ENDODONTICS Key Points by Danesh Kumar-JSMU || Chapter 01

• Pulpal cells--- odontoblast, from neural crest cell origin, produce mineralized dentin, express
TLR, cytokine, collagen type 1& 2.
• Sclerosis with time --- tertiary dentin.
• A fibers ( in periphery)for sharp response/ sensitivity & C fibers(at central pulp) for dull ache &
irreversible pulpitis.
• Terminal capillary network--- arterioles+ capillaries
• Dentinal permeability is greater close to pulp.
• Mechanical irritant--- deep scaling & curettage, trauma, hyper occlusion, over instrumentation of
root canal filling
• Open apices--- children—heal faster after major or minor trauma.
• Close apices--- older--- heal slowly because of less blood supply.
• Intrusive injuries—more pulpal necrosis than lateral or external injury.
• Inaccessible length of apex, lack of resistance, ortho movements---- damage to pulp.
• Cavity sterilizer--- sliver nitrate, phenol with or without camphor, eugenol.
• Chemical irritants--- antimicrobial agents, intra canal medications.
• Calcium hydroxide and antibiotic post---- conductive to cell proliferation
• Most infection by bacteria---activation of innate immune response (G protein & TLR-central role)
• Pulp necrosis/ inflammation depends upon--- virulence, host resistance, ability to circulate fluid
& lymph supply.
• Detection of microbes--- PAMPs & PRRs receptors
• Loss of integrity--- by caries, trauma, crack, anomalies, scaling, root planning, attrition, abrasion
• Caries—by common cause of pulpal exposure.
• Route of infection--- by caries, pocket, iatrogenic, apical foramen & lateral canal.
• Trauma----- cause pulp necrosis→ periapical or apical infection.
• Intra radicular infection--- by microbes cause primary infection
• Secondary infection--- by reminded microbes & cause complication like persistent exudation,
symptoms of flare up and failure of endodontics treatment.
• Goal of RCT---- removal of microbes and necrotic tissue
• Post infection after RCT--- because of loss of restoration, post placement without rubber dam,
failure of tooth structure, and recurrent caries.
• Extra radicular failure--- by invasion of microbes from pre inflamed peri apical tissues.
• Surface adhesion of microbial cells→ cell proliferation→ adhesion of other microbe→ Matrix
production→ colonization & maturation of microbes→ BIOFILM ( matrix= EPS).
• Exposure of specific microbes protein after bacteria cell reach threshold→ Qurum sensing
• Carious dentin→ lactobacillus, firmicutes, actino bacteria, & proteo bacteria.
• EBV → irreversible pulpitis & apical periodontitis, Papilloma & herpes→ acute apical abscess
• Symptomatic/ asymptomatic canal infection→ by provettela, porphyromonas, fusobacterium,
prepto coccuss.
• Microbes of endo infection---- prevetella, fusobacterium, porphyromonas, & streptococcus.
• Gram negative bacteria→ endotoxins ( LPS),first virulence factor.
• Normal pulp tissue→ fibroblast, odontoblasts, vascular element,stem cell, myelinated and un
myelinated fibers.
• Mediator of pulpal inflammation→ prostaglandins, neuro peptides, bradykin, cytokines & MMP
• Neuropeptide---- substances P & CGRP.
• Luxation injury→ Tooth with immature apex→ re vascularization quickly than mature apex
because of increased collateral blood supply.
• Secondary dentin and Pulp stone formation -→ because of increased re mineralization.

ENDODONTICS KEY POINTS BY DANESH KUMAR-JSMU 1

 • Excessive stones associated with caries, deep restoration, CVS disease, statin medication.
• Internal resorption→ osteoclasts & odontoblasts
• Dentin hypersensitivity, stone ,sharp pain→ reversible
• Internal resorption→ irreversible
• Irreversible pulpitis→ increased prostaglandins, bradykinin, MMP, no increase in leukotrienes.
• IL 10—central response of periapical lesion
• Root canal infection—multi species, bio film + ECM
• Reversible pulpitis→ mild hyperalgesia, elicited sharp pain < 20 minutes, unaffected by body
position, localized & non radiating.
• Irreversible pulpitis→ spontaneous, dull, > 20 minutes, affected by body position, difficult to
localization, radiating pain.
• Normal pulp→ cell free & cell rich zone, intact odontoblasts, absence of inflammation & necrosis
• Irreversible pulpitis→ internal resorption & hyperplastic pulpitis ( pulp polyps).
• Pulp polyp--+ children, pulp covered with desquamation of epithelium
• Hallmark of apical periodontitis---- bone resorption
• Periapical lesion to appear in radiograph→ 5-8 weeks
• Cytokines for bone resorption→ IL-1, 6, 11,17, TNF
• Cytokines limit bone resorption→ IL 4, IL-10.
• RNKL bind to RANK and cause osteoclasts differentiation & inhibition by OPG
• Periapical lesion consist of granulation, cyst, & apical abscess
• Cyst is of 02 types→ true cyst( don’t communicate with apical foramen) & pocket/ bay cyst (
Apex/ apical foramen directly into lumen of cyst).
• True cyst won’t respond to non surgical treatment→ require enucleation
• Apical abscess→ actinomyces species
• Symptomatic apical periodontitis—tender to percussion, mechanical allodynia, widened PDL
space, and abnormal radiolucency.
• Asymptomatic apical periodontitis→ furcation, necrotic pulp
• Acute apical abscess--- bacterial infection, swelling of facial spaces.
• IL -1 increase acute apical abscess.
• Chronic apical abscess→ drainage by pocket & sinus tract
• Condensing osteitis→ more sclerotic bone in apical region
• Non endodontics pathosis--- Intact lamina dura & normal pulp testing—e.g apical cemented
dysplasia, OKC, ossifying fibroma.
• Primary cause of Endodontics treatment failure-→ intra radicular infection in form of biofilm
• Extra radicular infection associated with long standing lesion and persistent root canal infection
• Altered tissue replaced by native tissue & complete restoration= Regeneration
• Odontoblasts--- first cell to overcome microbes
• Stem cells proliferation stimulated by PDGF-BB, VEGF, IGF-1, TGF- beta 1.
• Healing of periapical lesion--- cementum deposition, increased vascularity & fibroblastic activity.
• MMPS ,TMP1 & HSP27 for periapical tissues healing.
CHAPTER O2 HEALTH CONSIDERIN
• INR--- expressing the prothrombin time
• Heparin--- increase the PTT, aPTT
• Systemic condition affecting the most endo treatments—CVS problem & Diabetes mellitus
• Acute endodontic infection--- cellulitis
• Chronic endodontic infection--- chronic abscess, & sinus tract
• Sickle cell anemia---- 6% pulp necrosis
• Smoking—increase pain, swelling after endodontic treatment

