Transcript 投影片 1 - 口腔病理科教學網

口 腔 病 理 科
Infection of tooth:
Caries, pulpitis & periapical
lesions
齲齒、牙髓炎與根尖病變
陳玉昆教授: 高雄醫學大學 口腔病理科
07-3121101~2755
[email protected]
學 習 目 標 (1)
DENTAL CARIES
Etiology
Epidemiology
Clinical Types
Enamel Caries
Dentin Caries
學 習 目 標 (2)
PULPITIS
Reversible Pulpitis
Irreversible Pulpitis
Pulp Necrosis
Common Diagnostic Techniques
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
Histopathology of Pulpal Diseases
Acute Pulpitis
Chronic Pulpitis
Chronic Hyperplastic Pulpitis
學 習 目 標 (3)
Periapical Lesions
Chronic Apical Periodontitis
Periapical Granuloma
Periapical Cyst
Acute Periapical Conditions
Periapical Abscess
參考資料
References
1.
2.
3.
4.
5.
6.
7.
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14.
15.
Sapp JP: Contemporary Oral & Maxillofacial Surgery, p. 61-87
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
http://www.ne.jp/asahi/fumi/dental/
www.teethwhiteningkits.com/tooth_decay/t5_tooth_decay_children.htm
www.odonto-red.com/cariesdental.htm
www.lezerdent.hu/cariesn.htm
www.areadent.cl/
www.kavo.com/Es
www.uic.edu/classes/dh/dh110/Caries_files
http://iwate8020.jp/know/caries.html
http://www.suwaneedental.com/cariesprevention.htm
http://www.drfarid.com/fluoride.htm
Oral Pathology Department, Kaohsiung Medical University
Opal S, Garg S, Jain J, Walia I. Genetic factors affecting dental caries risk.
Aus Dent J 2015; 60:2-11
維基百科
Etiology
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 of infection with acidic and proteolytic
bacteria for enamel caries
Etiology
Refs. 3, 4
Etiology
Mechanism of dentin sensitivity
(Transient receptor potential channel, TRP)
• Neurogenic
• Hydrodynamic
• Odontoblastic
Refs. 1, 3
Etiology
Venn diagram showing interplay of genetic factors
Ref. 14
Etiology
http://www.experimentalgameplay.com/game.php?g=46
Refs. 4, 6
Etiology
Refs. 10, 11
Etiology
The Caries Balance
Pathological Factors
Protective Factors
Acidogenic bacteria
[Streptococci mutans]
Reduced salivary function
Frequency of fermentable
carbohydrate ingestion
Saliva flow & components
Proteins, calcium phosphate
fluoride, immunoglobulins
in saliva
Extrinsic chlorhexidine
Caries
No Caries
Saliva - contains materials for remineralization
- calcium and phosphate ions
Healthy tooth enamel rods
Refs. 5, 12
Enamel rods demineralized
(broken down by acid)
Enamel rods remineralized,
rebuilt, by fluoride & minerals in saliva
Etiology
製作氟托 (Fluoride tray)
Refs. 13
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
(i.e. certain segments of US, Western Europe,
New Zealand, and Australia)
Cause of decline?
It is attributed to fluoride
DENTAL PLAQUE =
gelatinous mass of bacteria
Ref. 5
Clinical Types
 Pit and fissure
 Smooth surface
 Cemental
 Recurrent
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
Clinical Types (2)
Ref. 6
Clinical Types (3)
Low laser
Ref. 8
Clinical Types (4)
Ref. 8
Clinical Types (5)
Ultrasonic caries detector
檢查前先將受檢牙齒吹乾、棉卷擦乾，
再將感應器放置在頰側並且直接面對受檢鄰接面
Ref. 2
Clinical Types (6)
Smooth surface caries: less common
:occurs on the labial
surface & proximal area
Ref. 1
Clinical Types (7)
Refs. 1, 6
Clinical Types (8)
Cemental (root) caries
1. 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
Clinical Types (9)
Recurrent caries arises around an existing restoration
as a result of marginal leakage
Marginal leakage is a situation predispose the tooth to
accumulate bacteria (av. diameter: 2000 nm), and food
Clinical Types (10)
Acute (rampant) caries and chronic caries are terms used
to denote the rate that dental caries progresses in patients
Ref. 4
Clinical Types (10)
Rampant caries
Frontal view
Upper view
Lower view
Ref. 13
Enamel Caries (1)
Smooth surface enamel caries is most commonly located on
the 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
Arrested form
- chalky appearance
Advanced form
- Cavitation
Ref. 1
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 hard
Active caries - cavitated, weak enamel, surface is soft
Ref. 1
Enamel Caries (3)
Hypocalcified enamel –
restore only for esthetics
Incipient caries –
 anti-microbial (remineralization)
 restore (after remineralization)
 only for esthetics
Arrested caries (remineralized) –
 restore only for esthetics
Active caries –
 anti-microbial + restorative
Enamel Caries (4)
Histopathology – Four zones on ground section
1.
