Endodontics Flashcards
What is the definition of endodontics?
The prevention diagnosis and treatment of the dental pulp and their sequelae
What is involved during endodontic treatment
Preserving all/parts of the pulp in health
Removing all of the pulp in irreversible disease
Carrying out further treatment to preserve teeth which have failed to respond to nonsurgical endodontics or developed new lesions: root canal retreatment or periradicular surgery
What are the reasons to perform endodontics?
Pain relief
Prevent adverse signs or symptoms
remove root canal contents
Promote healing and repair of periradicular tissues
What is the mantra behind endodontics?
Apical periodontitis is caused primarily by bacteria in Root canal systems If bacteria in canal systems are reduced to levels that are not detected by culturing, then high success rates are observed • Best documented results for canal disinfection are chemo‐mechanical debridement with Ca(OH)2 for at least 1 week • Mechanical instrumentation alone reduces bacteria by 100‐1,000 fold. But only 20‐ 43% of cases show complete elimination • Do mechanical instrumentation and add 0.5% NaOCl produces complete disinfection in 40‐60% of cases • Do mechanical instrumentation with 0.5% NaOCl and add one week Ca(OH)2: get complete disinfection in 90‐100% of cases
What is the evidence behind endodontic treatment diagnosis?
Koch’s postulates cannot be applied to establishing a bacterial origin of AP
• Mantra misses host response contributions (eg; Stashenko’s P or E‐selectin knockout
showed increased AP due to bacteria (thus, phagocytic leukocytes help to minimize AP via protection
against microorganisms; implies host defenses regulate the development of AP)
• What is the clinical significance of a “non‐cultivable” root canal sample when organisms can reproduce
in <12h?
• Implication: the “mantra” is focused on what the clinician can accomplish with current methods (eg.,
reduction‐disruption of a bacterial ecosystem). It only provides general guidance for developing better
therapeutic methods, and it cannot predict clinical success in cases where immunocompetence is
altered.
• Given a polymicrobial aetiology and a disease‐modifying host capacity, it is overly simplistic
to correlate one bug with given signs or symptoms. [Recall Sundqvist (1992) used odds ratio analysis &
concluded that bacterial pairings in infected root canal systems are not random, but appear to be due
to forces such as ecological commensalism. Since pairings can occur, correlational analysis between
bugs and signs ‐symptoms may be confounded if one bug is more easily cultivable than another]
Explain the 5 stage process of endodontic diagnosis?
- The patient tells the clinician the reasons for seeking advice.
- The clinician questions the patient about the symptoms and history
that led to the visit. - The clinician performs objective clinical tests.
- The clinician correlates the objective findings with the subjective
details and creates a tentative list of differential diagnoses. - The clinician formulates a definitive diagnosis.
What key symptoms will the patient complain of that may suggest pulp involvement?
Pain Swelling No sleep Broken tooth Discomfort from hot or cold Tooth colour change
What questions should the clinician ask the patient about symptoms and history?
SOCRATES Site: quadrant Onset: when it started and does it get better/worse Character: describe the pain? Radiation: pain to other parts of body? Association: other signs and symptoms Timing: when pain worst? Exacerbate: what sets of the pain? does anything help reduce the pain? Severity: 0-10 scale
Differential diagnosis for pulpal pain - referred pain?
Referred pain:
muscle trigger point referred to tooth and mimicked endo involvement
Sinusitis
Acute dental pain can be referred to opposite arc in same side
Name the 4 differential diagnoses for pulpal pain?
Referred pain
Neuropathic pain
Cancer
Other
Differential diagnosis for pulpal pain - neuropathic pain?
MS Trigeminal sensory neuropathy Trigeminal neuralgia Herpes Atypical odontalgia Atypical facial pain Phantom tooth pain
Differential diagnosis for pulpal pain - cancer?
Numbness of lower lip - common feature of metastatic CA
Metastatic breast cancer from mandibular pain
Malignant mediastinal lymphoma as mandibular pain
Metastatic carcinoma as PARL on mandibular molar (later paresthesia)
Necrosis: metastasis occluding BF
Differential diagnosis for pulpal pain - Other?
Eagle’s syndrome
Alveolar cavitational osteopathies
Neuralgia inducing cavitational osteonecrosis
Munchausen’s syndrome
Name the 3 causes for pulpitis?
Physical irritations from extensive decay
Trauma
Anachoresis (retrograde infections)
Name 5 key symptoms for pulpitis?
Pain on biting Pain when chewing Sensitivity with hot or cold Facial swelling Discolored tooth
What difficulties arise for pulpitis localisation?
Referred pain & the lack of proprioceptors in the pulp
localising the problem to the correct tooth can often be a
considerable diagnostic challenge
• Also of significance is the difficulty in relating the clinical status of a
tooth to histopathology of the pulp in concern
• Unfortunately, no reliable symptoms or tests consistently correlate
the two.
Name the 7 classifications for pulpal disease?
1) Healthy pulp.
2) Reversible Pulpitis.
3) Symptomatic Irreversible
4) Asymptomatic Irreversible
5) Pulp Necrosis
6) Previously Treated
7) Previously Initiated Therapy
Name the 6 classifications for periapical disease?
1) Normal Apical Tissues
2) Symptomatic Apical Periodontitis
3) Asymptomatic Apical Periodontitis
4) Chronic Apical Abscess
5) Acute Apical Abscess
6) Condensing Osteitis
What to do if the tooth is not restorable or periodontally unsavable?
EXTRACTION
Name 4 types of special investigations for pulpitis?
Tap the tooth – percussion test
• Feel the surrounding hard tissue – palpation test
• Testing movement of the tooth – mobility test
• Shine a light through the tooth ‐ transillumination
Name and describe the categories for percussion?
None (-): tap on incisal edge of tooth with end of mirror causes no discomfort
Mild (+): tap on incisal edge of tooth with end of mirror causes little discomfort
Moderate (++): tap on incisal edge of tooth with end of mirror causes noticeable discomfort
(painful)
Severe (+++): tap on incisal edge of tooth with end of mirror causes definitive
discomfort
(very painful)
Name and describe the categories for palpation?