ENDODONTICS KEY POINTS BY DANESH KUMAR-JSMU 2

 • IL1 beta allele 2 associated with reduced treatment after Endodontic treatment
• 66-70 Gy dose of radiation--- decreased pulp vitality testing
• Calcific metamorphosis--- denticles ( stone—in coronal pulp) & diffuse (linear- in radicular pulp)
• With aging--- decrease in diameter of canal apically.
• Age changes in pulp--- decreased vascularity, decreased no of odontoblasts, fibroblast, &
calcification.
• Pulp space decrease in occlusal apical direction with ageing.
• Working length difficult in older because of increased cementum deposition, modifying apical
anatomy.
CHAPTER 03 ENDODONTIC RADIOLOGY
• CBCT---- extra oral radiology, modification of CT, utilizes a pyramidal-shaped X-ray beam ,
Pixel called voxel, used for diagnosis of apical lesions, Crown morphology, pulp chamber, root
resorption, broken instrument, obturation, peri apical surgery.
• Disadvantages of CBCT—high cost, image noise, movement and metal defect, increased
radiation dose, loss of definition of structural edge.
• Comparison of receptor--- FILM( higer dose, chemical generation, delayed view, thin & flexible,
common error: film placement & horizontal overalp) , CCD( Charge couple device--small dose,
computer generated, reusable), PSP( photo stimulable phosphor—laser scanner generated).
• Major bio risk from x ray used for endodontics imaging--- stochastic
• PA--- paralleling technique ( receptor placed parallel, beam @90° require device) & bisecting
technique—receptor against lingual side of crown & mucosa & no device is request).
• Durability--- wall mounted x ray > hand handled x ray unit
• Tube shifting--- technique to locate the buccal & lingual portion of object
• Needs for endo imaging--- diagnosis, locating canals, roots, treatment evolution, finding WL,
obturation evolution.
• Imaging choice for endodontic evolution---- Periapical
• Intraoral Radiographs---Intraoral Periapical (IOPA), Occlusal Radiographs,Bitewing Radiographs
• Extraoral Radiographs----- Panoramic Radiographs
• Vertical angulation---Elongation----too little angulation corrected by increasing the vertical
angle of the central ray & Foreshortening---too much angulation corrected by decreasing the
vertical angle of the central ray.
• Horizontal angulation---- Clark’s rule, SLOB rule, Cone shift technique, Tube shift technique,
Buccal object rule.
• Slobe rules--- The object that moves in the SAME direction as the cone is located toward the
LINGUAL side.The object that moves in the OPPOSITE direction as the cone is located towards
the BUCCAL side.
• Uses of slobe rule--- Identification and separation of superimposed canals, Working
length,Undiscovered canals, Canal curvatures & Calcified canals.
• Diagnostic radiograph----Ideally should be taken using paralleling technique.
• Working radiograph----Used for determining position of instruments during procedure, Should
be taken without removing rubberdam, Bisecting angle technique can be used, Can use a
hemostat or a film holding device (Endoray)
• Advantage of using hemostat---Film easier to place,Mouth can be slightly closed allowing film
placement further apically, Handle of hemostat can help as a guide to align cone in vertical and
horizontal angulation & Less risk of distortion and film displacement.
• Post operative radiograph---Used for evaluation of endodontic treatment, Taken after removing
rubber dam, Paralleling technique should be used, Can be compared with diagnostic radiograph.

ENDODONTICS KEY POINTS BY DANESH KUMAR-JSMU 3

 • Follow up radiograph----For evaluating prognosis of endodontically treated teeth, Before
procedures like core-build up, crown placement etc,Health of periodontium, continued disease,
root resorption, treatment failures.
CHAPTER 04 || ENDODONTIC DIAGNOSIS & TREATMENT PLANNING
• Dental history---chief complain, past history & social history.
• Pain---- most common reason, history of pain includes it’s location, duration, onset, severity,
quality, intensity, exacerbating and relieving factors.
• A stoma / parulis--- visible point of drainage of a sinus tract & indicate presence of necrotic pulp
and chronic apical abscess.
• Non endodontic pathology--- periodontal abscess, Vertical root fracture (VRF), osteomyelitis.
• Endo perio Lesions present with a wider area of attachment loss.
• Mobility--- indicate limited periodontal support or underlying root fracture.
• Discolored crown---- indication of pulp pathosis.
• The most common etiology of pulpal involvement are caries, fractures, or deep restoration.
• Clinical test--- pulp test( cold, heat & EPT) , peri apical test( percussion, palpation, bite test).
• Ibuprofen affect the results of cold , percussion and palpation testing.
• Percussion is commonly performed by tapping on incisal or occlusal surface with end of mirror
handled parallel or perpendicular to crown..
• Palpation—by firm finger tip pressure on buccal or facial mucosa overlying apex.
• Bite test include cotton rolls, cotton swab, or plastic tester, pain on bite indicate coronal fracture.
• Measure to detect vascular components by spectrophotometry, pulse oximetry, laser Doppler
flowmetry.
• Cold testing---- most reliable, using refrigerant spray, MOA= hydrodynamic theory, Normal
response is sharp and quick, no response= pulp necrosis, false negative response because of
calcific metamorphosis, false positive in cold contact adjacent tooth & gingiva.
• Gingival recession & loss of attachment decrease sensitivity to cold testing.
• Heat testing-- less reliable, heated GP applied to buccal /facial Crown, MOA= hydrodynamic
theory, vital pulp shows sharp and non lingering pain.
• EPT--- adjunct, less accurate than cold, don’t difference between pulpitis & normal pulp, need
toothpaste, can’t contact composite or metallic restoration, MOA= ionic Changes in dentinal
fluid, more accurate with calcific metamorphosis, low reading= vital, high reading= necrosis.
• Adjunctive test--- dentin stimulation, test cavity, caries removal, selective anesthesia,
transillumination, and staining.
• A soft carious pulp exposure after complete excavation of caries--- Asymptomatic irreversible
pulpitis
• Periapical inflammation results in bone resorption & resultant periapical Radiolucency.
• Condensing osteitis--- reaction to pulp or periapical inflammation & increased density of
trabecular density as diffuse medullary pattern, resolve in 50%.
• CBCT --- used for detect external root resorption
• Extensive diffuse calcification in chamber, pulp canal obliteration indicate long term low grade
irritation related to deep restorative treatment.
• Normal/ Reversible pulpitis--- vital pulp, slight hypersensitivity in reversible pulpitis.
• Reversible pulpitis--- May or may not have slight symptoms to thermal stimulus, No periapical
changes Responds to changes.
• Irreversible Asymptomatic---Similar to reversible (diagnosed by caries excavation to reveal
exposure) None or slight periapical changes ,responds to pulp tests.
• Irreversible Symptomatic pulpitis--- Severe pain to thermal stimulus, spontaneous pain, None or
slight or slight periapical changes, One exception: occasional condensing osteitis, may have
severe pain with thermal; often spontaneous pain on pulp test, RCT is indicated.

