2. Dental caries
“It is an infectious microbiologic disease of
the teeth that results in localized dissolution
and destruction of thecified tissues.”
2
3. Classification
natomic site
Pit & fissure
Smooth surface
Proximal
Cervical
Root surface
of progression
Active or Acute
Arrested or Chronic
3
4. classification
Hard tissue involved
Enamel
Dentin
Cementum
Etiology
Radiation
According to age
Nursing bottle
Geriatric caries
4
8. Few facts
Sucrose greatly stimulates plaque metabolism
Periods of demineralization & remineralization
Some 200 to 300 species of bacteria, yeast & protozoa present in
oral cavity
sm associated with caries in man
8
11. rning the etiology of caries
ic plaque hypothesis
l plaque is pathogenic
plaque hypothesis
Recognizes plaque as pathogenic only when signs of
associated disease are present
11
12. ment Based on the Medical
Model
Etiology MS infection
Symptoms Demineralization lesions
ment, symptomatic Restoration of cavitated
lesions
ment, therapeutic Eliminate MS infection
atment assessment, Examine teeth for new
lesionssymptomatic
Bacteriologic testing for MSatment assessment,
therapeutic
12
14. Acidogenic theory
Dental decay is caused by acids produced by microbial enzymatic
action on ingested carbohydrates. These acids will decalcify the
inorganic portion of the teeth; then the organic portion is
disintegrated, creating cavities.
14
15. Proteolysis theory
Organic portion of the tooth is attacked first by certain
lytic enzymes, leaving inorganic portion without a matrix
ing it to be washed away, creating cavities
15
16. Micrbiotic Secretions theory
Metabolic products of MO have the ability to chealate
calcium from tooth substances, leaving the organic matrix
to be disintegrated
16
17. ace without caries.
of demineralization.
face has broken down.
demineralization has not been stoppe
5. The demineralization proceeds and undermines the
tooth. 6. The tooth has fractured.
18. chanism of DENTAL CARIES
Host ( tooth)
Parasites ( plaque mo)
Medium ( carbohydrates)
18
25. Stephan’s curve
Demonstrates the acid production of bacteria
(pH decrease) with a glucose swallow & the
gradual rise due to salivary buffering.
25
30. Smooth enamel surfaces
Presence of caries in these areas usually is indicative of a caries
active mouth.
The proximal enamel surfaces immediately gingival of the
contact area
Col
In very young patients, the gingival papilla completely fills
the interproximal space under a proximal contact
30
39. Subgingival areas
ulcus habitat is unique
Initial occupants of the sulcus are only an extension of the
plaque community on the immediately adjacent surface of the
tooth
Immunologic materials may change some characteristics of the
adjacent plaque by removing the most susceptible organisms.
Plaque changes progressively from cocci in the supragingival
plaque to filamentous bacteria & spirochetes in subgingival
plaque
39
40. ve as ecologic determinants
Oral hygiene
Available nutrients
Sulcular fluid
Saliva
Bacterial clearance
Direct antibacterial activity
Buffers
Remineralization
40
42. es/white spot lesion
al carious lesion
limited to enamel
intact surface but a
porous subsurface.
Chalky white, opaque
Seen only when the
surface is desiccated
42
45. Arrested lesion
It is an intact, but discolored, usually brown or
black spot
e, hard on excavation
Should not be restored unless esthetically
objectionable
45
49. Active lesions
White spot lesions that have a matte or visibly
frosted surface or are plaque covered after
drying or application of a disclosing agent.
Cavitated lesions, including micro cavities as
well as cavities exposing dentin.
hery in consistency
ntin on bitewing radiograph
49
61. Dentinal caries
Normal Dentin
Deepest area
Normal odontoblastic processes
No crystals are in the lumen
Intertubular dentin has normal cross banded
collagen
Normal dense apatite crystals
No bacteria
f dentin produces a sharp pain
61
62. btransparent Dentin
Demineralization of the intertubular dentin
Initial formation of very fine crystals in tubule
lumen
Damage to the odontoblastic process is evident
No bacteria are found
Stimulation of the dentin produces pain
Dentin is capable of remineralization
62
63. Transparent Dentin
Zone of carious dentin softer than normal Shows
further loss of mineral from intertubular dentin Large
crystals in the lumen
Stimulation of this region produces pain
No bacteria
This region remains capable of self repair provided the
pulp remains vital.
63
64. ne 4: Turbid Dentin
bacterial invasion
Distortion of dentinal tubules which are filled with
bacteria
Very little mineral present & collagen is irreversibly
denatured
o self repair
oved before restoration
64
65. e 5: infected Dentin
Consist of decomposed dentin teeming with bacteria
No recognizable structure to dentin & collagen
Mineral seem to be absent
oval is essential
ushy in appearance.
