RMRM
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DR. F.M.TAN
Primitive Oral Cavity
• Stomodeum (or Stomatodeum)
• Slit-like space lined by
ectoderm in the 3–4-week-old
human embryo
Morphodifferentiation Enamel Organ
• Cell form changes
•
Primitive Embryo
Vestibular lamina (the
future oral vestibule)
• Dental lamina (the future
dentition)
• Mesenchyme
• IDE → ameloblast → enamel
Dental Papilla
• Odontoblast → dentin-pulp
complex
Dental Follicle
Cellular Proliferation
• Cells divide (mitotic division)
Histodifferentiation
• Cells change into different
types of cells/tissues
Tooth Bud – will become the
Enamel Organ (EO)
Tooth Germ is composed of:
1. Enamel Organ (EO)
2. Dental Papilla (DP)
3. Dental Follicle (DF)
• Fibroblasts → PDL
• Cementoblasts → cementum
• Osteoblasts → alveolar bone
Periodontium includes
1. Periodontal Ligament
2. Cementum
3. Alveolar Bone
4. Gingiva
DEVELOPMENTAL STAGES OF THE TOOTH
1. Initiation Stage
➢ In the developing MX and MD, there is an ectodermal thickening that will form a U-shaped oral
thickening called Primary Epithelial Band
Primary
Epithelial
Band
➢ Primary epithelial band will give rise to:
i. Vestibular lamina (the future oral vestibule)
ii. Dental lamina (the future dentition)
➢ Dental lamina will have localized epithelial thickening creating Dental Placodes
➢ Starting stage to form tooth bud
2. Bud Stage
➢ Dental placodes proliferate (increase in number) and invaginates to ectomesenchyme creating
a knob-like projection, Tooth Bud
i. Tooth Bud – will become the Enamel Organ (EO)
➢ Ectomesenchymal condensation will occur, it is the merging of the ectoderm and the underlying
mesenchyme. This condensation forms the Dental Papilla
i. Dental Papilla (DP) (future dentin and pulp)
3. Cap Stage or Proliferation Stage
➢ Epithelial cells that became Short Columnar Cells at the concave region of the Cap-shaped
Enamel Organ forms the Inner Dental Epithelium (IDE)
➢ While epithelial cells that became Short Cuboidal Cells lying at the convex region of enamel
organ forms the Outer Dental Epithelium (ODE)
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Outer Dental
Epithelium (ODE)
DR. F.M.TAN
EO
DP
Inner Dental Epithelium (IDE)
DF
➢ IDE and ODE secretes glycosaminoglycans into their extracellular compartment, where it pulls
water from their surroundings into the enamel organ causing the cells to force apart that forms
the star-shaped Stellate Reticulum
➢ Cells of the ectomesenchyme surrounding the EO and DP is the Dental Follicle (DF) or Dental
Sac
i. Dental Follicle (future periodontal tissues of the tooth)
➢ Tooth Germ is Composed of:
i. Enamel Organ (EO)
ii. Dental Papilla (DP)
iii. Dental Follicle (DF)
4. Early Bell Stage
➢ Invagination deepens until the organ takes on a bell-like form.
➢ Histodifferentiation
i. Dental papilla will differentiate to be odontoblast with cytoplasmic extensions
• These cytoplasmic extensions will soon line the pulp and spreads to the dentin,
making the dentin-pulp complex vital.
ii. Short Columnar Cells of Inner Dental Epithelium (IDE) will differentiate into Long
Columnar Cells of Ameloblasts
• These ameloblasts will become the enamel
➢ Morphodifferentiation
i. Dental crown form is determined as guided by the IDE space.
EO
DF
DP
5. Late Bell Stage
➢ Initiation of mineralization will occur as odontoblasts forms the dentin along the future
Dentinoenamel Junction (DEJ); ameloblasts, forming the enamel.
6. Root Formation
➢ Cervical Loop at the junction of IDE and ODE will form the Hertwig’s Epithelial Root Sheath
(HERS) and it will continue to proliferate turning medially before it grows vertically, growing
coronally for the root formation. Enamel and dentin will reach the future cementoenamel junction,
and some cells will differentiate to become the future odontoblastic layer, dentin, cementum, and
periodontal ligament fibers.
7. Tooth Eruption
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Intrinsic
-
DR. F.M.TAN
Extrinsic
Genetics, hereditary, systemic, congenital
(not all congenital are inherited), metabolic
dysfunction
-
Generalized (Anomalies)
Due to infections, external factors
-
Usually hereditary (intrinsic)
True
DEVELOPMENTAL DISTURBANCES OF THE TEETH
ALTERATIONS IN SIZE (usually Intrinsic)
Anomaly
Clinical
Types
Features
1. 1. Generalized microdontia
2. - More common than generalized macrodontia
3. - All teeth are smaller than normal
Conditions Associated
Clinical
Management
Significance
1. Down Syndrome (Pegshaped laterals)
Microdontia
4.
5.
6.
7.
8.
Tooth/teeth
are smaller
than
the
normal size
2. Focal microdontia
2. Ectodermal Dysplasia
- One or group of teeth (regional but not all)
- More common is one tooth only than group of teeth - Affects nails, enamel, etc.
- Posterior teeth most commonly affected
- E.g. MX 3rd molar, MX laterals
3. Disproportional microdontia
- Relative generalized
- Normal, but looks not because of disproportion
- Bigger jaw (inherited) so there is spacing
Orthodontic
treatment
Dental
- Decreased restorations
masticatory such
as
function
crowns
or
- Esthetics
bridges
3.
Chondroectodermal
Esthetic
dysplasia
(Ellis-van
dentistry
Creveld Syndrome)
such
as
- Jaw develops from
veneers
Meckel’s cartilage
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1. Generalized macrodontia
- Less common than generalized microdontia (rare)
- All teeth are bigger than normal
2. Focal macrodontia
- One or group of teeth (regional but not all)
- More common is one tooth only than group of teeth
- Posterior teeth most commonly affected, MX 3rd 1.Gigantism
molar
(Hyperpituitarism)
- Generalized
2. Hemifacial hypertrophy
Tooth/teeth
– Focal
Macrodontia
are bigger
(Megadontism) than
the
normal size
3. Disproportional macrodontia
- Relative generalized
- Normal, but looks not because of disproportion
- Smaller jaw (inherited) so there is crowding
DR. F.M.TAN
- Esthetics
- Occlusal
issues,
improper bite
alignment
Difficult
dental
treatments
due to larger
size of teeth
(more
complex)
Orthodontic
treatment
- Selective
tooth
reduction
Dental
restorations
such
as
veneers
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DR. F.M.TAN
ALTERATIONS IN NUMBER AND ERUPTIONS
Anomaly
Clinical Features
Types
Conditions Associated
Clinical
Significance
Management
- They occupy
space
When
impacted, they
may block the
eruption
of
other teeth
- May cause
delayed
eruption of adj.
teeth
- May cause
malalignment
of the dentition
Tooth
extractions
- Orthodontic
treatment for
teeth
that
became
misaligned due
to
supernumerary
teeth
9. 1. Mesiodens
- Most common supernumerary
tooth
- Bet. two MX central incisors
th
1. Cleidocranial
Dysplasia
2. MX 4 molar
2nd
most
common
- Extra tooth/teeth that supernumerary tooth
can be found in any
location in the oral cavity.