ENDODONTICS KEY POINTS BY DANESH KUMAR-JSMU 4

 • Novel technique--- vital pulp therapy using MTA as a viable mean of definitive treatment.
• Pulp stones—discrete Calcified bodies found in pulp chamber, non pathologic, associated with
CVS disease, dentinogenesis imperfecta, hypercalcemia, renal disease, corticosteroids.
• Internal root resorption---loss/ damage of pre dentin with pulpal injury( because of trauma, bur
usage without coolant), abnormal altered pulp , enlarged pulp chamber& Radiolucency due to
localized pulpal inflammation / necrosis & dentinoclastic activity.
• External root resorption---- loss or damage to precementum with inflammation of adjacent PDL,
apically due to periapical inflammation, laterally due to luxation type or avulsive injury, mottled
appearance.
• Extensive ERR cause Replacement resorption & ankylosis.
• ERR→ Pressure Resorption (it occurs due to direct damage to cementum by ortho tooth
movement, misaligned tooth movement, slow growing tumors or cyst.)
• ICRR( invasive cervical root resorption)--- asymptomatic, because of loss of pre cementum &
inflamed junctional epithelium, associated factors (ortho, Trauma, intracoronal restoration, non
vital bleaching, dento alveolar injuy, herpes, bisphosphonates etc, treated by trichloroacetic acid
& restoration.
• ICRR lesion classification---class 1= small & localized, Class-2= localized but approach pulp,
Class-3= into coronal 1/3rd , class-4= beyond 1/3rd of root.
• A visible sinus tract---- indicate chronic apical abscess.
• Symptomatic apical periodontitis--- pain on percussion, sensitivity to percussion, RCT indicated.
• Diagnosis of longitudinal fracture---- probing, clinical, x ray, restoration removal,
transillumination, wedging Forces & staining with methylene blue or caries detection dyes.
• Types of longitudinal fracture----- craze line, fractured cusp, cracked tooth, split tooth, VRF.
• Except VRF ,all in mesio distal direction & VRF in facio lingual direction.
• Craze lines---- in posterior teeth, cross marginal ridges, extend bucco lingual surfaces, affect only
enamel, asymptomatic, & no treatment is required.
• Fractured cusp--- complete/ incomplete, from Crown & extending Subgingivally, occurs in teeth
with extensive caries, removal of fracture segment in complete fracture, RCT/ viral pulp therapy.
• Cracked tooth--- Incomplete, not all surfaces, extended Subgingivally & Mesiodistally, fracture
os more centered and more likely expose the pulp.RCT is indicated. If fracture extend to floor or
canal, then will be extraction of tooth.
• Split tooth---- Complete, extension & end result of a cracked tooth, split tooth can’t be saved,
saved if fracture more cervical ,extraction if fracture beyond cervical 3rd.
• VRF--- complete/ incomplete fracture & J-shaped lesion--- facio lingual fracture at any level
of root, fracture may extend to PDL & cause soft+ hard tissue damage & bacterial penetration,
VRF may mimics periodontal disease or failed RCT.
• Tooth with VRF may have history of post restoration & have deep defects of narrow or
rectangular pattern.
• Best determinant for VRF--- flap reflection, visualization of fracture, punched out bony
defects.
• Endodontic pathosis—discovered incidentally on routine examination.
• Peri apical index---- 1= normal structure, 2= small changes in bony structures, 3= change in
bone with mineral loss, 4= periodontitis with well defined radiolucent area, 5= severe
periodontitis
• Peri apical lesion---- acute = widening of PDL space, chronic condition(cyst, granuloma,
abscess), bone loss is a predominant feature with radiopacity.
• Peri apical lesion of endodontic origin—1) RADIOLUCENT LESION (Apical lamina dura
absent, A ‘hanging drop of oil’ shape, Radiolucency ‘stays’ at the apex regardless of cone

ENDODONTICS KEY POINTS BY DANESH KUMAR-JSMU 5

 angulation, pulpal necrosis, CYST-- > 200mm3, more radiolucent, round, well defined Borders
& dystrophic calcification.. GRANULOMA—small, ill defined border.
2) RADIOPAQUE LESION---(condensing osteitis):Opaque diffuse appearance & borders,
Roughly concentric arrangement around apex, Pulp is often vital and inflammed.
• Periapical lesion of non endodontic origin: Positive vitality & intact lamina dura
1) RADIOLUCENT LESION: ossifying fibroma, OK, LPC, DC, bone cyst, ameloblastoma etc
2) RADIOPAQUE LESION: osteosclerosis, unerupted tooth, foreign body, hypercementosis etc
• Primary endodontic infection---- necrotic pulp, chronic apical periodontitis, drainage sinus tract
through PDL & gingival sulcus, no crestal bone loss, negative pulp test, RCT preferred.
• Primary Endo + Secondary Periodontal--- non diagnosed primary endo infection, & 2° perio
problem because of plaque & calculus, bone loss, negative pulp test, deep pocket, RCT & root
planning is done.
• Primary perio --- defects are of periodontal origin, wide & v shaped. Step down pattern of crest
as probe reach deeper, pocket depth decrease in step up pattern.
• Primary perio with endodontics involvement----1° perio Lesions involve necrosis, pulpal
necrosis because of periodontal therapy, mixed pulp vitality both endo & perio therapy.
CHAPTER -05 DIFFERENTIAL DIAGNOSIS OF PAIN & RADIOLUCENCIES OF NON
PULPAL ORIGIN
• The frequency of continuing orofacial pain after Endodontic treatment has been 5%, 62% were
found to be non odontogenic.
• OPPERA study( orofacial pain, prospective evolution & risk assessment)---for disorders of
orofacial region .
• Algesia (any pain experience after a stimulus), allodynia (Painful response to non painful stimuli)
• Most common cause of pain in orofacial origin---- dental pathology
• Pain of pulpal tissues & periodontium is acute & may be localized.
• PDL pain is dull, aching pain in & around the teeth, tenderness of tooth to percussion.
• Musculoskeletal conditions are the major cause of non odontogenic pain in orofacial region.
• SNOOP( systemic symptoms, neurologic sign, onset sudden, onset after 40, pattern change)--- for
intracranial and headache pain.
• Myofascial pain is the most common muscle pain disorder of orofacial region.
• Orofacial pain is present in 15-40% .
• Oral splint can be helpful in diagnostic process of toothache when endodontic testing is resulting
inconsistent results.
• Dentigerous cyst is most common inflammatory odontogenic cyst of gnathic region.
• Ameloblastoma & odontogenic keatocyst ----- multilocular & traumatic bone cyst--- unilocular
CHAPTER 07 II ENDODONTIC ARMAMENTARIUM
• Hand Operated-Include K-type reamers & files, broaches &Hedstorm-type files.
• Engine Driven-Latch that inserts into a slow speed such as Gates Glidden burs & Peeso-reamers.
• Ultrasonic & Sonic-Diverse in design, insert into a vibratory handpiece & resembles broach type
instruments, files & diamond coated instruments.
• Nickel Titanium-Cross over design adapted both for hand & rotary use such as Protapers,
Profiles & GT files.
• Diamond Burs→ Round (sizes # 2 & # 4) & Tapered fissure burs, caries removal ,create initial
external outline shape, penetration through the roof & de-roofing, access through porcelain,
tapered fissure for axial wall extensions & refinement.
• Carbide Burs→ Round (sizes # 2, 4 & 6) & tapered fissure burs, access through metal &
amalgam, other uses are similar to diamond burs.
• Endo Burs=> Endo Z & Endo Access bur = Carbide burs with safety tips (non end cutting, axial
wall extensions, bur can rest on the floor ,entire wall can be refined in one plane ,

