1.
DENTAL CARIES
A PRESENTATION BY DR.J. O. OLAOYE

2.
Outline
 INTRODUCTION
 Aetiology
 Pathophysiology
 Signs and Symptoms
 Diagnosis
 Treatment

3.
Introduction
Dental caries simply means tooth decay.
 It is infectious, slowly progressive,
communicable.
 The development is dynamic, resulting
from interplay of four (4) principal factors.
 Results from imbalance between
demineralization and remineralization
process.

4.
Enamel is the hardest substance in the body
and is composed of 96 % minerals and the
remnant being organic substance.The
enamel is rightly classified as acellular
tissue.The mineral component is basically
hydroxyapatite, this forms the hard tissue
structure of the tooth.These minerals
become soluble in acidic environment.

5.
Normal Anatomy

6.
Aetiology of Dental Caries

7.
Aetiology
For dental caries to occur there must be
interplay of four main factors:
 Susceptible tooth surface
 Fermentable carbohydrate
 Caries causing bacteria
 Time
Though the above factors must be present for

8.
caries to occur, it is not definite that
cavity must form.There are other
determinant factors that
influence the process…The shape
of the teeth, level of oral hygiene
and buffering capacity of the
saliva.

9.
Susceptible Tooth Surface
 Some areas are rough naturally, for instance the
pits and fissures. Other areas are made rough by
:plaque and calculus formation, poorly cleansed
areas, friction due to rough diet.
 Certain diseases and disorders make teeth
vulnerable to decay e.g. Amelogenesis
imperfecta.
 Gingival recession expose root surfaces to decay,
decay is faster here due to absence of enamel.

10.
Caries Causing Bacteria
The oral cavity contains a wide range of
microorganism but only few species
of bacteria has been implicated in
caries formation, e.g. Streptococcus
mutans, Lactobacilli acidophilis,
Actinomyces isreali.These bacteria
has the ability to produce high level of
lactic acid following the breakdown of

11.
Dietary sugars.They are resistant to the
effect of low ph.These bacteria
collect around the teeth in a sticky
creamy coloured mass called plaque
which serves as biofilm.The pits and
fissures provide high retention site.

12.
Fermentable Carbohydrate
 If left in contact, the aforementioned
bacteria acts on fermentable
carbohydrate (glucose, fructose and
sucrose) and convert it acids (lactic
acid) through a glycolytic process
called fermentation.The acid formed
causes demineralization with teeth.

13.
If this is one time process over a long
time, there is possibility of
remineralization. But when the rate of
demineralization is higher than
remineralization, the amount of hard
tissue component lost is high leading
to disintegration of the organic
component left behind thereby
forming cavity.

14.
Time
 This has to do with frequency at which the
teeth is exposed to cariogenic
environment and the duration of exposure.
After a refined carbohydrate rich meal, the
bacteria in the mouth converts the
fructose, sucrose and glucose into acids
resulting in drop in pH.The higher the
frequency, the higher the chances of caries
formation.

15.
Stephan Curve

16.
 The curve shows sudden decrease in
plaque pH following a glucose rinse,
which returns to normal after 30-60
mins. Net demineralization occurs at
below the critical pH of 5.5.This
happens in reality after consumption
of our usual soft drink and refined
juice.

17.
Other factors
 Disease condition associated with reduced
salivary flow, under this circumstance the
buffering effect of saliva is lost. Examples
include Sjogren syndrome, diabetes
mellitus, sarcoidosis.
 Medications, such as antihistamines and
antidepressants can reduce salivary flow.
Tetrahydrocannabinol found in cannabis
impair salivary flow.

18.
Pathophysilogy
The bacteria in the saliva consumes refined
carbohydrate, utilizing it for its energy
needs, acid is produced. Acid produced
causes demineralization of hard tissue
structure of the teeth.When the rate of
demineralization is faster than
remineralization, the mineral content is
lost, leading to crumbling of the remaining
organic structure.

19.
Enamel:
The rate of progression here is slow. Enamel
rods which are the basic unit of the enamel
structure, run perpendicularly from the
surface of the tooth to the dentine.The
demineralization follows the direction of
enamel rods,the different triangular patterns
between pit and fissure and smooth-surface
caries develop in the enamel because the
orientation of enamel rods are different in the
two areas of the tooth.

20.
Dentine:
Unlike enamel, the dentin reacts to the
progression of dental caries. Presence
of caries in dentine can initiate a
process leading to formation of
sclerotic and tertiary dentine.This is
aimed at reducing the rate of
progression and prevent the exposure
of the pulp.

21.
Sign and Symptoms
The earliest sign of tooth decay is the
appearance of chalky white spot on the
surface of the tooth, indicating an area of
demineralization. If the oral hygiene
improves at this stage this spot will turn
brown(shiny), the progression
stops.Otherwise the demineralization will
continue till cavity is formed.When once
cavity is formed, there must be intervention.

22.
When the cavity is restricted to the enamel,
in about 98% of the cases the individual is
not aware of the cavity. Enamel being
acellular, nil sensation. As the caries
progresses into the dentine the individual
will experience different level of sensation
on exposure to fluids and chewing.The
pain becomes throbbing when the pulp is
exposed.

23.
Diagnosis
Presentation is highly variable. Primary
diagnosis is made using a good light source,
dental mirror and explorer.
Dental x-rays are used for less visible areas and
to judge the extent of destruction.
Large dental caries are visible to the naked eye.
Visual and tactile inspection along with
radiographs are used in diagnosing pit and
fissure caries. Lasers can also be used.

24.
Treatment (Restoration)
No carious
lesion
NoTreatment
Carious lesion Inactive lesion No treatment
Active lesion Non cavitated lesion Non operative
treatment
Cavitated lesion Operative
treatment
Existing filling No defect No replacement
Defective filling Ditching, over hang No replacement
Fracture or food
impaction
Repair or replace
filling
Inactive lesion No treatment
Active lesion Non cavitated lesion Non operative tx
Cavitated lesion Repair or replace
filling

25.
Treatment
 Root canal treatment
 Extraction

26.
REFERENCES
 British Dental Journal 2013
 Journal of American Dental Association 2010
 Dental Caries Article by Prof. Dickson
Ufomata
2000