- More on MX than MD
2. Gardner’s Syndrome
1. True Supernumerary 3. Peridens
- Resembles like a tooth - Erupts outside the dental arch
(in form and structure)
(ANTERIORS)
- Canine most common tooth
3. Down Syndrome
(Trisomy 21)
Supernumerary
2. False (Rudimentary)
Supernumerary
- Odd shaped, small
4. Mesiomolar or Distomolar
- Found in molar region, like extra
molar
5. Paramolars
- Erupt on buccal, lingual, or
proximal to one of the molars
(POSTERIOR)
- Usually, PMs not molars
4. Crouzon Syndrome
(Craniofacial
Dysostosis)
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DR. F.M.TAN
6. Paramolar tubercle
- Fused with a permanent molar
- Usually, found in molars not
PMs
1.
Generalized
(Complete)
Anodontia
- Intrinsic, systemic (hereditary)
- True anodontia, rare
1. Ectodermal Dysplasia
Anodontia
- Congenital absence of
teeth
- Caused by failure of
tooth buds to develop
- May involve both
deciduous
and
permanent dentition
- Hereditary (except false
anodontia)
2. Focal/Localized (Partial) 2. Cleft Lip and Palate
Anodontia
- Regional, one or group of teeth
- Hypodontia (1), or oligodontia (2
or more)
Failure
of
Permanent
Teeth Eruption
causes
- Loss of space
- Overcrowding
3. Cleidocranial
SuperDysplasia
numerary and
Frequency of Missing
supplemental
3. Pseudoanodontia
Teeth
teeth
- Tooth/teeth absent clinically
1. 3rd molars
- Retention of
because of impaction/delayed
2. MD 2nd PM
deciduous
eruption
3. MX Laterals
4.
Ellis-van
Creveld predecessor
- Hindered by adj. tooth, tissue, Syndrome
4. MD Centrals
or bone
5. MD Laterals
- Scarred tissue is hard to erode
when tooth is extracted during
childhood
- Prosthodontics
- Orthodontic
treatment for
partial
anodontia
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DR. F.M.TAN
4. False Anodontia
- Exfoliated/extracted teeth
- Induced anodontia
- Teeth are prevented from erupting by: adj. teeth or if crowded (lack of space); early extractions which forms scarred
tissue
- Tooth impaction have clinical significance: pain and discomfort, infection and inflammation, misalignment of teeth, cyst
tumor formation
- Dental management includes: surgical tooth extractions, orthodontic treatment, surgical exposure (for forced eruption)
MANDIBULAR 3RD MOLAR IMPACTION
Pell & Gregory Classification – Ramus Relationship (1st Name)
Landmarks:
• Point A - Distal of the 2nd molar
• Point B - Anterior border of the ramus
Impaction
enough space
Less than MD dia.
Of 3rd molar crown
2/3s of the 3rd
molar is located
within the ramus
1. Class I
- There is sufficient amount of space bet. the anterior border of the ramus and the distal portion of the 2nd molar for the
accommodation of the MD dia. of the crown of the 3rd molar.
2. Class II
- The space bet. the anterior border of the ramus and the distal portion of the 2nd molar is less than the MD dia. of the
crown of the 3rd molar.
3. Class III
- Tooth is located completely within the anterior border of the ramus
- 2/3s is located within the ramus
- Least accessible, most difficult to extract
RMRM
OP1
DR. F.M.TAN
Pell & Gregory Classification – Impaction depth in bone (2nd Name)
Landmarks:
• Point A – Occlusal plane of the 2nd molar
• Point B – Highest point of the impacted 3rd molar
in level or above
occlusal plane of
2nd M
below the occlusal
plane but above
cervical line of 2nd M
below cervical line
of 2nd M
1. Position A
- The highest point of the impacted 3rd molar is in the level or above the occlusal plane of the 2nd molar
2. Position B
- The highest point of the impacted 3rd molar is below the occlusal plane but above the cervical line of the 2nd molar
- The highest point of the impacted 3rd molar is bet. the occlusal plane of the 2nd molar and its cervical line
3. Position C
- The highest point of the impacted 3rd molar is below the cervical line of the 2nd molar
Winter’s Classification (3rd Name)
- In relation to the long axis of the 2nd molar and impacted 3rd molar
1. Mesioangular
3. Vertical
2. Distoangular
4. Horizontal
7. Linguoangular
- 3rd molar impaction where the crown is towards the lingual
5. Inverted
6. Buccoangular
RMRM
OP1
MAXILLARY 3
RD
DR. F.M.TAN
MOLAR IMPACTION
Based on the relative depth in bone (1st Name)
Landmarks:
• Point A – Occlusal plane of the 2nd molar
• Point B – Lowest point of the impacted 3rd molar
in level or below
occlusal plane of
2nd M
above the occlusal
plane but below
cervical line of 2nd M
above cervical line
of 2nd M
1. Position A
- The lowest point of the impacted 3rd molar is in the level or below the occlusal plane of the 2nd molar
2. Position B
- The lowest point of the impacted 3rd molar is above the occlusal plane but below the cervical line of the 2nd molar
- The lowest point of the impacted 3rd molar is bet. the occlusal plane of the 2nd molar and its cervical line.
3. Position C
- The lowest point of the impacted 3rd molar is above the cervical line of the 2nd molar
Winter’s Classification (2nd Name)
- In relation to the long axis of the 2nd molar and impacted 3rd molar
1. Mesioangular
3. Vertical
2. Distoangular
4. Horizontal
7. Linguoangular
- 3rd molar impaction where the crown is towards the lingual
5. Inverted
6. Buccoangular
RMRM
OP1
rd
Proximity with the Floor of the Sinus (3 Name)
Landmarks:
Point A – Bone
Point B – Floor of the sinus
1. No Sinus Approximation (NSA)
- 3 mm or more bone is present bet. the sinus floor and the impacted 3rd molar
bone present
2. Sinus Approximation (SA)
- No bone or less than 3 mm of bone is present bet. the sinus floor and the impacted 3rd molar
no bone
present
DR. F.M.TAN
RMRM
OP1
Identify the developmental anomaly (if present) and classify what type of 3rd molar impaction is shown (Both MX and MD).
