GOOD

MORNING
 DISEASES OF PULP

GUIDED BY PRESENTED BY
Dr.Girija.S.Sajjan Dr.M.Mobeena
Prof & HOD
 Contents

 Introduction
 Anatomy of pulp structures
 Diseases of pulp
* Classification
* Acute pulpitis
*Chronic pulpitis
*Chronic hyperplastic pulpitis
* Pulp calcification
* Pulp necrosis
 Clinical diagnostic methods
 Conclusion
 References
INTRODUCTION..
 PULP: Pulp is soft mesenchymal
connective tissue mass that occupies
the central area of the teeth.

 It is contained within the pulp chamber

and the root canals of the tooth.

 The shape of the pulp therefore

resembles the shape of the tooth in
which it is housed.
Microscopic anatomy of pulp

 Cells: Odontoblasts.
Fibroblasts.
Undifferentiated mesenchymal cells.
Defense cells.

 Inter-cellular substances:
Fibers
Ground substances
Blood vessels
Lymph vessels
Nerves
 Functions of Pulp:

 Inductive- differentiation of dental lamina & enamel organ

formation.

 Formative- dentin

 Nutritive- blood vascular system

 Protective –sensory response with pain to all type of

stimuli.

 Defensive / reparative- formation of reparative or sclerotic

dentin to noxious stimuli.
ETIOLOGY :

1. Physical
a a. Mechanical
b. Thermal
c. Electrical
2. Chemical
a) Erosions(acids)
b) Phosphoric acid, acrylic monomer
3. Bacterial
a) Toxins associated with the caries
b) Blood born microbial colonization
Sequale of pulpal infection
External stimuli

degranulation of mast cells

release of chemical mediator

vasodilatation

increased blood pressure and vascular leakage with edema

Increased pulpal pressure could compress venous return

Self strangulation
Pulpal necrosis
Pulpal response to inflammation differs
because:
Pulpal connective tissue is surrounded by the hard
dentinal wall  therefore it is unable to expand.

Pulp lacks collateral circulation  therefore healing

capacity is limited.

Pulp responds to irritation by  formation of reparative

dentin.

MEDICAL ORAL PATHOLOGY 2004;9 :52-62.

HYPOTHETIC MECHANISM OF THE PATHOPHYSIOLOGY OF PULPAL DISORDE

Kim, S;JOE,11;465,1985
Hemodynamic Changes In The Pulp During Caries
• The vascular component of the immune response in the dental
pulp is critical to planning or executing vital pulp therapy.

Blood Flow
-Measuring blood flow in dental pulp, is a difficult procedure.

-Using plaque extract to initiate inflammation in rat incisor model

Kim et al reported a 40% Increase in blood flow in moderately
inflamed pulp but 35% reduction in partially necrosed pulp.

-A study by Bletsa Et Al, in a similar model, showed that

application of LPS to the pulp resulted, after 10min in reduction
of blood flow that continued for 3-hour duration.
Interstitial fluid pressure
-The healthy dental pulp has interstitial pressure of 5-10mm
Hg.

-One of the key changes during inflammation is movement of

fluid from within the capillaries into interstitial space.

-By the law of physics, increasing the amount of fluid in a rigid

chamber leads to an increase in pressure.

-Such a pressure rise in the pulp would cause compression of

the blood vessels leading to vascular stasis and necrosis.
Effect of Pulp Pathosis on IPP
Classification Clinical Nature of pulp Average IPP
consideration (mm of Hg)
Normal pulp Structure- intact 10 (8-15 mm of
Tissue – resilient Hg)
extirpation in one
piece
Reversible Transient pain, Structure- intact 13
pulpitis hyperreactive Increased
pulp requires vascularity
stimulus
Irreversible Pain – Structure- intact 34.5
pulpitis spontaneous areas of necrosis
persistent or abscess
response to cold formation

Non vital Vitality –ve Dry granulated negative

dehydrated periapical tissue
radiolucency
maybe present
-Pressure change could lead to strangulation of the vessels at
the apex causing necrosis in areas of pulp not directly affected
by bacterial toxins.

