Pulpal & periapical diseases

BY

DIAA ELDIN

TEACHING ASSISTANT, NUBENDODONTIC DEPARTMENT

Introduction

Structure & function of the dentin

pulp complex

Inflammation & histopathology of

inflammation

Pathways of the pulp & etiology of

pulpal pathosis

Structure & function of dentin pulp complex

Dental pulp complex

Dentin structure

&Permeability

Dental pulp :

(histology ,function &special environment)

Dental pulp complex

Protective barrier

If communication

Pathological pulp condition

Dentin structure & permeability

A) dentin structure

component

D.T : (number ,diameter)

B) factors affecting dentin permeability

-number of D.T

-thickness

-exposed dentin-smear layer

Dental pulp

A) histology :

1- cellular structures

a) fibroblast

b) odontoblast

Arises from ???

Where ???

Shape

function

c) Immunocompetent cells

d) Reserve cells

2) extracellular matrix

3) pulp microvasculature & lymph

4) nerves of the pulp : (sensory & sympathetic)

C fibersA delta fibers

0.4-1.2 UM2-5 UMdiameter

0.5-2 M/S12-30 M/Sspeed

NOYESmyelinated

Throbbing,achingSharp,pricklingpain

highlowthreshold

painPain,temperature,touchresponse

b) Functions of the dental pulp

1) formative

2) nutritive

3) defensive

4) nervous

4) nervous

Dentin innervation

Hydrodynamic theory

Dentinoblastictransduction

Predentin – inner dentinal zone

Subdentinoblastic,dentinoblastic

Chemical –

electrical -mechanical

Thermal stimulation

hot cold

Pulpal & periapical inflammation

Definition

Is there difference ??

Objectives of inflammatory

Histopathology of inflammation

1) preinflammatory

2) inflammatory

b) proliferative

a) exudative

early

late

1) Exudative phasea) Early exudative phase

[ Blood ]

• SERUM -COMPLEMENT-FIBRINOGEN-KININOGEN

• PNLS – MONOCYTES

[ Damaged tissues ]

• BRADYKININ - LYSYLBRADYKININ - ARACHIDONIC ACIDS

• HISTIOCYTES - RESERVE CELLS

[ Suppuration ]

(neutrophils)

b) Late exudative phase

• SENSITISED LYMPHOCYTES :

{ B - CELLS PRODUCING ANTIBODIES }

OPSONINS - AGGLUTENINS - PRECIPTINS - ANTITOXINS

{ T - HELPER - T - SUPRESSIVE - T - KILLER CELLS -

- CELLS PRODUCING LYMPHOKINS -OAF - MAF -MIF }

2- - Proliferative phase

Significances pf pulp anatomy in inflammation

compliance temperature

Collateral circulation

repaire

Etiological factors of pulp diseases

1) living irritants

Open cavity haematogenousperiodontal Adjacent

teeth

Through open cavity

Periodontal membrane

Adjacent teeth

Haematogenousinfection

2) non-living irritantsa) mechanical irritation

2) odontoiatrogenic1) accidental

b) Thermal irritationodontoiatrogenic

Electrical irritation Aeronautical irritation

Chemical irritation

odontoiatrogenic idiopathic

PULPAL PATHOSIS

PULPAL

INFLAMMATION

PULPAL NECROSIS

PULPAL IRRITATION

PERIAPICAL PATHOSIS

PROGRESSION OF PULPAL

PATHOSIS Bacteria +Byproducts in deep layers of Dentin

Pulp is affected by bacterial byproducts before actual bacterial invasion

(via exposed D.T.)

Local cellular invasion

When actual exposure occurs, pulp is locally infiltrated with PMNs

Followed by liquefaction necrosis at site of exposure

Eventually necrosis spreads all across pulp then if not treated to periapicaltissues

CLASSIFCATION OF DISEASES

OF THE PULPGrossman’s Clinical

Classification

Pulpitis

Reversible Irreversible

Acute Chronic

Pulp Degeneration

Pulp Necrosis

Inflammatory diseases of the pulp

according to

Severity & duration:

i) Acute ii) Chronic iii)Subacute

Presence or absence of symptoms:

i)Symptomatic ii)Asymptomatic

Ability to heal:

i)Reverible ii) Non reversible

1-Inflammatory diseases of the pulp(Pulpitis)

