DENTAL CARIES AS

FOCUS OF SEPSIS

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 Definition

• Dental caries is defined as a microbiological disease

of the hard structure of teeth, which results in localized
demineralization of the inorganic portion and destruct
on of the organic substances of the tooth.

• Cariology is a science which deals with the study of

etiology, histopathology, epidemiology, diagnosis,
prevent on and treatment of dental caries.

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 Sites of Dental caries
• Pits and fissures on occlusal surfaces of molars and premolar

• Buccal pits of molars

• Palatal pits of maxillary incisors

• Enamel of the cervical margin of the tooth just coronal to the gingival
margin

• Proximal enamel smooth surfaces apical to the contact point

• In teeth with gingival recession occurring because of periodontal disease

• The margins of restorations predominantly which are defcient or

overhanging

• Tooth surfaces adjacent to dentures and bridges. 3

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 Etiology of Dental Caries Possible interventions

Reduce Strep. mutans

numbers by:
Possible interventions
Reduction in sugar intake
Reduce intake of cariogenic
Active or passive
sugars Particularly sucrose
immunization
Diet Bacteria

Caries

Possible interventions
Water + other types of
Susceptible
Time Fluoridation
Surface
Possible interventions (Host) Prevention during post-
eruptive maturation
Avoid frequent
Fissure sealing
sucrose intake
(snacking) Properly contured
restorations
Stimulate salivary flow 5
+ sugar clearance
 Etiology of Dental Caries

Plaque

Acidogenic Enzymes Food Acids Tooth Carious

Bacteria
Lesions

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 Theories of Dental caries

1. Acidogenic theory

2. Proteolytic theory

3. Proteolysis-chelation theory.

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 Acidogenic Theory
 1890

 WD Miller

 dental decay is a chemoparasitic process consisting of 2

stages

1. Decalcification of enamel results in total destruction

decalcification of dentin as a preliminary stage
2. Followed by dissolution of softened residue of
enamel and dentine

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 Factors that cause decay

(1)Role of carbohydrates

(2)Role of microorganisms

(3)Role of acids

(4)Role of dental plaque

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 Role of Carbohydrates
Carbohydrates exert cariogenic effect which depends upon the
following factors:
1. Frequency of intake

2. Chemical composition, for example, monosaccharides and

disaccharides are more carious than polysaccharides

3. Physical form like solid, sticky jelly like or liquid

4. Time of contact of carbohydrate with the tooth

5. Presence of other food components like presence of high fat or

proteins makes carbohydrate less cariogenic.
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 Role of microorganisms
 caused by acid resulting from action of microorganisms on
carbohydrates
 S. mutans has been proved for the initiation of caries
Initiation of Dental Caries Progression of Dental
Caries
Streptococci Streptococcal species:
• S. mutans Streptoccal species in
• S. milleri deep dentinal caries
• S. mitior and root caries
• S. sanguis
• S. salivaris
Lactobacilli Lactobacilli in dentin
• L. acidophillus • L. acidophillus
• L. casei • L. casei
Actinomycoses Actinomycoses
• A. viscosus • A. Israeli
• A. naeslundii • A. odontolyticus
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 Role of Acids

 play most important role in pathogenesis of dental caries

 pH 5.5 is called critical pH

 Below this pH demineralization of tooth substance begins

found
on uncleaned tooth surfaces

 appear as tenacious, thin film

 may accumulate within 24-48 hours

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 Role of Dental Plaque

Dental plaque also known as microbial plaque is important

for beginning of caries because it provides the environment
for bacteria to form acid, which causes demineralization of
hard tissue of teeth.

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 Proteolytic Theory

 proteolysis of the organic components of tooth as an

initial process
 than actual demineralization + dissolution of
inorganic substances
 proposed that enamel lamellae or rod sheath
(proteins) may be lysed
 which means proteolysis as first event in further
progression of bacterial invasion + demineralization
carious lesions

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 Proteolysis Chelation Theory
Suggests that caries is caused by simultaneous event of
proteolysis + chelation
Proteolysis
destruction of organic portion of tooth by proteolytic
microorganisms
Chelation
removal of calcium by forming soluble chelates

 oral bacteria attack organic component of enamel

(proteolysis)

 breakdown products have chelating ability and this dissolves

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Local factors affecting the incidence of
caries
• Tooth (Host)
– Variation in morphology
– Composition
– Position.

