Endodontics

W7 Lesions that mimic endodontic pathosis

W7 Endo-Perio Lesion

W8 Managing Iatrogenic Events

W8 Endo retreatment and apicectomy

W10 Photodynamic therapy

W11 Advanced endo Rotary and Obturation

W12 Traumatic Dental Injuries

 Week 7 - Lesions that mimic endodontic pathosis

Limits of radiology
- Can’t demonstrate periapical lesion in cancellous bone until mineral loss causes lesion to be 1-7mm
- Different anatomical locations have different likelihood to identify a radiolucent lesion
- In some scenario, the PDL can be widened/displaced prior to pulp necrosis due to cytokine cascade from inflamed pulp
- Periapical periodontitis = unilocular and no response to pulp test
- If its multilocular, its likely not of endodontic origin

Cysts aren’t as good with bone healing as granulomas

Multilocular radiolucency
- Non inflammatory aetiology
- Can present as a unilocular lesion in early stage
- If seen on PA, should refer for OPG or CBCT to confirm growth and determine extent
- Most common 3 are:
1) Odontogenic keratocyst
2) Ameloblastoma
3) Central giant cell lesion

(1) Odontogenic Keratocyst

- Developmental cyst
- 3-11% of all odontogenic cysts
- Most common as a solitary lesion between 10-40
- Well defined radiolucency that can be anywhere but most common in posterior body and ramus of md
- Small OKC can be unilocular and asymptomatic
- Larger OKC have classic multilocular appearance
- Pulp is vital

(2) Ameloblastoma
- Most common odontogenic tumour
- Benign and slow growing but can be large/disfiguring if untreated
- Often infiltrate normal bone resulting in extension beyond radiographic margins and higher recurrence rates
- Can be found anywhere but most are in posterior md
- Small one can be unilocular and asymptomatic
- Larger ones cause painless swelling and expansion of cortical plate
- Pulp is vital
(3) Central Giant Cell Lesion
- Unknown aetiology
- Most are in md and cross the midline
- Curettage is most common tx but extensive surgery may be needed for aggressive or recurrent lesions

Radiopacities in Periapical region

Endodontic lesions of inflammatory origin often present as radiolucent lesion without radiopacity. Exceptions to this are:
1. Condensing Osteitis
o Area of sclerotic bone in periapical region that results from inflammatory stimulus secondary to chronic pulpal inflammation or
necrosis, consistent with an osteoblastic response to low-grade stimulus
o Commonly in premoalr and molar region of md
o Asymptomatic but involved tooth can be painful due to pulpal inflammation or necrosis
o Necrotic pulp

2. Idiopathic Osteosclerosis
o Incidental finding
o Increased bone density of unknown etiology
o Most lesion remain unchanged or enlarge slightly until normal growth/development are complete
o No tx needed
o Common in first molar region in md
o Tooth is vital

Maxillary sinusitis of endodontic origin

- Inflammatory disease of microbial origin caused by necrotic pulp or RCT tooth with post tx disease
- Teeth closely associated with mx sinus are second molar, first molar and second premolar
- Close anatomical proximity of root ends to mx sinus and thin plate of bone separating roots from sinus lining means that an endodontic
infection can cause bone destruction and hence, a communication through the sinus floor
- Research – as much as 86% of sinusitis has potentially odontogenic origin
Odontoma
- Developmental abnormality (not neoplasm)
- Composed of tissues found in normal teeth (enamel, dentine, pulp, cementum)
- Compound odontoma – multiple structures that resemble teeth and common in anterior mx
- Complex odontoma – unorganised aggregate of enamel and dentine often in molar region
- Tx is surgery

Fibro-osseous Lesions
1) Periapical cemento-osseous dysplasia
- Early stage lesions radiolucent
- Intermediate stage is mixed radiolucent radiopaque
- Late stage is radiopaque with a radiolucent border
- Asymptomatic, teeth vital

2) Florid cemento-osseous dysplasia

- Bilateral multifocal involvement of md
- All 4 quadrant can be affected
- Can be asymptomatic or pain/exposed bone
- Similar radiographic maturation to PCOD
- Vital teeth

Periapical cysts and granuloma

- Granuloma = accumulation of inflamed granulation tissue as a result of necrotic pulp. Pulp should be non responsive unless partial
necrosis
- Biopsy is gold standard to differentiate cyst and granuloma as we can’t differentiate with radiography
 Week 7 – Endo Perio Lesions