A- HYPERALGESIA- HYPERSENSITIVITY- REVERSIBLE PULPITIS-HYPERSENSITIVE DENTIN-HYPEREMIA- HYPERACTVE PULPALGIA

B – IRREVERSBLE PULPITIS

a) SYMPTOMATIC PULPITIS :PAINFUL PULPITIS: ACUTE PULPITIS

b) ASYMPTOMATIC PULPITIS: NON PAINFUL PULPITIS: CHRONIC PULPITIS-

i. CHRONIC ULCERATIVE PULPITIS

ii. CHRONIC HYPERPLASTIC PULPITIS

iii. CLOSED FORM OF CHRONIC PULPITIS

A- HYPERSENSITIVITY- REVERSIBLE PULPITIS- HYPERSENSITIVE

DENTIN-HYPEREMIA- HYPERACTVE PULPALGIA

Definition: A clinical diagnosis based on

subjective and objective findings indicating

that the inflammation should resolve and the

pulp return to normal

Etiology:

Histopathology: Range from hyperaemia to

mild to moderate inflammatory changes limited

to the are a of involved D.T., V.D.→ ↑I.P.P.

→ Oedema → W.B.C.s infiltration

→followed by odontoblast differentiation and reparative dentin formation

B – IRREVERSBLE PULPITIS

SYMPTOMATIC IRREVERSBLE PULPITIS :PAINFUL

PULPITIS: ACUTE PULPITIS

Definition: A clinical diagnosis based

on subjective and objective findings

indicating that the vital inflamed

pulp is incapable of healing. (lingering

thermal pain, spontaneous pain,

referred pain)

Etiology:

Histopathology:

B – IRREVERSBLE PULPITIS

b) ASYMPTOMATIC PULPITIS: NON PAINFUL PULPITIS:

CHRONIC PULPITIS-

Definition: A clinical diagnosis based on

subjective and objective findings

indicating that the vital inflamed pulp is

incapable of healing. (no clinical

symptoms)

i. CHRONIC ULCERATIVE PULPITIS

ii. CHRONIC HYPERPLASTIC PULPITIS

iii. CLOSED FORM OF CHRONIC PULPITIS

• Etiology:

CHRONIC PULPITIS

Examination & diagnosis:

Non painful - mild discomfort

Spontaneous pain

Heat elicits pain

Exacerbation with lowered

body immunity

Delayed reaction to EPT

X - ray may be -ve , internal

resorption or condensing osteitis

CHRONIC ULCERATIVE PULPITIS

Chronic inflammation with

abscess formation at the

exposure site, and the

abscess is surrounded by

granulomatous tissues

Examination & diagnosis:

Painful with food impaction

All signs of chronic pulpitis

CHRONIC HYPERPLASTIC PULPITIS

Seen in young permanent cariouslyexposed teeth

It is an attempt of healing and repair by walling off the irritation

Proliferative reaction of the pulpal granulation tissue with formation of a polyp

May become epithelialized from desquamated epithelial cells

PULP NECROSISDefinition: A clinical diagnostic category in dicating death of the pulp. The pulp is usually nonresponsive to pulp testing. 2 types are present.

LIQUEFACTIVE NECROSIS

(WITH GOOD BLOOD SUPPLY.)

COAGULATIVE NECROSIS

(WITH DIMINISHED BLOOD SUPPLY.)

Examination & diagnosis:

If not treated ►►►Periapical leson of endodontic origin

Usually non painful untill the periapex is envolved.

Radiographic findings are -veunless there is a concomitant periapical disease.

-Ve with EPT except (some times) in liquefactive necrosis &multi rooted teeth.

RETROGRESSIVE PULP CHANGES(Pulp Degeneration)

1 - ATROPHY AND FIBROSIS Definition: waisting away or decrease in sze of the

pulp, with age.

MAY BE CONSIDERED AS AGE CHANGES.

Histopathology:

Mature collagen incrase / unit area and the cells

deminish in no. And size.

Excessive secondary dentin deposition deminishes the

size of the pulp chamber & canal lumen.

Decrease in blood supply.

2- CALCIFICATIONS

DYSTROPHIC CALCIFICATION

IN DEAD OR DEGENERATING TISSUES.( LOCAL ALKALINITY).

DENTICLES

According to location:

FREE

EMBEDED

ATTACHED

According tostructure:

True

False

INTERNAL RESORPTION ETIOLOGY:

Unknown , often histore of trauma Or chronic pulpitis. Or

pulpotomy

Examination & diagnosis

The pulp is vital .

