Disease of Dental Pulp powerpoint presentation

dental pulp diseases

1. DISDISEASES OF DENTAL PEASES OF DENTAL P ULPULP
DR AMIT KUMAR GARGDR AMIT KUMAR GARG
PROFESSOR & HEADPROFESSOR & HEAD

2. INTRODUCTIONINTRODUCTION
Inflammation of pulp and periapical tissue is one
of the most common diseases encountered in our day
to day practice.
To give proper and effective treatment one has
to diagnose correctly. Arriving at a correct diagnosis
requires knowledge, skill, art and experience;
knowledge of the diseases and their symptoms, skill
to apply proper test procedures, the art to correlate
the facts and experiences to reach proper conclusions.

3. PULPAL PATHOSISPULPAL PATHOSIS
“ The pulp lives for the dentin and the dentin lives
by the grace of the pulp. Few marriages in nature are
marked by a greater affinity.” - Alfred L. Ogilvie

4. According to Grossman
PHYSICAL
a) MECHANICAL
a) Trauma
b) Pathological wear
c) Cracked tooth syndrome
d) Barometric changes
b) THERMAL
a) Heat from cavity preparation
b) Exothermic heat from the setting of cement
c) Conduction of temperature through deep fillings
d) Frictional heat caused by polishing of restoration
ETIOLOGY OF PULPAL DISEASES

5. c) ELECTRICAL
a) Galvanic Current
CHEMICAL
a) Phosphoric acid, acrylic monomer
b) erosion
 BACTERIAL
a) Toxins associated with caries
b) Direct invasion of pulp from caries or trauma
c) Anachoreses

6. PULPAL PATHOPHYSIOLOGY
irritation to clinical crown
localized pulpal inflammation
increased local tissue pressure
initial
insult
venous collapse stasis ischemia local necrosis
release of intracellular inflammatory agents
localized
effect
Circumferential vascular disturbance
Increased tissue pressure
Necrosis of additional tissue
Total pulpitis
Mechanism
Of spread

7. CLASSIFICATION OF PULPAL DISEASES
According to Grossman
I] PULPITIS
a) REVERSIBLE
1. Acute (symptomatic)
2. Chronic (asymptomatic)
b) IRREVERSIBLE
1. Acute
- Abnormally responsive to cold
- Abnormally responsive to heat
2. Chronic
- Asymptomatic with pulp exposure
- Hyperplastic pulpitis
- Internal resorption

8. II] PULP DEGENERATION
Calcific (Radiographic diagnosis)
Others (Histopathologic diagnosis)
III] PULP NECROSIS

9. REVERSIBLE PULPITIS

A mild to moderate inflammatory condition
of pulp caused by noxious stimuli in which pulp is
capable of returning to the uninflamed state
following removal of the stimuli. Also, referred as
“PULP HYPERAEMIA”.

10. ETIOLOGY
1.Trauma
2.Thermal shock
3.Excessive dehydration
4.Galvanism
5.Chemical stimulus
6.Bacteria
7.Circulatory disturbances
8.Local vascular congestion

11. Symptoms
Sharp pain lasting for a moment
More often brought on by cold than hot food
Does not occur spontaneously
Does not continue when stimulus has been removed
Teeth are not tender on percussion
Histopathology
Hyperaemia - mild to moderate inflammatory changes are limited to the
area of involved dentinal tubules
Reparative dentin, dilated blood vessels, disruption of odontoblast layer
Extravasation of edema fluid
Immunologically competent chronic inflammatory cells
Presence of acute inflammatory cells

12. DIAGNOSIS
1. Pain: Sharp pain, lasts for a few seconds
Cold, sweet or sour causes pain
2. Visual examination & history:
Examine for caries, restorations, fractures or traumatic occlusion
History of past dental treatment
3. Clinical tests:
Cold test is excellent way to locate pain
Normal to percussion, palpation and mobility
4. Radiographically : No changes
5. Vitality test:
More readily response to cold stimulation than normal teeth
EPT requires minimal current to initiate positive response