DR. F.M.TAN
RMRM
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FURCATION
-
DR. F.M.TAN
IMPERFECTA
where roots of a multi-rooted
tooth meet
-
OBLITERATE
medical suffix used in naming conditions with
abnormalities in structure or function of affected area
-
to destroy, wipe out
DEVELOPMENTAL DISTURBANCES OF THE TEETH
ALTERATIONS IN SHAPE AND FORM
Anomaly
Clinical Features
Conditions
Associated
Etiology / Types
Clinical
Significance
Management
SHAPE OF THE CROWN
Gemination
(double teeth,
double
formations,
joined teeth,
fused teeth or
dental twinning)
Fusion
etiology:
nutritional,
endocrine
influences,
infectious/inflammatory
processes,
ingestion
of
medicines,
hereditary or congenital diseases, local
- fusion of two teeth trauma, and ionizing radiation
from a single enamel
1. Partial Cleavage
organ
- one tooth, 2 - appearance of two crowns that share the
No specific
same root canal
crowns
association
- 2 teeth, one tooth
germ
– common MX
anterior
- joining of two
developing
tooth
germs
- union between
dentin and enamel
of two or more
developing teeth
more
on
deciduous
dentition, anteriors
- Root canals may
also be separated
or shared
– etiology: local trauma
1. Complete (Total / True Fusion)
- fusion begins before calcification stage
- crown incorporates enamel, dentin,
cementum and pulp of both the teeth
No specific
association
crowding
disease and
alignment
issues
- orthodontic
treatment,
restorative
procedures
like bonding
or veneers
- orthodontic
treatment
crowding
- restorative
disease and
options like
alignment
veneers
or
issues
crowns might
be considered
RMRM
- may involve the
entire length of the
teeth, or roots only,
in
which
case
cementum
and
dentin are shared
OP1
2. Incomplete (Partial / Late Fusion)
- occurs at a later stage
- tooth have separate crowns and limited
to root alone with fused or separate pulp
canals
DR. F.M.TAN
- etiology: thought to be influenced by
of genetic factors during tooth development
Taurodontism
(Bull Tooth)
Talon’s Cusp
failure
appropriate
invagination
of
Hertwig’s epithelial
root sheath (HERS)
- enlarged pulp
chamber,
apical
displacement of the
pulpal floor, and lack
of constriction at
the
cementoenamel junction
- elongated crowns
or apically displaced
furcations, resulting
in pulp chambers
that have increased
apical-occlusal
height
1. Hypotaurodontism
- mild form, shorter roots
- only the pulp chamber is enlarged
2. Mesotaurodontism
- medium sized roots
1. Klinefelter
syndrome
2. Tricho-DentoOsseous syndrome
3. Down syndrome
4. Van der Woude
syndrome
5. Hypophosphatasia
- difficulties in
endodontic
treatment
- can affect
occlusion
and chewing
efficiency
- endodontic
treatment
- orthodontic
evaluation
- can cause
problems
with
occlusion,
increase the
risk
of
- restorative
procedures,
oral hygiene,
orthodontic
consideration
3. Hypertaurodontism
- root furcation occurs in close
proximity to the root apices due to the
disproportionately enlarged crown and
pulp chamber
- Anterior region
1. Rubinstein and
lingual surface
- etiology: developmental factors during Taybi
- common in MX tooth formation
2. Berardinelli-Seip,
laterals
Mohr
- “claw of bird of 1. Type 1: Talon
3. Ellis-van Creveld
prey”
4. Sturge-Weber
RMRM
- Teeth may also
exhibit extra small
enamel projections
called tubercles
- excessive folding
or invagination of
the dental enamel
organ
OP1
- projects from the palatal (or facial) 5. Incontinentia
surface of a primary or permanent pigmenti achromians
anterior tooth
- extends at least half the distance from
CEJ to the incisal edge
DR. F.M.TAN
fractures, and
complicate
oral hygiene
practices
2. Type 2: Semi talon
- additional cusp of a millimeter or more
- extending less than half the distance
from CEJ to the incisal edge
- may blend with the palatal surface or
stand away from the rest of the crown
3. Type 3: Trace talon
– an enlarged or prominent cingula and
their variations, i.e. conical, bifid or
tubercle-like
Dens
Evaginatus
(tuberculated
cusp, accessory
tubercle,
occlusal
tuberculated
premolar,
Leong’s
premolar,
evaginatus
- common than dens
invaginatus
- affects PMs
formation
of
accessory cusp
- often bilateral,
anomalous tubercle,
or cusp, located at
the center of the
occlusal surface
- cusp is composed
of normal enamel
etiology:
both
environmental factors
genetics
and
Location:
1. A cone-like enlargement of the lingual
No specific
cusp
association
- reducing the
cusp's
prominence,
- can increase
restoring with
the risk of
disease
composite
caries
and
material, or
pulp
even
exposure
extracting the
affected tooth
if necessary
RMRM
odontoma, and
occlusal pearl)
OP1
and
dentin 2. A tubercle on the inclined plane of the
containing
varying lingual cusp
extensions of pulp
tissue
- due to abrasion, it
wears
away
causing accessory
pulp exposure
3. A cone-like enlargement of the buccal
DR. F.M.TAN
cusp
4. A tubercle on the inclined plane of the
buccal cusp
5. A tubercle arising from the occlusal
surface obliterating the central groove.
Dens
Invaginatus
uncommon
compared to dens
evaginatus
- dens in dente or
tooth within a tooth - etiology: genetic factors involved in
No specific
represents
an some cases
association
exaggeration
or
accentuation of the
lingual pit
- permanent MX
laterals, next are
- cleaning
and
disinfecting
increases the
the
invagination
disease
susceptibility followed by
to caries and sealing it with
infection
a filling
material to
prevent
decay
RMRM
OP1
DR. F.M.TAN
endodontic
treatment
other
anterior,
bilateral commonly
seen
1. Type I
- enamel-lined minor form occurring
within the confines of the crown
- not extending beyond the CEJ
2. Type II
- enamel-lined form which invades the
root but remains confined as a blind sac
- may or may not communicate with the
dental pulp
3. Type III A
- penetrates through the root and
communicates laterally with PDL space
through a pseudo-foramen.
- no communication with the pulp, which
lies compressed within the root
4. TYPE III B
- penetrates through the root and
perforating at the apical area through a
pseudo-foramen.
- invagination may be completely lined by
enamel, but frequently cementum will be
found lining the invagination
Peg-shaped
Lateral
- undersized,
- etiology: predominantly genetically
tapered, maxillary
determined and can also be caused due to
lateral incisor
endocrinal disturbances
- conical in shape;
broadest cervically
1. Tooth agenesis,
2. Canine
transposition
3. Over retained
deciduous teeth
- can impact
aesthetics
and
alignment
cosmetic
bonding,
veneers,
or
crowns
RMRM
OP1
DR. F.M.TAN
and tapers incisally
to a blunt point
- single lobe instead
of four
- etiology: systemic, from mother to
fetus during the development of incisors
- Central incisors
are
notched,
smaller than normal
- Widely spaced and
shorter than lateral
incisors
- yellow-brown or
amber coloration
- enamel might be
hypoplastic (thinner
or less mineralized),
leading
to
more
translucent
appearance
1. Congenital syphilis
- can have
implications
for diagnosis
and
health
assessment
diagnosis
and medical
evaluation,
oral hygiene,
restorative
treatment
- Multiple rounded - etiology: systemic, from mother to
fetus during the development affecting
rudimentary
molar formation
enamel cusps
- molars can also be
discolored,
often
with a yellowishMulberry Molar
1. Congenital syphilis
brown hue
- enamel may be
hypoplastic, leading
to
increased
susceptibility
to
wear and decay
- can have
implications
for diagnosis
and
health
assessment
diagnosis
and medical
evaluation,
oral hygiene,
restorative
treatment
Hutchinson’s
Incisors
RMRM
OP1
DR. F.M.TAN
SHAPE OF THE ROOT
- etiology: space restriction during
development, local trauma, excessive
occlusal force, or local infection
1. True/developmental concrescence
- occurs during tooth development
- close proximity of developing roots of
the adjacent teeth
Concrescence
Enamel Pearl
- a form of fusion
- cemental union
- take place before
or after eruption
No specific
and is believed to be
association
related to trauma or
overcrowding
2.
