infection of teeth

8/3/2019 Infection of Teeth

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Caries, pulpitis & periapical

lesions

:07-3121101~2755

[email protected]


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(1)

DENTAL CARIES

Etiology

Clinical Types

Enamel Caries

Dentin Caries

Epidemiology


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(2)

Reversible Pulpitis

Irreversible Pulpitis

Pulp Necrosis

PULPITIS

History and Nature of Pain

Reaction to Thermal Changes

Reaction to Electric Stimulation

Reaction to Percussion of tooth

Radiographic Examination

Visual Examination

Palpation of Surrounding Area

Acute Pulpitis

Chronic Pulpitis

Chronic Hyperplastic Pulpitis

Histopathology of Pulpal Diseases

Common Diagnostic Techniques


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(3)

Periapical Lesions

Chronic Apical Periodontitis

Periapical GranulomaPeriapical Cyst

Periapical Abscess

Acute Periapical Conditions


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1. Sapp JP: Contemporary Oral & Maxillofacial Surgery, p. 61-87

2. Matalon S et al. Detection of cavitated carious lesions in approximal

tooth surfaces by ultrasonic caries detector. Oral Surg Oral Med Oral

Pathol Oral Radiol Endod 2007;103:109-13

3. http://www.ne.jp/asahi/fumi/dental/

4. www.teethwhiteningkits.com/tooth_decay/t5_tooth_decay_children.htm5. www.odonto-red.com/cariesdental.htm

6. www.lezerdent.hu/cariesn.htm

7. www.areadent.cl/

8. www.kavo.com/Es

9. www.uic.edu/classes/dh/dh110/Caries_files

10.http://iwate8020.jp/know/caries.html

11.http://www.suwaneedental.com/cariesprevention.htm

12.http://www.drfarid.com/fluoride.htm

References


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It is a multifaceted disease involving an interplay among

the teeth, oral host factors of saliva, microflora, and external

factors of diet.

It is a unique form ofinfection with acidic and proteolyticbacteria for enamel caries

Etiology


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Etiology

Refs. 3, 4


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Etiology

Refs. 1, 3


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Etiology

Refs. 4, 6

http://www.experimentalgameplay.com/game.php?g=46


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Etiology

Refs. 10, 11


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Etiology

Saliva - contains materials for remineralization- calcium and phosphate ions

Protective FactorsThe Caries Balance

Caries No Caries

Acidogenic bacteria[mutans Streptococci]Reduced salivary functionFrequency of fermentable

carbohydrate ingestion

Pathological FactorsSaliva flow & componentsProteins, calcium phosphatefluoride, immunoglobulinsin saliva

Extrinsic chlorhexidine

Healthy tooth enamel rods Enamel rods demineralized( broken down by acid)

Enamel rods remineralized,

rebuilt, by fluoride & minerals in saliva

Refs. 5, 12


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Epidemiology

1 of common chronic diseases in the world Prevalence - increased in modern times

Increase associated with dietary changes

Trend beginning to decline in some countries

y(i.e. certain segments of US, Western Europe,

yNew Zealand, and Australia)

Cause of decline?

It is attributed to fluoride

DENTAL PLAQUE =

gelatinous mass of bacteriaRef. 5


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Clinical Types

Pit and fissure

Smooth surface

Cemental

Recurrent


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Clinical Types (1)

Pit and fissure caries : the most common type: appear at an early age

: on the occlusal & buccal

surfaces of the molars

Refs. 1, 4


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Clinical Types (2)

Ref. 6


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Clinical Types (3)

Ref. 8


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Clinical Types (4)

Ref. 8


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Clinical Types (5)

Ultrasonic caries detector

Ref. 2


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Clinical Types (6)

Smooth surface : less commoncaries : occurs on the labial

surface & proximal area

Ref. 1


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Clinical Types (7)

Refs. 1, 6


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Clinical Types (8)

Cemental (root) caries1. Found in older people, especially, gingival recession

2. Progress differently than enamel & dentin caries because

root surfaces are soft, thin, and subject to chemical

erosion and abrasive action during tooth brushing

3. Both acid and enzyme producing bacteria and thin layer of

dentin results in rapid progression into pulp

Ref. 1


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Clinical Types (9)

Recurrent caries arises around an existing restorationas a result of marginal leakage.