None (-): feeling buccal and lingual gingiva apical to a tooth with the oad of the finger causes no discomfort at all
Mild (+): feeling buccal and lingual gingiva apical to a tooth with the oad of the finger causes little discomfort
Moderate (++): feeling buccal and lingual gingiva apical to a tooth with the oad of the finger causes noticeable discomfort (painful)
Severe (+++): feeling buccal and lingual gingiva apical to a tooth with the oad of the finger causes definitive discomfort (very painful)
Name and describe the categories for mobility?
Grade 0 – no apparent mobility
• Grade 1 ‐ mobility less than 1mm buccolingually
• Grade 2 ‐ mobility between 1 – 2 mm buccolingually
• Grade 3 ‐ mobility greater than 2 mm buccolingually AND apical
movement greater than 1 mm
What is the definition of sensibility testing?
e help to determine the pulpal status…alive or dead
What are the limitations for a sensibility test?
Can't differentiate between: “alive & healthy” “alive and diseased” “alive but just about to snuff it” or “in the process of dying
What is the definition of vitality, sensibility and sensitivity testing?
Vitality: blood supply present in tissue
Sensibility: ability to respond to a stimuli
Sensitivity: responsiveness to a stimuli
What is the true determinant for pulp vitality?
Vitality
Explain how the laser doppler flowmetry works?
Measures BF
Uses He neon laser beam directed onto tooth
Light contacts a moving object, is Doppler shifted
and a signal is produced.
As red blood cells are the majority of moving
objects, signal measures flow rate of blood
Explain how the vitality test works?
The pulse oximeter sensor consists of two light‐emitting diodes,
one to transmit red light (640 nm) and the other
to transmit infrared light (940 nm) and
a photodetector on the opposite side of the vascular bed.
The light‐emitting diode transmits red infrared light
through a vascular bed such as the finger or ear.
Oxygenated hemoglobin and deoxygenated hemoglobin
absorb different amounts of red infrared light. The
pulsatile change in the blood volume causes periodic
changes in the amount of red infrared light absorbed by
the vascular bed before reaching the photodetector.
The relationship between the pulsatile change in the
absorption of red light and the pulsatile change in the
absorption of infrared light is analyzed by the pulse oximeter to determine the saturation of
arterial blood.
Explain how the sensibility test works?
Thermal and electrical tests assess whether the pulp nerve fibres can
respond to a stimulus when applied to the tooth, hence they are
sensibility tests
Explain how the sensitivity test works?
Thermal and electric pulp tests are NOT sensitivity tests, although
they can be used to test the sensitivity of a tooth
Name the 8 ideal characteristics for an ideal sensitivity pulp test?
Simple Objective Standardised Reproducible Inexpensive Non‐painful Non‐injurious Accurate
Why can pulpitis diagnosis be wrong sometimes?
Diagnosing pulpal and periradicular symptoms is extremely difficult
because the histopathological condition of the pulp cannot be
determined by clinical means
How can special investigations help with diagnosis?
Sensibility tests are used to try and reproduce the pain the
patient is having & so confirm the source and reason for the
pain
Tooth localisation
How do nerve fibres reach the pulp and innervate the teeth?
Hundreds of sensory trigeminal afferent axons enter
through the apical foramen & branch through the
pulp following the distribution of the pulpal blood
supply.
Ultimately reaching coronal dentine where the plexus
of Rashkow is formed
Here they terminate as free nerve endings that
synapse onto and into the odontoblast cell layer
Explain how the sensibility test works physiologically?
aim to stimulate the A‐delta (Aδ) +/‐ C fibres
Due to the location of the C fibres & their stimulation
threshold, it is easier to stimulate the A‐delta fibres
Explain the Brännströms hydrodynamic theory?
Proposed pulpal pain results when A‐delta nociceptors are
activated by fluid movement within patent dentine tubules
Hence, for this to elicit pain, odontoblasts must be intact –
i.e. pulp is alive
Gives indirect information on the pulp status a positive
response does not guarantee a healthy pulp
It only tests if A‐δ nerves can respond to a stimulus
What should be included during a sensibility test to look out for?
Use control teeth
Use the information from the history, clinical examination
and findings, other special tests/investigations
When is a sensibility test useful or indicated?
When a patient has unlocalised or referred dental pain
To aid in diagnosis between odontogenic and non‐odontogenic pain
To confirm apparent radiographic periradicular pathology in the absence of any clinical signs/symptoms
To confirm pulpal status when there are clinical signs/symptoms but no apparent radiographic changes
periradicularly
To discern between a periodontal abscess and an endodontic abscess & help confirm when a perio‐endo
lesion is suspected
To assess the pulpal status of a tooth prior to crowning.
Monitoring the success of pulp caps/ pulpotomies (ensuring that the pulp has not become necrotic)
Monitoring traumatised teeth/ revascularization cases
(usually over several months).
Monitoring teeth following orthognathic surgery/ OS procedures/ facial fractures/ tooth transplantation
To confirm profound pulpal anaesthesia.
When is a sensibility test not indicated?
Electric pulp testers DO NOT interfere with pacemakers
Name 2 types of sensibility tests?
Thermal
Electrical
Name and explain 5 types of cold sensibility tests?
Ice sticks (not could enough) Ethyl Chloride EndoIce (TFE) EndoFrost (PBM) Dry Ice (very rapid sensory response)
What are the pros and cons for a cold sensibility test?
Superior to Hot test
Colder the test more reliable
Cold stim causes a rapid outward flow of dentinal fluid:
- test a delta fibres, respond to fluid movement, info extrapolated to consider pulp is vital
Name and explain 5 types of hot sensibility tests?
Warm Gutta percha (place vaseline first)
Warmed instrument
Electrical heat sources
Rubber prophy cup (frictional heat)
What are the pros and cons for a hot sensibility test?
Less useful than cold Initially stims A delta fibres Prolonged heat stims C fibres Excessive heat can cause pulpal damage An exaggerated and linegring response to heat is indicative of pulpitis
Explain how the electric pulp tester works?
A battery operated device passes a small electrical current along the enamel prisms & dentinal tubules
to pulp tissue
Current causes an ionic shift across the neural membrane inciting an action potential at the nodes of Ranvier
in myelinated nerves
This stimulates the A‐delta fibres
EPTs have a rheostat showing the relative amount of current applied on various scales
How to explain and complete the cold test procedure on a patient?
Explain test and why it's necessary Patient will feel cold Isolate and dry tooth Find a control tooth Tweezers and cotton wool Spray cold stim onto wool and place onto tooth
Where should you place the cold sensibility test stimuli on the tooth?