Acquired/post
inflammatory
- MX 2nd and 3rd concrescence
molars
- after root formation
- may result from a chronic inflammatory
response to a non-vital tooth
- may occasionally
be found on the - etiology: developmental factors during
tooth formation, during root sheath
roots of teeth
- most commonly in differentiation and enamel deposition
the bifurcation or
trifurcation of teeth
No specific
but may appear on
association
single-rooted
PM
teeth as well
MX
molars
commonly affected
than MD molars
- if problems
arise,
- can lead to extraction
challenges
might
be
during
considered,
disease
extraction
possibly
and
followed by
orthodontic
replacement
treatment
with
a
prosthetic
option
- can lead to
challenges
during
disease
extraction
and
orthodontic
treatment
surgical
removal if not
causing
periodontal
issues
RMRM
Dilaceration
OP1
- extraordinary
curving or
angulation of tooth
roots
- apical 1/3 for
anteriors
- middle 1/3 for 1st
molars
- coronal 1/3 for 3rd
molars
- root dilacerations
more common in
posterior,
permanent
crown
dilacerations
common
in
permanent
MX
incisors the MD
incisors (anteriors)
- MX incisors show
lingual deviation
MD
incisors
incline labially
DR. F.M.TAN
- etiology: hereditary (few cases only),
trauma
during
tooth
development,
mechanical trauma (E.g., laryngoscopy and 1. Smith Magenis
endotracheal intubation in primary teeth)
syndrome
2. Hypermobility type
of Ehlers-Danlos
syndrome
3. Axenfeld-Rieger
syndrome
4. Congenital
ichthyosis
- etiology: hereditary, trauma, crowding,
abnormal habits such as thumb sucking
Flexion
Ankylosis
- can lead to
difficulties in - orthodontic
tooth
treatment,
eruption,
extraction or
alignment
replacement
issues
No specific
association
- can lead to
challenges
during
disease
extraction
and
orthodontic
treatment
- orthodontic
treatment
might
be
used to align
the affected
tooth
properly
- fusion of the root - etiology: hereditary, trauma, idiopathic
(dentin
or causes
cementum) of a
No specific
tooth to bone
association
- appears to be in
lower level (height)
than the other ones
- can cause
orthodontic
disease and occlusal
issues, and
affect
eruption
- monitoring
the affected
tooth's
growth and
considering
orthodontic
treatment
- deviation or bend
of a tooth that is
restricted to the root
portion of a tooth
RMRM
OP1
DR. F.M.TAN
MACANANG, RIZA MAE R. | DMD4F
OP1 LEC Activity 2
DR. F.M.TAN
ALTERATIONS OF ENAMEL AND DENTIN
Anomaly
Etiology / General
Characteristics
Types / Clinical Features
Radiographic Features
Histopathologic
Features
Clinical
Significance
Management
- can result in
enamel
defects,
causing teeth
to be more
prone
to
wear,
sensitivity,
and decay
esthetic
restorations
like crowns,
veneers, or
bonding
ENAMEL
- etiology: hereditary
patterns
(cell
mutation
–
DNA
alteration) autosomal
dominant or recessive
to X-linked dominant or
recessive
AMELOGENESIS
IMPERFECTA (AI)
(Hereditary Enamel
Dysplasia,
Hereditary Brown
Enamel, Hereditary
Brown Opalescent
Teeth)
- affects both primary
and
secondary
dentition
enamel
appears
reduced in bulk, thin
layer over occlusal
and
interproximal
surfaces
- although enamel is
soft and irregular, teeth
are not caries prone
due
to
lack
of
interproximal
contacts (wear)
- dentin and pulp
appear normal
- Note: enamel: 9899% inorganic mineral
and less than 2%
organic matrix and
water
1. ENAMEL HYPOPLASTIC
AMELOGENESIS IMPERFECTA
(QUANTITATIVE)
- alteration occur during enamel matrix
secretion
- insufficient amounts of enamel
- normal enamel
- form pits and grooves (prone to staining
as the stain can be absorbed easily)
- rough or smooth and glossy, squareshaped crown
- yellowish-brown color
1. ENAMEL HYPOPLASTIC
AMELOGENESIS
IMPERFECTA
(QUANTITATIVE)
- presence of thin radiopaque
layer of enamel with normal
radiodensity
very
thin
enamel
irregularly
arranged
enamel prisms
- DEJ show
some
pits
grooves
exaggerated
2. ENAMEL HYPOCALCIFICATION
2. ENAMEL
scalloping
AMELOGENESIS IMPERFECTA
HYPOCALCIFICATION
areas
of
(QUALITATIVE)
AMELOGENESIS
homogeneous
- alteration occur during calcification IMPERFECTA (QUALITATIVE) aprismatic
stage
- thickness of enamel is enamel or fused
- weaker than hypomaturation AI
normal but radiodensity of indistinct prisms,
- enamel quantity = normal
enamel is less than that of with “a reduction
soft
and
friable,
deficiently dentin
in
distance
mineralized
between enamel
- fractures easily and wears readily
rod incremental
- white opaque to yellow to brown
lines”
- abnormal contour and absent
interproximal contact points
- “picket fence” appearance
- teeth appear like crown preparations
- sensitive
Soft, “cheesy
enamel”
MACANANG, RIZA MAE R. | DMD4F
OP1 LEC Activity 2
3. ENAMEL HYPOMATURATION
3. ENAMEL
AMELOGENESIS IMPERFECTA
HYPOMATURATION
(QUALITATIVE)
AMELOGENESIS
- alteration occur during maturation IMPERFECTA (QUALITATIVE)
stage
- radiodensity of enamel is
- mineralization begins but maturation similar to that of dentin
into dense crystal structure
- enamel quantity = normal
- mottling, opaque white to brownish
yellow discoloration (chalky)
- primary teeth: ground glass opaque
white appearance
- permanent teeth: mottled yellow
white, may be darkened with absorption
- tight contact point
- looks like fluorosis
DR. F.M.TAN
mottled
enamel
ENVIRONMENTAL
ENAMEL
HYPOPLASIA
LOCALIZED
ENAMEL
HYPOPLASIA
etiology:
not
hereditary
malnutrition,
bacterial
/
viral
infections,
trauma,
and
other
severe
illnesses experienced
during childhood
regional
or
generalized
etiology:
not
hereditary – local
infection, trauma to a
developing tooth, or
disruptions during tooth
formation
- affects single tooth
- more susceptible to
decay
- insufficient amounts of enamel
- horizontal grooves located on middle linear
radiolucencies
third to incisal third of the tooth
crossing the crown
- pits, or lines on the tooth's surface,
very
due to interrupted enamel formation
enamel
- more caries susceptible
- can indicate
periods
of
thin severe
physiological
stress during
tooth
development
esthetic
restorations
like crowns,
veneers, or
bonding
- can provide
insights into
periods
of
thin
localized
stress
or
trauma
during tooth
development
esthetic
restorations
like crowns,
veneers, or
bonding
horizontal
grooves
- insufficient amounts of enamel
- Turner’s Tooth
- vary in size and shape
- white, brown, or yellow spots
Turner’s
Tooth
linear
radiolucencies
crossing the crown
very
enamel
MACANANG, RIZA MAE R. | DMD4F
OP1 LEC Activity 2
DR. F.M.TAN
DENTIN
1. Type I
- collagen gene mutation
- syndrome-associated (osteogenesis
imperfecta – OI – brittle bone disease)
- normal dentin sialophosphoprotein
etiology:
gene (DSPP)
mutations responsible - primary teeth more affected than
permanent
for dentin formation
- roots may be short or blunted
amber
like - not sensitive
- caries resistant
appearance
- yellowish to brown
opalescent dentin
- affects both primary
and
secondary
2. Type II
dentition
enamel
looks - dentin sialophosphoprotein (DSPP)
chemically
normal gene mutation
DENTINOGENESIS but fractures easily - dentin abnormality only but no bone
disease
IMPERFECTA
due to wearing off
(Hereditary
tulip-shaped, - normal dentin collagen fibers
Opalescent Dentin) bulbous
crown - patients have only dentin abnormality
constricted
to but no bone disease
- not sensitive
cervical area
- either too big or too - caries resistant
small pulp chamber
- Note: dentin: mineral
(70%), organic matrix
(20%),
and
water
(10%)
- organic matrix:
collagen & dentin
protein
(dentin
sialophosphoprotein)
1. Type I
- partial or total obliteration
of pulp chamber and root
canals
irregular
shaped dentinal
tubules
filled
with inorganic
tulip-shaped
crown
substance
obliterated
pulp
- some areas
are sclerotic –
completely
2. Type II
- partial or total obliteration of obliterated by
pulp chamber and root canals calcification
- loss of enamel
due to flat and
smooth DEJ
weak
attachment of
enamel
to
obliterated
pulp
dentin
- bacteria has
direct access to
pulp due to thin
dentin
(shell
opalescent
teeth)
for
Type
III
3. Type III
3. Type III
- Brandywine Type
- multiple pulp exposures, making prone
to
periapical
- shell teeth
periapical radiolucencies
lesions
- dentin sialophosphoprotein (DSPP) - large pulp chambers
gene mutation
- dentin abnormality only but no bone
disease
shell teeth
large pulp
chambers
- can lead to
weakened
dentin,
making teeth
susceptible
to fractures
and wear
- diagnosis
and
evaluation,
restorative
treatments,
endodontic
treatments
MACANANG, RIZA MAE R. | DMD4F
OP1 LEC Activity 2
1. Type I (Radicular Type)
- roots are short and may be
more pointed than normal
- root canals and pulp
chambers are absent
1. Type I (Radicular Type)
- except for a chevron-shaped
- rootless teeth
remnants of pulp tissue –
- both dentitions are of normal color
- crowns appear to be normal in color horizontal radiolucencies
and shape
- premature exfoliation may occur due to
short roots or periapical inflammatory
short roots,
lesions
obliterated pulp
- caries resistant
1.
