1. Pulp diseasesLP DISEASES
Most common cause of dental pain

2. Significance of pulp anatomy
There are special anatomical features makes the response of the pulpal inflammation have a special way:
Significance of pulp anatomy

3. 1. The pulp lies in rigid chamber, to decrease the accommodation ion of the inflammatory fluid exudates, Rapid degeneration and necrosis.
2. Have constricted narrow apical formen, limits the blood supply.
3. No collateral circulation, low resistance of the pulp.
4. Decrease below 20C and above 45C pulp hyperaemia

4. Aetiology of pulp diseases
Living irritants (M.O) Non living irritants
Physical :Mechanical, thermal, electrical, aeronautical and irradiation
Chemical: Acids , alkalies and poisons
Enter pulp through:
An open cavity
Via the p.lig.
Adjacent teeth Haematogenous

5. Through an open cavity Fracture and pulp exposure
Caries which exposes the pulp
Pulp exposure during operative work

6. Via the p.lig.
Bacteria present in deep pockets are close to the periapical area
and enter the pulp from the apical foramen

7. Spread from adjacent teeth
Due to the intercommunication of blood and lymph systems Also, pressure of the periapical infection of one tooth pushes bacteria to the adjacent tooth

8. Haematogenous infection
In Tonsilitis Meningitis influenza and diphteria
bacteria circulating in the blood stream localizes
in irritated pulp
and periapical areas and this is called
ANACHORESIS
PHENOMENON

9. Non-living irritants

10. Physical A-Mechanical: Pulp exposure Grinding of tooth
1-Accidental Fall or blow to the face
2-Odontoiatrogenic: dentist induced pulpitis examples:
Pulp exposure
Grinding of tooth
Rapid separation of teeth
High speed instruments
Traumatic occlusion

11. B-Thermal irritation (Odontoiatrogenic)
Heat by bur or stone
Large metallic fillings without lining
Prolonged cooling of teeth with ethyl alcohol
Rapid polishing
Prolonged thermal pulp testers
Using lazer for tooth ablation

12. C-Electric irritation
Gold and amalgam come in contact with each other
electric current pulp necrosis or pulp will attract bacteria which irritate the pulp
Saliva

13. D-Aeronautical irritation
In flying personnels

14. In submarines (low pr. chambers)

15. Which teeth will be affected?
Carious or recently filled teeth contain
nitrogen bubbles or fat emboli which expand
under low pressure
and press on nerves)

16. What to do? Avoid heat during cavity prep. Avoid chemical irritation
Insert Zn Oxide and oil of clove after preparation to prevent pain
It is better to do a temporary filling to give chance for pulp to heal then fill it permenantly

17. Odontoiatrogenic Idiopathic
Chemical irritation
Odontoiatrogenic Idiopathic
Alcohol or chloroform *Bacteria in caries
to dry the cavity * Gingival recession
which exposes
Improper mixing of cementum to
Zn Ph cement or silicate irritants in food
cement

18. The main cause of pulp diseases is Caries

19. Diseases of the pulp Acute Closed Chronic Open
Focal reversible pulpitis
B-Communication with the oral cavity
A-Type of inflammation
Open
Closed
Chronic

20. Focal reversible pulpitis (or Pulp Hyperaemia)
Focal : localized under the carious lesion
Reversible if irritant is removed before pulp is severely damaged
Early form of pulpitis

21. Clinical picture
Deep caries or large metallic restorations without isolation or restorations with defective margins
Transient pain on cold only

22. Histologically
1-Intact odontoblastic layer 2-Vasodilatation (V.D) 3-Inflamatory fluid exudate (I.F.E) leaks out from b.v leading to hemoconcentration and increase in blood viscosity

23. 4-Then thrombosis will occur . It is due to:
1-Inc. in bld. viscosity
and slow down of blood
2-Inflamatory fluid exudate (I.F.E) outside presses on the b.v

25. Acute pulpitis
Follows hyperaemia if virulence of bacteria increases and resistance of the body is decreased
May be an acute exacerbation of a chronic condition
It begins in the part of the pulp below the carious process PARTIAL ACUTE PULPITIS

26. Aetiology
Pulp is capped following traumatic exposure Remnants of caries Haematogenous i.e Trauma caries anachoresis odontoiatrrogenic

27. Clinically Hotness No Swelling
Spontaneous , severe, continuous and throbbing pain
Pain increases if the patient is lying down and with change in temperature
Electric pulp tester reacts at a lower level