On sound tooth structure Incisal edge or incisal 1/3 anteriors Mid third buccal surface premolars Mesio‐buccal cusp tip molars Hold pellet in place until the patient feels the stimuli or for a few seconds if no response
Describe a normal pulpal reaction to a cold stimuli?
A sharp, sharp cold/pain sensation which
immediately ceases when the stimuli removed
Describe a pulpitis reaction to a cold stimuli?
A severe, prolonged, exaggerated response to cold
Describe a non-responsive reaction to a cold stimulus?
Pulp necrosis
Previous pulpotomy or previous pulpectomy
False negative
How to explain and complete the electric pulp test on a patient?
Explain procedure and why it is necessary
Patient may feel tinge or warm sensation
Dry and isolate tooth + control tooth
Place interprox celluloid strip where required
Place conducting interface medium on tooth
Place tip of EPT on conducting medium and patient completes circuit by earling the lip clip or touching the probe
Increase current slowly
Let patient respond at pre-pain sensation
Where should you place the electric pulp tester on the tooth?
On sound tooth structure
Incisal edge or incisal 1/3 anteriors
Mid third buccal surface premolars
Mesio‐buccal cusp tip molars
Describe a normal pulpal reaction to an electric pulp tester?
Sharp warm/hot/tingle or throbbing sensation which immediately ceases when stimulus removed
Describe a pulpitis pulpal reaction to an electric pulp tester?
A severe prolonged exaggerated response
Describe a non-responsive pulpal reaction to an electric pulp tester?
Pulp necrosis
Previous pulpotomy or previous pulpectomy
False negative
What are the 2 reasons for a false +ve result for a sensibility test?
Anxious or young patient
Multirooted tooth
What are the 8 reasons for a false -ve result for a sensibility test?
Incomplete root development Traumatised tooth Orthodontic tooth movement Heavily restored Pulpal obliteration Periodontal disease (decreased intensity of pain response to cold) Pre-medications Psychosis
Name 1 reason for a false -ve electric pulp test result?
Improper use/technique
Name 5 reason for a false +ve electric pulp test result?
Improper use/technique Pus in canal, as it can conduct to periapical tissues Metal splints Bridges Ortho arch wires
What is the definition of sensitivity?
Proportion of positives correctly identified
What is the definition of specificity?
Proportion of negatives correctly identified
What is the definition of a periradicular lesion?
Develop near the tips of root (where canal communicates with periodontium via apical foramen)
Where is a inflammatory periodontal lesion usually found?
Emerge at other anatomical or iatrogenic openings:
- lateral aspects of root
- furcations of multirooted teeth
How does apical periodontitis develop?
Following pulp tissue breakdown and the emergence of root canal infection
Can be symptomatic or asymptomatic
Bone resorption part of process
Explain how an RCT can be used to treat apical periodontitis?
Eliminate bacteria via RCT:
- active inflammatory lesion subsides
- bone regeneration takes place
What are the active immunocomponents found in the histopathology of a periradicular pathology?
Macrophages: - HLA-DR+ cells - CD14+ Dendritic: - HLA-DR+ - CD83+
What is the role of a mature dendritic cell in a periradicular lesion?
Regulate specific immune responses
- initial phases of apical periodontitis
Explain the activation phase for a periradicular lesion?
Antigen specific T cells are cloned in regional lymph nodes
- travel to lesion site
- become dominant in lesion
More CD4 cells than CD8 cells
Explain the established chronic phase for a periradicular lesion?
More CD8 than CD4
Suggests that CD4 are active during the expansion of the inflamm process
Involved with bone-resorptive process by activating macrophages producing bone resorbing mediators
Name 3 microscopic level different structural frame-works of apical periodontitis?
Apical granuloma
Apical abscess
Apical cyst
Clinically and radiographically these histopathological entities cannot be
distinguished from each other or recognized
What is the definition of an apical granuloma?
Consists of an inflammatory lesion dominated by:
- Lymphocytes,
- Macrophages and
- Plasma cells
Numerous fibroblasts and connective tissue fibres usually present
- + many capillaries.
Around the edge an encapsulation attempt may often be found
The epithelium originates from the epithelial cell rests of Malassez
Influenced by cytokines & growth factors released in the inflammatory process
the normally resting cells divide and migrate.
- They may form more or less continuous
- Random course
- May also become attached to the root surface
Polymorphonuclear leukocytes are found in varying numbers
Abscess formation can be a transient or persistent event within an
existing apical granuloma
What is the definition of an apical abscess?
Pus within the lesion
Abscess formation = cellular dynamics within apical granuloma or direct outcome of an acute primary infection
High influx of PMNs (with high phagocytic activity of PMNs)
PMNs die and release tissue-destructive elements
CT are degraded
Tissue in centre of lesion liquefied
COntinuum exists between apical abscesses and apical granulomas
What is the definition of an apical cyst?
Epithelium-lined cavity Contains fluid or semi-solid material Surrounded by CT: - infiltrated by mononuclear leukocytes and PMNs - cavity lined with stratified squamous epithelium - originates from epithelial rest of Malassez - can be lined with ciliary epithelium Lining can be be: - continuous - disrupted - completely missing Some cysts never become steady (consume bone or slowly expand)
Name the 2 types of apical cysts?
Pocket and True
What is the definition of a true apical cyst?
Located within the periapical granuloma
No apparent connection between
their cavity and that of the root canal space.
What is the definition of a pocket cyst?
An apical inflammatory cyst
Contains a sac‐like, epithelium‐lined cavity
Open to and continuous with the root canal space.
How is an oblong needle-like crystal formed?
The crystals are thought to derive from disintegrating red blood cells in stagnant vessels of the lesion.
But could be from inflammatory cells and/or circulating plasma lipids
Explain the nutritional deficiency theory for apical cyst formation?
Assumes that epithelial proliferation
results in an epithelial mass that is too large for nutrients to reach its core,
resulting in necrosis and liquefaction of the cells in the center. PMNs are
attracted by the necrotic material, which, together with tissue exudate,
result in microcavities that eventually coalesce to form the cystic cavity
Explain the abscess theory for apical cyst formation?
Assumes that tissue liquefaction occurs first, at the
central part of an abscess. The peripheral aspect of the cavity is later lined by proliferating epithelium, owing to the inherent nature of epithelial cells to cover exposed connective tissue surfaces
Why do the size of radicular cysts slowly increase?
