1.
DISEASE OF HARD TISSUES
OF TEETH AND PERIAPICAL
AREA
Dr Birke Bogale

2.
Objectives
 Define Dental caries
 Explain Causes, Risk factors and
Prevention of Dental caries
 Explain - Presentation
- Diagnosis
- Treatment of dental caries,
diseases of the pulp and
periapical tissue
 Identify different types of caries, diseases
of the pulp and periapical tissue

3.
DISEASE OF HARD TISSUES OF
TEETH
Dental Caries
Also called tooth decay.
It usually occurs in children and
young adults, but can affect any
person.
It is a common cause of tooth loss
in younger people.

4.
Facts, WHO 2003
 Dental diseases are the most
prevalent chronic diseases worldwide,
and a costly burden to health care
services.
 Expensive treatment: 5 -10% of total
health care expenditures in
industrialized countries.
 Dental caries: High prevalence rate in
most developing low-income countries
more than 90% of caries is untreated.
 An estimated 5 billion people worldwide
suffer from dental caries (tooth decay).

5.
Etiology
Common Bacteria:
Streptococcus species ; S. Mutans
Lactobacillus species Bacteria
Actinomyces species
Other Risk factors
Teeth Anatomy Sugar Time
Life style (Frequency of snacking, OH, infant feeding,
etc.)
Carbohydrates, sticky foods
Systemic Ds. (Metabolic, eating do, Immunity, etc.)
Worn dentures, appliances & fillings
Fluoride
D.
Carie
s

6.
 Bacteria: Normally present in the
mouth.
Convert all foods especially
sugar and starch into acids.
 Bacteria, acid, food debris and saliva
combine in the mouth to form a sticky
substance called plaque that adheres
to tooth surface.
 It is most prominent on molars, just
above the gum line on all teeth and at
the edges of fillings.

7.
The acids in plaque dissolve the enamel
surface of the tooth and create holes in
the tooth (cavities).
Cavities are usually painless until they grow
very large and affect nerves or cause a
tooth fracture.
Untreated tooth decay also destroys the
internal structures of the tooth (pulp) and
ultimately causes the loss of the tooth.

8.
Medical factors associated with
increased caries risk
Factors Risk increasing observation
Gender Female > Male
Age Children and adolescents
are more prone
Fluoride exposure No or less fluoride in
drinking water
Smoking Risk increases with intake
Alcohol Risk increases with intake
General Health Chronic illness and
debilitating disease
Medication Medication- w/c decrease
salivary flow E.g.-Atropine
-Antiepileptics
-Pills /hormone

9.
Clinical sites for caries initiation
1. Pit and fissures of enamel – most
susceptible
2. Smooth surface of crown (proximal) –
Second susceptible
3. Root surface (cervical area) –
Third susceptible site
4. Sub gingival area

10.
Presentation
 Highly variable.
 Risk factors and stages of development
are similar.
 Initially it may appear as a small chalky
area (Incipient caries), large
cavitation.
 With continued acid attack the surface
changes from being smooth to rough and
may become stained.

11.
Note: -
Penetration of enamel caries into the dentino-
enamel junction rapid lateral
expansion
DEJ has least resistance to caries attack.
Progression and morphology of carious lesion
is variable depending upon;
-Site of origin
-The condition of the mouth (oral
hygiene).

12.
Diagnosis
 Visual inspection: white spots or darker
inactive lesions
 Probing: soft surface and cavity
 Radiographic exam. (Bitewing or OPG) :
essential for interproximal caries,
◦ current radiographic techniques lack
sensitivity in recognizing non-cavitating
lesions or root surface caries.
 Newer techniques: quantitative light-
induced fluorescence and fiber-optic trans
illumination are currently under
development and may improve caries
detection.

13.
* Rampant caries
Acute and rapid infectious process,
usually involving several teeth. It is
usually occurred in children or infants.
Causes: -
Dietary habits
Poor oral hygiene
Systemic illness

14.
*Secondary caries
It is caries of filled teeth.
It may occur due to defective margin of
restoration and if caries is not completely
removed before cavity preparation.

15.
*Arrested Caries
Under favorable conditions,
a lesion become inactive, even regress.
Clinically arrested dentine caries has a
hard or leathery consistency and is darker
in color than soft, yellow active decay.
Arrested enamel caries can be stained
dark brown.

16.
Prevention
Three main approaches are possible:
1. Tooth strengthening or protection
2. Reduction in the availability of microbial
substrate.
3. Removal of plaque by physical or chemical
means;
practically: dietary advice,
fluoride,
Pit and fissure sealing
regular tooth brushing.
The relative value of these varies with age of the
individual.

17.
Saliva
1.Has buffering action (effect) against bacteria
and act as intra-oral antacid due to its alkali
PH at high flow rate
2.Has flushing effect – wash away bacteria and
decrease plaque accumulation.
3.Produce antimicrobial products such as IgA,
lysozyme, lactoferin, agglutins and
lactoperioxidase
4.Has remeneralization effect, as it is
supersaturated with calcium, phosphate and
fluoride ions which give opportunity for
remeneralization of enamel.