• Periodontium and pulpal space are 2 main sites of infection. They communicate through apical foramen, dentinal tubules, crack lines,
etc, where bacteria and microbial irritants trigger inflammatory responses in surrounding tissues

1. Endo-Perio
o Persistent infection in pulp tissue -> secondary infection and breakdown of periodontium (extra radicular and furcal bone
loss, suppuration, increased pocket, draining fistula)
o Necrotic
o Radiograph may show generalised periodontal disease with angular defect at site of initial endo involvement
o Tx for both endo and Perio
2. Perio – Endo
o Severe periodontal disease -> initiate or exacerbate inflammatory pulpal changes (less common, some researchers disagree
and say pulp can withstand insults from periodontal disease)
o Pathologic changes only occur in pulp if main canal is involved (i.e. Perio bacteria reach apical foramen in apical 1/3)
o Deep pocking and extensive periodontal disease
o Prognosis worsens as periodontal destruction progresses
3. True Combined Lesions
o Clinically indistinguishable
o Pulpal and periodontal disease occur independently or concomitantly in same tooth
o Prognosis determined by periodontal destruction
o Concomitant pulpal and periodontal lesion = both disease state exist but didn’t cause one another
Differential Diagnosis

1. Root Fracture
o Diagnosis difficult because unable to be seen by clinical inspection nor radiography
o Localised deep pocket

2. Lateral Periodontal Cyst

o Asymptomatic or gingival swelling on facial aspect that shows pain and TTP
o Ovoid radiolucency with sclerotic margin
o Slow growing
o Tx is excision
o Tooth is vital
o 3 possible etiologies:
i. Reduced enamel epithelium
ii. Remnants of dental lamina
iii. Cell rest of Malassez
 Week 8 – Managing Iatrogenic Events

• Iatrogenic event – medical condition or harm unintentionally caused by medical treatment or procedures
• Iatrogenic events can’t be prevented but can be greatly reduced with training, technique and technology (TTT)

(1) Sodium Hypochlorite • Extrusion in peri-radicular tissues causes rapid response – hemolysis, ulceration, damage to endothelial
and fibroblast cell, inhibit neutrophil migration
• Patient reaction to fluid insult = severe and immediate pain, oedema and bruising on face, cheek, lip, etc.
• Always do master GP cone fit/tug back with EDTA, not NaOCl
• The amount extruded, spatial location of fluid and proximity to sensitive anatomic structures dictates
severity and duration of rxn
• Paraesthesia (transient/permanent) can occur
• In md teeth, extension to submd, submental or sublingual area can compromise the airway and cause life
threatening episode. Must need surgical intervention to prevent life threatning episode
• Prevention:
o When irrigating woth positive pressure, use a small side vented needle, no closer than 2mm
from WL and express liquid slowly
o Assess canal for signs of perforation or other large portal of fluid egress
o Don’t wedge needle in canal and don’t insert beyond WL
o Confirm solution before injection or irrigation
• Tx:
o cease tx, get saline to irrigate canal and dilute sodium hypochlorite, LA/analgesics, cold
compress
o After 1 day, warm compress and warm salt water rinse (to stimulate local microcirculation)
o Antibiotics such as corticosteroids usually prescribed
o Pt should be monitored closely and an increase in swelling or signs of impeding airway
obstruction will need immediate referral to hospital or maxillofacial surgeon

(2) Instrument Separation • Common causes – overuse of instrument, too much radicular pressure, inadequate access (no straight
line access)
o Contributing factors – operator, rotational speed, canal curvature (radius), instrument, torque
setting, manufacturing process, type of NiTi alloy, continuous/reciprocating rotation, type of
tooth, glide path
• Endo instruments fracture due to either: cyclic fatigue, torsional fatigue, or both
o Cyclic fatigue = repetitive compressive and tensile stresses acting on the outer portion of a file
rotating in a curved canal, leading to cyclic failure without previous signs of plastic
deformation

o Torsional failure = tip of the instrument binds but the shank of file continues to rotate
o Clinically, cyclic fatigue more common in curved root canal but torsional failure can happen in
even a straight canal
• Non surgical tx
o Tools such as extraction tubes, wire loops, post removal systems, ultrasonic tips
o Main goal is to bypass the instrument
o Create a staging platform to extract separated instrument
o E.g. endo-cowboy (syringe with loop at end)