ENDODONTICS KEY POINTS BY DANESH KUMAR-JSMU 6

 • Long Shank Burs=> LN (long neck) bur & Goose neck bur, removing calcification, troughing of
floor.
• Ultrasonics=>CPR tips & ProUltra tips, Removal of calcification, Troughing of floor, Broken
instrument removal, Post removal.
• Endodontic Explorers, DG 16, Orifice location, Dislodgment of calcific deposits.
• Group I- Hand & finger operated instrument=> Barbed Broaches, K-type Instruments, H-
Type Instruments
• Group II-Low speed instruments with latch type attachments=>Gates Glidden (GG) burs,
Pesso Reamers
• Group III-Engine driven similar to hand & finger instruments=> Rotary instruments, Latch
type & mainly NiTi.
• Instrument Taper→ 2% taper for ISO standardized files, 0.02 mm increase in diameter/mm of
file, taper of newer non traditional instruments varies.
• Tip Geometry→ Non cutting tips/Batt Tips, tip design of newer instruments varies.
• Size→File tip diameters increase in 0.05mm increments up to size 60, file tip diameter increase in
0.10mm increments up to size 140, cutting edge is 16mm long.
• GATES GLIDDEN BURS→Elliptically flame shaped burs, latch attachment, long shank,
straight line access ,open orifice, flaring of coronal & middle third, always keep before curvature,
usually fracture from shank, available in 15 & 19mm lengths.
• PEESO REAMERS→ Similar to GG burs, latch attachment, parallel cutting sides, uses are
similar to GG burs, less flexible ,less controlled then GG burs, both instruments are aggressive,
rapidly enlarge canal.
• BARBED BROACHES & RASPS→ Manufactured by cutting sharp , angulated barbs into
metal wire blanks, broach has a taper of 0.07-0.01 mm, rasp has a taper of .015-0.02 mm with
shorter barb height, cut or snag tissue, don’t cut or machine dentine, used for pulp extirpation ,
removal of cotton & paper points, weak instrument, break easily.
• FILES & REAMERS→ K-files, Hedstorm-files (H files), K-Reamers.
• Taper→Amount the file diameter increases each millimeter along its working surface from the
tip towards the file handle, E.g. # 25 file with 0.02 taper have a 0.27 mm diameter 1 mm from
apex & 0.29 mm 2 mm from apex. Formula: tip diameter + (0.02 x length). Taper can be
expressed in percentage 0.02 taper=2% taper. ISO standardized file has a 2% taper for 16 mm.
• Flute→ Groove in the working surface, collect soft tissue, dentine chips & debris, effectiveness
depends upon its depth, width configuration & surface finish.
• Edge/Cutting Edge→ Blade of file, surface with greatest diameter that follows the groove as it
rotates, forms & deflects soft tissue & serve or snags soft tissue.
• Rake Angle→If the file is sectioned perpendicular to its long axis the angle formed by the
leading edge & the radius of the file is rake angle.
• +Ve Rake Angle→ If the angle formed by the leading edge & surface to be cut is OBTUSE then
the rake angle is positive or cutting, negative rake angle→ ACUTE rake angle or scraping.
• K-FILES→More flute/ length than reamer, use for shaping root canal system& for penetrating &
enlarging root canals, less sharper edges, triangular tip, work in anticlockwise rotation, can be pre
curved, 6→Pink, 8→ Grey, 10-Purple, 15- white, 20- yellow, 25-red, 30- blue, 35- green, 40-
black.
• H-FILES→ cut dentine when pulled or rotated clockwise, file is ineffective when pushed or
rotated counterclockwise, sharper edges then K file, square tip, can’t be pre curved.
• NiTi alloy→ exotic metal, super elasticity, shape memory, tough & flexible, as rotary instrument.
• Examination kit contain a mouth mirror, periodontal probe, dental probe/ explorer & cotton plier.
• In 1838 , Edwin maynard fabricated first endodontic instrument.