28. Pain is due to:
Oedema is compressed in a rigid chamber
Histamine and Serotonin act upon the nerve endings

29. Mic. Appearance V.D and I.F.E goes out of blood vessel
Swelling of odontoblastic nuclei due to osmotic imbalance
Disintegration of
nuclei (so in acute pulpitis
the odontoblastic layer is interrupted)

30. Pavementation of PNL Diapedesis Migration
These changes are first localized and the remainder of the pulp is normal then it becomes generalized

33. Hypremia Acute Pulpitis
Pain transient spontaneous Continuous &throbbing
On cold on cold & hot
V.D + I.F.E V.D + I.F.E + PNL
Intact od. Layer interupted
Reversible Irreversible

34. Pulp Abscess Abscess occurs first
at the pulp horn (area of minimum drainage)
If drainage is inadequate and the enterance to the pulp is minute
(small carious exposure)

35. Mechanism of abscess PNL X M.O
PNL die and are called pus cells and release
proteolytic enzymes cause
liquifaction to the necrotic pulp tissue, then pus is formed

36. Liquified necrotic tissue
Very important
Pus is formed from
Dead and living PNL
Liquified necrotic tissue
Dead and living M.O

37. Abscess is formed of pus surrounded by inflammatory cells

38. Collagen fibers surround the abscess
Sometimes
Collagen fibers surround the abscess
Abscess gets calcified and isolate the necrotic tissue
The remainder of the pulp shows V.D and CH. Inf. cells

39. Later on multiple abscesses are formed followed by complete liquification of the pulp tissue TOTAL SUPPURATIVE PULPITIS

40. CHRONIC PULPITIS

41. Classification
Closed Open
Ulcerative Hyperplastic

42. Chronic pulpitis Aetiology is as acute pulpitis BUT
The irritant is of low virulence
The body resistance is high

43. Characteristics of chronic pulpitis:
Destructive
changes Repair
(granulation tissue or fibrosis )

44. Closed pulpitis

45. Mechanism and Microscopic picture of chronic closed pulpitis
In chronic caries, toxins are not strong enough to destroy the odontoblasts, but irritate them
Odontoblasts lay down tertiary or reparative dentine
D.tubules are sealed by sclerotic dentine
This reduces the access of irritants to the pulp

46. Mild Caries

47. Microscopic appearence
B.V are dilated
Lymphocytes &plasma cells invade
the pulp
Fibrosis &collagen fiber bundles
are prominent in order
to wall off the inflammatory process

48. Clinical pict. Intermittent dull aching pain
Less sensitive to hot and cold than acute pulpitis due to degeneration of nerves
Tooth responds at a higher level to electric pulp testers than normal
TTT: As acute pulpitis endo. ttt or extraction

49. Chronic closed pulpitis

50. Chronic Open Pulpitis (Ulcerative)
chronic inflammation
The area of carious exposure is replaced with G.T infiltrated with inflammatory cells
Symptoms range from none to minimum bec. Edema escapes from the area of exposure
Pain worsens by thermal changes

51. Chronic Open hyperplastic pulpitis ( PULP POLYP)
Criteria:
1-Deciduous molars & first perm. molars (children & young adults)
2-Wide apical foramen
(excellent bld. supply)
3-Large carious exposure (excellent drainage)

52. So
Pulp is replaced by Granulation Tissue which becomes hyperplastic due to the Good blood supply so it extends from the pulp and forms a polyp and gets covered by epithelium

53. Gradually the surface gets epithelialised as a result of implantation of epithelial cells on its surface
Source of epith:
Desquamated epith. cells in saliva
Rubbing between the polyp & oral mucosa
Epithelium Protects the nodule of pulp from infection

54. Clinical pict.
Globular mass of tissue protruding from the pulp chamber & filling the entire cavity
Pink in colour
When young , it bleeds easily
With age, it becomes
pedunculated and lobulated

55. On palpation with a probe, it is slightly sensitive because the hyperplastic tissue contains few nerves.

58. Alveolar abscesses are not associated with this condition because here the vitality of the tooth is maintained.

59. Microscopic features
G.T covered by Keratinized stratified squamous epith.
Components of G.T:
Newly formed capillaries
Newly formed collagen fibrils
Proliferating fibroblasts

60. Pulp polyp is a misnomer?
Because polyp means a mucous membrane projection and pupl is not a mucous membrane

61. Thank you