(3) Ledge Formation
(4) Radicular Extrusion of
Root Canal Filling Material
• Separated instrument doesn’t mean failure of RCT
• The closer the CMP is, the better the outcome of instrument separation (as the bacteria is all cleaned)
• If canal isn’t affected, and no apical periodontitis, then a separated instrument shouldn’t affect prognosis
• Prognosis depends on removal of microbes, not removal of instrument!
• Ledge = artificial irregularity created on the surface of the root canal wall that impeded the placement of
an instrument to the apex
• Hinders adequate shaping and cleaning of canal in areas radicular to the ledge (hence, possible
unfavourable RCT outcome)
• Causes
o Curved canal
o Failure to pre-curve instruments and achieve a proper glide path to apex
o Forcing large file into canal
• Extrusion beyond radicular foramen
• When GP is extruded into peri-radicular tissue, there can be severe inflammation and GP should be
retrieved immediately
o This can be attempted by inserting a H file with a gentle clockwise motion to a depth 0.5-1mm
beyond the radicular constriction. The file is then slowly and firmly withdrawn with no
rotation
• If open apex -> MTA plug to prevent extrusion
• Sealer extrusion is ok as its resorbable
(5) Sinus perforation • Close proximity of mx premolar and molars to sinus and apices of teeth can be 2mm from sinus
• Pathologic destruction of sinus floor can predispose mx sinus communication and cause OAC
• Surgical intervention to remove extruded RCT filling material

(6) IAN injury • Anatomical proximity between apices of md posterior teeth and md canal
• IAN lesions due to RCT need urgent management
• Early surgical removal of excess endodontic material in centact with nerve allows best recovery prognosis
(72h). beyond this, irreversible nerve lesions prevail and medical symptomatic tx is needed
• Prevention
o Always assess proximity of tooth apex to IAN and assess root morphology and bone factors
contributing to leakage of chemicals adjacent to IAN
o Minimise apical breach
o Consider immediate exo of tooth and lavage of socket with additional medical tx if pt
develops sensory neuropathy within 3 day of endo tx
Alveolar Dome
= anatomical projection of root into floor of mx sinus
• First and second mx molars present a greater prevalence of alveolar domes, especially buccal roots,
followed by third molar and second premolar
 Week 8 – Endodontic Retreatment and Apicectomy

Microbial goal of Endodontic tx = eradicate bacterial colonisation or reduce bacterial load to levels that permit peri-radicular tissue healing

1. Primary infection 2. Secondary Infection

• Caused by microorganisms that • Microorganisms not present in the primary infection but introduced in the root canal
initially invade and colonise the at some time after the intervention
necrotic pulp tissue • Due to operator, poor temp resto, rubber dam, etc.

3. Persistent Infection
• Caused by microorganisms that were part of primary or secondary infection and resisted intracanal antimicrobial procedures. They
endured period of nutrient deprivation in treated canals

Causes for Failure of RCT

1. Iatrogenic procedural error (e.g. poor access cavity)
2. Untreated canal
3. Poorly cleaned and obturated canal
4. Complications of instrumentation (ledge, perforation, separated instrument)
5. Overextension of root canal filling
6. Coronal leakage
7. Persistent intra and extra radicular infection and radicular cysts (apical surgery is only way to treat extra radicular biofilm)

Treatment options for endodontic post-treatment disease

1) Do nothing
2) Extract tooth
3) Non-surgical retreatment
4) Surgical retreatment
Non-Surgical Retreatment
• Need to regain access to apical area of root canal space in previously treated tooth (if you cant reach critical zone, then refer for surgery)
• Coronal access (straight line access), remove all root canal filling (chloroform or orange oil dissolves GP), obstructions should be
managed, etc
• If tooth need retreatment but it has a full coverage restoration, the clinician can decide whether to preserve or replace restoration
• For GP removal, the crown down technique is done in reverse (from large to small file)

Post Removal
• 2 categories of post:
1) Prefabricated post (stainless steel, gold, titanium, ceramic, zirconia, fibre reinforced composite post)
2) Custom cast post (made in lab of precious or non-precious metal)
• Do apical surgery if cant remove post
• Can vibrate post out with ultrasonic or use needle bur to drill around it