Type
I
(Radicular
Type)
- short and
irregular
2. Type II (Coronal Type)
dentinal
mutation
or
deciduous
roots
are tubules
normal color
odontoblast
has
extremely short, pulps are - thin enamel
abnormal
almost completely obliterated
characteristics
- permanent dentition are 2.
Type
II
2. Type II (Coronal Type)
- abnormal pulpal
large
pulp (Coronal Type)
- dentin sialophosphoprotein (DSPP) abnormally
morphology
chambers in the coronal - normal root
gene mutation
portion of the teeth
dentin
- primary teeth: opalescent
- exhibits a thistle tube pulp
- permanent teeth: normal
configuration
with
radiopaque
globules
of
abnormal dentin
- etiology: genetic,
hereditary,
autosomal dominant,
or mutation
DENTIN
DYSPLASIA
opalescent in
primary
short roots,
pulp
obliteration
(primary)
Thistle tube
configuration
(secondary)
DR. F.M.TAN
- weakened
teeth that are
more prone
to decay and
fractures
regular
dental
check-ups
restorative
procedures
or, in more
severe
cases,
extraction
and
prosthetic
options
MACANANG, RIZA MAE R. | DMD4F
OP1 LEC Activity 2
DR. F.M.TAN
ENAMEL & DENTIN
- small, and distorted
- etiology: rare, local - soft on probing
circulatory
- irregular contour with surface pits and
disorders,
viral grooves
infections,
local - discolored, yellow or yellowish-brown
trauma,
- translucent or opaque with a mottled
pharmacotherapy
or pitted appearance
REGIONAL
during
pregnancy,
ODONTODYSPLASIA
facial asymmetry or a
(RO)
combination of these
(Odontogenic
factors
Dysplasia,
- regional, not all
Odontogenesis
teeth
Imperfecta, Ghost
- generally, it is
Teeth)
localized in only one
arch
- delayed or failed
eruption
due
to
arrested
root
formation
- disorganized
or
irregularly
- ghostlike
arranged
- faint, fuzzy outline
odontoblasts
pulp
chambers
are - thin enamel,
enlarged, and the roots dentin,
and
might be shorter
cementum
pulp
may
extend into the
roots of the
teeth
in
an
irregular
manner
- in some cases,
short roots,
the
affected
large pulp
teeth
might
chambers
exhibit
the
presence
of
cellular fibrous
tissue instead of
normal
dental
pulp
esthetic
concerns,
risk
of
infection,
pain
and
discomfort
- restorations,
endodontic
treatment,
orthodontic
treatment,
regular dental
check ups
MACANANG, RIZA MAE R. | DMD4F
OP1 LAB Activity 3
DR. F.M.TAN
HARD TOOTH TISSUE REDUCTION
Anomaly
ATTRITION
Tooth wear is an irreversible, non-carious, destructive process, which results in a functional loss of dental hard tissue.
Radiographic /
Conditions
Clinical
Etiology / Description
Clinical Features
Histopathologic
Associated Significance
Features
Etiology:
- Flat and smooth
- flattened and shorter - Bruxism or - Tooth
- Parafunctional activities
- Shiny wear facet on amalgam contacts coronally with reduction night grinding sensitivity
- Mastication (repetitive chewing)
- Possible fracture of cusps or in the size of the pulp - Clenching
- Changes in
- Fibrous diet
restorations
chambers and canals due
tooth shape
- Tobacco and bettlenut chewing - Enamel and dentin wear at the same to
deposition
of
- Fractures
- Bruxism or night grinding
time
secondary dentin
- Dentin may be yellow or brown stained - pulpal structures can
Description:
I. Anatomical Involvement
become
completely
- Latin verb: attritum / atterere – 1. INCISAL ATTRITION
obliterated (depends on
action of rubbing against another - Lack of supporting occlusion as in the degree)
surface
absence of posterior teeth
1. INCISAL ATTRITION
- Wearing away of a tooth as a - Surface of MD ant. teeth is worn
result of tooth-to-tooth contact.
obliquely
- Occlusal, incisal, and proximal
surfaces
- Lingual surface of ant. MX teeth
- Labial surface of ant. MD teeth
- Deciduous and permanent
2. OCCLUSAL ATTRITION
dentition
2. OCCLUSAL
- Due to functional mastication
- Usually, age-related process
ATTRITION
- Physiologic – aging
- Pathologic – affects esthetic
appearance and function
- Factors accelerating destruction:
fluorosis,
environmental
/
hereditary enamel hypoplasia,
3. PROXIMAL ATTRITION
premature contacts (edge-to-edge
- Due to friction caused by tooth
occlusion)
3. PROXIMAL
movement during mastication
- Shortening of length of dental arch and ATTRITION
Bite Force Studies
reduction in MD dia. ff the teeth
- 58 lbs. of force during chewing
- 68 lbs. during swallowing
- 85 lbs. biting on anteriors
- 150-175 lbs. biting on posteriors
- 70-900 lbs. during sleep
Management
Orthodontic
management
- Restorative
Management
(crown
replacement
or onlays)
Therapy
(bite / night
guard)
MACANANG, RIZA MAE R. | DMD4F
OP1 LAB Activity 3
II. Degree of Anatomical Involvement
1. FIRST DEGREE
- Incisal edge / Cusp are worn out flat
- No dentin exposure
2. SECOND DEGREE
- Incisal edge / Cusp are worn out
- Primary dentin are exposed
3. THIRD DEGREE
- Ring of secondary dentin is visible
4. FOURTH DEGREE
- Pulpal Involvement
DR. F.M.TAN
MACANANG, RIZA MAE R. | DMD4F
Etiology:
- Aggressive toothbrushing +
abrasive toothpaste + heavy
pressure + horizontal tooth
brushing stroke
- Pencils, toothpicks, pipe stems,
bobby pins, tobacco chewing,
cracking nuts, biting fingernails
ABRASION
(mechanical
wear)
Description:
- Latin verb: abrasum / abradere –
to scrape off, wear or partial
removal
through
mechanical
process
- Pathologic wearing of teeth
caused by an abnormal habit or
abnormal
use
of
abrasive
substances orally
- Location and pattern are directly
dependent on the cause
- Degree of lost is greatest on
prominent
teeth:
cuspids,
bicuspids, teeth adj. to edentulous
area
- Can be diffused or localized
- More commonly seen on left side
of right handed persons
- Affects teeth in groups (often
unilateral)
OP1 LAB Activity 3
Toothbrush
Abrasion
(Horizontal
Brushing Technique)
- Horizontal cervical notches on buccal
surface of exposed radicular cementum +
dentin
- Sharply defined margins
- Hard smooth surface
Thread Biting / Use of Bobby Pins
- Rounded or V-shaped notches in
incisal edges of anterior teeth
Use of Pipe
- Notching
Cigar Chewing
well-defined
semicircular or semilunar
shape radiolucent defects
in cervical level of the
tooth
- borders are radiopaque
- pulp chamber may be
partially
or
fully
sclerosed in severely
affected teeth
- Tooth
sensitivity
- Caries
susceptibilit
y
DR. F.M.TAN
- Composite
restoration
- Porcelain –
buccal or
labial up to
incisal with
metal at the
back
- Modified
cleaning
habits
MACANANG, RIZA MAE R. | DMD4F
OP1 LAB Activity 3
Etiology:
Maxillary Anteriors
- Multifactorial
- Shallow spoon-shaped depressions in
- External – work environment, cervical portion of crown
e.g.,
battery
manufacturing,
competitive swimming, professional
wine tasters; diet, e.g., citrus fruits,
acid-containing soft drinks
- Internal – regurgitation of gastric
contents (involuntary or voluntary)
- Dental Tetralogy
EROSION
(chemical
erosion)
Description:
- Latin verb: erosum / eroder – to Posterior Teeth
corrode, gradual destruction of - Extensive loss of occlusal surface
surface by chemical or electrolytic
process
- Loss of tooth structure through
a nonbacterial chemical process
- Most commonly, acids are
involved in the dissolution process
from an external or internal source.
