infection of teeth
TRANSCRIPT
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Caries, pulpitis & periapical
lesions
:07-3121101~2755
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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
Diagnostic Techniques (5)
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
Diagnostic Techniques (6)Radiographic Examination
Ref. 4
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Common
Diagnostic Techniques (6)Radiographic Examination
Ref. 4
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Common
Diagnostic Techniques (6)Radiographic Examination
Ref. 3
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Common
Diagnostic Techniques (6)Radiographic Examination
Ref. 3
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Common
Diagnostic Techniques (6)Radiographic Examination
Ref. 3
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Common
Diagnostic Techniques (6)Radiographic Examination
Ref. 3
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Common
Diagnostic Techniques (7)
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
Diagnostic Techniques (8)
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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