pulp and periapical diseases from a deeper scope.

2. Pulp & periapical
Diagnoses
Presented by:
Dental Intern/
Asmaa A.Rahman Elshawarby
Future University IN Egypt
Ahmed Maher Educational Hospital

3. Etiology

4. Etiology
Microbi
al
factors
•Ingress of Bacteria through( main Apical foramen -lateral canals-Dentinal
tubules)
•Septicemia( bacteria circulating through the Blood stream)
Physical
factors
•Acute(Vigorous polishing-)
•Chronic( Bruxism- abrasion ( abnormal brushing) – attrition(food)
Thermal
factors
•tooth preparation with (No-insufficient) coolant
•-Restoration with insuffient insulation.
Chemic
al
factors
•Bleaching agents with high concentration (hydrogen peroxide).
•Zinc phosphate cement.
Trauma
tic
factors
•Tooth responds with)Necrosis-calcification-no respond)

5. Can Pulp heal by its self ?
According to severity of the situation:
The low compliance and the enclosed environment of
the Pulp & lack of collateral circulation make repair
impossible if severely damaged .

6. Classification of pulp
diseases
Ability to heal
Reversible
irreversible
Extension
•Focal(partial)
•subtotal
•Total(Generalized)
Communication with
the oral environment
•Open(pulpitisAperta)
•Closed (pulpitis Clausa)
Severity
•acute
•Chronic
•Sub acute

7. PULP diseases
1)Inflammatory diseases of the pulp:
• Hyperemia
• Acute pulpitis
• Sub acute
• Chronic pulpitis
2)Additional pulp diseases:
• Necrosis.
• Retrogressive pulp changes
(calcification)
• Internal Resorption

8. Hyperemia
(focal pulpitis)
• Mild, transient , localized inflammatory response.
• Pathogenesis:
1. Dilation of blood vessels
2. Increase intravascular fluid (subliminal increase in intra pulpal pressure)
3. edema fluid collection .
4. Extravasation of RBCs and WBCs.
• Pain:
I. Cold
II. Sweets
III. Doesn’t linger
• Pulp tester : Responds at lower level of current.
 Visual examination:
 Deep carious lesion.
 Deep restoration without a base.
 Incipient caries
• Treat:
• Remove the cause.
!

9. Acute irreversible
pulpitis” Generalized””
• Definition:
A clinically detectable severe, painful & irreversible acute
inflammatory response of the pulpal C.T to an irritant, which
exudates are hyperactive& play a dominant role.
• Pathogenesis:
• Vasoldilatation
• Increased capillary permeability
• Leukocytic infiltration
• Increased fluid exudate
• Congestion of blood vessels leads to local necrosis.
• Increased intrapulpal pressure as pus formed.
• Extended inflammation leads to pulpal necrosis due to decreased blood flow.

10. Acute irreversible
Pulpitis follow”
Pain
Early stage:
cold :elicits pain increase due to hydrodynamic theory(movement of
fluids in dentinal tubule result in deformation of A fibers .
Hot :pain increase, due to increased vasodilatation & increased
pressure on c fibers.
Late stage:
Cold: relieves pain due to vasoconstriction of blood vessels leads to
decreased intra pulpal pressure.
Hot :pain increased due to increased, vasodilatation
&increased pressure(Hot Tooth).

11. Acute irreversible
Pulpitis “follow”
Examination & Diagnosis:
1)History &visual examination:
a-History of carious cavity.
b-Recent deep filling with no base.
c-Trauma.
d-Crown reduction without cooling
Sign & Symptoms:
*Severe or sharp throbbing pain characterized by:
a-Spontaneous.
b-Caused by irritant but linger.
c-Pain increased at night or when patient lies down.
d-Diffuse or referred pain
percussion: -ve
Sensitivity to pulp testing: Respond at very low levels of current
Vitality: vital
Radiograph: Normal
Treatment: RCT or extraction