- The pattern of erosion associated
with vomiting – generalized tooth
loss on lingual surfaces of MX
teeth
- All surfaces may be affected
- Facial and palatal surfaces of MX
ant. teeth
- Facial and occlusal surfaces of
MD post. teeth
Erosion related to Acid in soft drinks
- Affects teeth in groups (lingual
uppers / buccal lowers)
Note:
- Critical pH of enamel – 5.5 pH
- Any solution with a lower pH
value
may
cause
erosion
(especially when repeated or long
duration)
- Saliva and the salivary pellicle
counteract the acid attacks
- Saucer shaped lesions
have a smooth featureless
surface as well as craters
and dimples
- First area to be affected
is the peritubular dentin
Progression
makes
dentinal tubules become
enlarged but disruption is
also
seen
in
the
intertubular areas
- Bulimia –
self-induced
vomiting
- Anorexia
nervosa
- GI
disorders –
peptic ulcers,
gastritis
- Chronic
Alcoholism
- Pregnancy
(hyperemesis
gravidarum)
- Tooth
sensitivity
- Change in
tooth color
DR. F.M.TAN
- Crowns (if
dentin is not
exposed)
- Restorative
managemen
t
- Less intake
of acidic
sources of
food
MACANANG, RIZA MAE R. | DMD4F
Etiology:
- Repeated tooth flexure with
failure of enamel and dentin at a
location away from point of loading
- Occlusal forces are applied
eccentrically to a tooth
- Tensile stress concentration at
cervical fulcrum (causing flexure)
- Produce disruption in chemical
bonds of enamel crystals in
cervical areas
Description:
- Latin words: ab + fractio – away
ABFRACTION + breaking
- Latin verb: frangere – to break
(stress
- Loss of tooth structure from
corrosion)
occlusal stresses
- The harder it is, the more prone
to microfractures
- Dentin is able to withstand
greater tensile stress than enamel
- Cracked enamel can be lost or
more easily removed by erosion or
abrasion
- Predominantly affects: facial
surfaces of bicuspids and molars
- Affects single teeth (often upper
PM first)
OP1 LAB Activity 3
- Wedge-shaped defects limited to
cervical area of teeth
- Deep, narrow and V-shaped
- Occasionally lesions are subgingival
- Bruxism
- Gum
recession
- Tooth
sensitivity
- Caries
susceptibilit
y
DR. F.M.TAN
- Composite
restoration
- Night
guards
Desensitizin
g agents
- Fluoride
treatments
- Dental
bonding
- Restorative
Management
(crown
replacement
or onlays)
MACANANG, RIZA MAE R. | DMD4F
OP1 LAB Activity 3
DR. F.M.TAN
RMRM
OP1
DR. F.M.TAN
ABNORMALITIES OF THE DENTAL PULP
ABNORMALITIES
DESCRIPTION / ETIOLOGY
•
•
PULP
CALCIFICATION
CLASSIFICATIONS
BASED OF FORM
(Radiographic / Naked eye)
Calcified
deposits
form inside the pulp
DENTICLES
Etiology: Unknown, but
(Pulp Stones / Endoliths)
some conditions are
• Globules, discrete rounded structures, rounded nodules, foci (more common)
associated with pulp
BASED ON COMPOSITION
calcifications, no clear
BASED ON LOCATION (Radiographically)
(Histologically)
pathophysiology
1. Free – floating, incorporated within the
• Aging,
1. True Denticles – structures similar to
pulp tissue
inflammation,
dentin
2.
Attached – attached to the pulp cavity
nutritional
2. False
Denticles
–
calcified
wall / dentin wall
deficiency,
substance only, not identifiable as
3.
Embedded – incorporated within dentin,
genetics, etc.
dentin
radiopaque than the surrounding dentin
DENTICLES
DIFFUSED CALCIFICATION
DIFFUSED
CALCIFICATIONS
CLINICAL SIGNIFICANCE
1. Impediments / difficulty in endodontic treatment (may bara); endodontic treatment may not be done in some cases
o Endodontic treatment difficulty still depends on the SIZE AND LOCATION of calcified tissue
• Example:
Located in pulp chamber, free floating – you can scoop it out, endo is possible
Located in pulp chamber, attached – you can bur it out using endodontic burs
o Hardest to treat – endodontic problems associated with pulp calcifications located in the root canal portion
2. Pain and sensitivity due to pulp inflammation
o Because it is enclosed in a hard tissue cavity, it causes impingements of the nerve fibers, triggering slight to intense pain
3. Tooth fracture
•
Runs parallel to
the long axis of
the blood vessels
in pulp canal
RMRM
OP1
•
•
•
TOOTH
RESORPTION
Involves resorptive cells (-clast)
May happen inside and outside the tooth
WILL NOT OCCUR IN NON-VITAL PULP (necrotic pulp), as
resorptive cells need nourishment from blood supply
DR. F.M.TAN
PHYSIOLOGIC PROCESS
1. Resorption in deciduous dentition for the eruption of permanent
dentition
2. Orthodontic treatment where the teeth move, PRESSURE causes
the resorption
PATHOLOGIC PROCESS
• It destroys the inside tooth and bone
INTERNAL RESORPTION
EXTERNAL RESORPTION
• Within pulp chamber or root canal
• Within the root portion (cementum / alveolar bone)
• Odontoclasts
• Osteoclasts, cementoclasts
CLINICAL SIGNS AND SYMPTOMS
WHAT AFFECTS TREATMENT OR PROGNOSIS OF EXTERNAL
1. Pain and discomfort
RESORPTION?
