endo note 2 iintroduction
TRANSCRIPT
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Biology And Clinical RationaleFor Root Canal Therapy
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Functions of the pulp
Induction(Odonogenesis and Amelogenesis)
Formation of dentine (Primary, Secondary-reactionaryand Tertiary-reparative).
Maintenance of dentine (fluid environment).
Defence mechanism by inflammatory andimmunological
Sensation from dentine and enamel (pain, warning).
Age changes (peritibular dentine, more solid tooth)(Walton and torabinjad – 1996).
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Induction (Odonogenesis and Amelogenesis)
Dental pulp 25mm3
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Formation of dentine (coronal and radicular).
Predentine thickness 15µPrimary dentine during development 4µ/dayRegular Secondary dentine after develop 0.8µ/dayIrregular Secondary dentine due to stimuli 3µ/day
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Formation of dentine (coronal and radicular).
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Formation of dentine (coronal and radicular).
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Maintenance of Dentine (fluid environment).
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Maintenance of Dentine (fluid environment).
Pulpal end D-E JunctionTubules 65000 /mm2 15000/mm2
Diameter 3µ 1µSurface area 45% 1%
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Maintenance Dentine (fluid environment).
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Defence mechanism (IIry dentine, reparative dentine, fluid flow).
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Sensation (pain, warning).
1 axon innervate 100 dentinal tubules and penetrate up to 100-200µ
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Age changes (peritibular dentine, more solid tooth).
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Theories of dentine hypersensitivity• Classic theory – (Direct innervations)
A-δ fibres -sharp, localized pain (drilling, probing, air drying,application of hyper osmotic fluids heating and cooling thedentine electrical pulp testing)
C- fibres -dull less localized pain (thermal, mechanical andchemical stimuli)
A-β myelinated fibres-non-noxious mechanical stimulation(mastication and loading of teeth)
• Odontoblast as receptors – (neural crest)
• Hydrodynamic theoryRapid movement of fluid of in the dentinal tubulescause mechanical distortion of tissue
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Sensation (pain, warning).
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Differential diagnosis of acute pains
Condition
Odontalgia
Trigeminal
neuralgia
Cluster
headache
Acute otitis
Bacterial
Nature
Stabbing, throbbing, Hot,cold and non-episodic.
Lancination, electrical,
episodic
Severe ache, retro-obital
component, episodic
Severe ache, throbbing,.deep to ear, nonepisodic
Severe ache, throbbing.in maxillary posterior
Triggers
Toothpercussion
Light touch on
trigger zone
Sleep, alcohol
Lowering head,barometric pressure
Lowering head,tooth percussion
Duration
Hours-days
Seconds
30-45 min
Hours-days media
Hours-days sinusitis
teeth, nonepisodic
Cardiogenic Short-lived ache left Exertion Minuteposterior mandible
Sialolithiasis Sharp, drawing, salivary Eating, induced Low ache
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sharp swelling, episodic
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salivation when triggered
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Differential diagnosis of chronic painsCondition
Odontalgia
Nature
Dull ache,
Triggers
Hot, cold, tooth
Duration
Days-weekspercussion
TMJ pain
Myalgia
Atypical facial P
Phantom tooth P
Allergicsinusitis
Causalgia
Dull ache, sharp episodic
Dull ache, degree varies
Dull ache severe episodes
Dull ache severe episodes
Dull ache in maxillaryposterior teeth
Burning
Opening chewing
Stress, clenching
Spontaneous
Spontaneous
Lowering head
Post trauma,
Weeks-years
Weeks-years
Weeks-years
Weeks-years
Weeks-monthseasonal
Weeks-yearspost surgical
Post herpiticneuralgia
Cancer associatedfacial pain
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Deep boring ache withburning
Variable,motor difficult,paresthesia
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Spontaneousafter shingles
Spontaneous
Weeks-years
Days-months
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Aetiology of pulp & periapical diseaseBacteria
Trauma
Chemical
1-Coronal ingress(caries)
1-Accident
1-Filling material
2-Radicular ingress (PDD)
2-Physiological
2-Erosion
Iatrogenic 1-Cavity preparation (type of bur, speed, duration, nature of burcontact, cutting technique, amount vibration and cooling)
2-Restoration4-Prosthetic treatment6-Orthodontic movement8-Periodontal treatment
3-Surgical trauma5-Radiation7-Electric9-General Anaesthesia
Others
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1-Ageing
3-External resorption
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2-Internal resorption
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Bacteria
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Bacteria
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Chemical-Filling material
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Cavity Preparation
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Restoration
Post operative complications of restorations are, Marginal staining, dentine hyperSensitivity,, corrosion and degradation, secondary caries, pulp inflammation anddeath (Gulabivala-2004).