12. Sub acute irreversible
Pulpitis
• Mild to moderate pain
• Needs RCT

13. Chronic (Open) pulpitis
hyperplastic Pulp polypulcerative

14. Chronic ulcerative
Pulpitis
• Definitin :An inflammatory response of pulpal C.T. to an irritant in which proliferative
forces are hyperactive.
• Clinicalpicture
• Non prominent, mild , dull ache
• Reaction to thermal changes is reduced due to degeneration of nerves
• Responds at high current rate :pulp sensitivity
• -ve response on percussion
• Wide carious cavity +pulp Exposure= little pain
• Bleeding from the RC on probing with little pain.
• Painful with food impaction.
• Pathogenesis:
1-Zone of necrosis ( necrotic tissue – exudate )
2-Zone of contamination ( chronic inflammatory cells – exudate)
3-Zone III ( granulation tissue )(young fibroblast , young BVs , young nerve
fibers)

15. Chronic Hyperplastic
pulp polyp))pulpitis
• Characterized by overgrowth of granulomatous tissue( chronic
inflammatory cells+fibrous tissue) into the carious cavity, forming a
polyp.
• Clinical picture:
• Pinkish globule of tissue protruding from the carious cavity.
• Easily bleeds
• Proximal cavity
• Deciduous molars and 1st permanent molar (young children (high
tissue reactivity+ excellent blood supply)
• Misdiagnosis( gingival tissue growing into a carious lesion
• )!!!Probing (pain) +bleeds Easily )

16. Chronic Hyperplastic
pulp polyp))pulpitis
• Diagnosis and examination
• Little pain due to little nerves remaining.
• -ve response on percussion.
• Normal radiograph.
• Pulp sensitivity: delayed response to electric pulp tester and
at higher levels )
• Treatment:
• RCT after removal of the polyp by electric or thermal cautery ,
surgical , curettage or by “ Round bur “.
• Extraction

17. Dead tooth))Necrosis
necrosis
Liquifactive(good blood) )
supply)acute
inflammation( false + ve)
Coagulative ( Gangrenous)
(poor blood
supply)(trauma)
necrosis
+ve Response))Partial
multirooted teeth)
total
Death of pulp tissue as a sequel of:
Acute & chronic inflammation
OR
Immediate arrest of circulation due to traumatic injury.

18. (Gray tooth)
• This discoloration typically develops weeks or months
after the injury and is caused by incorporation of
pigments (hemosiderin) from hemoglobin released
during the breakdown of RBCs into the dentin.
• Asymptomatic
• -ve to sensitivity testing
• -ve response on percussion.
• Normal radiograph.
• TTT: RCT+ internal bleaching

19. Pulp calcification
Definition
Calcium deposits in the pulp chamber or root canal.
Classification:
1-Pulp stone denticles.
• in pulp chamber ( can’t detect orifice )
• According to location
• ( Free or Attached or Embedded
• According to structure :
• True (due to odontoblasts forming dentin)
• False (dead pulp tissue and alkaline media , calcium salt starts to
precipitate Called (dystrophic calcification or calcific metamorphosis) )
2-Diffuse calcification.( inside root canals ( Narrow ).
Etiology
Trauma
Natural phenomenon.

20. Pulp calcification
• Diagnosis
• History : Trauma
• Clinical examination : tooth looks lifeless ( chalky white).
• Asymptomatic unless impingement on the nerves occurs.
• -ve on percussion .
• -ve to sensitivity testing or ( respond at very high current)
• TTT
• RCT using
• C files
• gates Glidden
• Ultrasonic +)
• Retrograde cavity .

22. internal Resorption ))
(Pink spot )
Etiology
It may be due to
- Trauma
-Inflammation
-Idiopathic
Pathogenesis:
Trauma causes:
1)Intra-pulpal hemorrhage.
2)Loss of predentin.
3)Extravasation of blood , which change into granulation tissue.
4)This tissue proliferates lead to stimulation of U.M.C. and
will differentiate into dentinoclasts leads to resorption of interior wall.

23. Internal Resorption .
• Diagnosis
asymptomatic unless perforation of the root occurs and periodontal lesion
results.
• -ve to percussion .
• +ve response to electric pulp tester. Because some vital pulp is still present ,
• False -ve if coronal pulp is necrotic but remaining pulp is still vital.
• Radiograph : wide radiolucency inside root canals.
• TTT:
• immediate RCT before perforation occurs.
• Ultra sonic irrigation ( acoustic streaming )
• Intra canal medication with calcium hydroxide/
• Obturation using thermoplastisized Gutta-percha technique (Obtura )
• Surgical exposure.
• Extraction .

