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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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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&not 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.

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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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