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Restoration
If the thickness of dentine is <5mmCa(OH)2 sub lining and ZnO/E dressing
should be placed. Most effective materialpreventing microbial leakage
LCC and GIC cause more damage toodontoblasts (Gulabivala-2004).
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•
•
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Responses To Injury
Depend on,
The state of the pulp,
Previous history of irritants and repair,
The nature of the stimulus,
Duration of the irritation,
Any treatment provided.
Mild injury –Odontoblast die,
Acute inflammation in sub odontoblast layer,
Resolution
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•
•
•
•
•
•
Major Acute InjurySome pulp tissue die,
Acute inflammation in adjacent tissue,
Walling off affected area (fibrosis),
Pulpal abscess; pressure, pain,
Repair – depend on tissue capacity to repairand toxicity of necrosis (repair by fibrosis orreparative dentine),
If no repair, spread of necrosis to whole pulp.
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A -
B -
E -
Why Does The Pulp Die?No drainage within the pulp, (fluid can onlymove through rest of pulp),
Limited access for repair (from apicaldirection only),
C - Pulp is surrounded in three dimensions(by hard tissue),
D - Stimulus is concentrated in the pulp(diffusion through tubules from large areaand concentrated on small tissue),
Limitations of dental materials available fortreatment.
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a)
c))
d)
e)
f)
g)
Classification Of Pulp & Periapical Disease
Clinical normal pulp,
b) Reversible pulpitis 1-Acute 2-Chronic
Irreversible pulpitis 1-Acute 2-Chronic 3-Necrobiosis
Pulp necrosis 1-With & 2-Without infection
Degenerative changes 1-Atrophy2-Hyperplasia (pulp polyp)3-Calcification (partial, total)4-Internal resorption.
Previous RCT 1-Satisfactory (with & without infection)2-Unsatisfactory (with &without infection)
Perio-endo lesion 1-Endodontic origin2-Periodontc origin3-Combine P-E (do¬ communicate)
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•
•
•
•
•
Reversible Pulpitis
Short duration pain
After stimulation remove pain relieve
Tooth no tender to percussion
Difficult to localized the pain
Exaggerated respond to vitality test
Periapical area is normal in x-rays
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•••••••
Recent Restoration
High filling or pointsMicro leakageMicro exposureThermal or mechanical injury to pulpInadequate lining under metalic restorationChemical irritation from lining or filling materialGalvanic current
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Irreversible Pulpitis
• Early stages spontaneous pain last fewsecond to hours, radiate and difficultlocate the tooth
• Latter stage hot thing pain, cold relievethe pain patent able to locate the toothand tender to percussion
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Dynamics of Pulpal Responses
Reversible IrreversibleBacteria Low-grade
inflammation UntreatedResistance Chronic
pulpitisVirulence
TreatedAcute
Resolutionmild
pulpitis
Short-terminsult
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Major
Acuteinflammation
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Partialnecrosis
Totalnecrosis
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Indicators Of Pulpitis
Indicator
Sensitivity to thermal stimulation
Respond to thermal stimulation
Irreversiblepulpitis
Yes
Reversiblepulpitis
Yes
a) Lingering
b) Short
Previous history of pain
Intensity of pain a) Severe
b) Mild
Nature of pain – Spontaneous
Tenderness to percussion
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Yes
No
Yes
Yes
No
Yes
Not always
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No
Yes
No
No
Yes
No
Rarely
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Peri-apical Defence Mechanism
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a)b)
a)
c)
Classification Of Periapical Periodontal Disease
Clinical normal periodontal tissue,Apical periodontitis1-Acute2-Chronic - Granuloma
Radicular cyst - Apical true cyst- Apical pocket cys
3-Condensing osteitisPeriapical abscess1- Acute 2-Chronic
b) Facial cellulitisExternal root resorption1- Surface3- Replacement5- Pressure7- Physiologic
2- Inflammatory4- Invasive6- Orthodontic
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Dynamics Of Periapical Inflammation
Draining
Sinus
Bacterial Resistance ChronicInsult apical Cyst
periodontitisVirulence
Systemic
Short-term
insult
Acute apical
periodontitis
illness
Facial
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2.
6.
General Order Of Treatment
1.
3.4.5.
Pain reliefRemove infectionCaries controlPeriodonticsEndodonticsOrthodontics / Surgery
7. Prosthodontics
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Aims Of Endodontic Treatment• Biologic aims
a) To remove all the debris support to bacterialgrowth
b) To destroy all micro-organisms from the rootcanal
• Mechanical aimsc) Prepare root canal space for three
dimensional fillingd) To obturate prepared canal in order to
completely seal from both apical (at thecemento-enamel junction) and coronal seal
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• Root treated with a poor obturation butgood coronal restoration had prognosisthan good obturation and poor coronalrestoration (Ray and Trope-1995).
• Whatever the obturation system used ifthe canal system has not been adequatelycleaned healing may not occur(Carrotte-2004)
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