13. Treatment
-Prevention
-Removal of the noxious stimuli
-Check for vitality
-Periodic care to prevent caries
-Proper insulation of the restoration
-Desensitization
Prognosis
Good - if irritant is removed earlier
Otherwise condition may develop to Irreversible pulpitis

14. IRREVERSIBLE PULPITIS
A persistent inflammatory condition of the pulp,
symptomatic or asymptomatic, caused by noxious stimulus.
May be
Acute or chronic
ETIOLOGY
Caries
Chemical, thermal and mechanical injuries
Sequelae of reversible pulpitis

15. HISTOPATHOLOGY
Both acute and chronic inflammatory stages are seen
dentin
Chronic inflammatory
response
Caries not removed
inflammatory changes will increase
in severity
Post capillary venules
become congested
Affect circulation - Necrosis
Attract
PMNL’s
Acute
Inflammatory
reaction
Phagocytosis by PMNL ‘s
PMNL ‘s
Die & release
lysosomal
enzymes
lysis
pusmicroabscess
Carious process
continues
Chronic ulcerative
pulpitis

16. SYMPTOMS OF IRREVERSIBLE PULPITISSYMPTOMS OF IRREVERSIBLE PULPITIS
Early stages – Pain can be spontaneous in nature
which is sharp, piercing, intermittent or continuous in
nature.
Pain exacerbated on bending down or lying down
Presence of referred pain
Later stages  Pain is more severe, boring, throbbing
in nature.

17. Diagnosis
Deep cavity extending to the pulp.
Decay under filling.
Greyish scum like layer.
An odor of decomposition.
Probing into the area is not painful.
Deep probing will result in pain & haemorrhage.

18. History-
-May reveal previous symptoms or a traumatic experience
Radiographic examination:
-May not show anything of significance.
-It may disclose an interproximal cavity or caries under a filling
Percussion:
-Tenderness

19. Vitality test:

Thermal test:
As pulpal inflammation progresses, heat will intensify the responses.
Cold will tend to relieve the pain in advanced stages of pulpits.
Electric test:
Early stages – response to less current.
Later (Necrotic tissue)- more current is required.
Treatment:
Pulpectomy.
Surgical removal should be considered if the tooth is unrestorable.

20. POTENTIALLY REVERSIBLEPOTENTIALLY REVERSIBLE PROBABLY IRREVERSIBLEPROBABLY IRREVERSIBLE
Pain Pain Sharp, Momentary : dissipates readily Sharp, Momentary : dissipates readily
after removal of stimulusafter removal of stimulus
Continuous, throbbing : Persists Continuous, throbbing : Persists
minutes to hoursminutes to hours
Stimulus Stimulus Requires external stimulusRequires external stimulus
(cold, heat, sweet) (cold, heat, sweet)
Spontaneous : dead or injured Spontaneous : dead or injured
tissue in chambers or canal. tissue in chambers or canal.
Intermittent : Spontaneous pain Intermittent : Spontaneous pain
of short duration. of short duration.
History History Recent dental procedure, cervical Recent dental procedure, cervical
abrasionabrasion
Extensive restoration, pulp Extensive restoration, pulp
capping, deep caries, traumacapping, deep caries, trauma
Electric test Electric test Premature responsePremature response Premature, delayed or mixed Premature, delayed or mixed
responseresponse
Referred painReferred pain Negative Negative Common Common
Lying down Lying down NegativeNegative Increases painIncreases pain
Color Color Negative Negative May be present due to tissue lysis May be present due to tissue lysis
& intrapulpal haemorrhage. & intrapulpal haemorrhage.
Radiograph Radiograph Restoration ,caries, periodontal Restoration ,caries, periodontal
pocket, cupping of alveolar crest pocket, cupping of alveolar crest
Deep restoration, caries Deep restoration, caries
Periapex - NormalPeriapex - Normal Periapex – widening of PDL Periapex – widening of PDL
Endodontic Therapy Franklin S. Wein 6
th
edition

21. CHRONIC HYPERPLASTIC PULPITIS (Pulp
Polyp)

Chronic hyperplastic pulpitis is a productive pulpal inflammation
due to an extensive carious exposure of a young pulp.
Characterized by - development of granulation tissue, covered at
times with epithelium and resulting from long standing, low
grade irritation.