2. Discoloration
• Time when the process of resorption is discovered
• Appears pink because dentin is resorbed
• E.g., 3rd molar horizontal impaction that resorbs the root of 2nd
making hard tissue to become soft tissues, attracting /
molar
forming abundant capillaries / blood vessels (granulation
o Early detection, good prognosis (regardless of location)
tissue)
o Late detection, poor prognosis (regardless of location)
• Area of resorption becomes highly vascular, and since it
comes near with the enamel surface, it appears pink as it
reflects the color of the inside tooth structure
3. Prone to fracture
• Enamel is brittle, dentin gives the support for the enamel not to
be fractured (shock absorber)
WHAT AFFECTS TREATMENT OR PROGNOSIS OF INTERNAL
RESORPTION?
• TIME when the process of resorption is discovered, extent
of damage depends on the time (routine radiographic
examination is important
o Early detection, good prognosis (regardless of location)
TREATMENT
o Late detection, poor prognosis (regardless of location)
• Regardless of time, whether caused by age, trauma, systemic
• LOCATION will determine if prognosis is good or bad, including
disorders, or idiopathic, it has POOR PROGNOSIS
the root canal area, or damage within the dentin
1. Extraction (poor prognosis)
TREATMENT
1. Endodontic Treatment (good prognosis)
2. Extraction (poor prognosis)
Poor Prognosis
RMRM
OP1
GENERALLY, WHICH HAS BETTER PROGNOSIS IF BOTH DISCOVERED EARLY, INTERNAL RESORPTION OR EXTERNAL RESORPTION?
• Internal resorption, because early detection problem can be resolved (endodontic treatment)
• Prognosis of resorption is case to case basis, it depends on the TIMING AND LOCATION
• RCT is feasible if you detected resorption early and it depends on the location
DR. F.M.TAN
RMRM
OP1
DR. F.M.TAN
PULP
UNIQUE CHARACTERISTICS OF THE PULP
1. ENCLOSED WITHIN A RIGID / SOLID / HARD CAVITY
▪ Why pain in the pulp can be very intense?
▪ It does not allow / accommodate swelling caused by
inflammation, no room for expansion, resulting to
impingements of nerve fibers due to increased vascular
pressure
2. HIGHLY VASCULAR soft tissue containing blood vessels,
lymphatic vessels, and nerve fibers
3. Has TERMINAL BLOOD VESSELS
▪ Why pulp undergoes necrosis once it is damaged?
▪ It has only one main vessel (without collateral circulation) or
backup blood supply; so, there will be no revascularization
(e.g., trauma due to intrusion)—causing necrosis
▪ But if it is in the case of traumatized developing tooth with an open
apex, revascularization is still feasible, there will be backup blood
supply
▪ Fully developed tooth with closed apex is not feasible to be
revascularized
4. Has FREE NERVE ENDINGS only
▪ Why pain is the only type of sensation felt in the pulp?
▪ Free nerve endings are pain receptors; all stimuli are
interpreted / perceived as pain
5. Has NO PROPRIOCEPTORS, location detector
▪ Sometimes you cannot pinpoint where the pain is coming
from
▪ Pain felt is diffused or referred pain (not localized)
CAUSES OF PULP DISEASE
1. Physical (No bacteria on the first place)
o Mechanical
o Thermal
o Electrical
2. Chemical (Erosion) (No bacteria on the first place)
3. Bacterial (Bacteria is the direct cause)
• Type of pulpitis depends on the intensity of damage
• Exposed dentin is prone to pulp diseases as odontoblastic
processes are exposed and bacteria has a direct access up to the
pulp due to the dentinal tubules.
• Bacteria is not always the main cause, but this will intensify the
severity of pulpitis
INFLAMMATION OF THE PULP
• As the bacteria / irritant has been detected by the defense cells, they go out of
the circulation reacting with the irritant
• The interaction between the defense cells and pulp irritant increases blood flow
in the area, causing SWELLING
• Swelling causes impingement of the nerve fibers present in the pulp, resulting
to PAIN
GOOD EFFECT OF INFLAMMATION (FUNCTIONAL)
• We need inflammation TO ELIMINATE THE BACTERIA in our body
• If there is no inflammation, there will be a rapid infection
SIDE EFFECTS OF INFLAMMATION
• Depends of the virulence or the extent of the irritation or inflammation
• Cardinal signs of inflammation:
o REDNESS (Rubor); HEAT (Calor); SWELLING (Tumor); PAIN (Dolor); Loss of
function
WHICH IS MORE PAINFUL, INFLAMMATION IN SKIN OR IN PULP?
• Pulp, because there will be an increase pressure in the blood supply; and
remember that the pulp is enclosed within a solid cavity, so there will be no room
for expansion caused by the increased pulp volume which causes swelling,
making the nerves of the vital pulp to be impinged, causing mild, moderate, to
severe pain
▪ VIRULENCE OF BACTERIA / HOST RESISTANCE WILL DETERMINE IF THE
DISEASE WILL BE REVERSIBLE OR NOT.
▪ Severity of inflammation is directly proportional to the intensity of pain
• Prognosis is better if the area of inflammation is in the area where there is high
vascularity
Which will have more severe bacterial invasion, the fractured tooth with exposed dentin
or pulp in the oral cavity, or exposed pulp due to wrong preparation done by the dentist
(properly isolated, sterile burs are used)?
•
•
Fractured tooth, because bacteria (from the saliva) will have a direct access up to
the pulp (even if dentin is the only part the is exposed) due to open dentinal tubules.
Thus, this will have more intense inflammation, so more intense pain.
Bacterial invasion can be prevented in an exposed pulp caused by wrong tooth
preparation by placing pulp medicaments as soon as possible. (Good prognosis)
RMRM
OP1
DR. F.M.TAN
DISEASES OF THE PULP
PULP DIAGNOSES
1. NORMAL PULP
2. REVERSIBLE PULPITIS
- Bacteria has pulp access
via open dentinal tubules
- Tubules widens apically,
bacteria spread faster
3. SYMPTOMATIC
IRREVERSIBLE PULPITIS
(Acute, rapid onset, dentin
is not yet broken / opened)
- Continues
bacterial
invasion, slow process
- Host response, virulence of
bacteria affects the process
4. ASYMPTOMATIC
IRREVERSIBLE PULPITIS
(Chronic, dentin is broken,
opened, pulp exposed,
pressure released)
5. PULP NECROSIS
6. PREVIOUSLY TREATED
PULP
7. PREVIOUSLY INITIATED
THERAPY
DESCRIPTION /
SIGNS / SYMPTOMS
PULP TESTING
(PULP VITALITY TEST)
Electric, hot, cold test
(+)
Normal pulp, no
problem
Reaction for a few seconds,
pain does not linger upon
removal of stimulus
Inflamed but can still
be treated, can recover
back to normal (also
with the help of defense
mechanism)
(+)
Inflamed and cannot
be recovered due to
severe inflammation
(terminal stage)
In symptomatic IP:
Severity may progress
into Hyperplastic (Pulp
Polyp) Asymptomatic
Irreversible Pulpitis or
Pulp Necrosis
Can be caused by the
progression of
irreversible pulpitis, or
trauma, etc.
