DENTAL CARIES SIDDHARTH GAUTAM-76.

DEFINITION
Microbial disease of the calcified tissues of the teeth, characterized
by demineralization of the inorganic portion and destruction of the
organic portion of the teeth
DMF INDEX
The most commonly employed method to measure the extent of
previous damage to permanent dentition.
DMF(T) – decayed, missing, and filled teeth
DMF(S) – decayed, missing and filled surfaces
The def(t) and def(s) – primary dentition
FACTORS AFFECTING
CARIES
PREVALENCE
Race – American blacks have fewer carious lesions than whites.
Age – cumulative with age
Gender – females
Familial – siblings of individuals with high caries susceptibility are
also caries active, whereas siblings of caries immune individuals
exhibit low caries rate.
EARLY THEORIES
THE LEGEND OF WORMS – Caries is caused by worms 5000 BC
ENDOGENOUS THEORIES –
Humoral theory – Greek physician – caries produced by
internal action
of acids and humors
Vital theory of tooth decay – tooth decay originated like a bone
gangrene, from within the tooth itself – Greek physician
CHEMICAL THEORY – An unidentified chymal agent was responsible
for caries – Parmly 1820s. Robertson 1835 proposed that decay was
caused by acid formed by fermentation of food particles.
 MILLER’S ACIDOGENIC THEORY /
MILLER’S CHEMICO-PARASITIC
•

•
Dental caries is chemoparasitic process
• It is a 2 stage process – decalcification of enamel
which also results in the destruction of dentin by the
acid attack
• Dissolution of the softened residue of enamel and
dentin is carried
• by the proteolytic action of the bactereia.
PROTEOLYTIC THEORY
Enamel contains 0.56% of organic matter
Microorganisms produce proteolytic enzymes which destroy the
organic matrix of enamel, loosening the apatite crystals which are
eventually lost and tissue collapses.
Organic portion of enamel – enamel lamellae and enamel rods prove
to be the pathways for the advancing microorganisms.
PROTEOLYSIS – CHELATION
THEORY
Proposed by Schatz and his co-workers in 1955
Chelation – it is a process in which there is complexion of the metal
ions to form complex substances through coordinate covalent bond
which results in poorly dissociated or weakly ionised compound.
The bacterial attack on the surface of enamel results in the
breakdown of the protein, chiefly keratin and results in the formation
of soluble chelates with calcium which decalcify enamel even at
neutral pH.
Mucopolysaccharides may also act as secondary chelators.
BASED ON ANATOMIC SITE
OF THE LESION
 Pit and fissure caries
 Smooth surface caries
 Cervical caries
 Root caries
PIT AND FISSURE CARIES
Develop on the occlusal surface
of molars and premolars, the
buccal and lingual surface of the
molars and the palatal surface
of the maxillary incisors.
Prone to caries – poor self
cleansing
May appear brown or black and
feel slightly soft and catch to a
fine explorer.
SMOOTH SURFACE CARIES
Proximal surface of teeth just
below the contact point or on the
gingival third of the buccal and
lingual surfaces
Generally preceded by formation
of a microbial plaque
CERVICAL CARIES
It is typically a crescent shaped
cavity beginning as a slightly
roughened chalky area which
gradually becomes excavated.
It is always an open cavity
It can occur on any tooth without
predilection and is directly
related to lack of oral hygiene.
ROOT CARIES
A soft progressive lesion that is
found anywhere on the root
surface that has lost connective
tissue attachment and is exposed
to the oral environment.
Predominantely seen in older age
groups with significant gingival
recession and exposed root.
BASED ON SEVERITY AND
RATE OF PROGRESSION
 Acute dental caries
 Chronic dental caries
ACUTE DENTAL CARIES
It is the form of dental caries
which runs a rapid course and
results in early pulp involvement.
Children and young adults
No reparative dentin
Dentin is light yellow stained
Pain is not an invariable finding
CHRONIC DENTAL CARIES
It progresses slowly and tends to
involve the pulp much later
Sclerosis of the dentinal tubules
and deposition of reparative
dentin
The carious dentin is often
stained dark brown
OTHER CLINICAL VARIANTS
 Rampant caries
 Nursing bottle caries
 Adolescent caries
 Recurrent caries
 Arrested caries
 Radiation caries
RAMPANT CARIES
Sudden, severe destruction of
teeth, affecting surfaces that are
relatively caries free
A caries increment of 10 or more
new carious lesions over a
period of one year is
characteristic.
Primary dentition of young
children and permanent dentition
of teenagers.
NURSING BOTTLE CARIES
A form of rampant caries
affecting decidous teeth
Attributed to prolonged use of
nursing bottle containng milk or
milk formula, fruit juice or
sweetened pacifiers,
breastfeeding and sugars.
ADOLESCENT CARIES
Acute exacerbation in caries rate
usually seen at 4 – 8 years of
age and 11 – 18 years of age.
Relatively small opening in the
enamel and with extensive
undermining of enamel
RECURRENT CARIES
Reccurent caries is that type
which occurs in the immediate
vicinity of a restoration.
It is usually due to inadequate
extension of the margins of the
restoration or poor adaptation of
the filling material to the cavity
which produces leaky margins.
ARRESTED CARIES
It has been described as caries
which becomes static and does
not show any tendency for
further progrssion.
Eburnation of dentin –
superficially softened and
decalcified dentin is gradually
burnished until it takes on a
brown stained, polished
appearance.
RADIATION CARIES
The development of rampant
caries in patients undergoing
radiation therapy in the head and
neck region.
Involves the cusp tips, incisal
edges and the cervical areas