually determined by vascular supply, which may be intact during injury but neural response be impaired-pulp tests should be repeated at 3 weeks, 3 months, 6 months, 1 year, and yearly intervals

Uncomplicated Fractures-fracture w/o pulpal involvement1) Infraction: incomplete crack of enamel w/o loss of tooth structure2) Ellis Class I: fracture involving only enamel

-treated by smoothing rough edge or restoring tooth if needed (good prognosis)3) Ellis Class II: crown fracture involving enamel and dentin, but no pulp

-treated w/ restoration using bonded technique (good prognosis unless luxated)

Complicated Fractures-fracture that involves enamel, dentin, and pulp (Ellis class III) -treated via vital pulp therapy or RCT depending on several factors

a) stage of tooth development: immature teeth should use vital pulp therapy if possibleb) time btw accident and txt: if within 24hrs, should use vital pulp therapy b/c should be limited contamination and less then 2mm pulp inflammation; after 24 hrs can do RCTc) concomitant perio injury: compromises nutritional supply of pulp and should do RCTd) restorative txt plan: if complex restoration to be placed, RCT recommended

Horizontal Root Fracture-fracture limited to root only (cementum, dentin, and pulp involvement)-may have bleeding from sulcus1) Consequences

a) coronal segment of tooth is usually displaced but apical portion is usually notb) pulp necrosis of coronal segment may result (25%)c) pulp necrosis in apical segment is rare b/c blood supply is not disrupted

2) Diagnosisa) may be missed on a PA radiograph b/c fracture usually oblique from facial to palatalb) radiographic exam should include 1 occlusal and 3 Pas (at 0 degrees, +15, and -15 degrees)

3) Healing Patterns (4 types)a) Healing w/ calcified tissue: ideal healing type; calcified callus forms at fx site on root surface and inside canal (successful)b) Healing w/ interproximal connective tissue (successful)c) Healing w/ bone and CT (successful)d) Interproximal inflammatory tissue w/o healing (unsuccessful)

4) Treatmenta) Coronal root fracture: stabilize coronal segment w/ rigid splint for 6-12 wks

-if reattachment of coronal segment not possible, extract coronal segment and if possible try to restore apical segment by ortho extrusion or perio surgery

-coronal fractures have poor prognosisb) Midroot fracture: stabilize for 3 weeks

-pulp necrosis occurs in 25% of cases (often limited to coronal segment)-in rare cases where both coronal and apical segments are necrotic, RCT through fracture

is difficult and both portions should be removedc) Apical root fracture: have best prognosis b/c pulp will mostly be vital and have little mobility

5) Prognosisa) Improves as fracture extends apicallyb) Horizontal fracture is better than verticalc) Nondisplaced better than displacedd) Oblique better than transverse

Luxation (Ellis Class V)-effect on tooth that tends to dislocate tooth from alveolus -concussion: no displacement or mobility, normal cold response but sensitive to percussion

-pulp blood supply likely to recover-treatment: occlusal adjustment possible, but no immediate txt needed; should let tooth rest (avoid bite) then follow-up

-should take baseline radiographs and vitality tests

Subluxation-tooth has been loosened, but not displaced-treatment: baseline vitality tests/radiographs, occlusal adjustment, splint for 3 weeks-rarely results in pulpal necrosis

Extrusive/Lateral Luxation-tooth is partially extruded from socket, occasionally accompanied by alveolar fracture-usually, crown is displaced palatally and root apex labially (extrusive luxation)

-lateral luxation is displacement in any direction other than axially-treatment: radiograph, reposition tooth and splint; RCT may be necessary-pulpal outcome: 65% rate of necrosis in extrusive luxation; 85% rate in lateral luxation

Intrusive Luxation-apical displacement of tooth (pushed into socket)-treatment:

a) immature teeth w/ open apex: allow to re-eruptb) ortho repositioningc) surgical repositioningd) RCT

-have very high rate (96%) of pulpal necrosis

Avulsion (Exarticulation)-complete separation of tooth from alveolus by traumatic injury (Ellis Class VI)1) Treatment: first priority is to protect viability of PDL

a) Reimplant immediately if possible-immediate implantation improves PDL healing and prevents root resorption

b) If can’t reimplant immediately, then store in media and take to dentist-success rates of extraoral dry-time:

i) less than 15 mins: 90% successii) 30 minutes: 50% successiii) over 60 mins: less than 10% success

-storage media:i) optimal storage environment (OSE): maintains and reconstitutes metabolites

-Viaspan, Hank’s balanced salt solution (best)ii) other wet environment: just maintains viability of PDL

-milk>saline> saliva> water (least desirable-as bad as dry storage) -saliva and water are hypotonic and cause cell lysis and inflam.