Increased osmosis leading to passage of fluid from the surrounding
tissue into the cyst lumen is likely to occur owing to breakdown of
epithelial and inflammatory cells
Release of bone‐
resorbing factors from mononuclear leukocytes present in the cyst wall,
including interleukins, mast cell tryptase and prostaglandins.
What are the causes for apical periodontitis?
Most AP is due to microorganisms within the RC. Other occasional
causes include trauma, occlusal trauma, foreign body reaction
Bacteria in infected necrotic pulps predominately obligate anaerobes.
Different microorganisms display differing ability
to survive in the root canal system
More likely that
a community of microbes exists
Biofilms form in RCs. Biofilms protect bacteria from being destroyed
Name 6 microbial causes of primary apical periodontitis?
Carious lesions Cracks Traumatic exposure Accessory canals Exposed dentinal tubules Periodontal pockets to the apical foramen
Name 3 factors of selective pressures for microbial invasion of apical periodontitis?
Nutrition
Oxygen
Microbial interactions
Name 6 types of bacteria present in primary root canal infections?
- Spirochetes • Fusobacteria • Actinobacteria • Firmicutes • Proteobacteria • Bacteriodetes No more than 10 per canal and more are negative and are mostly anaerobic
What is a reason for persistent Apical periodontitis?
Microbes remaining within the canal system
What are the survivability characteristics for E. faecalis?
Possesses a “proton pump” which allows it to survive in high pH (i.e. can survive calcium hydroxide)
• Can survive in mono‐infection
• can survive long periods of low/no nutrition
Name 3 forms of non-microbial causes for apical periodontitis?
Periapical cysts – 15% of lesions (Nair 1996)
• Serial sectioning indicates two types – true cysts and pocket cysts
• Foreign Body Reactions
• Cholesterol Clefts
Name 8 non-specific mediators of inflammatory reactions?
neuropeptides, • fibrinolytic peptides, • kinins, • complement fragments, • vasoactive amines, • lysosomal enzymes, • arachidonic acid metabolites, • and various cytokines
Explain the root canal response to canal instrumentation cutting BVs in the PDL or bone?
This activates intrinsic and extrinsic coagulation pathways.
• Contact between the Hageman factor and:
• collagen of basement membranes,
• enzymes such as kallikrein or plasmin,
• endotoxins from inflamed root canals
can activate the clotting cascade and the fibrinolytic system.
• Fibrinogen molecules and fibrin degradation products are released during fibrin proteolysis by plasmin
these release fibrinopeptides
• Trauma to the periapical tissues during RCT can also activate the kinin system
• This will then activate the complement system.
• C3 complement fragments found in periradicular lesions.
• Products released from the activated systems contribute to the inflammatory process and cause
swelling, pain, and tissue destruction.
How do mast cells play their part in apical periodontitis?
Mast cells are normal components of connective tissues
• present in a normal PDL.
• also found within periradicular lesions.
• (Physical or chemical) injury causes the release of vasoactive amines
• e.g. histamine,
which are chemotactic for leukocytes and macrophages.
• In addition, lysosomal enzymes cause cleavage of C5 and generation of C5a, a potent chemotactic
component, and liberation of active bradykinin from plasma kininogen
• Periradicular lesions show increased levels of lysosomal hydrolytic arylsulfatase A and B compared to
normal tissues.
• Significant levels of PGE2 and leukotriene B4 are also present in these lesions.
What can you stain with immunohistochemical staining for an apical periodontitis?
PGE2, prostaglandin F2a
(PGF2a), and 6‐keto‐PGF1a
Explain the process of formation of a periapical granuloma?
Bacterial antigens come from the infected root canal
• taken by antigen presenting cells (APC),
• processed and
• presented to the T‐lymphocytes (T).
• A dual signal of antigen presentation with IL‐1 activates the T‐lymphocytes.
• Cytokines produced by these activated cells include
• (a) IL‐4, IL‐5 and IL‐6, which induce proliferation and maturation of a specific clone of B‐lymphocytes (B) that
were exposed to this specific antigen, to result in plasma cells producing IgG specific to this antigen;
• (b) INFγ which serves to activate macrophages which in turn will produce the IL‐1 essential for local
recruitment of circulating PMNs and IL‐8 which activates these PMNs.
Bacterial endotoxin derived from Gram‐negative bacteria, activates macrophages.
• All the above is aimed to allow effective specific phagocytosis by the PMNs of any
bacterium emerging from the apical foramen.
• Bone resorption is a side‐effect of the defensive process, mediated by TNFβ,
produced by the activated T‐lymphocytes and IL‐1β, produced by the activated
macrophages. Both activate osteoclastic bone resorption
Name the 2 agents responsible for bone resorbing activity?
IL‐1β (mainly produced by activated macrophages) and
• TNFβ(mainly produced by activated T‐lymphocytes
Describe the bacteria confined to the root canal space?
Rarely be able to survive and establish themselves in the apical lesion
• In the process of pulpal breakdown, eg after carious exposure, bacteria will gradually
gain terrain and move their front line towards the apex, depending on how effective the
host response is in limiting further bacterial colonization in the pulp tissue.
• The host tissue–bacterial front will be established in the vicinity of or at the exit of the
apical foramen.
• exact position of the bacterial front is unpredictable.
• Can often be well inside the apical foramen,
• PMNs engaged in phagocytic activities prevent dispersion of bacterial elements from the
root canal biofilm.
• Yet, PMNs have a hard time dealing with those organisms attached in a biofilm structure.
• this means that there is a constant battle between the spreading organisms and the host
defense
wHAT ARE THE 2 TYPES OF EXTRARADICULAR INFECTIONS?
Bacteria in chronic abscesses
Bacterial cluster formation?
What is the definition of bacteria in chronic abscesses?
with a persistent sinus tract.
• Viable bacteria can usually be isolated from the exudate
• The source may be bacteria that emerged from the root canal space
What is the definition of bacteria in cluster formation
Actinomyces israeli
• Propionibacterium propionicum can grow in clumps and thereby prevail
• Such aggregations may become too large for phagocytosis.