24. Pulpoperiapical pathosis
*It is an inflammatory response of the periapical C.T.,due to
a pulpal irritant.
Etiology:
1-Pulpal inflammation
2-Pulp extirpation
3-Over-instrumentation
4- Improper manipulation
5- Incomplete removal of the pulp tissue

25. classification
Pulpoperiapicalpathosis
Acute (symptomatic)
1-Acute apical periodontitis
2-Acute periapical abscess
3-Recrudescent (phoenix)
4-Subacute periapical
abscess
Chronic
(asymptomatic)
1-Chronic apical
periodontits.
2-Chronic periapical
abscess.
3-Periapical granuloma .
4-Periapical cyst
5-Condensing
osteitis:(pulpoperiapical
osteosclerosis)

26. Acute apical
periodontitis
• Painful inflammation of the periodontium as a result of irritation ,
infection or trauma through dental pulp regardless pulp is vital or
non vital.
• Diagnosis :
• Clinical Examination :
• Tooth is tender on percussion.
• Severe pain on closure of teeth
• Radiograph : may be Slight widening of PDL.
• No swelling or mobility .
• +ve In case of acute pulpitis with periapical periodontitis:
• Signs and symptoms of both is present
• or –ve on electric pulp testing.
• TTT: RCT “ intra canal medicaments (steroids) or Extraction

27. Acute periapical Abscess
Diagnosis:
1-Visual examination & history
-Redness & hotness
-Pain on palpation .
- Swelling of the oral mucosa & skin is noticed later.
- sinus tract formation intraoral/ extra oral .
Sign & symptoms
a) Sever throbbing pain increases, on biting
b)Feeling of fullness or elongation of the tooth
c)Fever , malaise or loss appetite
N.B. The most intense pain occurs, as the pus penetrates the outer plate of bone & begin to raise the
periostium .(severe pain )

28. Acute periapical
abcess”follow”
Percussion : Sever pain (touch tooth with your finger gently)
-Vitality test : -ve (most cases)
-Palpation & mobility: Swelling (fluctuant) &
transient mobility (after root canal therapy no mobility)
-Radiography: Normal or slight widening of PDL
TTT:
Relief pain by drainage
(1-access)
(2-file beyond apical constriction)
(3-incision and drainage by lancet)
(4-trephination to drain pus using round bur )
* RCT : irrigation by warm saline then NaHco3

29. Recrudescent Abscess
(Phoenix abscess)
*It is an acute exacerbation of a chronic lesion.
Etiology:
It ‘s developed as a granulomatous zone which becomes contaminated.
Diagnosis :
Similar to acute periapical absecess (Except a Large well defined radiolucent
area)
Treatment :
root canal therapy , Drain
1-access ,
2-violation of apical constriction ,
3-incision and drainage
4-trephination
irrigation with saline not Naocl (pus + sodium hypochlorite = clumping and
make blockage to canals.

30. Periapical Granuloma
• One of the most common sequalae of pulpitis.
• Formation of Granulation tissue apical in an attempt to localize the periapical
infection .
• Diagnosis:
• Asymptomatic unless acute exacerbation occurs .
• Sometimes pt presenting with mild sensitivity to thermal changes + pain on chewing
hard food.
• +ve on percussion
• -ve to electric/ thermal pulp testing.
• Discovered on routine radiographic examination
• Well defined radiolucency.
• No sinus tract is formed
• TTT:
• RCT
• Extraction.

32. Periapical cyst

33. Periapical cyst
• Pathological cavity lined by Epithelium .
• Contains fluid or gaseous content that’s not created by accumulation of
pus.
• After pulp necrosis.
• RG: Well corticated Radiolucency .
• Periapical cysts are treated by enucleation and curettage, either
through an extraction socket or via a periapical surgical approach when
the tooth is restorable ( RCT) or the lesion is greater than 2 cm in
diameter.
• Asymptomatic unless exacerbation by an acute infection ,it turns into
abscess that should by drained .
• The cyst is removed through a small incision inside the mouth and the
space that is left behind is cleaned out.
• If it is very large, or has caused damage, the surgeon may also remove
some teeth, roots and a section of jawbone.

34. Condensing
osteitis(pulpoperiapical
osteosclerosis
1-It is a productive response of the periapical bone.
2-Characterized by increased density of bone.
3-So increased bone at apex in the expense of bone
marrow space
4-Radiographically it appears radio-opaque.
5-Treatment:
1-remove irritant
2-root canal therapy

35. THANK you for your listening