Examination of the Teeth

• Preceeded by careful prophylaxis

• Be able to determine the normal

variations of the teeth in terms of:

• Color, size, form, structure and

number
 Color
• Primary teeth are generally bluish white
• Permanent teeth are generally more
opaque with variations of gray and yellow
hues as the person gets older
 Color changes in Teeth
Inherent color is determined by the
translucency and thickness of the enamel
and underlying dentin
• Alteration may be physiologic or
pathologic and intrinsic or extrinsic
• Qualitative and quantitative change in
dentin
• Yellowing of dentin, general loss of
translucency, pigmentation and inadequate
oral hygiene
 Disturbance in color due to Intrinsic
Factors
• Causes can either occur during tooth
development and those acquired later in life
– Dental caries
– Fluorosis
– Dental Trauma
– Pulp necrosis
– Internal resorption
– Root canal treatment
– Amalgam fillings
– Tetracycline and its derivatives
– Genetic disorders
 Dental caries
• Begins as an opaque white spot on the surface
of the enamel and as demineralization
progresses it cavitates and the underlying
brown color becomes visible
 Fluorosis

• Occurs when there is chronic and excessive

exposure to fluoride during tooth
development
– Appears as a small opaque white flecks on the
enamel surface and on severe cases it appears as
hypoplastic patches of enamel and is prone to
accumulation of surface stains
 Dental Trauma
• Appears as reddish discoloration or blue-
brown discoloration
 Pulp necrosis
• Teeth may turn grey weeks or months after
injury due to incorporation of pigments
released during the breakdown of pulpal
tissue and blood into the dentin
 Internal resorption
• Appears as a pink hue occurs when the dentin
is resorbed and replaced by a hyperplastic
vascular pulp tissue
 Root canal treatment
• Maybe due to incomplete debridement of the
necrotic soft tissue of the pulp or certain root
canal materials (gutta percha or canal sealer
cements)
 Amalgam fillings
• Amalgam pigments slowly leaches out casting
a shadow that is visible through the tooth and
make it appear darker
 Endogenous Stain
• It resu
• Characterized by bands
or zones of discoloration
that may vary in color
from yellow to brown
gray
 Genetic disorders
• Enamel hypoplasia
• Enamel hypocalcification
• Amelogenesis imperfcta
• Dentinogenesis imperfecta
• Congential porphyria (Gunther disease)
• Hyperbilirubinemia
• Thalassemia and sickle cell anemia
 Amelogenesis Imperfecta and
Dentinogenesis Imperfecta
• AI - Enamel is fragile, teeth appears yellow or
brown and surface stains build up easily

• DI – Defect in dentin formation and teeth may

appear discolored yellow brown, deep amber
or blue grey with increased in translucency
 Hypocalcified type:
(mottled enamel)

• Color is from white

to yellow to brown
• Chalky enamel
surface may be
gradually worn
away
 Radiographic features
(dentinogenesis imperfecta)
• Partial or complete absence of
pulp chambers and root canals
• Roots are short and occasional
root fracture seen.
Histologically,
Dentin is quite irregular with a
laminated appearance, tubules
are larger and fewer in number
than normal
 Congenital Porphyria
• Characterized by severe skin photosensitivity
that could lead to scarring and blistering
• Effect in the synthesis of RBC in the bone
marrow
• Treatment is blood transfusion or spleen
removal to reduce the amount of porphyrin
produced by the bone marrow. Avoid
exposure to sunlight
 Hyperbilirubinemia
• Bilirubin is incorporated into the dental hard
tissues during tooth formation causing yellow
green or blue green discoloration
Thalassemia and sickle cell anemia
 Disturbances in Color due to
extrinsic pigmentation
• Introduction of
medicaments
• Metallic staining
from ingestion or
inhalation of metals Excessive use of Chlorhexidine

on their salts due to

drugs or
occupational hazards
• Use of tobacco
Severe tobacco stain
 Anomaly according to size
• Microdontia-teeth
smaller than normal

• Macrodontia-
abnormal increase
in tooth size
Abnormalities in Tooth Shape
 Fusion

developmental anomaly in which at least 2 separate

tooth germs fuse together to form a common tooth
structure
 Gemination
• aborted twining of a
single tooth genes.
• Production of two
crowns on a single root
with complete or
incomplete separation
of the crown.
 Concresence
union of 2 adjacent
teeth by excessive
cementum
production
 Dilaceration
• An unusual bend or
position of a tooth
root
• Most often involve is
the third molar
 Dens en Dente
• Developmental
anomaly in which
there is invagination
of the enamel from
the crown portion
apically
 Enamel Pearl
• a discreet globule of
enamel that is
usually located near
the cemento-enamel
junction on the root
surface of the
maxillary molars
 Talon Cusp
• Commonly located
on the lingual
surface of maxillary
incisors and a pulp
horn often
accompanies the
cusp
 Anomaly according to number
• Anodontia- complete
• Hypodontia-absence of
one or few teeth
• Hyperdontia- extra or
supernumerary
deciduous or
permanent teeth
 Acquired Defects of Teeth
Noncarious Loss of Tooth Structure
 Abrasion
• pathologic loss of
tooth structure
caused by
abnormal
mechanical wear
 Attrition
physiologic wearing
down due to
frictional contact
 Abfraction
(stress induced cervical lesions)

pathologic loss of
tooth structure
caused by abnormal
biomechanical
loading
 Erosion

loss of tooth structure

caused by chemicals
, gastric, or
environmental acids
Acquired Defects of Teeth:
Carious Tooth
 Incipient, initial or primary carious
lesion

