dental

1. Pulp Diseases
BY
Dr: Hanan Eid Gamal

2. - The most common pulp disease is
pulp inflammation (pulpitis).
Pulpitis, if untreated, is followed
by death of the pulp and spread of
infection through the apical
foramina into the periapical
tissues.

3. Criteria of pulp
inflammation

5. • Absence of collateral circulation
This accelerates degeneration of pulp tissue if
subjected to irritation
• Constricted apical foramen
This limits the blood supply to the pulp and
venous return from the pulp
• Pulp is enclosed in a rigid chamber of dentine
This will not allow pulp tissue to swell if
inflammed and edema fluid will press on
blood vessels . So pulp inflammation usually
proceed into necrosis
• Pulp is not precisely presented in the sensory
cortex
This will leads to unlocalized type of pain on
the affected side by the patient.
Pain may be referred to distant sites as the
ear.

6. Etiology of Pulpitis

7. 1. Bacterial (Living Irritants)
• Bacteria can gain access into the pulp
through :
 Dental caries: the most common cause.
Tooth fracture:
• Fracture of crown or cusp
• Cracked tooth syndrome: minute invisible
cracks but allow bacteria to enter the pulp
Can be identified by applying pressure to
occlusal surface with burnisher to open up the
cracks, pulp pain then results.

9. Blood born infection (anachoresis):
It is settlement of bacteria circulating in
the blood(as in tonsillitis), in a
hyperaemic pulp facilitated by stasis
caused by hyperaemia .
-Through deep periodontal pocket via an
accessory root canal.
Iatrogenic comes from a Greek word that
means complication caused by a
physician.
-Odontoiatrogenic(complication caused
by a dentist) damage, in case of pulp
exposure during cavity preparation.

10. 2. Chemical causes
• Odontoiatrogenic damage
• Use of Irritant substances as alcohol or
chlorofom for drying cavities.
• Improper mixing of cements as zinc
phosphate cement.
• Erosion
It is a chemical destruction of tooth structure
by acids that causes variously shaped
depressions, generally at the cemento-enamel
junctions of teeth.

12. 3. Physical causes
Odontoiatrogenic damage
• Thermal irritants
Large metallic restoration without base
Heat generation during cavity preparation or
tooth reduction for crown construction
without cooling water spray.
• Electric stimulation:
 due to presence of two dissimilar metallic
restorations (Galvanism) without using
varnish.

14. 4. Mechanical causes
Trauma leading to crushing blood supply of
tooth.
Abrasion: is the loss of tooth structure by
mechanical forces (friction) from a foreign
element as toothbrushes and toothpicks.
Brushing too hard is a common cause of
abrasion.

15. 5. Aerodontalgia
Is a condition in which a toothache is
present in persons flying at high altitudes
and are recently subjected to recent filling or
carious teeth. As gas spaces may exist in
infected teeth or may enter around the edge
of the filling , gas expansion occur resulting
in severe pain.
It is recommended to insert pulp protector in
the cavity after preparation to prevent pain.

16. Classification of
Pulpitis

17. A. According to type of
inflammation
Focal reversible pulpitis
Acute pulpitis
Chronic pulpitis
Chronic hyperplastic pulpitis
Irreversible

18. B. According to extent of pulp
inflammation
 Partial pulpitis
The pulpitis is confined to part of the pulp
 Total pulpitis
The entire pulp is involved

19. C. According to communication
between the pulp and the oral cavity
 Closed pulpitis
No direct communication between the pulp
and the oral cavity
 Open pulpitis
The pulp is communicated (exposed) with the
oral cavity

20. Focal Reversible Pulpitis
( Pulp Hyperemia)
• Definition
 Is the active dilatation of the pulp blood
vessels representing the earlier stage of
pulpitis
 It is reversible condition provided that the
irritant is removed before the pulp is
severely damaged

21. Focal Reversible Pulpitis
( Pulp Hyperemia)
• Etiology
 Any cause of the previous causes
• Clinically
 The tooth is sensitive to thermal changes
particularly cold
 Pain is sharp shooting and disappears rapidly on
removal of the stimulus
 Pain can not be localized
 Tooth is more sensitive to electric pulp tester