Marginal leakage is a situation predispose the tooth to

accumulate bacteria and food.


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Clinical Types (10)

Acute (rampant) caries and chronic caries are infrequently used termsto denote the rate that dental caries progresses in patients

Ref. 4


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Enamel Caries (1)

Arrested form

- chalky appearance

Advanced form

- Cavitation

Smooth surface enamel caries is most commonly located onthe mesial and distal surfaces at the point of contact with the

adjacent tooth (interproximal caries).

The less common lesions on the buccal and lingual surfaces

Ref. 1


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Enamel Caries (2)

Hypocalcified enamel - structure is abnormal- not weakened, surface is hard

Incipient caries - porous weakened structure

- surface is softened

Arrested caries (remineralized) - strong, surface is hardActive caries - cavitated, weak enamel, surface is soft

Ref. 1


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Enamel Caries (3)

Hypocalcified enamelrestore only for esthetics

yIncipient caries

y anti-microbial (remineralization)y restore (after remineralization)

y only for esthetics

yArrested caries (remineralized)y restore only for esthetics

Active caries

anti-microbial + restorative


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Enamel Caries (4)

Histopathology Four zones on ground section1. Translucent zone: advancing front of initial demineralization

2. Dark zone: remineralization

3. Body of lesion: region of maximal demineralization

4. Surface zone: remain unaffected until it is collapsed forming a cavity

Enamel

Surface zone

Body oflesion

Dark zoneTranslucentzone

Ref. 1


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Enamel Caries (5)

Incipient Lesion - 4 ZonesZone 1 - translucent zone

Zone 2 - dark zone

Zone 3 - body of the lesion

Zone 4 - surface zone

body of lesion (B) appears dark beneath relatively INTACT SURFACE ZONE

lesion = cone shaped

B SZ

Ref. 9


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Enamel Caries (6)

Incipient Lesion - 4 ZonesZone 1 - translucent zone

Zone 2 - dark zone

Zone 3 - body of the lesion

Zone 4 - surface zone

TZ

DZ B

TRANSLUCENT ZONE (TZ) present at advancing front of lesion

DARK ZONE superficial to TZ

Ref. 9


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Enamel Caries (7)

Zone 1 - translucent zone1. deepest zone - closest to pulp

2. advancing front of lesion

3. appears structureless - (polarized light)4. pore volume - 1% - > 10v normal enamel

5. pores/voids form along prism boundary

due to ease of hydrogen ion penetration

from caries process


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Enamel Caries (8)

Zone 2 - dark zone1. does not transmit polarized light

2. caused by presence of lots of tiny pores

which are too small to absorb quinoline(polarized light)

3. air / vapor filled pores - opaque

4. pore volume - 2 to 4 %

5. remineralization - increase in size of darkzone

6. size of dark zone - indication of amount

of remineralization


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Enamel Caries (9)

Zone 3 - body of lesion1. largest portion of lesion

in demineralization phase

2. largest pore volume - 5% at periphery

25% at center

3. straie of Retzius well marked

4. first penetration of caries enters enamel

via the striae of Retziuswhich provides access to rod prism cores

5. BACTERIA may enter if pores large enough


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Enamel Caries (10)

Zone 4 - surface zone1. relatively unaffected by caries attack

2. lower pore volume than body of lesion

3. radiopacity - similar to unaffected enamel

4. surface in contact with saliva

hypermineralized by fluoride

5. serves as barrier to bacterial invasion

arresting caries processmay result in rough, but hard surface


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Dentin Caries (1)

This stage of caries progression requires a different mixtureof bacterial colonies than is necessary for enamel caries.

Bacteria strains capable to produce large amounts of

proteolytic & hydrolytic enzymes, rather than acid-producing

types of enamel caries.