• Substrate
(Environmental factors)
– Saliva
i.Composition
ii.Quantity
iii.pH
iv.Viscosity
v.Antibacterial factors.
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• Diet
i Physical factors
ii. Local factors
a.Carbohydrate content: Presence of
refined cariogenic carbohydrate particles
on the tooth surface
b.Vitamin content
c.Fluoride content.
d.Fat content

• Microorganisms: Most
commonly seen microorganisms
associated with caries are
Streptococcus mutans and
Lactobacillus.

• Time period. 18
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 Classification
(1) Depending on nature of attack

(2) Depending on progression of caries

(3) Depending on surfaces involved

(4) Based on direction of attack

(5) Based on number of surfaces involved

(6)GV Black Classification based on treatment and

restoration design

(7) Based on location of lesion

(8) Based on tissue involved 21

 (1) Nature of Attack
Old Theories

 Primary Caries

 incipient; initial

 first attack on tooth

surface

 Secondary Caries

 recurrent

 occurs on margins or
walls of existing
restorations
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 (2) Progression of Caries
Old Theories

 Acute
 usually pulp is involved at early
stage
• Rampant caries
• Nursing bottle caries
• Radiation caries

 Chronic
 lesions are long standing
 fewer in number
lesions are long standing
 fewer in number 23
 (3) Surfaces involved
Old Theories

 Pit and fissure

 Smooth surface caries

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 (4) Direction of caries attack
Old Theories
 Forward Caries  Backward Caries

 proceeds from  proceeds from DEJ

enamel to dentin towards enamel surface

 lesion is triangle in shaped  also triangle shaped with

with base of triangle at base at DEJ + apex
enamel surface + apex towards enamel surface
towards
dentin

 in pits + fissures base is at

DEJ + apex in the pit
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Old(5) Number of Surfaces involved
Theories
 Simple

 only one surface is

involved by caries

 Compound

 2 surfaces are involved

 Complex

 more than 3 surfaces

involved
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 (6) GV Black Classification
Old Theories

 Class I

 begin in pits, fissures

+ defective grooves

 seen in occlusal
surface

 occlusal two-thirds
of molars

 lingual pits of
incisors 28
Old Theories

 Class II

 lesions seen on
proximal aspects of
molars + premolars

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Old Theories

 Class III

 lesions involving
proximal aspects of
incisors

 do not involve or
necessitate removal of
incisal edge

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Old Theories

 Class IV

 lesions involving
proximal aspects of
incisors

 involve or require
removal of incisal
edge

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Old Theories

 Class V

 lesions present on gingival

third of all teeth

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Old Theories

 Class VI

 lesions found on
incisal edges + cusp
tips

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Old Theories
(7) Location of the lesion
 Pit and Fissure caries

 Occlusal
 Buccal or lingual pit

 Smooth surface caries

 Proximal
 Buccal or Lingual
surface

 Root caries
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Old Theories (8) Tissue involved

 Enamel Caries

 Dentinal Caries

 Cemental Caries

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 Zones in Enamel caries

• Zone 1: Translucent zone

• – Represent the advancing

front of the lesion

• – Ten times more porous

than sound enamel

• – Not always present.

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• Zone 2: Dark zone

• – It lies adjacent and superficial

to the translucent zone

• – Usually present and thus

referred as positive zone

• – Called dark zone because it

does not transmit polarized
light

• – Formed due to
demineralization.

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• Zone 3: Body of the lesion

• – Largest portion of the

incipient caries

• – Found between the surface

and the dark zone

• – It is the area of greatest

demineralization making it
more porous.

