DISEASE OF HARD TISSUES OF

TEETH AND PERIAPICAL AREA

Dr Birke Bogale
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
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.
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).
Etiology

Common Bacteria:
Streptococcus species ; S. Mutans
Lactobacillus species Bacteria
Actinomyces species
D.

Other Risk factors Teeth Anatomy Caries

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
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.
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.
Medical factors associated with increased caries risk 

Factors Risk increasing observation

Gender Female > Male
AgeChildren 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
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
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.
 
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).
 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.
 * 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
*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. 
*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.
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.
 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.
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 used
on back teeth
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.
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.
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.
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
 
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.
Rx: - Filling
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.
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
 
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.
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.
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
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 condition
 
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.