Ref. 1


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Dentin Caries (2)

Dentin caries advance through 3 changes1. weak organic acid demineralizes dentin

2. organic material of dentin (mostly collagen)

is degenerated and dissolved3. loss of structural integrity

followed by bacterial invasion


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Dentin Caries (3-1)

1234

5

Fivemicroscopic

zones

Enamel

Dentin

Ref. 1


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Dentin Caries (3-2)

Bacteria in

dentin tubules

Liquefaction

Zone 1: deepest zone, fatty degeneration

the earliest changes where bacterial enzymes in dentinal tubules

causing breakdown of cell membrane of dentin releasing lipid

Zone 2: translucent zone, a band of hypermineralized dentin and sclerotic

Zone 3: demineralization, softer dentin due to bacterial enzymes

Zone 4: brown discoloration, reduction of mineral with bacteria withindentinal tubules

Zone 5: cavitation, no mineralization and organic component is partially

dissolved by the bacteria

Ref. 1


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Dentin Caries (4)

Dentin - 5 zones of slowly progressing lesionZone 1 - Normal dentin

Zone 2 - Subtransparent dentin (affected)

Zone 3 - Transparent dentinZone 4 - Turbid dentin

(in advanced lesions - infected)

Zone 5 - Infected / Necrotic dentin


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Dentin Caries (5)

Zone 1 - Normal dentin dentinal tubules with smooth odontoblastic

no crystals in lumen

NO BACTERIA in tubules stimulation - elicits pain


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Dentin Caries (6)

Zone 2 - Subtransparent dentinAFFECTED - not infected

zone of demineralization - by acid from caries

capable of remineralization

damage to odontoblastic processes

NO BACTERIA

stimulation - elicits pain


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Dentin Caries (7)

Zone 3 - Transparent dentin softer than normal dentin

AFFECTED - not infected

zone of demineralization - by acid from caries

capable of remineralization

large crystals

NO BACTERIA

stimulation - elicits pain


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Dentin Caries (8)

Zone 4 - Turbid dentin

zone of bacterial invasion

filled with BACTERIA

very little mineral present collagen irreversibly damaged

will not self-repair / no re-mineralization

must be REMOVED


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Dentin Caries (9)

Zone 5 - Infected dentin NECROTIC dentin in advanced lesions

decomposed dentin

lots ofBACTERIA

no recognizable dentin structure

no collagen / no mineral

must be REMOVED


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Pulpitis

It is an inflammation of the pulpal tissue that may be acute orchronic, with or without symptoms, and reversible or irreversible.

Ref. 1


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Reversible Pulpitis

1.Whether pain is spontaneous or stimulated2.Duration of pain

3.Nature of pain described by patient

Decision of reversible or irreversible pulpitis1. Conservatively restore the defective tooth structure

2. Removed the disease pulp disease

3. Remove the entire tooth

Ref. 7


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Reversible Pulpitis

Reversible pulpitis / hyperemialimited inflammation of pulp

tooth can recover - if caries producing irritant removed

ASAP

clinically - pain that lingers


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Differences between Pain Symptoms

Reversible Irreversible

ElicitedSharp

< 20 minutes duration

Unaffected by body

position

Easily localized

SpontaneousDull

> 20 minutes duration

Affected by body

position

Difficult to localize Refs. 1, 3


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Pulp Necrosis

Discoloration

of tooth

It is the term applied to pulp tissue that is no longer living

A result of a sudden trauma (e.g. a blow to the tooth in

which blood supply has been severed), there will be

no symptoms for a time

Ref. 1


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Common

Diagnostic Techniques (1)1. History and nature of the pain

2. Reaction to thermal changes

3. Reaction to mild electric stimulation4. Reaction to percussion of the tooth

5. Radiographic examination

6. Visual clinical examination

7. Palpation of the surrounding tissue


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Common

Diagnostic Techniques (2)

History and Nature of Pain

Reversible pulpitis: sharp and intense

Irreversible pulpitis: dull, nagging, vague in location


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Common

Diagnostic Techniques (3)Reaction to Thermal Changes

Reversible pulpitis: immediate, sharp pain, last for

up to 20 minutes

Irreversible pulpitis: less sharp, last for a much

longer time


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Common

Diagnostic Techniques (4)Reaction to Electric Stimulation

Reversible pulpitis: nerves will be easily excitedrespond at a lower than normal voltage

Irreversible pulpitis: nerves severely damaged

a higher level of voltage


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Common


Reaction to Percussion of Tooth

Percussion pain indicates an inflammation in the apical

periodontal tissue.