Periradicular surgery – Apicectomy

o Indicated when non-surgical treatment is impractical or unlikely to improve previous result
o Surgical approach may be first choice for managing teeth with:
▪ Long post
▪ Irretrievable separated instruments
▪ Non-negotiable ledge and canal blockage
▪ Hard cement filling
▪ Failure of previous non-surgical treatment
o Even if surgical tx is definitive approach, non-surgical may be recommended to reduce number of microorganisms in root canal to allow
better prognosis
Week 10 – Antimicrobial Photodynamic Therapy in Endodontics

Properties of Laser
1. Monochromatic

2. Coherence

3. Collimation

Photodynamic Therapy
3 components
1) Laser
2) Photosensitizer (e.g. methylene blue - irrigate canal with this)
3) Oxygen
Cause bacterial cell damage (singlet oxygen production)
Light is distributed with an optical fibre in the root canal

Operator glasses block out red and infrared laser

Pt wear black glasses

Despite gram + being hard to remove with CMP, laser targets both gram positive and negative bacteria

PDT Procedure
1. CMP complete
2. Dry canal with paper point
3. Irrigate root canal with methylene blue
4. Pre-irradiation time (2 min)
5. Laser 660nm, energy 9J, 90 seconds
6. Final irrigation with NaOCl
 Week 11 – Advanced Endodontics

Criteria for Endodontic Success

- The crown down technique reduces the amount of necrotic debris that can be extruded through the apical foramen during
instrumentation

Primary Objectives in Cleaning and Shaping

1. Remove infected soft and hard tissue
2. Give disinfecting irrigants access to apical canal space
3. Create space for delivery of medicaments and obturation
4. Retain integrity of radicular structure

Endodontic Motions
(Reciprocating and Rotary)
- A disadvantage of reciprocating is that it tends to push debris
- Reciprocating – 150 degree forward and 30 degree back (net 120 degree forward)

Examples of Rotary File Systems

ProTaper Universal ProTaper Next ProTaper Gold

(progressive taper) (e.g. 0.18 tip is equivalent to file 18)

ProTaper Ultimate (used at JCU) Wave One Gold Reciproc Blue

- Resistant to cyclical fatigue as (single file system, reciprocating motion)
files are heat treated
- Scout canal to 2/3 of root
- SX is orifice opener to enlarge
coronal and middle 1/3
- Slider creates a glide path for
following files
- Don’t have to use all of F1/2/3
ProTaper Ultimate
- Has multiple tapers

Files are unable to touch all surfaces of the canal and debris can accumulate

XP Endo shaper and Finisher

- Are components of the XP Endo Shaper system
- M and A Phase (only finisher will expand like this)
o M Phase 20 degree celcius and has soft shape
o A Phase 35 degree celcius and during rotation at 800-1000rpm, expands in pt canal to a memorised shape that
touches all walls
- XP Endo Shaper
o Used for canal shaping
o It expand and touch all wall
o Non cutting tip
o 1% guiding taper
- XP Endo Finisher
o Used for final cleaning and finishing
o Used with NaOCl at end of CMP to agitate the NaOCl
o Flexible, ribbon like design that allows canal to conform to canals irregularities
o 0% taper for optimal expansion and canal cleaning
o Adapts to anatomical dimension
Sodium Hypochlorite
- Most common irrigants due to antibacterial capacity and ability to dissolve necrotic tissue, vital pulp and organic
components of dentin and biofilms in a fast manner
- If used without caution, it is very toxic and destructive to intraoral soft tissues, periradicular vasculature and cancellous
bone, it elicits severe inflammatory response and degradation of organic component

Glide Path
= File reaching apical foramen
= Appropriate glide path is indicated by the fact that a size #15 K file can passively and smoothly travel to WL with long in and out movements

Patency
= apical portion of canal is maintained free of debris by recapitulation with a small file through the apical foramen