-Tonder and Van Hassel measured interstitial fluid pressure in

the pulps of experimental animals showed that pressure in the
area beneath an injury a short distance(2mm) away, pressure
stays within normal limits.

-Even within areas of raised interstitial pressure , capillaries

remain patent because of balancing increase in inter-luminal
pressure.
Neural Changes During Pulpal Inflammation

 Sympathetic nerves control blood flow by constricting

precapillary sphincters and by interaction with other
elements of inflammation.
 Sympathetic activity inhibits the production of anti-
inflammatory cytokines.
 Sympathetic nerves have an inhibitory effect on
Odontoclasts and stimulate reparative dentin production.
 Afferent sensory fibers from trigeminal system also plays
an important role in response to toxins and injury.
 The afferent fibers release two important neuropeptides,
substance P and Calcitonin Gene Related Peptide
 Both cause vasodilatation and increased permeability.

 Sympathetic activity causes vasoconstriction and also

reduces the release of peptides from afferents.

 In injured pulps, there is an increased expression of

nerve growth factor and its receptors.
Diseases of the pulp

PULPITIS: Inflammatory reaction of pulp to an noxious stimulus

.
Classification :
 a. Acute pulpitis
 b. Chronic pulpitis
 Hyperplastic pulpitis
 Internal resorption.
 Pulpal degeneration:- a. calcific (radiographic changes)
b.others (histopathologic diagnosis)
 Necrosis
CLINICAL PRESENTATION OF
DISEASES OF PULP
 PAIN

 Any sensory response is interrupted as pain in dental

tissue.

 The dental pulp is innervated by the C fibers by 87%.

 The remaining 13% of its contributed by A-β (7%) and

A-δ (93%) fibers which are myelinated in nature.

 So the dental pain is generally slow and deep seated in

nature.
 PAIN

 Any sensory response is interrupted as pain in dental

tissue.

 The dental pulp is innervated by the C fibers by 87%.

 The remaining 13% of its contributed by A-β (7%) and

A-δ (93%) fibers which are myelinated in nature.

 So the dental pain is generally slow and deep seated in

nature.
 The nerve fibers are classified as regards diameter and
transport speed into A fibers(αβγδ) B and C fibers.

 The A fibers induce tactile and proprioceptive

reactions(they supply information to the musculoskeletal
structures, relative to presence, position and movement of
body)

 The A-δ and C fibers transmit pain, although they are not
specifically for pain.

 The A-δ myelinic fibers respond to mechanical and thermal

stimulus(pain quickly felt-pinprick sensation, sting).
 While, C amyelinic fibers respond to mechanical,
thermal and chemical stimulus(slow pain-burning
sensation)

 Only 13% of nerve fibers that enter human premolars

are myelinated; of these 93% are A-δ and remaining
7% are A-β fibers.

 Nair analyzing the neural elements of dental pulp and

of dentin, classified nerve fibers of mammals showing
type, diameter, speed and function.
CLASSIFICATION OF NERVE FIBERS
TYPE DIAMETER VELOCTY OF FUNCTION
(microns) CONDUCTION
(m/sec)

A alpha 12 - 22 70 – 120 Motor ,

proprioception

A beta 5 – 12 30 – 70 Touch , pressure

A gamma 3–6 15 – 30 Muscle spindles

A delta 2 -5 12 – 15 Pain , touch ,

temperature

B 1–2 3 – 10 Pre ganglionic

ANS

C < 1.5 0.5 - 2 Pain ,

sympathetic
 Aδ fibers - Myelinated, large diameter, specific for pain ,
low threshold.
 Location – periphery of the pulp
 Momentary sharp pain & stimulated by dentine
hypersensitivity.

 C fibers – Unmyelinated, small diameter, high threshold.

 Location – core of pulp
 Produce dull, throbbing pain.
 Stimulated by tissue inflammation and damage.
 The identification of pain or any sensory
stimulation occur in 5 stages
1. Initiation
2. Transduction
3. Transmission
4. Modulation
5. Perception
 Fields has described that the subjective
experience of pain arises by four distinct
processes
Transduction

Transmission

Modulation

Perception
 The perception of pain alone to any stimulus may be
explained by the fact that the initiation of stimuli
generally starts with hyperemia in closed pulp chamber
which triggers inflammatory response leading to release
of bradykinin which is a neurotransmitor.