65
66. Dentin
ected dentin
aminated with bacteria
Includes superficial granular necrotic tissue, &
softened, dry, leathery dentin
ected dentin
Comparatively hard, demineralized dentin that is not
yet invaded by bacteria
66
70. e) that may be associated with
caries
Sweet
-sharp, last seconds
♦Hot & cold
-sharp, lasts seconds
♦Hot & cold
-lingers, “throbbing”
♦Constant throb
-pain starts off by itself
♦Painful on biting
Severity does not always relate to extent and
“toothache” can present as any one of the above
71. Clinically, how would you treat the different
types of carious dentin ?
71
74. Caries diagnosis
ies diagnosis are to identify those
that require surgical treatment
lesions that require nonsurgical treatment
persons who are at high risk of
developing lesions.
74
75. sk assignment for caries
MS counts are found
of the following are found
Two or more active lesions
Large no of restorations
Poor dietary habits
Low salivary flow
75
76. W RISK PATIENT
avitated lesions
May have inactive white spots (smooth shiny).
Bacteria MS levels are low
Diet is normal sugar levels low
Normal Saliva levels
Low DMF
77. TE RISK PATIENT
avitated lesions
Some active white spot lesions (rough/chalky)
Bacterial MS levels elevated
erate sugar use
Saliva normal or reduced (xerostomia)
Moderate DMF
78. H RISK PATIENT
ore cavitated lesions
May have white spot lesions (active or inactive)
Bacterial MS levels are very high
ntake very high
Saliva levels low (xerostomia)
High DMF
85. can we do about caries?
1.Prevent
mount) of “substrates”(sugars)
r, tablets, mouthrinse, salt)
♦Regular visits to dentist, including placement of fissure
sealants
ve plaque removal
2.Treat
lling & Filling
♦Extract
89. o Difficulties
o place an initial restoration?
own of the outer enamel is an
clinical indicator of the treatment
to deal with severe caries?
Protection of dental pulp is the
primary goal
90. nt of Fissured Surface
es or Arrested Enamel Demineralization Cavitation or
n Fissures with or Questionable Caries in Caries in Dentin
ble Morphology Dentin
Low High Low HighOpen fissuresCaries Caries
with round burRisk? Risk?
enamelDemineralization dentin
involve
reatment Sealant RestorationEnamel PRR
98. Caries control restoration
The goal is elimination of the source of
cariogenic organisms by removal of caries
from all deep lesions and placement of
temporary restorations early in the treatment.
99. Caries Control Restoration
Cavity preparation is done quickly without
definitive cavity preparation.
Undermined enamel be left to aid in retention
of these treatment restorations, especially if
restoratives are used that bond
ooth structure.
100. Control Restoration
Restorative materials used for caries control
restoration.
CaOH
Reinforced Zinc Oxide-eugenol
Glass ionomer
Amalgam
102. Indirect pulp capping
All infected dentin is excavated with large round burs
and excavators, being careful not to expose the pulp.
Basic fuchsin effectively identifies infected dentin.
A small amount of firm caries (affected dentin) is left
over sites of potential exposure.
103. Indirect pulp capping
Calcium hydroxide liner is placed in the deepest areas.
The high pH of the CaOH will neutralize acid, kill
bacteria and stimulate formation of restorative
dentin.
The rein-forced ZOE, glass ionomer or amalgam
restoration is placed
108. Properties Of Cutting
Instruments
rt & ease of use
Discriminate & remove disease tissue
Painless, silent, req. minimal pressure
No heat or vibration
Affordable
109. hanical caries removal
a gel that selectively attacks denatured collagen in the
carious dentine, thus making the carious dentine
softer.
a set of specially designed
instruments used for
moval of the
ened material.
110. Carisolv gel consists of two carboxymethylcellulose based
gels:
gel containing :
amino acids (glutamic acid, leucine and lysine),
NaCl
NaOH
Erythrosine (added in order to make the gel visible during
use ).
aining sodium hypochlorite
111. The gels are mixed & then applied onto the exposed
carious dentine and left for 30 to 60 seconds then the
softened dentine is gently but firmly abraded away
leaving a hard, caries-free cavity
112. A soft caries lesion Gel application. Let gel slide onto the
lesion. Wait 30 seconds.
Re-applied gel stays clear. Cavityis gently scraped with
is hard with a probe.tar instrument
113. gel is removed with a
Complete caries removal is
dry pellet
checked with an explorer
cavity is cleaned with
Finished cavity
wet pellets
114. antages :
althy tooth structure,
Virtually no risk of inadvertent pulp exposure,
Reduce the need for anesthesia and allow for
same-visit cavity preparations on multiple
quadrants,
e post-operative sensitivity.
115. Sono abrasion
Sono abrasion technique is based on the
removal of tooth material by an air-
driven hand piece equipped with a
diamond-coated working tip that
removes tooth material by ultrasonic
netic energy.