• bacterial cells are out of reach for phagocytosis = chronic infection
• cannot be managed by endodontic treatment
Name the 7 factors needed for a tooth to be healthy?
comfortable to the patient • not tender to percussion or occlusal pressure • not sensitive to palpation. • Free from sinus tracts • Free from swelling • Has no painful symptoms. • Has normal pocket‐probing depths: • pocketing may also imply a sinus tract drainage along the periodontal ligament space.
Name the 5 different types of root canal infections?
asymptomatic apical periodontitis (chronic apical/periradicular periodontitis),
• symptomatic apical periodontitis (acute apical/periradicular peri‐ odontitis),
• acute apical abscess (acute periradicular abscess),
• chronic apical abscess (chronic periradicular abscess, suppurative apical/periradicular
periodontitis),
• condensing osteitis (focal sclerosing osteomyelitis, periradicular osteosclerosis, sclerosing
osteitis, sclerotic bone).
What are the radiographic findings for a normal periapical condition?
unbroken lamina dura
• distinct periodontal ligament space of normal width,
comparable to adjacent and contralateral teeth.
What is the definition of an asymptomatic apical periodontitis?
is longstanding periapical inflammatory
• Has radiographically visible periapical bone resorption
• has no clinical signs and symptoms.
• Is associated with a tooth with a non‐vital pulp (untreated or treated).
It might be suspected from a carefully taken disease history in cases when patient has
experienced a prior painful event.
What is the definition of an symptomatic apical periodontitis?
Symptomatic apical periodontitis may develop as a direct consequence of the
breakdown and infection of the pulp within a previously healthy periapical region.
• It reflects a response to an initial exposure of the periapical periodontium to bacteria
• or their products emerging from the infected root canal.
• may also appear in a tooth with previous asymptomatic apical periodontitis.
• Can be a natural shift in the balance previously established between the bacteria and
the host or occur in response to endodontic treatment (endodontic flare‐up).
• The typical symptoms include:
• pain (aching)
• may become severe or even unbearable.
• usually tender to percussion
• mucosa and bone overlying the apical area sensitive to palpation.
• premature occlusion
What is the definition of an acute apical abscess?
Characterized by:
• rapid onset,
• spontaneous pain,
• tenderness of the tooth to pressure,
• pus formation
• swelling of associated tissues.
• Initially, may be extremely painful, (pressure builds up in bone or periodontal space).
• Cortical plate may perforate and pus will accumulate under the periosteum producing a most severe painful condition.
• Only with the perforation of the periosteum will the pus be able to drain and allow pain to subside.
• Then a tender local swelling will appear.
• Sometimes, natural drainage will be established within a few days by perforation of the covering tissue.
• In other cases, the swelling will remain for some time before it gradually subsides.
• Drainage of an apical abscess will take the “path of least resistance”
• thickness of overlying bone
• Following penetration of the bone and periosteum, drainage will often be visible:
• in the oral cavity but it may also occur
• into perioral tissues or
• into the maxillary sinus.
What is the definition of an chronic apical abscess?
Typical feature = sinus tract.
• Drains into:
• mouth or
• extraorally through the skin
• A sinus tract may establish exit with drainage
• into the gingival sulcus,
• in a periodontal pocket or
• in a furcation area
• MUST be differentiated from periodontal disease and from a pocket associated with a
vertical root fracture.
• A sinus tract may also lead into the maxillary sinus and cause unilateral chronic sinusitis!
• Most commonly associated with an apical radiolucency (but not always)
• It is asymptomatic (or only slightly symptomatic)
• patient often unaware of its presence.
• This may last as long as the sinus tract is not obstructed.
What is the definition of cellulitis?
symptomatic edematous inflammation
• associated with diffuse spreading of invasive micro‐organisms through connective tissue and fascial planes.
• Its main clinical feature is diffuse swelling of facial or cervical tissues.
• Cellulitis usually follows an apical abscess that penetrated the bone,
• allows the spread of pus along paths of least resistance.
• Spreading infection may or may not be associated with systemic symptoms such as fever and malaise.
• Since cellulitis is usually a sequela of an uncontrolled apical abscess, other clinical features typical of an
apical abscess are also expected.
• Spreading of an infection into adjacent and more remote connective tissue compartments may, rarely, result
in serious or even life‐threatening complications.
• Cases of Ludwig’s angina
• orbital cellulitis
• cavernous sinus thrombosis
• and even death from a brain abscess
• originating from a spreading dental infection have been reported.
What is the definition of condensing osteitis?
diffuse radiopaque lesion
• believed to represent a localized bone reaction to a low‐ grade inflammatory
stimulus
• usually seen at an apex of a tooth (or its extraction site) in which there has been a
longstanding pulp disease.
• It is characterized by overproduction of bone in the periapical area, mostly around
the apices of mandibular molars and premolars that had long standing chronic pulpitis.
• The pulp of the involved tooth may be vital and chronically inflamed or may have
become necrotic with time, leaving the radiopaque area.
• Normally the condition does not prompt treatment
• unless the pulp necrosis.
• The radiopacity may or may not disappear after endodontic treatment or tooth
extraction
How are the periodontium and pulp connected?
Natural communications
Pathological and iatrogenic communications
As the periodontium and teeth develop, name the 3 natural avenues communication between pulp and periodontium?
Dentinal tubules
Apical foramen
Accessory canals
What can cause the dentinal tubules to become exposed?
Developmental
Disease
Periodontal surgery
Traumatic injury
Describe the 4 types of CEJ morphology?
I: cementum over enamel
II: edge edge cementum and enamel
III: gap between cementum and enamel
IV: enamel over cementum
What is the definition of the apical foramen?
Principle route of communication between pulp and periodontium
Pulpal inflamm can cause a localised inflammatory reaction
May be exposed due to severe loss of attachment
What is the definition of lateral canals?
Found apically
COntains CT and BVs
Don’t extend full width of dentine
What is the definition of a furcal canal?
All teeth with furcation involvement can potentially have exposed furcal canals
Lesions suggested radiographically may be due to infectious products from a necrotic pulp diffusing down a furcal or lateral canal
What teeth to test for exposed furcal canals?
Sensitivity test:
- Lower 46,36 (DL root)
Upper and lower premolars (1-3 roots)
Canines (2 roots)
Name the 6 bacteria present in teeth with chronic/asymptomatic PRP AND a chronic periodontitis?
Aggregatibacter actinomycetemcomitans P gingivalis Eikenella Fusobacterium P intermedia Treponema denticola
Name 5 pathological or iatrogenic pathways for communication between periodontium and the pulp?