 Substance p is associated with the unmyelinated C fibers

of pulp.

 All the various types of sensory stimuli may be

transmitted as they are but modulated as pain(OKESON)
 Clinical diagnostic methods
 History and record.
 Symptoms –
1. subjective
2. objective
 In objective symptoms :
Visual & tactile Inspection – color, contour, consistency
(3 c’s)
Palpation – Sensitivity over apex of tooth suggests
periapical inflammation. Firm or fluctuant swelling
consistent with abscess.
Percussion – Pain/sensitivity consistent with periapical
inflammation. Late stages of chronic pulpitis.
CLASSIFICATION OF DISEASES
OF PULP
 522 Diseases of pulp

 522.0 Pulpitis
Pulpal: Abscess
Polyp
 Pulpitis: Acute
Chronic (hyperplastic) (ulcerative)
Suppurative

 522.1 Necrosis of the pulp

Pulp gangrene
 522.2 Pulp degeneration
* Denticles
*Pulp calcifications
*Pulp stones
 522.3 Abnormal hard tissue formation in pulp
Secondary or irregular dentin
 According to WHO
*Initial Pulpitis
*Acute Suppurative(pulpal Abscess)

 According to Grossman
*Hyperemia
*Pulpitis
*Acute pulpitis
 According to Ingle
*Hyper-reactive pulpalgia
*Hypersensitivity
*Hyperemia
*Acute pulpitis
According to Seltzer&Bender
*Pulpitis
*Incipient form of chronic pulpitis
*Acute pulpitis
 According to Weine
*Hyperalgesia
*Hypersensitive dentin
*Hypereamia
*Painful pulpitis
*Acute pulpalgia
 According to Cohen&Burns
*Reversible Pulpitis
*Irreversible Pulpitis
 According To Estrella
*Hyper-reactive pulpalgia
*Chronic pulpitis
*Chronic ulcerative
*chronic hyperplastic(pulp polyp)
 HISTOPATHOLOGICAL CLASSIFICATION OF THE
DISESASES OF DENTAL PULP
A)
1 Pulp Hyperemia
2. Acute Pulpitis
*Serous
*purulent
3. Chronic pulpitis
*Ulcerative
*Hyperplastic
4. Pulp necrosis

1. Closed pulpitis
*Pulp Hyperemia
* Infiltrative pulpitis
* Abscessed pulpitis
2. Open pulpitis
* Ulcerous traumatic pulpitis
* Ulcerous non traumatic pulpitis
*Hyperplastic pulpitis
3. Pulp necrosis
1. Reversible pulpitis
2. Pulpitis in the transition period
3. Irreversible pulpitis
4. Pulp necrosis
 Classification of diseases of pulp

 (1) Based on Severity of Inflammation

 (2) According to Involvement

(1) Based on Severity of Inflammation

 (1) Reversible Pulpitis

 (2) Irreversible Pulpitis

 (3) Pulp Degeneration

 (4) Pulp Necrosis

(1) Based on Severity of Inflammation

 (1) Reversible Pulpitis

 Symptomatic (acute)
 Aysptomatic (chronic)

 (2) Irreversible Pulpitis

 Acute
• Abnormally responsive to cold
• Abnormally responsive to heat
(1) Based on Severity of Inflammation

 (2) Irreversible Pulpitis

 Chronic
• Asymptomatic with pulp exposure
• Hyperplastic
• Internal resorption
(1) Based on Severity of Inflammation

 (3) Pulp Degeneration

 Calcific

 (4) Pulp Necrosis

(2) According to Involvement

 (1) According to Involvement

 (2) According to Severity

 (3) According to presence or absence of direct

communication between dental pulp + oral environment
(2) According to
Involvement

 (1) According to Involvement

 Focal or Subtotal or
Partial Pulpitis

 Total or Generalized
Pulpitis
(2) According to
Involvement

 (2) According to Severity

 Acute
 Chronic
(2) According to
Involvement

 (3) According to presence or absence of direct

communication between dental pulp + oral environment

 Pulpitis Aperts (open pulpitis)