It is useful when pain is vague and offending tooth is

not apparent.


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Common

Diagnostic Techniques (6)Radiographic Examination

It is useful to determine if the inflammatory response has

reached the periapical tissue.

The presence of a radiolucency at tooth apex is a great help

to determine the vague pain in mandible or maxilla.


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Common


Ref. 4


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Common


Ref. 4


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Common


Ref. 3


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Common


Ref. 3


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Common


Ref. 3


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Common


Ref. 3


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Common


Visual Examination

It may reveal a cortical expansion of alveolar bone

A small, raised, reddish papule (parulis) over tooth apexindicating an opening of the sinus tract of periapical abscess

Ref. 1


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Common


Palpation of Surrounding Tissues

It indicates that the inflammation has reached the tissue

surround tooth apex

This is an indication that pulp is necrotic required treatment


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Histopathology of

Pulpal DiseaseAcute Pulpitis

Pulp horn

Intrapulpal

hemorrhage

Ref. 1


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Histopathology of

Pulpal Disease

Chronic Pulpitis

Spherical

calcification

Dystrophic

(linear)

calcification Ref. 1


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Histopathology of

Pulpal Disease

Chronic Hyperplastic Pulpitis

1. It is a rare condition that is primarily confined to the molars of children

2. It is the result of rampant acute caries in young teeth that quickly

reaches the pulp before it becomes completely necrotic.

Ref. 1


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Periapical Lesions

Major factors involve

Presence of an open or closed pulpitis

Virulence of the involved microorganisms

Extent of sclerosis of the dentinal tubules

Competency of the host immune response


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Chronic Apical Periodontitis

It is the earliest radiographic evidence of extension of theinflammatory process from the pulpal chamber into the

adjacent periodontal membrane around the apical foramen

Chronic Acute

Chronic apical periodontitis

Periapical granuloma

Periapical cyst

Periapical abscess

Osteomyelitis

Chronic

Osteomyelitis

Garre

Osteomyelitis

Cellulitis

Ref. 1


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Periapical Granuloma

1. It occurs when a pulpitis progresses into a periapicallesions

2. The most common lesion occurs after pulpal necrosis

3. It is usually painless, progresses slowly, and seldom

becomes very large

Well-defined radiolucency

with corticated outline

Radiography

Ref. 1


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Periapical Cyst

Histopathology

1. It is a common development of long-standing, untreatedperiapical graunoma

2. The epithelial lining is derived from rests of Malassez

3. The rests are stimulated to proliferate by low-grade

inflammation of the periapical granuloma

Epithelial proliferation

Cystic space

Epithelial

distintegration

Ref. 1


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Periapical Cyst

Histopathology

Cystic

lumen

Epithelial

lining

Cholesterol

Fibrous capsule

Ref. 1


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Radiography

Periapical Cyst

Ref. 1

A t P i i l C diti


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Acute Periapical Conditions

Factors associated

Young tooth with open tubules

Rampant caries

Closed acute pulpitis

Presence of high virulent microorganisms

Weakened host defense system

Ref. 3


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Periapical Abscess

Histopathology

1. It is the initial lesion that develops when the circumstancesare adverse.

2. The most painful patient condition and is potentially one of

the most dangerous

3. Progression of acute pulpitis that has exudates extending

to adjacent soft and hard tissues.

Ref. 1


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Periapical

abscess

Ref. 7


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Periapical

abscess

Ref. 7


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SUMMARY (1)

DENTAL CARIESEpidemiology

Clinical TypesEnamel Caries

Dentin Caries


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SUMMARY (2)


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infection of teeth

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