Preparation for obturation

- must get rid of smear layer as it interferes with adhesion and penetration of sealer into dentine tubules
- EDTA used after CMP as it can chelate and remove mineralised portion of smear layer
- EDTA used at 17% and remove smear layer when in direct contact with wall for 3 mins
- After using EDTA, irrigate with NaOCl to remove remaining organic component
- Additional method to remove smear layer is sonic and ultrasonic instruments for 30 seconds (2 cycles)
- use EDTA to check master cone tug back as NaOCl cause extrusion
- sealer used with GP and is condensed for 10 second
 Week 10 – Traumatic Dental Injuries

Classification of Dental Injuries

▪ Enamel Infraction
▪ Enamel Fracture
▪ Enamel-Dentine Fracture
▪ Enamel-Dentine-Pulp Fracture

▪ Crown-root fracture
▪ Root fracture
▪ Fracture of alveolar socket wall

Injuries to the tooth and supporting structure

- Concussion
- Subluxation
- Extrusive luxation
- Lateral luxation
- Intrusive luxation
- Avulsion

Questions to ask patient regarding trauma

• When did injury occur? (tells you about time – critical!)
• Where did injury occur?
• Was there a period of unconsciousness? How long? Amnesia? Vomiting? (these indicate brain concussion and need hospital referral)
• Any previous injuries to the tooth? (can help explain radiographic findings such as PCO and incomplete root formation in adult
dentition)
• What measures have been done to teeth since accident? (tooth reimplanted, stored, been to another clinic, etc.)
• Is there a change in occlusion? (can imply luxation, alveolar fracture, jaw fracture or luxation/fracture of TMJ)
• Is there increased reaction to cold or heat? (indicate dentine exposure)
• Ask about medical hx (allergy, blood disorder, medication, antitetnus vaccine)

Do a clinical exam, mobility test, percussion test (TTP = PDL damage), pulp test, radiograph (IOPA, OPG, CBCT)

Pulp Healing
1. Pulp healing and revascularisation
• After luxation, there may be partial or total disruption of neurovascular supply to pulp apically
• For partial disruption, reduced circulation can be maintained and pulp can revascularize
• Positive sensibility test after 2-3 months
2. Pulpal necrosis
• Radiographically – periapical radiolucency 2-4 wks after occurance
• Classic signs – crown discolouration (grey, blue, red), negative sensibility testing, apical radiolucency, TTP
3. Pulp canal obliteration (no pulp space)
• Common after trauma
• Yellow discolouration is common but doesn’t imply periapical disease
• Abcense of response in pulp test doesn’t mean pulp necrosis if PCO is present
• Usually asymptomatic
• RCT indicated if there is periapical disease
Transient Apical Breakdown
 When neurovascular supply to pulp is disrupted, the revascularisation process will involve osteoclastic activity at the base of socket
and apical foramen
 Doesn’t necessitate RCT and often these cases are common in open apex
 Process is transient and when revascualrisation is present, the radiolucency will disappear
 This is seen 2-12 months after injury and involves extruded and laterally young permanent teeth

Periodontal Healing
We don’t know what type of resorption will occur
3 Types of Resorption
1. Surface • Healing to a localised injury in PDL
resorption • Usually concussion and lateral luxation
• Also can occur after intrusion and replantation
(Repair related) • Identified 4 week after injury
• If tooth non-vital, RCT should be done

2. Inflammatory • Combined injury to pulp and PDL

resorption • Bacteria in root canal and dentine tubule trigger
osteoclastic activity on root surface
(Infected related) • Common in intrusion and reimplantation of
avulsed teeth
• Identifies 2-4 week after injury
• Total resorption of root may occur

3. Replacement • Response to extensive damage to innermost layer

Resorption of PDL
• root structure gradually replaced by bone at
(Ankylosis similar rate to bone remodelling speed
Related) • ankylosis is often after intrusion and reimplant
avulsed teeth
• radiographic diagnosis after 1-2 month

Transient Marginal Breakdown

- resorption process of injured socket wall occurs before healing
- after lateral luxation and intrusion
- radiographically, it is resorption of lamina dura
- will resolve after 1 month with reformation of socket bone
Concussion - injury to tooth supporting structures without increased mobility or displacement of tooth
- tooth in normal position but TTP due to PDL injury with edema and bleeding
- neurovascular supply may be damaged
Subluxation - injury to tooth supporting structures resulting in mobility but without displacement of tooth
- bleeding from gingival sulcus confirms diagnosis
- secondary effect can be total or partial rupture of neurovascular supply of pulp