 Pulpitis Clausa (closed pulpitis)

Acute Pulpitis

 Causes

 tooth with large carious

lesion

 defective restoration
where there has been
recurrent caries

 pulp exposure due to

faulty cavity preparation
Acute Pulpitis

 Clinical Features

 severe pain is elicited by

thermal changes

 pain persists even after

thermal stimulus
disappears or been
removed
Acute Pulpitis

 Clinical Features

 may be continuous

 intensity may be increased

when patient lies down

 application of heat may cause acute exacerbation of pain

Acute Pulpitis

 Clinical Features

 tooth reacts to electric pulp vitality tester at a

lower level of current than adjacent normal
teeth.
Acute Pulpitis

 Clinical Features

 pressure increases
because of lack of
escape of inflammatory
exudate

 rapid spread of inflammation

through pulp with pain
+ necrosis
Reversible Pulpitis

 mild to moderate inflammatory

condition of pulp

 caused by noxious stimuli

 pulp is capable of returning

to un-inflammed state

 following removal of stimuli

Reversible Pulpitis

 Causes

 agent capable of injuring pulp like:

• trauma
• disturbed occlusal relationship
• thermal shock
Reversible Pulpitis

 Clinical Features

 sharp pain lasting for

a moment

 often brought on by cold

than hot food or beverages
and by cold air
Reversible Pulpitis

 Clinical Features

 does not continues when the cause has been

removed

 tooth responds to electric pulp testing at lower

current
Reversible Pulpitis

 Management

 Removal of noxious
stimuli
 Prevention

 early insertion of filling

if a cavity has developed

Periodic care
Irreversible Pulpitis

 persistent inflammatory condition of pulp

 may be symptomatic or asymptomatic

 caused by noxious stimulus

Irreversible Pulpitis

 Causes

 bacteria involvement of
pulp through caries

 chemical

 thermal

 mechanical injury
Irreversible Pulpitis

 Clinical Features

Early Stage

 paroxysm of pain
caused by:

• sudden temperature
changes like cold,
sweet, acid foodstuffs
Irreversible Pulpitis

 Clinical Features

Early Stage

 pain often continues

when cause has been
removed

 may come and go

spontaneously
Irreversible Pulpitis

 Clinical Features

Early Stage

 pain

• sharp
• piercing
• shooting
• generally severe
Irreversible Pulpitis

 Clinical Features

Early Stage

 pain

• bending over exacerbates pain which

• lying down is due to change in
• change of position intrapulpal pressure
Irreversible Pulpitis

 Clinical Features

Late Stage

 pain

• more severe as if tooth is under

• throbbing constant pressure
Irreversible Pulpitis

 Clinical Features

Late Stage

 pain

• patient is often awake at night due to pain

• increased by heat and sometimes relieved by cold,

although continued application of cold may intensify pain
Irreversible Pulpitis

 Management

 complete removal of pulp

or pulpectomy

 root canal filing with inert material like gutta percha should be done
 What is a hot tooth?

The term ‘‘hot’’ tooth generally refers to a pulp

that has been diagnosed with irreversible pulpitis, with
spontaneous, moderate-to-severe pain. A classic example
of one type of hot tooth is a patient who is sitting in the
waiting room, sipping on a large glass of ice water to help
control the pain.

- In dealing with teeth diagnosed with irreversible pulpitis,

determining whether adequate local anesthesia has been
achieved before treatment is important.
 Few considerations should be taken in mind;

•The first consideration could be to change the local anesthetic

agents.

•The next strategy would be to change the injection technique in

attempting to block the inferior alveolar nerve.
•Accessory nerves have also been implicated as a potential reason for the failure
of the IANB.

•Increasing the volume of the local anesthetic delivered during the IANB has
also been found not to increase the incidence of pulpal anesthesia.