• Described as the caries

first attack on tooth
• Commonly seen in pits
and fissures
Recurrent, Secondary caries

• Usually observed under or around the

margins of the surrounding walls of an
existing restoration
 Acute or Rampant caries

• Rapidly invading
process that usually
involves several teeth
 Chronic caries

• Variable depth, longer standing and tend to be

fewer in number
 Senile carious lesion
• Associated with aging
process
• Almost at the root
• Follows the advanced
gingival recession
Diagnosis of Dental Caries
Armamentarium
1. Explorer- sharp
-press on the pits
and fissures with
forces parallel to
the blade
2. Radiographs
use of bitewings, periapical
radiograph

3. Discoloration
-gray hue on marginal ridge
-for older persons- leathery dark
brown color (organic material)
4. Patient’s Complaints
-sweet, hot, cold that may cause osmotic
pressure within the dentin causes
subjective complaints (suspect dentin
involvement)
5. Dental Floss
-fraying or shredding of the floss connotes
caries
6. Separation of the Teeth
- Use wedge or any
mechanical separator
to visualize if the
proximal surface have
caries
7. Transillumination
- light source is passed
lingually
- Shadow of caries can
be visualized
Evaluation of Pulpal and Periapical diseases

1. Subjective Examination
-pain description includes: intensity, spontaneity,
continuity of pain
(quality and quantity of pain)

2. Objective Examination
- examination of intraoral and extraoral tissue and be
able to compare bilaterally for presence and
absence of pathosis
3. Clinical Test

-includes the use of mouth mirror and

explorer to reveal gross and recurrent
caries, pulp exposures, crown fractures
and defective restoration
 CONTROL TEETH
• important adjunct to pulp and periapical
tests
• teeth are normal and healthy
• to determine the stimulus if it is capable of
invoking a response
• to observe the nature of the patient’s
response to certain stimulus
• similar tooth preferred
4. Periapical Tests
 Percusssion

• To determine the presence of periradicular pathosis

• Marked positive response indicates inflammation
• Periodontal Inflammation is more likely to moderate to mild
response
• Periapical inflammation is sharp, causing a withdtrawal response
 Palpation

• To determine how far the inflammation process

has extended periapically
 5. Pulp Vitality Test
• To determine the
response to stimuli and
occasionally can identify
the offending tooth by
an abnormal response
• Direct dentin
stimulation, cold and
hot or electricity
Hot Test
Cold Test
 Electric Pulp
Tester
 6. Periodontal Examination
• Important because
periapical and periodontal
lesions mimic each other
and require
differentiation
• Probing is necessary to
determine the pocket
depth
 7. Mobility
• to determine the status of the
periodontal ligament
 8. Radiographic Examination

• Allows evaluation of tooth related problems

• Periradicular lesions in its early stages are not

detected
Periradicular lesions of pulpal origin will give the
following characteristics:

1. Lamina dura is lost apically

2. Lucency ramains at the apex
3. Lucency resembles a hanging drop
4. Pulpal necrosis is sometimes evident
(more translucent)
 Pulpal Diseases

• Reversible
• Irreversible
• Necrosis
• Normal pulp – Pulp is symptom free and
normally responsive to vitality testing

• Symptomatic – Lingering pain, spontaneous

pain, referred pain

• Asymptomatic – No clinical symptoms but

inflammation produced by caries, caries
excavation, trauma is present
 Reversible Pulpitis
• Pulpal inflammation which resolves once the
etiology is removedMost common site

• Most common site of occurrence

– Primary and permanent teeth
– Site of recent of defective restoration
– Sites of recent trauma
• Signs
– Caries
– Exposed dentin

• Symptoms
– Non lingering pain to temperature
 Irreversible Pulpitis
• Pulpal inflammation which will not resolve
once the etiology is not removed
• Site of occurrence same with reversible
pulpitis
• Signs : deep caries
• Symptoms
– Intense, lingering pain to temperature changes
– Spontaneous sharp pain
– Diffuse pain
 Dx of Irreversible Pulpitis
• Pain from cold test lingers more than 30s
• May get pain from heat test
• May have spontaneous sharp
• Sensitive to percussion
• Radiographically or clinically visible deep
caries
• Accentuated by postural changes
 Pulp Necrosis
• Pulp non responsive to pulp testing and is
asymptomatic
• Pulp necrosis does not cause apical
periodontitis unless the canal is
infectedUnresponsive teeth to pulp testing
maybe due to calcification, trauma
Periradicular Diseases
• Acute Apical Abscess