2) Treatment in dental officea) Closed apex, extraoral dry-time less than 60 mins or stored in OSE, milk, or saliva

-don’t handle root surface or curette socket-remove coagulum from socket w/ saline-replant tooth slowly-stabilize w/ physiologic (semi-rigid) splint for 7-10 days-systemic antibiotic for 7 days (Pen VK)-refer to MD for need for tetanus booster

b) Closed apex, extraoral dry-time over 60 mins-remove debris and necrotic PDL, coagulum from socket-immerse tooth in 2.4% NaF solution (pH 5.5) for 5 mins, replant, splint 7-10 days-systemic antibiotic (Pen VK) for 7 days and refer to MD for tetanus booster

c) Open apex w/ extraoral dry-time less than 60 mins or stored in OSE, milk, saliva-clean root surface and apical foramen w/ saline-place tooth in doxycycline/saline solution-remove coagulum from socket w/ saline-replant tooth and stabilize w/ physiologic splint for 7-10 days-systemic antibiotic and tetanus booster

d) Open apex and extraoral dry-time over 60 mins-replantation not recommended

3) Endo txt after 7-10 days reimplanteda) Closed apex

-RCT initiated 7-10 days after reimplantation-if RCT is delayed for longer period than this or signs of resorption present, should give

long-term CaOH txt before doing RCTb) Open apex, less than 60 mins dry-time

-RCT should be avoided and signs of revascularization should be checked-at first sign of infected pulp, apexification procedure should begin

c) Open apex, over 60 mins dry-time-if RCT not performed on tooth out of mouth, the apexification procedure is initiated

External Resorption-destructive process initiated in periodontium-4 types: 1) Surface resorption

2) Replacement resorption (ankylosis)3) Cervical resorption4) Inflammatory root resorption

-external resorption always accompanied by bone resorption

Surface Resorption-transient phenomenon that is common, reversible, and self-limiting-due to mechanical damage to cementum surface and PDL which causes spontaneous destruction and repair

-repair occurs within 2 weeks and is not clinically significant

Replacement Resorption (Ankylosis)-caused by PDL damage/trauma, resulting in nonviable PDL

-occurs in 60% of replanted teeth-there is loss of root as it is replaced by bone, causing loss of cementum, dentin, and PDL as bone fuses to root defect-clinically, causes progressive submergence of tooth leading to infraocclusion, lack of physiologic mobility, as well as metallic sound on percussion-is irreversible process w/ no real feasible txt

Cervical Resorption-also called extracanal invasive resorption or subepithelial external root resorption-caused by a sulcular infection from trauma, ortho, perio txt, chemical injury (nonvital bleaching), or idiopathic-radiographically, appears similar to cervical caries or radiolucency around canal w/ irregular moth-eaten appearance around root-clinically, see crestal bone defect and possibly pink spot due to granulation tissue undermining enamel-pulp testing is WNL-usually begins at CEJ-treated by surgical removal of granulation tissue and repaired w/ restoration

Inflammatory Root Resorption-caused by necrotic pulp from trauma where bacteria initiate and follow ports of exit to affect periodontium -occurs at apical and lateral aspects of root, appearing similarly to cervical resorption radiographically-is a necrotic pulp, so treated by immediate RCT

-CaOH filling placed in canal and checked every 3 months for 1 year; if after year the resorption has stopped, gutta percha placed

Internal Resorption-destructive process initiated within root canal system-caused by inflammation from caries, attrition/abrasion, cracked tooth, trauma, pulpotomy, crown prep-can occur anywhere along root canal, but mainly in primary teeth-is generally asymptomatic, but can manifest as pink tooth from granulation tissue in coronal dentin undermining the enamel (can be misdiagnosed as cervical resorption)-radiographically, margins of canal are smooth but balloon out-usually tests vital, but may get negative vitality test if resorption has been longstanding and pulp is necrotic-treated by prompt RCT

Calcific Metamorphosis-pulp canal obliteration-occurs from subluxation-also increased likelihood from immature teeth, intrusions, and severe crown fractures

Pulpal Necrosis from Trauma1) Intrusion (96%)2) Lateral luxation (80%)3) Extrusion (65%)4) Subluxation (6%)5) Concussion (2%)-much less chance of necrosis in immature teeth than mature/closed apex teeth

Part 10: Adjunctive Endo TherapyVital Pulp Therapy Techniques1) Indirect pulp capping2) Direct pulp capping3) Partial pulpotomy4) Pulpotomy5) Apexogenesis