ENDODONTICS KEY POINTS BY DANESH KUMAR-JSMU 7

 •Non surgical RCT instrument= LA, explorer (DG 16), ruler, endodontic spreader—for lateral
condensation of GP, endodontic pulgger---for vertical GP condensation & plastic instrument.
• EAL( electronic apex locator)→ for to determine position of apical foramen/ constriction,
introduced by Sunada in 1962.
• Instrument for endodontic access→ high speed handpiece, diamond burs (approach best the
ceramic & porcelain restoration), Carbide burs acceptable for amalgam, gold or composite
restoration.
• Safe end burs( Endo Z) → Used after achieving access, for avoiding unnecessary damage to
floor of pulp chamber.
• Root canal localization is difficult because of pulp stone or dystrophic calcification, it’s removed
by munce burs, muller burs, swiss LN burs.
• Preparation of coronal & middle 3rd of canal is called straight line access, achieved by both hand
& rotary instruments.
• NaOCl → most common used irrigant, dissolve pulp tissue, lubricate root canal, bactericidal, can
penetrate deep dentinal tubules.
• 2% chlorhexidine→ antibacterial, less effective than NaOCl, can’t dissolve organic tissue.
• EDTA/ EDTAC→ chelate inorganic molecules & remove smear layer, no antibacterial & tissue
dissolving capacity.
• Sterile saline→ for irrigating root canal, intermediate between CHX & NaOCl.
• Irrigation needle between 25-31 gauge.
• Paper points used to dry the root canal space before obturation.
• Zinc oxide sealer is hydrophobic , applied inside root canal space to adhere GP to canal walls.
• CBCT is used for internal & external resorption, traumatic injury.
• Temporary coronal seal area material are Zinc oxide eugenol, intermediate restorative
material ( IRM), Cavit, GIC.
• Sanford Barnum invented rubber dam in 1862.
• Instrument for drainage/ incision→ scalpel handle, blade(12,15), periosteal elevator, suction
tip, needle holder, irrigating syringe, sterile solution.
• Instrument for apicoectomy→ scalpel, periosteal elevator, retractor, bone & periosteal curette,
micro mirrors, retro pluggers, needle holder, blades, air handpiece, burs, dye, hemostatic agents.
• Hemostatic agents→ epinephrine pellets, ferric sulphate, resorbable collagen.
• Lentulo spiral drill→ used to spin calcium hydroxide or sealer into canal.
• D11 handled spreader & fine finger spreader→ for lateral condensation.
• Apicoectomy include the placement of a retro filling material to seal the root canal apically.
• Angulated bone currette to facilitate removal of Granulation tissue from periapical lesion.
• Periodontal curette to scale root surface after apical resection & removal of Granulation tissue.
CHAPTER -08 LOCAL ANESTHESIA
• Factors affecting endodontic anesthesia→ anxiety, fatigue, tissue inflammation, previous
unsuccessful anesthesia.
• Classic sign of anesthesia→ lip numbness & dull feeling of tooth or quadrant.
• Initial management →by psychological approach through concern, communication, confidence,
topical anesthesia, gentle needle insertion, 27 gauge needle, controlled anesthetic delivery system
(CCLLAD), 02 stage injection.
 MANDIBULAR ANESTHESIA
• Most commonly used LA anesthetic agent is 2% lidocaine with 1:100,000 epinephrine.
• Lip numbness occurs 4-6 minutes after inferior alveolar nerve block.
• Pulpal anesthesia occurs in 5-9 minutes in the molars & pre molars, & 14-19 minutes in anterior.
• Successful duration for LA is 2 & ½ hour.

ENDODONTICS KEY POINTS BY DANESH KUMAR-JSMU 8

 • 02 stage injection→ initial very slow quarter cartridge , after regional numbness, remaining is
deposited.
• Increasing volume of anesthetic from 01 to 02 cartridges doesn’t increase the success rate.
• No improvement in pulpal anesthesia with higher concentration of epinephrine.
• Alternative solution→ 2% mepivacaine with 1:20,000 levonordefrin, 4% prilocaine with
1:200,000 EN, plain solution--- 3% mepivacaine & 4% prilocaine.
Others 4% articaine with epinephrine for inferior alveolar nerve block.
• Long acting agents→ bupivacaine & etidocaine.
• Buffered lidocaine→ with sodium bicarbonate, increase pH , less pain during injection.
• Gow gates & vizarani technique→ both requires 02 cartridges volume & supplemental anesthesia
& vizarani for trismus patient.
• Incisive nerve block/ infiltration @ mental foramen→ successful in 80-83% for anesthetizing
pre molar for 20-30 minutes, not effective for anteriors.
• Labial/ lingual infiltration of lidocaine solution are NOT effective for pulpal anesthesia in
mandible.
• Factors affecting the efficiency of LA→ needle placement, needle deflection/ bevel, accessory
& cross innervation, red hairs & patient positioning.
• Methods to increase success of IAN block→ supplemental buccal articaine infiltration, IO
injection of lidocaine & mepivacaine with Vasoconstrictors, PDL injection of 2% lidocaine, slow
inferior alveolar nerve block.
 MAXILLARY ANESTHESIA
• Maxillary anesthesia for restorative dentistry→ 2% lidocaine with 1:100,000 epinephrine.
• Maxillary infiltration success rate→ 87-92%, onset time→ 3-5 minutes,
• Maxillary anterior infiltration duration decline after 30 minutes & losing anesthesia by 01 hour &
for posteriors effective till 40-45 minutes.
• Alternative= Plain solution of mepivacaine & prilocaine→ for duration of 10-15 minutes, 4%
prilocaine, 2% mepivacaine, 4% atricaine.
• Others→ bupivacaine with epinephrine.
• Increasing duration of LA by increasing volume & epinephrine concentration.
• Adding a cartridge of 2% lidocaine with EN @ 30 minutes in anterior & 45 minutes in posterior
improve duration of pulpal anesthesia.
• Alternative injection technique→ posterior superior alveolar nerve block ( for 1st & 2nd molar),
infraorbital block, 2nd division block, palatal anterior superior alveolar, anterior middle superior
alveolar nerve block.
• Supplemental anesthesia→ by infiltration ( lidocaine in Maxilla & articaine in mandible), intra
osseous anesthesia, PDL injection, intra septal injection.
• PDL injection is less effective than intra osseous technique because more anesthetic solution can
be delivered to cancellous bone.
• Post operative pain in PDL injection in 1/3 or 2/3rd of patients with duration of 14 hours to 03
days.
• Anesthesia difficulties in Endodontics→ anesthetic solution don’t penetrate completely, local
tissue damage, hyperalgesia, apprehension, insufficient time allowed after injection.
• Most commonly used inhalation anesthetic agent is nitrous oxide. 30% NO= 10-15mg morphine
• Patients with symptomatic irreversible pulpitis have less successful anesthesia than with
asymptomatic irreversible pulpitis.
• Nitrous oxide administration helps to reduce pain during treatment in patients with symptomatic
irreversible pulpitis.
• With irreversible pulpitis, teeth most difficult to anesthetize is mandibular molars.
• Duration of anesthesia in Maxilla is less than in the mandible.