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• Zone 4: Surface zone

• – This is zone is not or least

affected by caries

• – Greater resistance probably

due to greater degree of
mineralization and greater
fluoride concentration

• – It is less than 5 percent

porous
• – Its radiopacity is comparable
to
adjacent enamel. 40
 Zones of Dental caries

• Zone 1: Normal dentin

• – Zone of fatty degeneration of

Tome’s fibers

• – Formed by degeneration of the

odontoblastic process

• – Otherwise dentin is normal

and produces sharp pain on
stimulation.

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• Zone 2: Zone of dentinal
sclerosis

• – Intertubular dentin is
demineralized

• – Dentinal sclerosis, i.e. deposition

of calcium salts in dentinal tubules
takes place

• – Damage to the odontoblastic

zone process is apparent

• – There are no bacteria in this

zone.
Hence, this zone is
capable of remineralization. 42
• Zone 3: Zone of
decalcif cation of
dentin

• – Further
demineralization of
intertubular dentin
lead to softer dentin.

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• Zone 4: Zone of bacterial
invasion

• – Widening and distortion

of the dentinal tubules
which are f lled with
bacteria

• – Dentin is not self-repairable,

because of less mineral
content and irreversibly
denatured collagen

• – This is zone should be

removed during tooth
preparation.
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• Zone 5: Zone of
decomposed dentin due
to acids and enzymes

• – Outermost zone

• – Consists of decomposed
dentin filled with bacteria

• – It must be removed during

tooth preparation.

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Clinical Features: Smooth Surface Caries

 Interproximal Caries

 opaque chalky region (white spot)

 some cases yellow or brown pigment area

 spots are generally located on outer surface of enamel

between contact point + height of free gingival margin

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 Cervical, Buccal, Lingual or
Palatal Caries
 Clinical Features:

 usually extends from

area opposite gingival
crest occlusally to
convexity
of tooth surface

extends laterally
towards proximal
surfaces
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 Clinical Features:

 usually occurs on cervical

area

 typical cervical lesion is a

crescent shaped cavity
beginning as slightly
roughened chalky area

 gradually becomes
excavated
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 Pit and Fissure Caries

 Clinical Features:

 appears brown or black

 feel slightly soft

 catch a fine explorer point

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 enamel bordering the
pit and fissure may
appear

• opaque
• bluish as it becomes
white undermined

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 lateral spread of caries at DEJ as well as
penetration into dentin along dentinal tubules
may be extensive

 without fracturing away overhanging enamel

 there may be large carious lesion with only a tiny point of

op4e7 ning
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 Root Caries

 also known as cemental

caries

 involves both dentin +

cementum

 Increase in number of people

exhibiting gingival recession
with clinical exposure of
cemental surface

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 Clinical Features:

 slowly progressing chronic lesion

 usually found in mandibular molar area +

premolar region

 gingival recession is associated with root surface

caries

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 Recurrent Caries

 occurs immediately adjacent

to restoration

 may be caused by inadequate

extension of restoration

 was not able to excavate or

removed well original carious
lesion

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 Clinical Features:

 restoration with
poor margins

• permitted leakage +
entrance of both
bacteria + substrate

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 Etiology:

 due to nursing bottle

containing milk or
milk formula, fruit
juice or sweetened
water

 sometimes it occurs
due to sugar or honey-
sweetened pacifier

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 Pathogenesis:

 child is put on bed at afternoon nap time or at night

with nursing bottle containing milk or a sugar containing
beverage

milk or sweetened liquid becomes pooled around

maxillary anterior teeth

carbohydrate containing liquid provide an excellent

culture medium for acidogenic microorganisms

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 Clinical Feature:

 prolonged feeding beyond usual time may result in early +

rampant caries

 early carious involvement of maxillary anterior, maxillary +

mandibular 1st permanent molars, mandibular canines

 carious process is so severe that only root stumps remain

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 Prevention:

 parent should start brushing the child teeth as soon as

they erupt in oral cavity

 discontinue bottle feeding as soon as child can drink from

a cup, at approximately 12-15 months of age

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 Rampant Caries

 suddenly appearing

 widespread

 resulting in early
involvement
of pulp

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 Etiology:  Clinical Features:

 may be due to  occurs in children with

nutritional deficiency poor dietary habits

 malnutrition
 extensive inter-proximal
 emotional + smooth surface caries
disturbances