Developmental Resorptive lesions Perforations Cracks Mucosal fenestrations
What is the definition of a developmental malformation?
Palatogingival groove
Usually maxillary lateral incisors
If epithelial attachment is breached, grooves becomes contaminated
Self-sustaining infrabony pocket develops
Loss of attachment can quickly extend to apical foramen
Difficult to treat as scaling and RSI does not work
What is a resorptive lesion and its 2 requirements for it to be one?
Injury Stimulus External inflamm resorption internal inflamm resorption Cervical inflamm resorption
What is the definition of internal inflammatory root resorption?
Associated with increased probing depths and BOP when resorptive process has perforated entirely through the root
What is the definition of an external inflammatory root resorption?
Depending on location, may be associated with increased probing depths and BOP
Late stages, can interfere with gingival sulcus and result in periodontal abscess
What is the definition of a cervical inflammatory root resorption?
Starts where the Je attaches to the root surface
Microbes in the gingival sulcus stimulate and sustain the resorptive process
Associated with increased probing depths, gingival swelling and BOP
What is the definition of perforations?
Caused pathologically by caries/resorption or iatrogenically by procedural errors
Present with perio abscess - pain, swelling, pus draining through PDL and with time infrabony pocket developing
Acute inflammatory action will occur
Closer to gingival sulcus more likelihood of apical migration of gingiva
What does the perforation prognosis depend on?
Location: - better in apical 1/3 Bad with advanced perio Time Ability to seal Chance of building new attachment Accessibility of the remaining RCs
What is the definition of a root fracture?
Horizontal:
Pocket formation may occur when fracture out with alveolar bone
Cornola 1/3 root fracture
Can present with perio abscess or sudden deepening of a perio pocket
Vertical:
Microbial colonisation of crack space = periodontal inflammation = breakdown of CT and alveolar bone leading to deep infrabony pocket
How to diagnose a vertical root fracture?
Take more than 1 x-ray
parallax increases yield
J shaped radiolucency
Can present initially with perio abscess or sudden deepening of periodontal pocket
Deep, narrow pocket, pain on biting, abscess and chronic sinus
Definitive diagnosis = surgical exploration Hopeless prognosis
What is the definition of mucosal fenestration?
Pathological condition characterised by the perforation of the alveolar bone plate and overlying the mucosa by the roots of the teeth
Asymptomatic but are PRFs
Name 6 aetiologies for mucosal fenestrations?
Root prominence Developmental Perio disease Biotype Chronic periradicular pathosis Ortho tooth movement
What is the treatment for mucosal fenestrations?
Endodontic Rx
Surgery
CT graft
Can periodontal disease affect the pulp?
Area of fibrosis
Areas of mineralisation
narrower canals
Reparative responses
If blood supply through apical foramen remains intact, pulp can withstand insult from perio disease
Pulpal necrosis only seen when perio disease advanced that microbes reach apical foramen
Can periodontal treatment affect the pulp?
RSI can remove cementum and expose dentinal tubules
Pulpal changes seen adjacent foci of inflamm +/- secondary dentine formation
How can scaling RSI and polishing affect the pulp?
Heat application to intact enamel can increase pulp temp between 5-17C causing irreversible pulpitis Frictional heat depends on: - speed - torque - amount of force Cause odontoblast death
How can endodontic pathology to affect the periodontium require?
A patent route to the periodontium
Infected root canal system
Sufficient virulent microbes to provoke a periodontal response
Do lateral canals cause infrabony defects?
Lateral canals in an infected/necrotic pulp may cause lateral periodontal lesions rarely
Can periodontal disease exert an effect on lateral canals?
Where the subgingival biofilm reached a lateral canal, the microcirculation was severed, but inflammation of the adjacent pulpal tissue was minimal
When the subgingival biofilm reached the apical foramen, the whole pulp became necrotic
Can endodontic disease affect the periodontium?
Loss of periodontal attachment directly correlated with the presence of endodontic infection
Patients have deeper pockets, increased CAL, higher freq of vertical/angular defects
Pulpal infections serve as a risk factor in patients prone to periodontitis (other papers say otherwise)
Both endo and perio disease is a microbial infection, microbes associated with a necrotic pulp are fewer than the complex biofilm in a deep periodontal pocket
Host response with be acute abscess or chronic inflamm response
How to drain an endodontic abscess?
Insert a GP cine and radiograph
Can drain through the PDL space to the sulcus
Can endodontic treatment affect the periodontium?
5-10C elevations in external root temo can produce damage to PDL Gutta percha increases flow Tip heated to 250-600C External root temp between 8.5-22.1 Ok to use with care
Name the 8 foreign body reaction in the periodontal and periradicular tissues?
Dentine and cementum chips Amalgam Root canal filling material Intracanal dressing, sealers and obturation materials Cellulose fibres Leguminous foods Calculus
Can cause acute or chronic reaction
Multinuc giant cells surround foreign body
What will influence the treatment options and prognosis?
Timing and amount of remaining perio support
What is the classification system for perio and endo lesions?
2017 World Workshop
Periodontitis associated with endodontic lesions
Explain the clinical examination for a possible endo or perio lesion?
Palpation
Percussion
pocket probing
Mobility
Sinus or pus draining through PDL
If sinus is present, palpate to see if discharging
If so, insert gutta percha cone and radiograph
Explain the diagnosis procedure for a possible endo or perio lesion?
Special tests
To differentiate between perio and endo
Sensitivity test
Higher false positives in teeth with advanced periodontitis
If perio only tooth will respond to sensitivity testing
Use 2 tests to increase reliability
Test cavities to differentiate between perio and endodontic pathosis
Both perio and endo affecting tooth form a perio-endo lesion
Characterised by CAL, bone loss and periradicular pathology
What symptoms should I suspect with a perio-endo lesion?
Hisotry of symptoms History of surgery deep pockets (average root lengths) furcation Pus exuding from deep pockets or swellings
Explain the plan of action for a perio-endo lesion?
Gather history and clinical information (endo and perio exam) 2 Sensitivity tests Radiograph periapical Make diagnosis Or further testing
What is the treatment plan for a perio-endo lesion?