ENDODONTICS KEY POINTS BY DANESH KUMAR-JSMU 9

 • Mandibular posterior teeth (inferior nerve block & long buccal injection), Maxillary posterior (
3.6ml/ doubled 2% lidocaine dose for buccal infiltration & palatal infiltration).
• In symptomatic pulp necrosis, IO, PDL & IP injections are contraindicated.
• Symptomatic pulp necrosis→ mandible= inferior alveolar nerve block & long buccal injection,
Maxilla if no swelling then conventional infiltration, if any swelling ( cellulitis/ abscess) then
infiltration on either side of swelling.
• Asymptomatic pulp necrosis→ Inferior alveolar nerve block & long buccal injection for
Mandible & infiltration in Maxilla.
• Articaine is best used for mandibular infiltration after a IANB.
• Cold testing for anesthesia should be done before beginning endodontic therapy.
• For IO injection→ lidocaine & mepivacaine used.
• 600 mg ibuprofen or with APAP 1000 mg is most effective in attenuating postoperative
endodontic pain.
• Periapical inflammation occurs 1-3 days after pulpal exposure.
• Localized periodontal abscess→ vital pulp
• Acute apical abscess→ non vital pulp.
• Treatment of flare up→ reassurance
• Incidence of flare up→ 3%.
• Flare up are uncommon in patients with vital pulp.
CHAPTER-10 MANAGEMENT OF VITAL PULP & IMMATURE TEETH
• Defense mechanism of pulp→ outward fluid flow, neurogenic inflammation, arteriole /
venule(AV) shunt & tertiary dentino genesis.
• Positive pressure maintained by pulp act to push microbes.
• Dentinal fluid carry important molecules e.g cytokines, immunoglobulin, & complement proteins.
• Bacteria mediated demineralization of dentin release non collagenous protein (NCP) that mediate
reparative response.
• Nociceptors cause neurogenic inflammation by releasing vasoactive peptides such as CGRP (for
vasodilation) & substance P (cause plasma extravasation).
• Nociceptive fibers extend up to 200 um into dentinal tubules.
• TLR recognize LPS or endotoxins from gram negative bacteria.
• TLR 4 activation→ fiber sensitization→ decreased activation threshold→ increase response
magnitude→ release of CGPR & substance P→ vasodilation → increased vascularity→ increased
outward fluid flow.
• Exaggerated response to noxious response→ Reversible pulpitis
• Odontoblasts may act as sentinels because these express many sub types of TLRs.
• Tertiary dentin is deposited in area of insult in form of either reactionary or reparative dentin.
• Primary dentin is formed during tooth development & secondary dentin is deposited at slow rate
after tooth maturation.
• The most superficial layer of dentin in contact with dental pulp is pre dentin, that’s formed by un
mineralized matrix secreted by odontoblasts.
• Mineralization of pre dentin= primary dentin & secondary dentin ( 70 % mineral, 20%
organic, 10% water).
• Tertiary dentin is secreted in response to any injury to dentin pulp complex.
• In vital pulp, due to trauma, progenitor cells differentiate into odontoblasts like cells, which
secrete matrix that upon mineralization form a mineralized bridge over the area of injury called
reparative dentin.
• Reparative dentin is atubular, rapid secretion, trap osteocytes like cells.
• Etiological factors for dentin pulp complex injury→ trauma, caries, dental anomalies or
iatrogenic factors.

ENDODONTICS KEY POINTS BY DANESH KUMAR-JSMU 10

 • Vital pulp therapy are not suitable for cases showing deep pulpal inflammation.
• The incidence of dental trauma is most common in boys, & anterior Maxillary teeth.
• The incidence of dental trauma has frequency of 5%( all ages), 17% in 0-6 years old.
• The traumatic injuries are more common in permanent (58%) than in primary teeth (17%).
• The Maxillary central incisor is more affected (66%) than lateral incisors (17%).
• Uncomplicated crown fracture (without pulp exposure) are most common traumatic injury.
• Pulp exposure after uncomplicated crown fracture is 2-5%.
• Luxation injury, chance of pulp necrosis in close apex( 55-65%) with open apex( 3.5-11%).
• The traumatized dental pulp in immature or open apex teeth will have greater chance to heal.
• Immature permanent tooth become necrotic 14-67% of time.
• Immature permanent tooth is avulsed & replanted, risk of pulp necrosis in 77%.
• Dens evaginatus which is occlusal tubercle formed during development by folding IEE into
stellate reticulum, most commonly in Mandibular secondary premolar, 1-4% of Asian.
• Dens invaginatus formed from infolding of IEE & odontoblastic layer in pulp, most found in
Maxillary lateral incisors, 1-10%.
• Radicular lingual grooves most commonly found in lateral incisors.
• Cutting with adequate cooling is less likely to damage pulp unless thickness of dentin between
preparation & pulp is less than 1mm.
• Examples of vital pulp therapy→ partial pulpotomy, full chamber pulpotomy, direct & indirect
pulp capping.
• Pulpectomy is not included in vital pulp therapy.
• INDIRECT PULP CAPPING→ no pulp contamination/ exposure, vital pulp, excavation of
infected dentin, RDT of at least 0.5mm, pulp capped with bioactive material, formation of
reactionary dentin, in young patients, step wise caries excavation, contraindicated in any signs of
pulpal/ periapical pathology, soft leathery dentin covering a very large area of the cavity & in a
non restorable tooth.
• DIRECT PULP CAPPING→ Pin point pulp exposure, vital pulp, excellent prognosis in
incompletely formed tooth, light bleeding, traumatic exposure in dry & clean field,
Contraindication--> Pain at night, spontaneous pain, tooth mobility, thickening of PDL,
intraradicular radiolucency, excess bleeding at the exposure site, purulent or serious exudate.
• PARTIAL PULPOTOMY→ or cveck pulpotomy, large exposure, recent trauma,
contamination, removal of diseased or irreversibly injured pulp followed by direct capping of
residual pulp. Cotton pellet soaked in NaOCl,→ 17% EDTA→ tri calcium silicate materials over
pulp→ Final coronal sealing material (composite). Reevaluated at 6-12 months.

ENDODONTICS KEY POINTS BY DANESH KUMAR-JSMU 11

 • PULPOTOMY→ Removal of coronal part of dental pulp followed by application of a
medicament. Indication--> Vital teeth, healthy periodontium, only coronal involvement,
contraindicated extraction, absence of infection/abscess/ fistula/ spontaneous pain/ involvement

of pulp floor/ inter-radicular bone loss.

• Ca(OH)2 apexification→ hard tissue apical barrier & multiple appointment, MTA apexification /
one step apexification→ apical barrier as collagen plug.
• Apexification contraindicated in short roots, marginal periodontal breakdown, vital pulp.
• Apexogenesis contraindicated in severe root fracture, un restorable carious tooth & necrotic pulp.
CHAPTER 11- MANAGEMENT OF TRAUMATIC DENTAL INJURY
• Post auricular ecchymosis is cardinal sign of Lefort 3.
• Step in borders of orbit, abnormal nose mobility, depression & mobility of zygomatic arch are all
indication of fractures.
• Abnormal mobility of segments of dentition indicate cortical plate fracture.
• Intrusion & ankylosis-→ metallic sound
• 0= physiologic tooth movement, 1= slight mobility (up to 1mm), 2= significant mobility (1-2
mm), 3= severe mobility (> 2mm) both horizontal & vertical.
• Displacement of teeth from their normal position→ Luxation
• PDL damage shows swelling, bleeding, ecchymosis, laceration.
• Palpation find critical plate & alveolar fracture.
• Useful test for finding PDL injury is percussion.
• Pulpal injury→ calcific metamorphosis ( yellowish color & narrowing/ disappearing of pulp
space) & pulp necrosis that lead to external inflammatory resorption.
• Pulpal blood supply provide better diagnostic test in determining pulp vitality.
• Blood circulation accurately detected by Doppler flowmetry & pulse oximetry.
• Nolla stages of odontogenic development→ 0= no bone crypt, 1= presence of crypt, 2= initial
calcification, 3= 1/3 crown completion, 4= 2/3 crown completion, 5= Crown almost complete,
6= crown completion, 7= 1/3 root complete, 8= 2/3 root complete, 9= root almost complete (open
apex), 10= root apex complete
• Chipping & cracks→ result of impact injury, damage to pulpal vessels.
• Uncomplicated crown fracture→ involve dentin & enamel, no pulp exposure, no urgent care,
no observable displacement, restoring missing structure.

