1. Why we need Root Canal Treatment ?

2. Aetiology of the pulp and periapical pathosis
Microbial: dental caries
Mechanical: operative procedure (iatrogenic), trauma
Chemical: pulpal (acid etching, bond), periapical (irrigation)

3. 1- Due to deep Caries

5. 2- Due to Leaked Restoration

6. 3- Due to Trauma

7. 4- Excessive force during ortho. treatment

8. EFFECT OF DENTAL MATERIALS ON PULP
GIC – Well tolerated by pulp
Calcium hydroxide – includes dentin bridge formation.
Zine oxide – eugenol- has an anti-bacterial effect.
Formocresol – Cause chronic inflammation of the pulp.
Dentin bonding agent – can irritate the pulp causing inflammation

9. Physiology of Pulpal Pain Odontogenic pain
myelinated A fibres (A-delta and A-beta fibres)
sensibility of the dental pulp
coronal portion of the pulp and concentrated in the pulp horns
2.Unmyelinated C fibres
2 types of sensory nerve fibres in the
core of the pulp extend into the cell-free zone underneath the odontoblastic layer

12. Dentin tubule fluid movement
Hyper-
osmoticsolutions
Dehydration Heat Cold
Dentinal
tubule
and fluid
Dentin
A-delta
fibers
Odontoblast
movement
Sensory nerves

14. Pain Location Onset Timing (frequency, duration)
Quality (sharp, dull, throbbing
Intensity (0-10)
Relieves / Aggravates
Associated symptoms
Pain

16. Referred Pain referred pain.
The perception of pain in one part of the body that is
distant from the actual source of the pain is known as
referred pain.
Referred Pain

17. Pulpal Status Vital Nonvital Normal Inflamed Necrotic Reversibly
Irreversibly
Inflamed

18. Pulpal Pain Deep, dull, aching pain of a threshold nature
Often difficult to localize
Occurs irrelevant to biomechanical(masticatory) functions

19. Common Characteristics of Pulpal Pain
1. Quality of pain is dull, aching, throbbing and occasionally sharp
2. An identifiable condition that reasonably explains the symptoms
3. Response to local noxious stimulation is proportionate and predictable
4. Pulpal pain tends to get better or worse, but rarely stays the same over time
5. Local anesthesia of the suspected tooth eliminates the pain

20. Site of Pain vs. Source of Pain
The location where the patient feels the pain
Easily located by asking the patient to point out the region of the body that is painful
Source of Pain
That area of the body from which the pain actually originates

21. Site (where it hurts) = Source (where it originates)
Primary Pain
Site (where it hurts) = Source (where it originates)
Eg./ cut finger
Heterotopic Pain
Site ≠ Source
Eg./ cardiac pain

23. Heterotopic Pain
Pain felt in an area other than its true site of origin (associated with deep, somatic pain).
Projected pain: perceived in the anatomic distribution of the same nerve that mediates the primary pain (painful adjacent teeth).
Referred pain: felt in an area innervated by a different nerve from the one that mediates the primary pain (teeth in opposing arch, face, head, neck).
Does not cross the midline.
Convergence of afferent neurons.

24. TERMINOLOGY
Dental pulp – Tissue within each tooth that contains the nerves, blood vessels, and cells that make the tooth a living organ
Pulpitis – A range of conditions from inflammation all the way to pulpal necrosis

25. TERMINOLOGY CON’T
Vitality – response of the pulpal tissue to a stimulus(healthy to nonresponsive)
Reversible/irreversible pulpitis – Reactions of a vital pulp to stimuli
Necrotic – death of the pulp
Periapical Tissue
chronic periodontitis
acute periodontitis

26. WHY PULPAL TESTING?
Pulp testing is done to determine the treatment need of the tooth

27. PAIN
An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.

28. Acute v Chronic

29. Acute Pain Associated with tissue damage or injury. Recent onset.
Limited duration.
Stimulation of peripheral and central nociceptors by algogenic substances (bradykinin, prostoglandin, leukotrienes, histamines, substance P, excitatory AAs).

30. Chronic Pain
Prolonged persistence of pain beyond the healing of tissue.
Frequently experienced in the absence of peripheral stimulation or lesions.
Result from changes in the dorsal horn and brain.

31. TOOTHACHE PAIN
Toothache of odontogentic origin can be visceral (pupal) or musculoskeletal (periapical or periodontal).
When the pulp is exposed to a noxious stimulus, there is a reactive inflammatory response.
The resulting edema is unable to expand because of the surrounding inflexible cementum → ↑ tissue pressure and ↓ blood flow that causes damaging effects to the pulp.

32. Considerations: Healthy pulp (cellular) v Aged pulp (fibrous)
As an increasing amount of pulp tissue is involved, the inflammatory process progresses apically, until it extends out into the periapical tissue → apex becomes sensitive to palpation and percussion.
Periapical inflammation from non-pulpal causes can exhibit similar symptoms:
Hyperocclusion
Bruxism

33. Pulpal Status Vital Nonvital Normal Inflamed Necrotic Reversibly
Irreversibly
Inflamed

34. CLINICAL CLASSIFICATION OF PULPAL AND PERIAPICAL DISEASES
Normal Pulp
Reversible Pulpitis
Irreversible Pulpitis
Necrosis
Pulpal Disease

35. PAIN Location Onset Timing (frequency, duration)
Quality (sharp, dull, throbbing, aching,burning, etc.)
Intensity (0-10)
Relieves / Aggravates
Associated symptoms

38. Reversible Pulpitis
Common causes:
Caries, recent restorative procedures, faulty restorations, trauma, exposed dentinal tubules, periodontal scaling.

39. Condition should return to normal with removal of the cause.
Pulpal recovery will occur if reparative cells in the pulp are adequate.

40. Treatment of Reversible Pulpitis

41. Remove irritant if present (caries; fracture; exposed dentinal tubules).
If no pulp exposure: CaOH, restore, monitor
If pulp exposure:
Carious: initiate RCT
Mechanical: >1 mm: initiate RCT
<1 mm crown planned: initiate RCT
<1 mm: direct cap or RCT
If recent operative or trauma – postpone additional treatment and monitor.

42. Irreversible Pulpitis

43. Pulpal inflamation and degeneration not expected to improve.
A physiologically older pulp has less ability to recover due to decrease in vascularity and reparative cells.
As inflammation spreads apically, cellular organization begins to break down.
Localized pressure slows venous return, resulting in buildup of toxins and lower pH that causes widespread cellular destruction.

44. Treatment of Irreversible Pulpitis
Ideal immediate treatment
(complete removal of pulpal tissue)completely relieve occlusion if have acute periapical peridontitis.

45. Pulpal Disease
Necrotic Pulp

46. Necrotic Pulp
Results from continued degeneration of an acutely inflamed pulp.
Involves a progressed breakdown of cellular organization and no reparative potential.
Commonly have apical radiolucent lesion. (always conduct proper pulp testing to rule out a non-pulpal origin).
With multi-rooted teeth, one root may contain partially vital pulp, whereas other roots may be nonvital (necrotic).

47. Treatment of Necrotic Pulp
Minimum immediate treatment (if not extraction)
Partial instrumentation of canals:
Place Ca(OH)² into all canals
completely relieve occlusion if have acute apical periodontitis.
Ideal immediate treatment
Complete instrumentation of canals:
completely relieve occlusion if have acute apical periodontitis.