2.
3.
4.
Translucent zone: advancing front of initial demineralization
Dark zone: remineralization
Body of lesion: region of maximal demineralization
Surface zone: remain unaffected until it is collapsed forming a cavity
Surface zone
Body of
lesion
Dark zone
Translucent
zone
Enamel
Ref. 1
Enamel Caries (5)
Incipient Lesion - 4 Zones
Zone 1 - translucent zone
Zone 2 - dark zone
Zone 3 - body of the lesion
Zone 4 - surface zone
B
SZ
lesion = cone shaped
Ref. 9
body of lesion (B) appears dark beneath relatively INTACT SURFACE ZONE
Enamel Caries (6)
Incipient Lesion - 4 Zones
Zone 1 - translucent zone
Zone 2 - dark zone
Zone 3 - body of the lesion
Zone 4 - surface zone
TZ
DZ
B
Ref. 9
TRANSLUCENT ZONE (TZ) present at advancing front of lesion
DARK ZONE superficial to TZ
Enamel Caries (7)
Zone 1 - translucent zone
1. deepest zone - closest to pulp
2. advancing front of lesion
3. appears structureless - (polarized light)
4. pore volume - 1% - > 10 normal enamel
5. pores/voids form along prism boundary
due to ease of hydrogen ion penetration
from caries process
Enamel Caries (8)
Zone 2 - dark zone
1. does not transmit polarized light
2. caused by presence of lots of tiny pores
which are too small to absorb quinoline
(奎林)
(C9H7N ) (polarized light)
3. air/vapor filled pores - opaque
4. pore volume - 2 to 4 %
5. remineralization - increase in size of dark
zone
6. size of dark zone - indication of amount
of remineralization
Ref. 15
Enamel Caries (9)
Zone 3 - body of lesion
1. 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 Retzius –
which provides access to rod prism cores
5. BACTERIA may enter if pores large enough
Enamel Caries (10)
Zone 4 - surface zone
1. 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 process –
may result in rough, but hard surface
Dentin Caries (1)
This stage of caries progression requires a different mixture
of 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
Dentin Caries (2)
Dentin caries advance through 3 changes
1. weak organic acid demineralizes dentin
2. organic material of dentin (mostly collagen)
is degenerated and dissolved
3. loss of structural integrity,
followed by bacterial invasion
Dentin Caries (3-1)
Enamel
Dentin
Five
microscopic
zones
5
4
3
2
1
Ref. 1
Dentin Caries (3-2)
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 within
dentinal tubules
Zone 5: cavitation, no mineralization and organic component is partially
dissolved by the bacteria
Bacteria in
dentin tubules
Liquefaction
Ref. 1
Dentin Caries (4)
Dentin - 5 zones of slowly progressing lesion
Zone 1 - Normal dentin
Zone 2 - Subtransparent dentin (affected)
Zone 3 - Transparent dentin
Zone 4 - Turbid dentin
(in advanced lesions - infected)
Zone 5 - Infected/Necrotic dentin
Dentin Caries (5)
Zone 1 - Normal dentin
 dentinal tubules with smooth odontoblasts
 no crystals in lumen
 NO BACTERIA in tubules
 stimulation - elicits pain
Dentin Caries (6)
Zone 2 - Subtransparent dentin
 AFFECTED - not infected
 zone of demineralization - by acid from caries
 capable of remineralization
 damage to odontoblastic processes
 NO BACTERIA
 stimulation - elicits pain
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
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
Dentin Caries (9)
Zone 5 - Infected dentin
 NECROTIC dentin in advanced lesions
 decomposed dentin
 lots of BACTERIA
 no recognizable dentin structure
 no collagen / no mineral
 must be REMOVED
Pulpitis
It is an inflammation of the pulpal tissue that may be acute or
chronic, with or without symptoms, and reversible or irreversible.