Delayed response to EPT

In the pulp chamber it forms the pink spot.

In the canal it may perforate causing a lateral lesion.

At the cervical level it may be mixed with external cervical

resorption.

Radiographically,in int. Resorption disrupts the canal while

in ext .Resorption the canal contour is unaltered.

Periapical disease

SYMPTOMATIC (ACUTE) APICAL

PERIODONTITIS SYMPTOMATIC (ACUTE) APICAL PERIODONTITIS

Definition: Inflammation of the apical periodontium

producing clinical symptoms including a painful

response to biting and/or percussion . It might or not

be associated with apical radiolucent area.

• Etiology:

• ) Histopathology: (as explained before)Inflammatory

reaction in apical periodontal ligament ? Dilation ob

B.V.? Exudation and accumulation of PMNs

?Distension of P.L. and extrusion of tooth ----with

continuous irritation ---?loss of alveolar bone

• Examination & diagnosis:

• : Treatment : R.C.T----

– TOOTH REDUCTION OUT OF OCCLUSION

ACUTE APICAL ABSCESS : Definition: An inflammatory reaction to pulpal

infection and necrosis characterized by rapid onset ,

spontaneous pain , tenderness to tooth pressure, pus

formation and swelling of associated tissues

• Etiology:

• Histopathology: Inflammatory reaction in apical

periodontal ligament ? Dilation ob B.V.? Exudation

and accumulation of PMNs ?Distension of P.L. and

extrusion of tooth ----with continuous irritation ---?loss

of alveolar bone---- localized area of liquefactive

necrosis containing PMNs , debris , cell remnants and purulent exudate

Examination & diagnosis: Tooth severely painful & tender

• Localized vestibular swelling or

facial cellulitis• Pain starts

severe and decrease after

swelling

• Patient may become febrile

with lympf nodes affection

• Tooth becomes loose

• -Ve EPT findings except in

liquefactive necrosis & multiple

canals

• Radiograph: HAZY APICAL RAREFACTION

RECRUDECENT ABSCESS(PHOENIX ABSCESS)

Definition: ACUTE EXACERBATION OF A PRE- EXISTING

CHRONIC PERIAPICAL PATHOSIS

RECRUDECENT ABSCESS

• Clinically often undistinguishable from AAA

• DIAGNOSIS IS BASED ON PATIENT HISTORY,

CLINICAL PICTURE AND RADIOGRAPHIC

FINDINGS REVEALING THE PREVIOUS

CHRONIC PERIAPICAL PATHOSIS

CHRONIC APICAL PERIODONTITIS Definition::Inflammation of the apical

periodontiumof pulpalorigin, that does not produce clinical symptoms and

radiographicallyappears as apical R.L. area

Inflammation of the apical

periodontiumof pulpalorigin, that does not

produce clinical symptoms and

radiographicallyappears as apical R.L. area

– asymptomatic or slight discomfort

– little or no pain on percussion

• X-ray:

– apical radiolucency or Condensing

osteitis: radiopaque

PULPOPERIAPICALOSTEOSCLEROSIS

• Productive response of

periapical bone to a low-grade

long standing pulpal irritation

• Increase in density of bone

due to osteoblastic hyperactivity

• Seen in young permenant

teeth with carious exposures & chronically inflammed pulps

CHRONIC APICAL ABSCESS(SUPPURATIVE APICAL PERIODONTITIS)

Nonpainful low grade long

standing chronic inflammatory

reaction to pulpal irritants

• It represents a balance between

body resistance and the periapical

pathosis

• Formation of pus that

drainsthrough a sinus tract

• Ill defined periapical

radiolucency

• The tooth may be slightly mobile

PERIAPICAL GRAMULOMA

• Examination & diagnosis:

• Non painful• -Ve EPT findings

• Well defined periradicular radiolucency•

Histopathology:

• periapical granulomatous tissue

• Encapsulated with a fibrous capsule

• May show epithelial strands

• May transform into a phoenix abcess if

infected or manipulated

PERIAPICAL CYST Definition::Inflammatory cyst due to extension of

infection from pulp into surrounding periapical

tissues

• Histopathology:

• Central fluid-filled epithelium-lined cavity

surrounded by granulation tissue and a fibrous capsule

• Forms on heals of a periapical granuloma

• Examination & diagnosis:

• Well defined apical radiolucency

• Non painful untill infected (phoenix abscess)

• Slowly growing destroying bone and moving teeth