Retain tooth
Extraction (vertical and horizontal bone loss)
Non-surgical endo/perio treat
Resection
Elim diseased root
Visible with fixed prosthesis (high smile line)
Buccal recession around implant
Consider condition for potential abutment teeth
Increased plaque, CAL and caries with RPDs
Explain the process of non-surgical endo and perio treatment?
Endo first and then perio
Cementum and intact PDL fibres may persist, can regenerate after perio treatment
Perio straight after endo, destroy fibres form long JE
Explain the process of root resection?
Allows functional retention of a multi-rooted tooth
Remove 1 or more roots
Use for furcated max molars
Always RCT first before resection
After treatment, cuspal coverage restoration
Important to remove any dentinal overhangs
Name the 7 indications for root resection?
Root fracture Perforation Root caries Root resorption Severe periodontal disease Grade II or III furcation Failed endodontic treatment
Name the 2 contraindications for root resection?
Medical/physical issues
Fused roots
How success are root resections?
62-100% success over 5-13 years
Resected teeth have better outcome with regular perio maintenance and Fl application
1:1 root:crown ratio is minimum acceptable
Long term tooth retention requires 50% bone support
Resected for perio better than non-perio
What is the definition of regeneration?
Aims to regenerate lost periodontal structures
Deep narrow defects favourable
endo first
Retract flap, scale, RSI, removal granulation tissue, type defect, bone graft and resorbable membrane
77.5% success over 5 years
What is the prognosis difference between single and multirooted teeth?
Better for single rooted
More success for perio than endo
Deep narrow pockets good prognosis
Name 7 factors does endo success depend on?
Reaching WL
Disinfecting full canal length
Keep all RCT material within root canals
Dense obturation with no voids within 2mm radiographic apex
Having enough dentine to achieve ferrule effect
Adequate coronal seal
Cuspal coverage
Name 7 factors does endo success depend on?
CAL Stabilisation of perio disease Reduction of perio pocket depth and lack BOP Effective perio maintenance Presence of furcation Morphology of lesion Sufficient bone
What is the definition of apical periodontitis?
Bacteria in the root canal system
Why to perform root canal treatment?
Remove/reduce the bacteria to an undetectable level
What is the best method to reduce bacteria in root canals?
C&S + NaOCl + one week later Ca(OH)2
What problems arise with our understanding of the root canal system?
Koch’s postulates (polymicrobial)
Missing the host response
Non-cultivable bacteria in root canal (immunocompetence alters response)
One bacteria can’t cause all these symptoms
Due to ecological commensalism (bacterial pairs)
What evidence supports root canal treatment to aim for the apex of the root?
Best amount of healing
Overfilled teeth have persistent inflammation
Sjorgen:
- 0-2 mm 94%
- > 2mm 68%
- overfilled 76%
Aim to fill between 0.5-2mm from the apex of the root
Where is the apex of the root found?
0.5 to 0.65 mm in elderly
0.59 mm
0.72 mm
0.8 mm
Apex changes in necrosis cases compared to normal
Changes in shape change the apex
Name the 8 cross-section shapes of a root filing tool?
K K-flex Flexofile Mwo Profile Protaper K3 Hero 642
What is the definition of a K file as a root tool?
Most common CAn be square, triangular or rhomboidal From 1.97-0.88 sharp grooves per mm 45 helical angle 21, 25 and 31mm length From 6-gauge to the 140th twisted instrument
What is the definition of a F-flex file (Kerr)?
Rhombus stem
Remove debris by increasing clearance between file and dentine wall
Sharp rhombus angle improve cut efficiency
From 6-gauge to the 80-gauge
Twisted
What is the definition of a Hedstroem file?
Drags large amounts of fabric in its traction cut
Helicoidal shape
Turned instrument
Cut in one direction only, of retraction, due to positive inclination of their groves
What motion is good for a SS file?
Bend to get round corners
What motion is good for NiTi files?
Straighten it
What gives a greater chance of separation via movement?
A CW rotation greater chance than CCW rotation
What are the pros of a tapers root file?
Better than straight
Less dentine removed
Less chance of perforation
Better debridement of apical prep
Danger zones vs safe zones?
Paper:
- Abou-Rass, Frack and Glick 1978
Explain the step-back (telescopic technique) for root filing?
Determine WL and develop apical stop to #25
Step-back by shortening 30, 35, 40 in 0.5 or 1-2mm increments
Recapitulate with #25
Coronal flare with #2 and 3 Gates-Glidden
Explain the step-down technique for root filling?
Passive use #15, 20 and 25 hedstrom in coronal 2/3 of canal system then irrigate
Coronal flare with #2 and 3 Gates-Glidden
Establish WL and prepare apical seat with standard serial filling
Step-back to blend apical and coronal segments
Recapitulate
Explain the crown-down pressureless technique for root filing?
Rotate straight file twice form larger to smaller sequence until 16mm
Coronal flare with GG
Establish provisional WL 2mm short of apex
Rotate stright file at WL
Finish apical prep at WL with file 2 sizes larger than first file to reach WL
Explain the balanced force technique for root filling?
Use FlexR files or FLexofile for non-cutting pilot tips of triangular file
Use crown-down to establish radicular access
Rotate straight file CW from 90-180 with light apical pressure to engage dentine
Shear dentine by 120 CCW rotation with apical force, flexing it to conform to canal curvature
Continue until get adequate apical enlargement at WL
Inspect file frew, do not go beyond #35 in curved canals
Explain the double-flared technique for root filling?
Passive use larger-smaller files in coronal 2/3 canal system then irrigate
Establish WL with small K file. Serial file to prepare apical stop and then step back to blend with coronal step-down flare
Circumferentially file with master K file
Explain the passive step-back technique for root filling?
Establish canal patency with small K file at WL then passive instrument with larger K files
Coronal flare with #2, 3 and possibly #4 GG in coronal 1/3
Confirm WL (typically reduced after coronal flare and curvature removal)
Increase straight line access with careful re-work with GG
Serial file to prepare apical stop and then step back to blend with coronal step-down flare
Explain the process of root filing for a Ni Ti file?