•Increasing the concentration of epinephrine (1:50,000), with the hopes of

keeping the anesthetic agent at the injection site longer, also showed no
advantage in the IANB.
So why then is it so difficult to achieve adequate pulpal anesthesia in
Mandibular teeth, even if the patient is asymptomatic?
- One theory to explain this is that the inflamed tissue has
a lowered pH, which reduces the amount of the base form of
the anesthetic needed to penetrate the nerve sheath and
membrane.

-Therefore, there is less ionized form of the anesthetic within

the nerve to produce anesthesia.
-
-This theory may explain only the local effects of inflammation
on the nerve and not why an IANB injection is less successful
when given at a distance from the area of inflammation (the hot
tooth).
Local Anesthesia Strategies for the Patient With a ‘‘Hot’’ Tooth
Dent Clin N Am 54 (2010) 237–247
 - Another theory is that the nerves arising from the inflamed
tissue have altered resting potentials and reduced thresholds of
excitability.

-It was shown that anesthetic agents were not able to prevent the
transmission of nerve impulses because of the lowered excitability
thresholds of inflamed nerves.

-To deal with the eventual failures found with the IANB injection,
the clinician needs to include the use of supplemental anesthesia
techniques

Dent Clin N Am 54 (2010) 237–247

 SUPPLEMENTAL INJECTIONS
Intraligamentary (Periodontal Ligament) Injection

- The success of supplemental PDL injections in helping

achieve anesthesia for endodontic procedures has been
reported to be 50% to 96%.
Intraosseous Injection

- Nusstein and colleagues found that a supplemental

mandibular IO injection using 1.8 mL of 2% lidocaine with
1:100,000 epinephrine had a 91% success rate in attaining
complete pulpal anesthesia when used after the IANB
injection failed.
Mandibular Buccal Infiltration Injection with
Articaine

-Kanka and colleagues reported a success rate of 91% with

4% articaine with 1:100,000 epinephrine.

Intrapulpal Injection

- The intrapulpal injection works well when it is given under

back-pressure. Onset of anesthesia is immediate.
Preemptive Strategies to Improve Success
of the IANB Injection

-The use of oral medications before treatment of a patient

with a tooth diagnosed with irreversible pulpitis in hopes
of improving the success rate of the IANB injection.

-Ianiro and colleagues used pretreatment oral doses of

Acetaminophen or a combination of Acetaminophen And
Ibuprofen versus placebo in patients undergoing
endodontic therapy.

- Higher success rates (defined as no pain upon entering

the pulp chamber) of 71% to 76%, respectively, as
compared with placebo (46%).
 - Galatin and colleagues used an IO injection of 40mgof
methylprednisolone (Depo-Medrol) and found that it
significantly reduced pain and use of medication in untreated
patients diagnosed with irreversible pulpitis when compared
with patients who received a placebo injection.

- Berthold et al. showed that pretreatment with sedative

drugs reduced pain sensation. Ketamine is one drug
that may reduce pain sensation.

Journal of Oral Science, Vol. 53, No. 4, 461-465, 2011

Conclusion:

 Diagnosis of pulp diseases at an early stage

will prompt so that adequate treatment of
the disease so that probable sequel of the
disease can be avoided. which on neglect can
lead to life threatening.
 The differential diagnosis is quite an
important aid to the dentist in successfully
treating the patient.
“PULP IS A SMALL TISSUE WITH
A BIG ISSUE”
-I.B.Bender
References

 Textbook of oral pathology Shafer’s ….6th edition.

 Text book of oral pathology – Neville,3rd edition
 Topazaina – Text book of oral and maxillofacial
infections
 Text book of endodontic practice - Grossman, 10th
edition.
 Text book of endodontics - Ingle 6 th edition
 Text book of principles of Oral and Maxillofacial
Surgery, Peterson 2nd edition, volume 1
 Text book of oral histology – orban’s
 Journal of indian acedamy of oralmedicine & oral
radiology 2011,23(1):54-56
 Journal of Oral Sciences 52, 411-416
 Journal of dentomaxillofacial radiology (2006)
35,326-333
 Journal of indian of oral medicine & oral radiology
2011,23(1):54-56
 Journal Of Endodontics 2009,35(12).
 International Endodontic Journal, 42, 555–567, 2009
THANK
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