18.
Treatment
1. Fillings : by removing the decayed tooth
part with a drill and replacing with filling
material.
 Aesthetic filling materials:
GIC, Porcelain and composite resin
More closely match the natural tooth
appearance and preferred for front
teeth.
 Non-aesthetic filling materials:
Silver amalgam (alloy) and gold
Considered to be stronger and are often

19.
2. Crowns or "caps"
 Used if tooth decay is extensive & limited tooth
structure, which may cause weakened teeth.
 Large fillings and weak teeth increase the risk of
the tooth breaking.
 The decayed or weakened area is removed and
repaired.
 A crown is fitted over the remainder of the tooth.
 Crowns are often made of gold, porcelain or
porcelain attached to metal.
 They are also used on fractured teeth due to
trauma.

20.
3. Root canal treatment
 Recommended if the nerve in a tooth dies.
 The center of the tooth, including the nerve and
blood vessel tissue (pulp), is removed along with
decayed portions of the tooth.
 The root chamber and canals are filled with a
sealing material.
 The tooth is filled and a crown may be placed
over the tooth, if needed.

21.
The development stages of
dental caries
a. Enamel caries: No pain
b. Dentine caries: maybe sensitive to
hot, cold and sweet foods/drinks and
eating hard things; there may be pain
c. Pulp involved: severe continuous or
throbbing pain
d. Abscess: deep acute pain which may
disappear after a while.

22.
Disease of the pulp and periapical
Tissues
I. Disease of the pulp (Pulpitis)
Pulpitis - Inflammation of pulp
Etiology: -Dental caries (primary cause)
-Tooth fracture; expose dental
pulp to oral fluids and bacterias
-Chemical irritation to pulp; filling
-Severe thermal change; common in
large metallic restoration

23.
Classification:
1. Pulp hyperemia (Focal Reversible
Pulpitis)
Earliest form of pulpitis
Cause: -Deep caries
-Large metallic restoration
(especially with no adequate
insulation)
-Restoration with defective margin
CF: -Sensitive to thermal changes, particularly
to cold, but disappears upon removal of the
stimulus or restoration of normal
temperature.

24.
2. Reversible pulpitis
CF:- Fleeting sensitivity / pain to hot, cold or
sweet with immediate onset
-pain usually is sharp and may be difficult
to locate
-Quickly subsides after removal of
stimulus (pain <10 min)
Rx:-Filling with sedative dressing (if needed)
or permanent restoration with suitable pulp
protection.

25.
3. Irreversible Pulpitis
CF:-Spontaneous pain which may last several hours
(>10 min), be worse at night and is pulsatile in
nature
-Pain elicited by hot and cold at first
-Heat will be more significant and cold may
actually ease symptoms in later stages .
-Localization of pain may be difficult initially,
- As the inflammation spread to the Periapical
tissue, tooth will become more sensitive to
pressure.
-Tender to percussion
Rx: -RCT, treatment of choice
-Extraction

26.
Diseases of periapical tissues
 Once infection has become established in the
dental pulp, spread of the process can be in
one direction through the root canals and into
the periapical region.
 Progression of irreversible pulpitis ultimately
leads to death of the pulp (pulpal necrosis).
 At this stage the patient may experience
relief from pain.
 If neglected, the bacteria and the pulpal
breakdown products leave the root canal
system via the apical foramen lead to
inflammatory changes and possibly severe
pain.

27.
Here a number of different tissue reactions
may occur, depending on the
circumstances
The periapical lesions don’t represent
individual and distinct entities, but rather
that there is a subtle transformation from
one type of lesion into another type in
most cases.
Note: - Sensitive to percussion is first
evidence that infection has spread beyond
the confines of the pulp.

28.
1. Apical periodontitis (Periapical granuloma)
Granuloma :-Essentially localized mass of chronic
granulation tissue formed in response to infection
CF:-Sensitive to percussion, due to edema,
hyperemia and inflammation of apical periodontal
ligament.
-Mild pain occasioned on biting or chewing solid
foods
-In some cases tooth feels slightly elongated in its
socket and may actually be so.
Rx: -Extraction
-RCT, under certain condition with or without
subsequent apicectomy

29.
2. Apical periodontal cyst
Cyst – Pathological cavity lined by epithelium and is
often fluid filled
APC- is common and developed over long period of
time.
Cause:- Sequela of periapical granuloma
- Necrosis of dental pulp
CF:-The majority is asymptomatic and present no
clinical evidence of their presence.
-Seldom painful even sensitive to percussion.
-Long standing may undergo acute exacerbation of
inflammatory process and develop rapidly into an
abscess may then proceed to a cellulites or draining
fistula.
Rx: -Extraction and curette of periapical tissue,
carefully
-RCT and apicectomy with inoculation in some

30.
3. Periapical Abscess (Dentoalveolar Abscess)
An acute or chronic suppurative process of the
dental periapical region.
CF:-Tooth is extremely painful
-Slightly extruded from its socket
-Seldom severe systemic manifestation, regional
lymphadenitis and fever may be present
-Rapid extension to adjacent bone marrow spaces
frequently occurs producing an actual
osteomyelitis.
Rx: -Drainage by either opening the pulp chamber
or extraction
-RCT, sometimes
Note: - If not treated, leads to Orofacial soft tissue
infections, osteomyelitis, bacteremia, etc.