Used for crown-down sequence
Estimate working length from pre-OP radio, subtract 3mm from this length - use this new length to work to for the coronal 2/3 prep
Initial negotiation by hand using ISO files 08-20 passive
Precurve
Use lubricant
Take S1/2 to 2/3 canal length turning clockwise until snug then pull from canal and clean
If further coronal flare required or relocation orifice use SX to 2/3
Length (WL minun 3mm), turning clockwise
Determine WL with apex locator and take ISO 09-20 to WL
S1 then S2 to WL turning clockwise as above
F1 to length
Gauge the size of the apical constriction using a 20K file, if this fits snugly, the prep can be complete at this stage
However, generally the apical size needs to be at least 30 to allow irrigation into the apical 1/3
Take F2 to WL and gauge the foramen using a 25 K file
If this fits snugly, the prep can be complete
Or Take F4 to WL and gauge with 30K file, i fits snugly can be completed
Use the same sized paper points for during the canal and same sized GP cone for obturating
Why to use F3 Ni Ti files?
150mm bacteria
What is the needle nominal O.D. for a 30 gauge needle?
0.312 mm
What is the needle nominal O.D. for a 27 gauge needle?
0.413 mm
What % does NiTi superflexible show for elastic ability?
8%
How does NiTi superflexible root file become to flexible?
Martensite heated becomes Austenite and then cools and changes structure, but when deforms reverts back
Name 4 1st generation NiTi root file?
ISO standard taper (0.4 and 0.6% tapers)
Lightspeed system
GT system
Quantec
Name and describe 5 2nd generation NiTi root file?
Active cutting edges Decreased number of instruments needed Asymmetrical cross section Greater cutting efficiency ProTaper Universal K3 Mtwo Hero Shaper iRace and iRace +
Name and describe 5 3rd generation NiTi root file?
EMphasis on NiTi metallurgy Heating and cooling methods to reduce cyclic fatigue Transition point between martensite and austenite optimised M wire tech R phase tech Twisted files K3 XF files Profile Gt Series X Hyflex CM Flex Files
Name and describe 4 4th generation NiTi root file?
Canal prep more efficient with reciprocation
Reciprocation is any repetitive up and down or back and forth motion
Liberator
Wave One
Reciproc
Self-adjusting File
Name and describe 3 5th generation NiTi root file?
Centre of mass or centre of rotation is offset
Produces a mechanical wave of motion that transverses along the length of the file
Improved cutting and removal of debris by increasing cross-sectional space
Reduce engage between file and dentine
Revo S
ProTaper Next
One Shape
What is the definition of a rotary file?
Full 360
What is the definition of a reciprocating file?
Angle of rotation are asymmetrical, CCW and CW
Rotary vs Reciprocation files?
CW rotation greater than CCW rotation
CW rotation it will screw in the canal
CCW rotation, will unscrew out of the canal
CW > CCW, end result is screwing in effect and advancement of instrument
Very little pressure necessary to advance
Advantages of Rotary over Reciprocation files?
Fast Flexible Less transportation and ledging Shapes canal uniformly Reduced operator fatigue Improved efficiency
Disadvantages of Rotary over Reciprocation files?
CAn't be used in all cases Build up debris NO beyond apical foramen Fracture can occur Cost Loss tactile sensation
What is the definition of LA?
The practice of various psychological, physical and chemical approaches to the prevention and treatment of preOP, OP and postOP anxiety and pain
Name 5 methods of pain control?
Anaesthetic agents Inhalation sedation Antianxiety agents IV sedation GA
Pros and Cons for GA?
R v B
Risk death
Pros and Cons for IV sedxation?
Training
R v B
Refer necessary
Name and describe 2 form of antianxiety agents?
Oral sedation Usually Benzodiazepine Augment anaesthetics Pre-Op amnesia Drug choice depend on individual and nature of procedure Should be avoided in CNS depression, sleep apnoea and compromised airway Temazepam* Diazepam
What is the definition of a topical LA?
Numb specific site Provides temp numbing effect on nerve endings on the surface of the oral mucosa Ointment Liquid Spray
Name the 7 key characteristics for a LA?
Be non-irritating to the tissues Minimal toxicity Rapid onset Profound Anaesthesia Sufficient duration Completely reversible Sterile
Name the 4 types of LA injections?
Infiltration
Block
intraligamentary
Intraosseous
What is the defintion of short-acting?
Less than 30 mins
WHat is the definition of intermediate-acting?
Less than 60 mins
What is the definition of long acting?
Greater than 90 minutes
Indications for lidocaine?
Normal procedures
Preferable for IANB
Indications for articaine?
Profound anaesthesia infiltration
Not IANB
Indications for mepivacaine?
Short anaesthesia, periodontal treatments
Indications for prilocaine?
Pulpal anesthesia for 10 mins
Name 4 types of CCLAD LA systems?
Comfort COntrol Syringe
QuickSleeper
Anaeject
Ora Star
What is the definition of a wand/compudent system?
Accurently manipulate fingertip accuracy and deliver LA with foot control
Pen-like grasp, providing greater tactile sensation
Flow rate remains constant and can be varied
Improved experience
What is the definition of a comfort control syringe?
no foot pedal
Aids with injection and aspiration controlled directly from syringe
No more helpful than a manual syringe
What is the definition of ‘Hot Pulp’
Inflamm changes within the pulp progressively worsen as a carious lesion near the pulp
Chronic inflammation is an acute exacerbation
Influx of neutro and release inflamm mediators (glandins and IL)
Proinflamm neuropeps:
- SubP
- bradykinin
Sensitive the peripheral nociceptors within the pulp
How often does LA failure for hot pulp in the mand first molar? first premolar? lateral incisor?
17% mand first molar
11% first premolar
32% lateral incisor
Explain the lowered pH theory for LA?
Reduced pH means there is less of the base form of anaesthetic
Base form is needed to penetrate the nerve sheath and membrane
Less ionised form of LA within nerve to produce anaesthesia
What other theories are available for the failure of LA?
Nerves arise from inflamed tissue have altered resting potentials and reduced thresholds of excitability
Not able to prevent the transmission of nerve impulses because of the lowered excitability thresholds of inflamed nerve
Presence of anaesthetic resistant Na chs and up reg of Na chls in pulp with irreversible pulpitis
How successful are supplement PDL LA injections?
Endodontic: 50-96%
Irreversible pulpitis: 74-96%
What is the definition of intraosseous LA injection?
Need 27 gauge making through bone with slow speed
Immediate onset
Distal to tooth as thinnest bone
What is the definition of intrapulpal injection?
Must be given under pressure
V painful
Is pre-emptive pharmacy useful for root canal treatment?
71-76% painless treatment vs 46% in placebo