Materials Used in Vital Pulp Therapy-attempt to stimulate dentinal bridge formation and maintain vital pulp1) Calcium hydroxide: used since 1930s as pulp capping material and very reliable

-has ph of 12.5 which cauterizes tissue and causes superficial necrosis, which encourages pulp to induce production of reparative dentin

2) Mineral trioxide aggregate: derivative of Portland cement-consists of calcium phosphate and calcium oxide (hydrophilic) which set in presence of moisture-nonresorbable, so makes great sealing agent and also not adversely affected by blood contamination-has high pH to induce hard tissue formation-also used for retrofilling of canals

Advantages/Disadvantages of MTA1) Advantages

a) radiopaque d) non-toxicb) hydrophilic e) induces hard tissue formationc) biocompatible

2) Disadvantagesa) hard to manipulateb) long setting time

Indirect Pulp Capping-material is placed on thin piece of remaining carious dentin that, if removed, would result in pulp exposure-indicated in teeth w/ deep carious lesion near pulp, but no signs of pulpal or periapical disease

-done on permt. teeth w/ immature apex-objective is to arrest the caries and allow remineralization/reparative dentin formation-wait 6-8 weeks for reparative dentin to form, then go back and remove remaining caries

Direct Pulp Capping-material placed directly over mechanical/traumatic pulp exposure-indicated if pulp has been exposed for under 24 hrs, pulp is healthy/asymptomatic, and exposure is small-thin layer of CaOH or MTA placed directly over exposure, then base, and final restoration-during follow-up visits, do pulp testing and take periapicals to visualize hard tissue barrier formation-survival of pulp depends on quality of seal of restoration against bacteria, degree of bleeding, and elimination of any inflamed pulp-indirect or direct pulp caps done only on permt. teeth b/c high pH of CaOH or MTA can induce internal resorption in primary teeth

-better results of pulp capping if exposure is accidental (non-carious) and of young child (not older adult)

Partial Pulpotomy (Cvek Pulpotomy)-surgical removal of small portion of coronal pulp tissue to preserve remaining coronal and radicular pulp tissue-indicated in teeth where inflammation less than 2mm into pulp chamber and not into root orifices, traumatic exposures less than 24 hrs, or immature permt. teeth-follow up w/ pulp testing and radiographs-good prognosis, depending on adequate removal of inflamed pulp, disinfection of dentin/pulp, avoidance of clot formation, and good seal on restoration

Pulpotomy-surgical removal of coronal portion of vital pulp to preserve vitality of radicular pulp-pulp usually removed to level of root orifices, but is arbitrary-indicated in teeth w/ vital pulp exposure after 72 hours, no pain, and no abscesses

-done in primary teeth w/ vital pulp or irreversible pulpitis or permt teeth w/ incomplete root formation or as emergency procedure until RCT can be done-pulpotomies not used as permt. txt in permt. teeth b/c can result in pulp obliteration, internal resorption, or necrosis and make canals inoperable to future RCT-primary teeth w/ less than 2/3 remaining root structure, internal resorption, furcation perforation, sinus tract, or periapical pathology contraindicated for pulpotomy

-if hemorrhage can’t be controlled, may need to complete over two appts-may need to remove more tissue apically, as all uninflamed tissue must be removed-if hemorrhage still won’t stop, use hemostatic agents of full RCT can be initiated

-problem is dentist can’t determine exactly if all diseased pulp has been removed

Apexogenesis-process of maintaining pulp vitality during pulp txt to allow for continued development of entire root

-tooth has open apex still (apical closure occurs 3 yrs after eruption)-indicated in immature teeth w/ incomplete root formation and damaged coronal pulp but health radicular pulp-procedure: 1) Access prep and pulp amputation

2) Control hemorrhaging 3) Place CaOH over radicular pulp stump and place coronal filling 4) Recall every 3 months and perform RCT when root development completed

-good prognosis in pulp cap or partial pulpotomy; conventional pulpotomy has slightly less success-contraindicated in avulsed, nonrestorable, necrotic, or horizontally fractured teeth

Nonvital Pulp Therapy1) Pulpectomy2) Apexification

Apexification-method used to stimulate formation of calcified tissue at open apex of pulpless tooth-creation of calcified barrier involves cleaning debris/bacteria from canal and placing material at apex to induce apical closure

-2 methods: 1) place dense CaOH paste into canal after instrumentation and then obturate in 3-6 months

2) Place artificial barrier (MTA) at open apex prior to obturation (obturate in 1-2 days)

-indicated in teeth w/ open apex and standard techniques can’t create apical stop to facilitate obturation