22. ETIOLOGY
Slow, progressive carious exposure.
Pulp polyp develops in a tooth with large, open cavity having
a young resistant pulp & a chronic low grade stimulus
Mechanical irritation & bacterial infection provide stimulus.
Symptoms
It is asymptomatic, except during mastication.

23. HISTOPATHOLOGY
Budding capillaries, proliferating fibroblasts & inflammatory cells
are seen.
Presence of granulation tissue – which is young vascular
connective tissue containing PMNL’s, lymphocytes & plasma
cells.
Collagenous fibres -rooted in
deeper tissue of pulp chamber.
Sensory nerve fibres are almost
absent near surface.
Surface is usually covered by
stratified squamous epithelium.

24. DIAGNOSIS
- Appearance of polyp tissue clinically, characteristic of a fleshy,
reddish, pulpal mass which fills most of pulp chamber.

- Radiographically- a large open cavity with direct access to the pulp
chamber.
-Thermal tests- Feeble or no response
- EPT : More current than normal may be required to elicit a response

Differential Diagnosis
- Proliferating gingival tissue (Gingival Polyp)

25. TREATMENT
• Elimination of polyp tissue with a sharp curette or spoon excavator,
followed by extirpation of the pulp, provided the tooth can be
restored.
• Bleeding can be controlled with pressure.
•pulpectomy can be completed in a single visit.

26. CHRONIC PULPITIS (CLOSED FORM)
Occur from operative procedures, trauma or periodontal lesions
extending apically to the foramina of lateral canals
Excessive orthodontic movement may affect the vascular supply to
the pulp producing localized areas of necrosis
Depending on the strength and duration of the inciting irritant,
pulpitis may be chronic from onset or become chronic after the acute
responses have subsided
Exacerbation – additional operative procedures
Minimal pulpal damage – resolution may occur

27. CHRONIC PULPITIS (ULCERATIVE OR OPEN FORM)
Is a chronic inflammation of the cariously exposed pulp
characterized by the formation of an abscess at the point of
exposure (ulcer).
Terms used are - Pulpal chronic abscess or pulpal granuloma.
The abscess is surrounded by granulomatous tissue
Can be partial or total.

28. INTERNAL RESORPTION
An idiopathic, slow or fast progressive resorptive process occurring
in dentin of the pulp chamber or root canals of teeth.
Synonyms: Internal granuloma, Odontoclastoma,
Pink tooth of mummary
ETIOLOGY:
Unknown, but patient often has a history of trauma.

TYPES- ( James L. Gutmann 1999)
•Root canal replacement resorption (Metaplastic resorption)
•Internal inflammatory resorption
(Quintessence Int ,1999 :vol 30)

29. MECHANISM OF INTERNAL RESORPTION

30. HISTOPATHOLOGY :
• Shows Osteoclastic activity.
• Resorptive lacunae may be filled in by osteoid tissues
• Presence of granulation tissue, multinucleated giant
cells ,dentinoclasts, chronic inflammatory cells.
• Metaplasia of pulp i.e. transformation to another tissue
SYMPTOMS
- Asymptomatic.
- In the crown, it is manifested as a reddish area called “pink spot”
representing the granulation tissue showing through the resorbed area
of crown.

