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.

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• 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

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• 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.

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• 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.

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• 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

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 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