Nonvital (Internal) Bleaching-indicated in teeth that have discoloration from internal source and have been treated endodontically-must place cement barrier (IRM or Cavit) to prevent cervical resorption from bleach penetrating into dentinal tubules-procedure: 1) Place rubber dam and remove coronal portion of gutta percha to place cement base

2) Bleaching agent placed in facial surfaces of access prep and temporary restoration placed 3) Tooth monitored for color change every 3-4 days, and bleaching agent removed when satisfactory results obtained

Nonvital (Internal) Bleaching Techniques1) Thermocatalytic technique: place oxidizing agent (30% H2O2/Superoxol) into pulp chamber and apply heat (2mm cement barrier needed when Superoxol used)

-complications: cervical resorption as bleach/heat damage cementum and PDL2) Walking bleach technique: place mix of sodium perborate and water in chamber and return in 2-6 wks

-several repetitions performed

Causes of Discoloration1) Necrotic pulp2) Intrapulpal hemorrhage3) Calcific metamorphosis4) Age5) Fluorosis6) Systemic drugs7) Tooth defects8) Blood dyscrasias9) Obturation materials

Part 11: Post-Treatment EvaluationCoronal Leakage-major cause of endo failures

-more endo treated teeth are lost b/c of restorative factors than endo factors-after RCT, internal chambers of tooth may become reinfected if coronal leakage occurs (saliva contaminated w/ bacteria can cause endo failure which increases w/ duration of saliva exposure)

-temporary restorations will not provide complete protection against occlusion forces, so when an immediate restoration isn’t possible, a bonded temporary restoration at canal orifice should be used-permt. restorations are best placed as soon as possible to seal tooth from contamination-when root canal space has been grossly recontaminated, retreatment should be considered

Structural Considerations-endo treated teeth do not become brittle; the moisture content of endo treated teeth isn’t reduced even after 10 yrs-teeth are weakened by loss of tooth structure

-loss of marginal ridges is major contributor to reduced cuspal strength-it is loss of structural integrity w/ access prep, rather than changes in dentin, that lead to higher occurrence of fractures-most impt part of restored tooth is the tooth structure itself; no restoration can substitute for tooth structure

Ferrule-when a crown is needed, the axial walls of crown engage axial walls of prepped tooth, forming the ferrule-the ferrule is a band that encircles the external dimension of the residual tooth, similar to metal bands around a barrel; it is formed by the walls and margins of the crown-a longer ferrule increases resistance to fracture

-fracture resistance increases with an increasing amount of tooth structure-a longer ferrule also resists lateral forces from posts and leverage from the crown in fxn-crown preps w/ 1mm coronal extension of dentin above margin of restoration have double the fracture resistance compared to when dentin core ends immediately above the margin

-the ferrule must encircle a vertical wall of sound toothy structure above margin and can’t end on restorative material-insufficient tooth structure to construct a ferrule should be evaluated for crown lengthening or ortho extrusion to gain additional root surface

Post Preparation-primary purpose of post is to retain a core-need for post is dictated by amount of remaining coronal tooth structure-posts weaken tooth by additional removal of dentin and by creating stress that predisposes the root to fx-at least 4-5mm of remaining gutta percha is recommended-all post deigns are predisposed to leakage-threaded screw posts increase likelihood of fracture compared to parallel/tapered posts

Causes of Endo Failures1) Inadequate seal of root canal system

-coronal seal more important than apical seal-obturation reported as most critical step to RCT success

2) Poor access 3) Inadequate debridement4) Missed canals5) Vertical fx6) Procedure errors (perforation, ledge, etc.)7) Leaking restoration8) Perio involvement9) Resorption10) Compromised host factors (systemic conditions)11) Misdiagnosis

Factors Influencing Endo Success1) Periradicular Pathosis (presence of PA lesion before txt reduces success rate by 10-20%2) Bacterial status of canal: presence of bacteria in canal before obturation decreases success3) Quality of endo work4) Quality of coronal seal

Classic Triad of Successful Endodontics1) Sterilization (microbe disinfection)2) Debridement (key to success)3) Obturation

Part 12: Root Canal AnatomyNumber of Canals for Maxillary Teeth1) Central incisor: 1 root, 1 canal (100%)2) Lateral incisor: 1 root, 1 canal (100%)

-root curves distally at apex3) Canine: 1 root, 1 canal (100%)

-longest tooth in arch4) 1 st premolar : 2 roots, 2 canals (75%)

-1 root, 1 canal (20%)-3 roots, 3 canals (5%)

5) 2 nd premolar : 1 root, 1 canal (75%)-1 root, 2 canals (25%)