ENDODONTICS KEY POINTS BY DANESH KUMAR-JSMU 12

 • Complicated crown fracture→ pulp exposure, factors to be noted are fracture extension, stage
of root development, & the time since injury occurred, smaller fracture restored by acid etch
restoration & by vital pulp therapy, extensive fracture require endo treatment, teeth with
incomplete root formation treated by shallow pulpotomy followed by acid etch restoration.
• Treatment of crown fracture→ pulp capping or a shallow pulpotomy or by conventional
endodontic treatment.
• Primary reason for considering vital pulp therapy is to preserve pulp tissues & important in teeth
with incomplete root formation.
• Pulpotomy→ removal of pulp tissue apical to CEJ & cvek pulpotomy→removal of minimum
tissue to point where hemostasis can be obtained.
• Cvek pulpotomy will preserve radicular & coronal pulp, allowing the opportunity for greater hard
tissue formation.
• Shallow pulpotomy→ for both mature & immature Tooth, & tooth with incomplete root
formation, pulp tissue is removed to a depth of 2mm below exposure, sealing with MTA or bio
ceramic putty. Evolution at 6 months. X ray evolution of root formation is indication of
successful treatment.
• Tooth with complete root formation can be treated by vital pulp therapy & by endodontic
treatment.
• Crown root fracture→ present in oblique direction, splitting of tooth, shattered crown, exposed
pulp, in molars & PM, detected by die, transillumination, in posterior teeth, it’s because of sharp
blow to chin, skin abrasion, vehicle accident. Managed by bonding loose tooth fragments,
incomplete root formed tooth treated by shallow pulpotomy, pulpectomy in case of fully formed
root,
• Root fracture→ also called intra alveolar root fracture/ horizontal root fracture/ transverse root
fracture. Oblique in direction often, x ray beam @ 45° to detect it, mobile or displaced teeth with
pain upon biting & possible occlusal interference. More coronal the fracture, more chances for
mobility & necrosis. Splitting is indicated for fracture occurring in cervical/ middle 3rd of root.
• In root fracture, splinting the displaced coronal segment & stabilization for 6 weeks.
• Calcific metamorphosis is common occurrence after a root fracture.
• Healing of root fracture will occur either through hard tissue healing or connective tissue healing.
• Hard tissue healing by deposition of Calcified tissue originating from apical pulp & PDL.
• Connective tissue healing is more likely to occur with greater degree of displacement, fracture
line visible on radiograph & intact lamina dura.
• Pulpal response to trauma→ calcific metamorphosis, pulp necrosis, & Crown discoloration.
• Unreliable response to pulp testing in erupting, developing teeth is due to late differentiation of
Ad fibers.
 Injuries to periodontium:
• CONCUSSION→ sensitivity to percussion, no mobility, no displacement, less severe.
• SUBLUXATION→ sensitivity to percussion, mobility, no displacement, sulcular bleeding.
• LUXATION( extrusion, lateral & intrusive)→ sensitivity to percussion, mobility & displacement.
• EPT for necrosis & Cold testing for differentiate vital & non vital tooth.
• CBCT doe in luxation & avulsion injuries & in alveolar fracture.
• External Resorption, inflammatory resorption & pulp space calcification is seen with trauma.
• Crown color change→ initial pink , grayish dark in necrotic pulp. Yellow to brown in calcific
metamorphosis.
• Treatment for concussion→ no treatment, soft diet for 14 days, chlorhexidine rinses & follow up.
• Treatment for sub luxation→ relieve occlusion, soft diet, apply splinting for 02 weeks, follow up.
• Extrusive luxation→ Partial tooth displacement from socket along long axis.

ENDODONTICS KEY POINTS BY DANESH KUMAR-JSMU 13

 • Lateral luxation→ displacement in any direction besides axially, by communicated fracture,
metallic sound on percussion indicate root tip forced in alveolar bone.
• Treatment of lateral luxation→ resposition, splinting for 4 weeks, soft diet, RCT.
• Intrusive luxation→ movement in apical direction, no mobility, resembling ankylosis.
• Treatment for intrusive luxation→ in open apex, reposition spontaneously, RCT if necrosis. In
case of closed apex( older than 17 years)- 85-100% tooth undergoes necrosis hence RCT is done.
• Avulsion/ exarticulation→ complete tooth out of socket, prognosis of tooth depends upon extra
oral day time & storage media.
• Avulsion→ Immediate replantation= splint for 02 weeks, tetanus shot, RCT within 7-10 Days.
• Replantation within 60 minutes of avulsion→ tooth with closed apex= tooth stored in HBSS
storage medium, stabilization for 02 weeks .
• Replantation within 60 minutes of avulsion→ tooth with open apex= tooth in physiologic saline,
cover root surface with tetracycline based antibiotics, replant with slight digital pressure, splinting
for 02 weeks.
• Replantation with dry time longer than 60 minutes→ tooth with closed apex→ stabilization for 4
weeks.
• Trauma-> closed apex tooth/ mature tooth= RCT after 7-10 days after replantation, immature
tooth / open apex= Ca(OH)2 apexification for 18 month, & MTA apexification, regenerative
endodontic treatment.
• External root Resorption seen in replanted avulsed teeth, 03 types→ surface, informatory &
replacement Resorption.
• Surface Resorption→ also called repair related Resorption, lacunae of Resorption shown in
cementum & not visible in radiograph.
• Inflammatory Resorption→necrotic pulp, injury to PDL, loss of bone & adjacent tooth
structure, RCT is recommended.
• External replacement/ PDL related Resorption→ ankylosis, metallic sound on percussion.
• Antibiotics for avulsed replanted tooth→ Under 12 years age= penicillin V 25-50 mg/kg body
weight & patients of 12 years or older--> doxycycline-100 mg 02 times a day.
• Primary tooth--- luxation injury are most common.
• Primary Crown fracture without pulp exposure—treated by smoothen the Sharp edges, seal
exposed dentin with composite restoration.
• Pulpal exposure→ partial pulpotomy with sandwich technique.
• Alveolar fracture→ resposition & splinting for 4 weeks.
• Replantation of avulsed primary teeth is not recommended because of risk of damage to
permanent successor.
• Prevention→ by Education, Early orthodontics treatment, protective devices.
• Teeth replanted, give Stony hard percussion→ because of replacement Resorption
• Contusion-→ from blunt trauma
• Apical root fracture in anterior is treated by→ extraction, splinting for 2-3 weeks, & endo treated.
• Endo treated tooth , more susceptible to trauma than untreated because of loss of coronal
architecture.
• Best prognosis-→ for fracture of apical 3rd of root.
• Most common age group for fracture of permanent teeth→ 8-12 years.
• Ellis classification→ 1= simple Crown, 2= extended Crown+ dentin fracture, 3= extended Crown,
dentin & pulp, 4= non vital, 5= avulsed tooth, 6= crown fracture ,7= tooth luxation without root/
Crown fracture, 8- cervical crown fracture, 9= traumatic injury of primary tooth.
• Mild child tooth fracture→ necrotic pulp, open apex→ apexification
• Secondary tooth with fracture involving apical 1/3rd of root → vital & functional
• Period of immobilization for reimplantated mature tooth→ 7-10 days.