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Sequelae of Dental Caries
 Sequelae of Dental Caries

Enamel Caries

Dentine Caries

Pulpitis
Acute Chronic

Acute Apical Peridontitis

Chronic
Periapical Periapical Granuloma
Abscess
Acute Chronic
Acute Osteomyelitis Chronic

Periapical cyst
Periosteitis

Cellulitis Abscess
 FOCAL REVERSIBLE PULPITIS:

• due to dentinal and pulpal

irritation
• pulp hyperemia

C/F:
• Tooth sensitive to thermal
changes
• Responds to low current in EPT
• Application of ice results in pain
but disappears
on removal
 ACUTE PULPITIS:
• extensive acute
inflammation of pulp
• frequent sequel of focal
reversible pulpitis
• Pain is due to pressure built
up due to lack of
exudate escape

C/F:
• pain persists even after
removal of thermal stimuli
• Lacinating or throbbing
type pain
• Responds to low current in
EPT
 CHRONIC
3.
PULPITIS:
• Due to quiescence of a previous
acute pulpitis or may be chronic from
onset

• Reduced pain and reaction to

thermal change due to degeneration of
nerves

• Granulation tissue formation

• Response to high current in EPT

 APICAL PERIODONTITIS :

• Inflammation of the
periodontal ligament around
the root apex
• Due to spread of infection
following pulp necrosis
• May be ACUTE or
CHRONIC

A. Acute apical periodontitis:

• Tenderness on mastication
• May cause reabsorption of
surrounding bone
• Widening of periodontal
space
Chronic apical periodontitis (periapical
granuloma):

• Common sequelae of
pulpitis
• Localized mass of chronic
granulation tissue at the
apex of non vital tissue
• Thickening of ligament at
the root apex
 APICAL PERIODONTAL CYST
(PERIAPICAL CYST)
• Due to bacterial infection and
necrosis of pulp
• Usual sequela of the
periapical granuloma
• Lined by epithelium and fluid
filled
• Lining epithelium is derived
from epithelial rests of
Malassez
 PERIAPICAL ABSCESS
(ALVEOLAR ABSCESS):
• Acute or chronic
suppurative process of
the periapical region.

• May develop from

acute periapical
periodontitis or
• from periapical
granuloma.

• Localized collection of pus

in the alveolar bone at the
root apex following death
 Osteomyelitis:

• Inflammation of bone and bone marrow

• Sequela of periapical infection resulting in diffuse
spread of
infection throughout the medullary space
• Necrosis of jaw bone
 Cellulitis:
• Inflammation of soft tissues which
tends to
spread through tissue spaces and
facial planes
• Caused by organisms producing
hyaluronidase and fibrinolysins
• Cellulitis of face and neck occurs as
sequela of an apical abscess or
osteomyelitis
Prevention/Management of Dental Caries

 Restorative Treatment

 Tooth Brushing

 Mouth Rinsing

 Dental Floss

 Topical Fluoride Application (Pedo

Patients)

 Pit and Fissure Sealants

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 Different ways of caries prevention
• Chemical Method
• Fluoride: Fluoride alters the tooth surface or/and tooth structure to
increase resistance to demineralization and prevent dental caries.
Fluorides are used in the following forms:

a.Fluoridation of water supplies

b.Topical application of fluoride
i. Sodium fluoride (NaF)
ii.Stannous fluoride (SnF2)
iii.Acidulated fluorido-phosphate
iv.Prophylactic paste
v.Fluoride dentifrices
vi.Fluoride mouthwashes or
rinses.
• Chlorhexidine
• Zinc chloride
• Caries vaccine 75
Dietary Method
Caries can be prevented by the restriction of intake of
refined carbohydrate. Sucrose is most cariogenic
carbohydrate, hence its use in food should be
restricted.

Mechanical Methods
• Tooth brushing
• Dental floss
• Mouth rinsing
• Pit and fissure sealants

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Thank you