6) 1 st molar : most often 3 roots, 4 canals (2 in MB root) (60%)-can have 3 roots, 3 canals (40%)-4 roots, 4 canals (rare)

7) 2 nd molar : 3 roots, 3 canals (60%)-3 roots, 4 canals (2 in MB root) (40%)-can also have 2 roots w/ 2-3 canals or 1 root, 1 canal

Number of Canals for Mandibular Teeth1) Central incisor: 1 root, 1 canal (95%)

-1 root, 2 canals (5%)2) Lateral incisor: 1 root, 1 canal (70%)

-1 root, 2 canals (30%)3) Canine: 1 root, 1 canal (95%)

-1 root, 2 canals (5%)4) 1 st premolar : 1 root, 1 canal (80%)

-1 root, 2 canals (20%)5) 2 nd premolar : 1 root, 1 canal (90%)

-1 root, 2 canals (10%)6) 1 st molar : 2 roots, 3 canals (2 in M root) (70%)

-2 roots, 4 canals (2 in M and D roots) (30%)-can have 3 roots and 4 canals (2M, 1DB, 1 DL)

7) 2 nd molar : 2 roots, 3 canals (2M, 1 D) (90%)-2 roots, 4 canals (2M, 2D) (5%)-C-shaped single orifice w/ 3 canals (5%)

Access Preparation Shapes1) Maxillary

a) CI: triangularb) LI: narrow triangle to ovoidc) Canine: narrow triangle to ovoidd) 1PM, 2PM: ovoide) 1M, 2M: triangle

2 Mandibulara) CI, LI: narrow triangle to ovoidb) Canine, 1PM, 2PM: ovoidc) 1M, 2M: trapezoid

Maxillary Molar Facts-MB root of max. molars is most complex root in entire dentition b/c 90% have 2 canals or major fins

-should always assume 2 MB canals until proven there is only one-MB canal hardest to locate and located under MB cusp

-MB2 located just lingual to orifice of MB1 canal

-max. 1st molar is posterior tooth w/ highest endo failure rate-palatal root is longest, has largest diameter, and easiest access of 3 rootsMandibular Molar Facts-in 40% of cases, mand. molars have 2 canals is distal root (always 2 in mesial)-lingual wall of mand. teeth most easily perforated due to lingual inclination of teeth

-mesial wall also frequently overcut-mand. 1st molar is tooth most frequently requiring RCT in whole mouth

Maxillary First Premolar-PM most likely to have 2 canals, w/ 60% having 2 roots

-other 40% have one root w/ 2 separate canals-easily perforated on mesial due to concavity on mesial side of crown

Maxillary Anteriors-all have distal axial inclination, so bur should be angled slightly to distal when accessing to prevent mesial perforation

Mandibular Anteriors-roots/accesses are always wider labiolingually and thin mesiodistally

Apical Terminology1) Anatomic apex: most apical end of root (also known as radiographic apex)2) Apical foramen: rarely coincides w/ anatomic apex and usually about 0.5mm short of it3) Apical constriction: located about 0.5mm from apical foramen

-is a natural stop in RCT and is detected by apex locator-RCT and obturation should stop about 1mm short of radiographic apex (apical constriction is 0.5mm short of apex and apical foramen is 0.5mm short of constriction)

Part 13: Hand and Rotary InstrumentsHand Instruments1) Broach: thin, flexible, tapered and pointed metal instrument w/ sharp projections/barbs along length of instrument

-used to remove pulp tissue from wide canals-not meant to be used for canal enlargement -must be used w/ extreme care not to fracture

2) Reamer: made by twisting a tapered triangular or square wire for form instrument w/ sharp cutting edges-used w/ reaming action only to enlarge canals-differs from K-files in having fewer spirals/flutes per unit length

3) K-file: has tightly spiraled cutting edges that cut wither in reaming or filing motion-cross-sectional configurations include diamond, square, and triangular-most useful instruments for removing hard tissue-strongest of all instruments and cut least aggressively

4) Hedstrom file: made by cutting spiral flutes into shaft of tapered wire to produce elevated cutting edges that appear to form a series of intersecting cones

-cutting occurs only on pulling strokes (only to be used in filing motion)-cuts more aggressively than K-file, but more prone to breakage

*all above instruments made of stainless steel

Rotary Instruments1) NiTi files: made by cutting spiral flutes into round wire composed of superelastic nickel-titanium alloy

-remain better centered, produce less transportation, and instrument faster than stainless steel files due to better flexibility and resistance to fracture

2) Gates-Glidden burs: composed of stainless steel shank w/ cutting bulb and pilot-tip-designed so that a fracture occurs near hub than btw shank and cutting bulb