22. Focal Reversible Pulpitis
( Pulp Hyperemia)
• Histopathology
 Dilated blood vessels
 Presence of inflammatory fluid exudate (edema)
 No extravasation of RBCs
 Intact odontoblastic layer.
• Treatment
 Removal of the cause
• Prognosis
 Very good, the condition is reversible if the insult
is removed

24. Acute Pulpitis
• Definition
 An acute inflammation of the pulp
• Etiology
 Any of the previous causes
 The condition may follow pulp hyperemia
or representing acute exacerbation of
chronic pulpitis

25. Acute Pulpitis
• Clinically
In early irreversible pulpitis:
• Sharp, severe pain upon thermal stimulation
especially cold although heat, sweet or sour
foods also can produce pain.
• The pain continues after the stimulus is
removed.
• The pain may be spontaneous and may be
exacerbated when the patient lies down.

26. 
In the later stages of irreversible pulpitis:
•The pain increases in intensity and is
experienced as a throbbing pain that can keep
patients awake at night.
•The patient is unable to identify the offending
tooth within a quadrant.
•At this point, heat increases the pain; however,
cold may produce relief.
Pain is due to :
- Pressure on irritated nerve endings by
inflammatory exudate
- Release of pain mediators as bradykinine and
serotonine from the damaged tissues
- Tooth is more sensitive to electric pulp tester
- Tooth is not sensitive to percussion

27. Acute Pulpitis
• Histologically
 Destruction of odontoblastic layer
 Dilatation of blood vessels
 Inflammatory edema
 Acute inflammatory cellular exudate (PNLs)
 Focal areas of liquifactive tissue necrosis forming focus of
pus (pulp abscess)
 Pus is consists of necrotic pulp tissue, dead and alive PNLs
and dead and alive bacteria
 Multiple foci of pus are formed which fuse together and total
liquifaction of pulp occurs ( suppurative pulpitis )
• Treatment
 Extraction or endodontic treatment

29. Pulp Abscess

30. Total Pulpitis
1. Dilated BVs 2.Dense PNLs infiltrate
3. Loss of odontoblastic layer

31. Suppurative Pulpitis
1
2
3
1. Pus Cells in center
2. Pyogenic membrane
3. Inflammatory cells

32. Chronic Pulpitis
• Definition
 is a chronic inflammation of the pulp
 The inflammation is persistent with
continuous attempts of repair
• Etiology
 It may follow acute pulpitis or arise de
novo due to low virulent bacteria

33. Chronic Pulpitis
• Clinically
 Pain is dull aching, and is intermittent
 Reduced reaction to thermal changes and electric pulp tester
 Tooth is not sensitive to percussion
• Histologically
 The pulp is gradually replaced by granulation tissue due to
increased activity of fibroblasts
 Granulation tissue is formed of :
 Proliferating fibroblasts
 Proliferating blood capillaries
 Delicate collagen fibrils
 Chronic inflammatory cells

34. Chronic Pulpitis
• As there is low-grade irritation so,
considerable amounts of reactionary dentin
continue to form . The dentin bridges is poorly
formed, and inflammation progresses beneath
it.
• Treatment
 Endodontic treatment or extraction
• Fate
 Acute exacerbation
 Pulp necrosis

36. Chronic Hyperplastic Pulpitis
• Definition
 It is a hyperplasia of chronically inflammed pulp
• Etiology
4 pre-requests should be fulfilled:
 Good sheltered area of the newly formed tissue
 Wide apical foramen for good blood supply
 Wide pulp exposure to allow protrusion of the new
tissue
 Young aged patient for good proliferative power

37. Chronic Hyperplastic Pulpitis
• Clinically
 Usually affects children and young adults
 Common teeth are deciduous molars and first permanent
molars
 A swollen tissue is extruded from the pulp and is present in a
wide carious cavity
 The lesion is insensitive to manipulation as it contains few
nerve endings
• Differential diagnosis
It should be differentiated from gingival polyp which is:
 Attached to gingiva
 More sensitive to manipulation

38. Chronic Hyperplastic Pulpitis

39. Chronic Hyperplastic Pulpitis
• Histologically
 Granulation tissue with chronic
inflammatory cells
 Epithelialization of this tissue occurs by
time. The source of epithelium is :
1. Desquamated epithelial cells found in saliva
2. Implantation of epithelial cells during rubbing
of the cheek with the mass of granulation
tissue
• Treatment
 Extraction or endodontic treatment

41. Chronic Hyperplastic Pulpitis

42. Thank you