1. Diseases of the Pulp Asalaam Alekum Dr. Gaurav Garg, Lecturer
1/04/2014
Asalaam Alekum
Diseases of the Pulp
Dr. Gaurav Garg, Lecturer
College of Dentistry, Al Zulfi
Majmaah University

2. Contents: Dental Pulp Pathophysiology of pulpal diseases

3. Pulp is the formative organ of the tooth.
DENTAL PULP
Pulp is the formative organ of the tooth.
It occupies the centre of each tooth.
Consists of soft connective tissue.

4. Dental papilla differentiates to form pulp.
Its development starts at about the 6th wk of intrauterine life during the initiation of tooth development.
Dental papilla differentiates to form pulp.

5. Pulp organ consist of two parts :-
Coronal pulp - located centrally in the tooth
Radicular pulp- located in root.
It extends from cervical region of crown to the apex and is continuous with periapical C.T through apical foramen and accessory canals.

6. Structure of pulp Consists of :- Fibroblasts
Undifferentiated mesenchymal cells
Odontoblasts
Defense cells
Intercellular substance
Blood vessels
Lymph vessels
Nerves

7. Central region of pulp contains large nerve trunks and blood vessels.
Peripherally ,the pulp is circumscribed by the specialized odontogenic region composed of
Odontoblasts
Cell free zone (Weil’s zone)
Cell rich zone

8. Functions of Pulp
Inductive
Formative
Nutritive
Protective
Defensive

9. Pain fibers in pulp A-delta fibers C fibers Myelinated Unmyelinated
In odontoblastic & throughout the
subodon. zone pulp tissue
(peripherally) (centrally)
Fast (2-30)m/sec Slow(0.4-2)m/sec
Carry initial sharp continuous or
momentary pain throbbing pain

10. A-delta fibers C-fibers
Can be stimulated associated with
without injuring the tissue injury and
tissue inflammation.
Low excitability High
threshold
Respond to electric Do not
vitality tests

11. A-delta fibers C-fibers
Response to cold Negative
sensitivity tests is
positive.
Immediate & first Delayed and
response to heat Prolonged.

12. Pulpal Pathophysiology
Irritation to clinical crown (tooth preparation, caries)
Release of inflammatory mediators ( 5-HT, Histamine, PG’s)
Release of neuropeptides
Localized pulpal inflammation
(Hyper-excitation, vasodilatation, vascular leakage)
Increased local tissue pressure

13. Total Pulpitis Increased local tissue pressure
Venous collapse Stasis/decrease blood flow ischemia
Release of inflammatory agents
Local necrosis
Vascular disturbances
Increased tissue pressure
Necrosis of tissue
Total Pulpitis
Franklin S Weine; endoodontic therapy,5th edition

14. Diseases of the pulp Pulpitis (Inflammation) Reversible Pulpitis
-Acute (symptomatic)
-Chronic (Asymptomatic)
B. Irreversible Pulpitis
-Acute
a. Abnormally responsive to cold
b. Abnormally responsive to heat
-Chronic
a. Asymptomatic with pulp exposure
b. Hyperplastic pulpitis
c. Internal resorption

15. 2. Pulp degeneration 3. Necrosis A. Calcific (radiographic diagnosis)
B. Others (histological diagnosis)
3. Necrosis

16. Etiology of Pulpal inflammation
1 .Physical
A. Mechanical
a. Trauma
b. Pathological wear
C. Cracked tooth syndrome
d .Barometric changes (Barodontalgia)
B. Thermal
a. Heat from cavity preparation
b. Exothermic heat from setting of cements
c. Conduction of heat and cold through deep restorations
d. Frictional heat produced during polishing
C. Electrical – Galvanic current

17. 2. Chemical
- Acids from cements
- Erosion
3. Bacterial
-toxins associated with caries
-direct invasion in pulp
-by blood borne microorganisms (anachoresis)

18. Reversible pulpitis
Definition:-it is a mild to moderate inflammatory condition of pulp caused by noxious stimuli in which the pulp is capable of returning to uninflammed state following removal of the stimuli.

19. Histopathology Slight disruption of odontoblast layer
Dilation of blood vessels
Hyperemia
Extravasation of odema fluid
Presence of acute and Chronic inflammatory cells

20. Clinical features Sharp/ shooting pain
-which is often brought about by cold rather than hot foods.
-does not occur spontaneously.
subsides as soon as stimulus is removed.
Pain is often localized.
Tooth reacts to vitality tester at lower level than normal ,indicating increased sensitivity.