• Acute Apical Periodontitis

• Chronic Apical Abscess

• Chronic Apical Periodontitis

 Normal Apical Tissues
• Symptoms None
• Radiograph No periapical change
• Pulp test Responds normally
• Periapical test (-) percussion, palpation
• Lamina dura Intact
 Acute Apical Abscess
• Formation of purulent exudate (PUS)
• Swelling of associated tissues
• Rapid onset
• Spontaneous and severe pain
• Tenderness of tooth to pressure
• No response to pulp test
• There may be no radiographic sign
• Fever, malaise, lymphadepathy
 Chronic Apical Abscess

• Gradual onset of infection

• Little or no discomfort
• Intermittent discharge pus with associated
sinus tract
• Osseous destruction (radiolucency)
 Symptomatic Apical Periodontitis
• Inflammation of the periodontium
• Painful response to biting and percussion
• May or may not be associated with apical
radiolucency
Asymptomatic Apical Periodontitis
• Appears as a radiolucent area
• Does not produce clinical symptoms
• Inflammation and destruction of apical
periodontium
 Pulpal Diseases
Clinical Vitality Test Percusion Radiographic
signs and Palpation Interpretation
symptoms
Hot Cold Test
Cavity
Clearly
delineated canal
Mild to moderate transient (-) when that tapers
Within Asymypto response to thermal and percussed smoothly
Normal matic electrical stimulus is removed and toward the apex.
Limit Response subsides almost palpated No evidence of
immediately when the stimulus calcification or
is removed root resorption.
Lamina dura is
intact
 Clinical signs Vitality Test Percus Radiographic
and symptoms sion Interpretation
Palpa
tion
Hot Cold Test
Cavity
Quick, sharp, Clearly
hypersensitive (-) (+) (-) delineated canal
response that Moment when that tapers
subsides as soon ary pain Percus- smoothly
Reversible as the stimulus is sed and toward the apex.
Pulpitis removed (usually palpa No evidence of
cold) ted calcification or
root resorption.
Otherwise Lamina dura is
asymptomatic intact
No spontaneous
pain
 Clinical Vitality Test Percusion Radiographic
signs and Palpation Interpretation
symptoms
Hot Cold Test
Cavity
(+) percus Thickening of
Necrosis Asympto (-) (-) (-) sion periodontal
matic (-) ligament,
palpation tenderness to
mastication
 Percussi
Clinical Signs Hot Cold Test on/ Radiographic
and Symptoms Cavity Palpatio Interpretation
n
Pain Not significant
lingers Advanced stage
Maybe acute or after of symptomatic
subacute or (+) stimulus (+) (-) irreversible
Irreversible chronic is (+) pulpitis-
Pulpitis removed thickening of the
(symptomatic) Symptomatic apical portion of
Spontaneous the periodontal
(unprovoked) ligament
intermittent or
continuous
Moderate, severe,
sharp or dull,
localized or
referred.
 Percus
Clinical Signs Hot Cold Test sion/ Radiographic
and Symptoms Cavity Palpa Interpretation
tion

With Internal
Irreversible prolonged resorption,
Pulpitis e.g. Symptoms Canal
(Asymptomatic) hyperplastic (-) (-) (-) (+) to calcification-
pulpitis, percussion identified in the
(-) palpation radiograph
internal
resorption,

canal
calcification
 Periapical Disease
Disease Clinical Signs Vitality Per Palpa Mobility Radiographic
and symptoms cussion tion Interpretation
Acute Apical Painful May occur Periodontal
Periodontitis inflammation of in vital and ligament may
periodontal non-vital appear normal,
ligament teeth (+) (-) (-) or only slightly
around the apex widened on the
pretreatment
radiograph

Due to:
Extension of pulpal disease into periapical tissue,
overextension of the endo material
or occlusal trauma such as bruxism
Disease Clinical Signs Vitality Percus Palpa Mobi Radiographic
and sion tion lity Interpretation
Symptoms
Painful, May
purulent occur in
exudates vital and Increas Normal lamina
Acute around the non-vital (+) (+) ed in dura
Alveolar apex due to teeth mobilit (slightly
Abscess acute apical y thickened)
periodontitis
from a
necrotic
pulp
rapid onset of
slight
swelling,
moderate to
severe pain
Disease Clinical Vita Percus Palpa Mobi Radiographic
Signs and lity sion tion lity Interpretation
Symptoms
Chronic Apical
Periodontitis
Large diffuse,
Chronic small or
Alveolar abscess Asympto- Non- tender tender slight circumscribed
or matic vital periapical
radiolucency
Granuloma
(gum boil or
fistula)
Disease Clinical Vita Percus Palpat Mobility Radiographic
Signs and lity sion ion Interpretation
Symptoms

Phoenix
Abscess No sinus Non-
tract vital (+) (+) (+) Large diffuse,
Pain small or
With Identical to circumscribed
history of acute periapical
Chronic apical radiolucency
Alveolar abscess
Abscess
Disease Clinical Vita Percus Palpat Mobility Radiographic
Signs and lity sion ion Interpretation
Symptoms

Periapical
Osteo Asymp- Vital Diffused
Sclerosis tomatic Tooth (+) (-) (-) radiopacity

(excessive
bone
minerali-
zation)