ENDODONTICS KEY POINTS BY DANESH KUMAR-JSMU 14

 • Stabilization of avulsed tooth→ 1-2 weeks
• Child → avulsed tooth= HBSS, 2nd Medium→ milk
• Most of fracture of replanted tooth due to external Resorption.
• Replacement resorption → tooth ankylosis
• Apical surgery best indicated in Mandibular pre molar.
• Apicoectomy is indicated in overfilled canal, perforation at apical 3rd & contraindicated in
extensive bone loss.
• Good prognosis of broken instrument if present at apical 3rd of canal.
• Endodontic surgery is avoided in short rooted tooth, teeth with periodontal disease.
• Hemisection is indicated after a endodontic treated tooth.
• Standard approach for apicoectomy→ rectangular & semilunar Incision.
CHAPTER -12 ROOT CANAL ANATOMY
• Weine’s classification→ Type1= 1-1, type2= 2-1, type 3= 2-2, type 4= 1-2.
• Vertucci’s classification→ 1→ 1-1, 2→ 2-1, 3→ 1-2-1, 4→ 2-2, 5→ 1-2, 6→ 2-1-2, 7→ 1-2-1-2,
8→ 3-3.
• Pulp chamber in anatomical crown & root canal space found inside radicular part.
• In pre molars & molars, pulp chamber present a square shape with 06 sides.
• With ageing, decrease in pulpal space due to reactionary or physiologic dentin formation.
• Biological width→ gingival epithelium+ connective tissue
• Law of centrality→ floor of pulp chamber located at center of tooth @ level of CEJ.
• Law of concentricity→ walls of pulp chamber are concentric to external tooth surface at CEJ.
• Law of CEJ→ distance from external surface of crown to wall of pulp chamber is same @ level
of CEJ. { CEJ is most consistent, repeatable landmark for locating position of pulp chamber}.
• Law of symmetry 1→ except for Maxillary molars, orifices of canal are equidistant from a line
drawn in mesiodistal direction through the pulp chamber floor.
• Law of symmetry 2→ except for Maxillary molars, orifices lie on line perpendicular to a line
drawn in mesiodistal direction.
• Law of color change→ color of pulp chamber floor is always darker than walls.
• Law of orifices location→ 1= Orifice@ junction of wall & floor. 2= orifices@ angle in floor
wall junction, 3= orifices@ terminus of root developmental fusion line.
• Root canal comprised of main canal & lateral components ( isthmus, accessory canals---furcation,
lateral & secondary canal, recess of flattened & oval shape canal.
• Canals are usually broader facio lingually than in mesio distal plane.
• Canal shape may be round, oval, flattened or irregular.
• Mean aspect ratio= ratio of major to minor canal diameters
• Minor apical diameter→ apical constriction, major apical diameter→ apical foramen.
• Oval shaped canals have aspect ratio between 1-2, long oval canal—2-4, flattened canal- > 4.
• Isthmus/ transverse anastomosis→ narrow ribbon shaped, communication between 02 canals that
may contain vital tissue, necrotic pulp, biofilm or residual filing material.
• Hu & kim classification of isthmus→ type 1= 02 canals with no communication/ incomplete, type
2- hair thin connection, 3- short, presence of 03 canals, 4- isthmus with extended canal, 5- true
communication or wide corridor.
• Unfilled isthmus can be commonly observed after root end resection in cases referred for
apicoectomy treatment.
• Accessory canal→ branch of root canal that communicate with PDL, lateral Canal is an accessory
canal located at coronal or middle 3rd of canal.
• Accessory canal present as potential pathway for bacteria.

ENDODONTICS KEY POINTS BY DANESH KUMAR-JSMU 15

 • Canal connecting pulp chamber to PDL in furcation region of multi rooted tooth are called
furcation canal, which are derived from entrapment of periodontal vessels during fusion of parts
of diaphragm which will become floor of pulp chamber.
• Furcation canals are associated with primary endodontic lesion in intra radicular region of multi
rooted tooth.
• Furcation canals in 13% of mandibular first molar.
• Main root canal end @ apical foramen/ major foramen, which open laterally on root surface at
mean distance of 0.2- 3.8 mm from anatomic apex.
• Apical foramen coincide anatomic apex in 67- 46%, it’s diameter is 0.21-0.39 mm.
• The mesial root of mandibular molar, maxillary PM & mesio buccal roots of maxillary molars
present with highest % of multiple apical foramen.
• Number of foramina on each root varies from 1-16.
• The apical portion of root canal having narrowest diameter is called apical constriction/ minor
foramen, located 0.5- 1.5 mm from center of apical forame%n.
• CDJ ---- cementodentinal junction, at which pulp tissue end & periodontal tissue begin.
• Morphology in which the main canal is divides into multiple accessory canals called apical
ramifications of apical delta.
• In Maxilla, frequency of apical ramification from 1 ( CI) to 15.1% ( 2nd PM), where in Mandible
from 5% ( CI) to 14% ( distal root of 1st molar).
• All root canals are curved in apical 3rd in facio lingual direction.
• Schneider’s method for determining root canal curvature→ 1st line parallel to long axis of tooth,
2nd line connecting apical foramen to point in 1st line where canal begin to leave the long axis of
tooth, angle formed by these 02 lines was angle of curvature, straight= < 5°, moderate- 10-20°,
Severe – 25-70°.
• Another mathod→ Weine’s method-> more reliable than Schneider’s method.
• The highest degree of curvature in mesio buccal canal of Maxillary molar & in mesial canals
of mandibular molars.
•

ENDODONTICS KEY POINTS BY DANESH KUMAR-JSMU 16