21. Irreversible pulpitis
                                            
Definition:-It is persistent inflammatory condition of pulp, caused by noxious stimuli.

22. Histopathology Series of events Inflammation congestion necrosis
PMNs chemotaxis
phagocytosis
pus formation
                              

23. Symptoms
Sudden paroxysm of Pain which may be caused by temperature changes, packing food into the cavity etc.
Pain often continue even when the cause has been removed.
May occur spontaneously.
May intermittent or severe depending upon the degree of pulpal involvement.
Patient may also complain that change of position or bending over and lying down exacerbates the pain.

24. Pain may refer to adjacent teeth, temple region or to the ear.
Pain can be most intense when no outlet is present such as covering of decay with filling or because of food packed into the cavity.
In such cases patients are often kept awake at night by the pain which continues to be intolerable despite all analgesia.

25. Pain is increased by the heat.
It gets decreased after the exposure and drainage.

26. Radiographic changes
An interproximal cavity that is not clinically seen or can suggest involvement of pulp horn.
May show caries under the filling, deep cavity or filling threatening the integrity of pulp.

27. Clinical examination
Inspection generally discloses deep cavity or decay under the filling.
Pulp may already be exposed.
Exposed pulp may be covered by a greyish, scum like layer which is composed of food debris, degenerated PMNs, microorganisms and blood cells.
On probing deep into the pulp , pain and hemorrhage may be present.
Drop of pus may be expressed on exposing the pulp if it is already not exposed.

28. Differential diagnosis
From reversible pulpitis
Pain
-onset
-type
-duration
More response to cold than hot
Vitality testing

29. Chronic Hyperplastic Pulpitis
synonym:-pulp polyp
Definition:-it is productive pulpal inflammation due to extensive carious exposure of young pulp.
Characterized by development of granulation tissue ,covered at times with epithelium and resulting from long standing, low grade irritation.

30. Etiology Slow progressive carious exposure of the pulp is the cause.
For the development of Hyperplastic Pulpitis, a large open cavity, a young pulp and a chronic low grade stimulus are necessary.
Mechanical irritation from chewing and bacterial infection often provide the stimulus.

31. Histopathology Surface of polyp is covered by epithelium.
                              
Histopathology
Surface of polyp is covered by epithelium.
Epi. is usually stratified squamous and is derived from gingiva or freshly desquamated epi. cells of mucosa or tongue.
Tissue in pulp chamber is transformed into granulation tissue which is young vascular C.T containing PMNs, lymphocytes and plasma cells.
Nerve fibers may be found in epithelial layer.

32. Symptoms
Usually symptom less except during mastication when pressure of food bolus may cause discomfort.

33. Clinical features
Usually seen only in teeth of children and young adults.
Characteristic appearance:- a fleshy polypoid ,reddish pulpal mass fills most of the pulp chamber or cavity or even extends beyond the confines of the tooth.
At times mass may be large enough to interfere with closure of teeth.
Less sensitive than normal pulp.

34. Cutting of this tissue produces no pain but pressure transferred to the apical end of pulp may produce pain.
Tissue bleeds easily because of rich network of blood capillaries.
Tooth may respond feebly or not at all to the thermal test.

35. Radiographic features
Shows large ,open cavity with direct access to the pulp chamber.

36. Differential diagnosis
Appearance is usually characteristic and is easily recognized but must be distinguished from proliferating gingival tissue.
To differentiate it ,one should raise and trace the stalk of the tissue back to its origin, the pulp chamber.

37. Treatment
RCT/Pulpectomy

38. Internal resorption
Definition:-it is an idiopathic slow or fast progressive resorptive process occurring in the dentin of pulp chamber or root canals of tooth.
Cause:-is unknown but usually such patients have history of trauma.

39. Synonyms:- Odontoclastoma Pink tooth of mummery
Chronic proliferating hyperplasia

40. Etiology of internal resorption
Exact cause is unknown.
Possible contributing factors are:-
-trauma
-caries
-ortho treatment
-infection/pulpitis
-extreme heat

41. Clinical features Usually asymptomatic
First evidence may be the pink hued area on the crown of the tooth so called pink tooth which represent the hyperplastic vascular tissue.

43. Histological features
Microscopic examination shows variable degree of resorption of inner or pulpal surface of dentin and proliferation of pulpal tissue filling the defect.

44. Resorption is of irregular lacunar variety showing occasional osteoclasts or odontoclasts. Hence called “odontoclastoma ”.
Irregular lacunae like areas are completely filled with irregular dentin or osteodentin.
These exhibit alternating periods of resorption and repair.