Extrusive - tooth is partially displaced out of socket with mobility and bleeding from gingival sulcus
Luxation - radiographically dislocated and apical part of socket is empty
- PDL healing usually normal
- disruption of neurovascular supply often cause negative pulp sensibility.
▪ In open apex teeth, PCO is the result of successful revascularisation
▪ In closed apex, pulp necrosis will likely occur
- Treatment
▪ Tooth repositioned with axial finger pressure on incisal edge
▪ Check occlusion and stabilise tooth for 2 week with flexible splint
▪ Take PA to verify correct tooth position
▪ Monitor pulpal condition after 2-4wk, 6-8wk, 1yr, yearly for 5 years

Lateral - Lateral displacement of tooth in socket and fracture of alveolar bone plate
Luxation - Crown usually in palatal direction
- Tooth immobile due to locked position in bone
- Percussion is high tone and metallic
- Treatment
▪ Reposition bony lock using forceps or digital pressure in incisal direction over apex and
repositioned apically
▪ Occlusion check, Tooth splinted for 4 week with flexible splint, PA to check correct splint position
▪ Follow up 4 wk, 6-8wk, 6 month, 1 yr, yearly for 5 year

Intrusive - Tooth is forced into socket in position in bone

Luxation - Clinically, crown is short and there is bleeding from gingiva
- Tooth immobile
- Percussion tone is high and metallic
- Treatment
▪ Open apex: spontenous repositioning is possible for kids under 16. If no movement in 3 weeks,
use rapid orthodontic repositioning
▪ Closed apex: reposition orthodntically or surgically if deeply intruded
▪ Extrusion should be completed within 3 weeks after injury
▪ Prophylactic extirpation of pulp should be done as pulp usually will be necrotic
▪ Splinted 4-8 weeks with flexible splint
▪ Follow up after 2 wk, 6-8 week, 6 month, 1 year and yearly for 5 years
Root Fracture
- Injury to PDL, pulp, dentin, cementum
- Injury to coronal segment is considered a luxation injury with trauma to PDL and neurovascular supply to coronal pulp
- Apical fragment remains uninjured
- Semi-rigid splint for 4 week (if coronal fracture at the cervical area, a longer splinting time of 4 months is recommended)

Alveolar Process Fracture

- Fracture of alveolar process that may/may not involve alveolar sockets
- Clinically, teeth are displaced axially or laterally, resulting in occlusal disturbance.
- Fragment should be mobile
- Dull sound to percussion
- Fracture line can be seen on x-ray
- Bony fracture can disrupt the vascular supply which can cause necrosis
- Due to concomitant luxation injury and damage to PDL, root resorption can occur
- Treatment:
▪ Use regional block anaesthesia, the fragment is repositioned
▪ Disengage apice from bony lock via apical digital pressure or initial axial traction of the fragment, which is splinted
with a semi-rigid splint
▪ Splint removed after 3-4 weeks
▪ Pulpal and PDL healing should be monitored after 4wks, 8 wk, 6 month, 1yr and yearly for 5 years

Avulsion
- Immediately after avulsion, the PDL and pulp of avulsed tooth begin to suffer ischaemic injury, which is aggravated by
drying exposure to kill bacteria or chemical irritants, which can kill PDL and pulp cells even after a short extra-alveolar
period
- Tx outcome depends on length of dry extra-alveolar time and storage media
- Management
▪ Check for other injuries (i.e. head and neck)
▪ Don’t reimplant primary teeth
▪ Don’t scrape or handle the root
▪ Rinse tooth with dairy milk, saliva or saline. No water. Don’t let tooth dry out before it is reimplanted.
▪ Reimpant ASAP
▪ Ensure tetanus up to date
▪ Prescribe antibiotics
• Doxycycline orally 1x day for 7 days
o Adult or child >8 and >35kg: 100mg
o Child >8 and <25kg: 50mg
o Child >8 and 26-35kg: 75mg
If doxycycline contraindicated (e.g. kid under 8)
• Amoxicillin 500mg orally 8-hourly for 7 days
o Child: 15mg/kg up to 500mg

Splinting
- Indicated in all cases of repositioning after a luxation, avulsion, root/bone fracture
- Flexible splint can optimise pulp and PDL healing
- RHS photo is example of splint called Ribbond