31. DIAGNOSIS
- Recognized during routine radiographic examination
- Affects either crown or root or both.
- It is slow & progressive or develops rapidly to perforate the
tooth .
- Most commonly involved - maxillary anterior teeth.
RADIOGRAPHICALLY
- Pulp chamber / root canal with a round or ovoid radiolucent area.
DIFFERENTIAL DIAGNOSIS
- External resorption

32. TREATMENT
- Extirpation of pulp, stops the internal resorptive process.
- Routine endodontic treatment is indicated, but in advanced
cases -calcium hydroxide paste dressing
- Repair is completed when calcific barrier is present.
- Later the canal with its defect is obturated with plasticized gutta
percha.
PROGNOSIS
Is favourable, before perforation occurs.

33. RETROGRESSIVE PULP CHANGES (PULP DEGENERATION)
Pulp degeneration is induced by attrition, abrasion, trauma,
operative procedures, caries, pulp capping and reversible
pulpitis. Generally present in older people .
May occur in the following forms

Atrophy CalcificationsFibrosis

34. ATROPHIC DEGENERATION
-Is observed histopathologically in pulps of older people.
-Fewer stellate cells are present
-Intercellular fluid is increased.
-Pulp tissue is less sensitive than normal.
-No clinical diagnosis exists.
FIBROUS DEGENERATION
-Is characterized by replacement of cellular elements by fibrous
connective tissue.
-Pulp has a characteristic appearance of a leathery fibre.
-Reduction in size of pulp chamber.
-Decrease in nerve supply or blood supply.
-There are no distinguishing symptoms.

35. CALCIFICATIONS
Here a part of pulp tissue is replaced by calcific material, i.e. pulp
stones or denticles are formed, either within pulp chamber or
root canal.
3 types
-Dystrophic, Diffuse, Denticles / pulp stones

DYSTROPHIC CALCIFICATIONS
Occur by deposition of calcium salts in dead or degenerated tissue
Occur in minute areas of young pulp affected by minor
circulatory disturbances, in blood clot or around a single
degenerated cell.
It can also begin in the connective tissue walls of blood vessels
and nerves and follow their course

36. DIFFUSE CALCIFICATIONS
Generally observed in root canals
The deposits become long, thin and fibrillar on fusing

37. DENTICLES / PULP STONES
True denticles are composed of dentin and formed by detached
dentinoblasts or fragments of Hertwig’s sheath which may
stimulate undifferentiated cells to assume dentinoblastic
activity.
False denticles are formed when a degenerating tissue structure
serves as a nidus for deposition of concentric layers of calcified
tissue
Pulp stones are considered harmless, although
referred pain in few patients has been reported.

38. structure
size location
true
false
Local
diffused
free
attached
embedded
DENTICLES

39. NECROSIS OF PULP
Necrosis or death of the pulp tissue is a sequela of acute and
chronic inflammation of the pulp or an immediate arrest of circulation
by traumatic injury .
- It may be partial or total.
ETIOLOGY
1)As a Sequelae to inflammation
2) Bacteria, trauma and chemical irritation.: causing an ischaemic
infarction & resulting in dry gangrenous necrotic pulp.

40. TWO TYPES

LIQUEFACTION NECROSIS
Tissue converted into softened mass
Good blood supply.
Inflammatory exudate.
COAGULATION NECROSIS
Tissue converted into solid mass
Less blood supply to the area.
Cheesy consistency.

41. SYMPTOMS :
- No painful symptoms.
- Discolouration of tooth is first indication that pulp is dead.
- Dull or opaque appearance of the crown – lack of normal
translucency
- Grayish or brownish discoloration may cause tooth to lack its
usual brilliance and luster
HISTOPATHOLOGY
- Necrotic pulp tissue, cellular debris and microorganisms are
seen
- Periapical tissue may be normal or slight evidence of
inflammation of apical PDL

42. DIAGNOSIS
-Pain is absent with total necrosis
Swelling - negative
Mobility - negative
Tenderness to percusion - negative
Radiographic findings are normal except if there is apical
periodontitis.
No response to vitality tests.
Sometimes positive electric test as result of liquefaction necrosis.
Discoloration - as result of haemolysis of RBC s or
decomposition of pulp tissue (grey/ brown)

TREATMENT - Root Canal Therapy

43. HANK
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