45. In coronal resorption ,enamel may also get resorbed.
In root resorption ,perforation of dentin and cementum may occur which if left untreated results in mobility of segment
When the root surface is perforated it is impossible to determine whether it is external or internal.

46. Radiographic feature

47. Treatment Extirpation of pulp stops the resorptive process.
In case of root perforation, Calcium hydroxide paste is placed in canal until the defect is repaired by calcific barrier. the canal is finally obturated.
Repair by MTA

48. Pulp degeneration Usually present in teeth of older people. Types:
Calcific degenerations
Atrophic degenerations
Fibrosis

49. Calcifications
In calcific degeneration part of pulp is replaced by calcific material called Pulp stones or Denticles
Denticles are nodular calcified masses appearing in either or in both the pulp chamber and radicular pulp.
Seen in functional as well as unerupted embedded teeth.
Pulp stones have been noted in patients with systemic or genetic diseases such as dentine dysplasia, dentinogenesis imperfecta and in certain syndromes such as Van der Woude syndrome
Exact cause is unknown

50. Hyalinization of injured cells
PROPOSED MECHANISM OF FORMATION OF PULP STONES
Localized metabolic dysfunction
trauma
Hyalinization of injured cells
Vascular damage
fibrosis
mineralization (nidus formation)
Growth with time
Pulp stone
shafer:; textbook of oral pathology

51. Classification Pulp stones are classified According to structure:-
True denticles
False denticles
Diffuse calcifications
2. According to location
Free
Attached
Embedded

52. True Denticles Are comparatively rare
Usually located close to apical foramen.
Structure is similar to dentin, in that they exhibit dentinal tubules containing odontoblastic processes.
True stones are formed by inclusion of remnants of the epi. root sheath with in the pulp which in turn induce the cells of the pulp to differentiate into odontoblasts which then forms the denticles.

53. False Denticles
Do not exhibit tubules but appear as concentric layers of calcified tissue.
In centre of these calcified masses there may be remnants of necrotic and calcified cells.
Some may arise from blood vessels (Thrombi).
All denticles begin as small nodule but increase in size by incremental growth on the surface.

54. Diffuse calcifications
Appear as irregular calcific deposits in pulp tissue, usually following collagenous fiber bundles and blood vessels.
Usually persists as fine calcified spicules but may also develop into large masses.
Mostly found in radicular pulp whereas pulp stones are more frequent in coronal pulp.

55. Incidence as well as size of pulp stones/ Calcifications increases with age.
10-30 yrs of age - 66 %
30-50 yrs of age- 80%
over 50 yrs- 90%
No treatment required
Endodontic treatment is difficult in presence of Pulp Stones

57. Necrosis of pulp Definition :-death of pulp Types :-two types
Coagulation necrosis
Liquefaction necrosis
Causes:-can be caused by any noxious stimuli which is injurious to the pulp such as bacteria, trauma and chemical irritation.

58. In coagulation Necrosis, the soluble portion of tissue is precipitated or converted into a solid material.
Liquefaction necrosis results when Proteolytic enzymes convert the tissue into soft mass or liquid.
Can be partial or total depending upon the involvement of part of pulp.

59. Clinical features Discoloration of tooth –indicates dead pulp
May be asymptomatic.
Tooth with partial necrosis can respond to thermal changes but in case of total necrosis no sensitivity to thermal or vitality testing is there.

60. Radiographic changes Generally shows large cavity or filling.
Periapical tissue may be normal or thickening of PDL can be there.
Some teeth have neither filling nor cavity but pulp may have died because of trauma.
                              

61. Thorough clinical examination Histopathology :-
Diagnosis :-
Proper history
Vitality testing
Thorough clinical examination
Histopathology :-
pulp cavity contains necrotic pulp tissue, cellular debris and microorganisms.
Treatment
Preparation and obturation of root canal.

62. 1. Asymptomatic pulp exposure Others (Atrophic &Fibrous)
Pulpal Diseases
Pulpitis
Reversible
Acute/Chronic
Irreversible
Acute
Chronic:
1. Asymptomatic pulp exposure
2. Hyperplastic
3. Internal resorption
Pulp Degeneration
Calcific
Others (Atrophic &Fibrous)
Necrosis

63. References Pathways of pulp; Stephen Cohen
Endodontics; Franklin S. Weine
Textbook of Endodontics; Ingle & Bakland

64. THANK YOU!