Ref. 1
Reversible Pulpitis
Decision of reversible or irreversible pulpitis
1. Conservatively restore the defective tooth structure
2. Removed the disease pulp disease
3. Remove the entire tooth
1. Whether pain is spontaneous or stimulated
2. Duration of pain
3. Nature of pain described by patient
Ref. 7
Reversible Pulpitis
Reversible pulpitis/hyperemia
limited inflammation of pulp
tooth can recover - if caries producing irritant removed
ASAP
clinically - pain that lingers <10 seconds
hyperemia = increased blood flow and volume
pulp surrounded by dentinal walls
which limits drainage of this increased
blood flow/ volume
Irreversible Pulpitis
Inflammation of pulp
Tooth can NOT recover– if caries producing irritant
removed ASAP
Clinically - pain that lingers > 10-15 seconds
Throbbing, continuous pain
Pain upon heat relieved by cold
Partial / total pulp necrosis
Treatment – endo / extraction
Ref. 3
Differences between Pain Symptoms
Reversible
Irreversible
Elicited
Sharp
< 20 minutes’ duration
Unaffected by body
position
Easily localized
Spontaneous
Dull
> 20 minutes’ duration
Affected by body
position
Difficult to localize
Refs. 1, 3
Pulp Necrosis
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
Discoloration
of tooth
Ref. 1
Common
Diagnostic Techniques (1)
1. History and nature of the pain
2. Reaction to thermal changes
3. Reaction to mild electric stimulation
4. Reaction to percussion of the tooth
5. Radiographic examination
6. Visual clinical examination
7. Palpation of the surrounding tissue
Common
Diagnostic Techniques (2)
History and Nature of Pain
Reversible pulpitis: sharp and intense
Irreversible pulpitis: dull, nagging, vague in location
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
Common
Diagnostic Techniques (4)
Reaction to Electric Stimulation
Reversible pulpitis: nerves will be easily excited
respond at a lower than normal voltage
Irreversible pulpitis: nerves severely damaged
a higher level of voltage
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.
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.
Common
Diagnostic Techniques (6)
Radiographic Examination
Ref. 4
Common
Diagnostic Techniques (6)
Radiographic Examination
Ref. 4
Common
Diagnostic Techniques (6)
Radiographic Examination
Ref. 3
Common
Diagnostic Techniques (6)
Radiographic Examination
Ref. 3
Common
Diagnostic Techniques (6)
Radiographic Examination
Ref. 3
Common
Diagnostic Techniques (6)
Radiographic Examination
Ref. 3
Common
Diagnostic Techniques (7)
Visual Examination
It may reveal a cortical expansion of alveolar bone
A small, raised, reddish papule (parulis) over tooth apex
indicating an opening of the sinus tract of periapical abscess
Ref. 1
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
Histopathology of
Pulpal Disease
Acute Pulpitis
Pulp horn
Intrapulpal
hemorrhage
Ref. 1
Histopathology of
Pulpal Disease
Chronic Pulpitis
Spherical
calcification
Dystrophic
(linear)
calcification
Ref. 1
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
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
Chronic Apical Periodontitis
It is the earliest radiographic evidence of extension of the
inflammatory process from the pulpal chamber into the
adjacent periodontal membrane around the apical foramen
Chronic
Chronic apical periodontitis
Periapical granuloma
Periapical cyst
Acute
Periapical abscess
Osteomyelitis
Chronic Cellulitis Garre’
Osteomyelitis
Osteomyelitis
Ref. 1
Periapical Granuloma
1. It occurs when a pulpitis progresses into a periapical
lesions
2. The most common lesion occurs after pulpal necrosis
3. It is usually painless, progresses slowly, and seldom
becomes very large
Radiography
Well-defined radiolucency
with corticated outline
Ref. 1
Periapical Granuloma
Histopathology
Remodeling cortical bone
Fibrous tissue
Granulation tissue
Root apex
Ref. 1
Radicular (Periapical) Cyst
1. It is a common development of long-standing, untreated
periapical 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
Histopathology
Epithelial proliferation
Cystic space
Epithelial
distintegration
Ref. 1
Radicular (Periapical) Cyst
Histopathology
Cystic
lumen
Epithelial
lining
Cholesterol
Fibrous capsule
Ref. 1
Radicular (Periapical) Cyst
Radiography
Ref. 1
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
Periapical Abscess
1. It is the initial lesion that develops when the circumstances
are 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
Histopathology
Ref. 1
Periapical
abscess
Ref. 7
Periapical
abscess
Ref. 7
下列何者是reversible pulpitis的特徵?
a)Difficult to localize
b)Sharp pain
c)Dull pain
d)Spontaneous pain
e)Long duration
(1) a, b, d (2) b (3) c, d (4) e
SUMMARY (1)
DENTAL CARIES
Epidemiology
Clinical Types
Enamel Caries
Dentin Caries
SUMMARY (2)
PULPITIS
Reversible Pulpitis
Irreversible Pulpitis
Pulp Necrosis
Common Diagnostic Techniques
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
Histopathology of Pulpal Diseases
Acute Pulpitis
Chronic Pulpitis
Chronic Hyperplastic Pulpitis
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