Reaction for a minute or two,
pain disappears after
removal of stimulus
(-)
(still confined within the pulp)
Pain lingers for a long time
(provoked) even after
removal of stimulus, or
unprovoked pain without
stimulus; intense, sharp,
shooting, pulsating pain
Response may be similar to acute
apical periodontitis
(+)
(-)
Parang brain dead na ito,
pero buhay pa
(still confined within the pulp)
(-)
May elicit pain, if there are
remaining pulp that is not
dead i.e., accessory canals
May still elicit pain, if there are
remaining pulp debris (not
properly prepared canal)
(-)
RCT on going
(-)
(still confined within the pulp)
PALPATION TEST
To check swelling
or tenderness on
the tissue area (-)
RADIOGRAPHIC
FINDINGS
No findings
Radiograph:
Normal, intact,
no remarkable
changes
No findings
Radiograph:
Normal, intact,
no remarkable
changes
No findings
Radiograph:
Normal, intact,
no remarkable
changes,
restorations can
be seen if with
large caries
No findings
Radiograph:
Normal, intact,
no remarkable
changes
No findings
Radiograph:
Normal, intact,
no remarkable
changes
No findings
Radiograph:
Normal, intact,
no remarkable
changes
No findings
Radiograph:
Normal, intact,
no remarkable
changes
(+)
(-)
RCT done
PERCUSSION TEST
(PERIAPICAL TISSUE TEST)
Non-affected tooth first, so there
will be basis for comparison (pain)
May still elicit pain since
ongoing treatment, if there are
remaining pulp tissue
Can be false positive
(-)
(-)
(-)
RMRM
OP1
1. INTERNAL RESORPTION
•
•
•
DR. F.M.TAN
ASYMPTOMATIC IRREVERSIBLE PULPITIS
2. HYPERPLASTIC PULPITIS (PULP POLYP)
Starts from reversible pulpitis first, slow process
Resorption may have pain or no pain
No symptoms but pulp cannot be recovered
•
•
•
•
•
Starts from symptomatic irreversible pulpitis: mild, moderate, intense pain
Long standing inflammation, inflammation is still on going
PRESSURE is released, thus, asymptomatic (since there is no impingement of
nerve fibers present)
Inflammation causes hyperplastic reactions of pulp producing more fibers +
dead bacteria + chronic inflammatory cells, forming granulation tissue
Common in newly erupted 1st molar, open apex
NOTE:
• Subjective Symptoms – Varies (Depends on the patient’s pain threshold, immune system, etc.), not reliable source
• Objective Symptoms – All the same, with the help of clinical tests
• You cannot apply medicaments in pulp with disease, especially worse cases
• Inflammation does not always mean that the site has bacteria. Sometimes it is just secondarily infected by bacteria.
• Symptomatic = Acute, painful, intense
• Asymptomatic = Chronic, not painful
• Infection always finds a path with least resistance
RMRM
OP1
DR. F.M.TAN
PERIAPICAL DISEASES (APICAL PERIODONTITIS)
•
•
•
•
Untreated necrotic pulp / symptomatic /
asymptomatic irreversible pulpitis can lead
to periapical diseases
May not always arise from a diseased pulp
o E.g., due to trauma; normal tooth, with
periodontal disease
Periapical diseases do not eliminate the
bacteria, they just confine it
Bacteria continue to build up + dead tissue
will drain to the root apex
o Going to the thin layer of periodontal
ligament tissue, reacting with the
inflammation
o Due to its thin / small area, few tissues, it
cannot confine the infection, so the
infection will progress to the surrounding
bone
o Radiographically, it is seen as the widening
of periodontal ligament space, as the bone
is will be destructed / destructed already
DISTINCT FEATURE OF PERIAPICAL DISEASE (RADIOGRAPHICALLY)
• Periapical Radiolucency
1. Cyst
2. Granuloma
3. ABSCESS
• ILL-DEFINED MARGIN, it blends with the surrounding tissue; spreads faster
CHRONIC ASYMPTOMATIC LESIONS
• Slow growing, long duration
• Has SCLEROTIC MARGIN – WELL-DEFINED SCLEROTIC BORDER; represents
new layer of bone, osteoblasts lay down new bone since the lesion is slow growing
1. CYST
2. GRANULOMA
• To know if granuloma or cyst, do histologic examination
IMPORTANCE
• Confines the bacteria discharged from the root canal space
• Prevents bacteria from spreading into adjacent bone marrow spaces and other
surrounding tissues
IN RETURN
• Bone will be destroyed / resorbed, bone will sacrifice
Cyst / Granuloma
Abscess
RMRM
PERIAPICAL DISEASES
(APICAL PERIODONTITIS)
1. SYMPTOMATIC
APICAL
PERIODONTITIS
(ACUTE)
Periodontal
ligament
tissue is only a thin layer
so the spread of
infection spreads faster
to the adjacent bone
structure
• If it will confine
bacteria, CAP
• If not, AAA
OP1
DESCRIPTION / SIGNS /
SYMPTOMS
Initial time of entry,
inflammatory products has
reached the apical tissue
(PDL),
Intense pain
(No space in the periapical
area, inflammation causes
pressure)
No bone destruction yet
PULP TESTING
(PULP VITALITY
TEST)
Electric, hot, cold
test
Can be false
positive, not
always (-)
Response may be
similar to
symptomatic
irreversible pulpitis
(for early stage only
of AP)
DR. F.M.TAN
PERCUSSION TEST
(PERIAPICAL TISSUE TEST)
Non-affected tooth first, so
there will be basis for
comparison (pain)
PALPATION TEST
To check swelling
or tenderness on
the tissue area
RADIOGRAPHIC FINDINGS
Normal (early stages), but
there can be slight periodontal
ligament space widening
(for later stages)
With or without slight
periapical radiolucency (not
well-defined)
(+)
(+)
(pressure = pain)
(apical)
Cyst or Granuloma, well-defined
sclerotic border, periapical
radiolucency (hallmark of
periapical disease)
2. ASYMPTOMATIC
APICAL
PERIODONTITIS
(CHRONIC)
Bone will be resorbed in
return
to
bacterial
confinement
and
infection spreading
(- / +)
Released Pressure =
No Pain
• Granuloma
• Cyst (has thick lining)
(Negative if
progressed from
necrotic pulp,
positive if
progressed from
irreversible pulpitis)
(-)
(-)
RMRM
3. ACUTE APICAL
ABSCESS
(SYMPTOMATIC)
• Pus – degradation
products
of Can be secondarily infected
inflammation, dead
granuloma / cyst from
bacteria
and existing periodontal disease
neutrophils
(due to virulence of bacteria)
Exacerbation of existing
• Abscess – lesion,
granuloma / cyst
localized collection
of pus
• Cellulitis – not
localized
pus,
spreads
OP1
Presence of
swelling
(- / +)
(Negative if
progressed from
necrotic pulp,
positive if
progressed from
irreversible pulpitis)
(+)
(+)
(apical)
(pressure = pain)
(-)
4. CHRONIC APICAL
ABSCESS
No Pain (there is drainage)
Abscess will find and area
with least resistance,
creating sinus tract
Fistula can appear on other
areas (not adjacent to the
infected tooth)
(- / +)
(Negative if
progressed from
necrotic pulp,
positive if
progressed from
irreversible pulpitis)
DR. F.M.TAN
Periodontal ligament space
widening, with radiolucency
(well-defined)
(-)
Presence of fistula,
draining sinus,
gingival swelling,
tenderness,
redness
Periodontal ligament space
widening, with radiolucency
(or mild pain)
Well-defined periapical
radiopacity, associated with
carious tooth
5. CONDENSING
OSTEITIS
Forms bone instead of
destructing, can be
cementoblastoma or
osteoblastoma
(-)
(+)
(process of inflammation)
(-)
If intact (vital) tooth, not
coming from a carious lesion,
tumor (i.e., cementoblastoma)
RMRM
OP1
NOTE:
• Granuloma can become cyst if it remains chronic, or directly become abscess (bacterial invasion)
o Proliferation of epithelial cells, connective tissues, inflammatory cells can transform into cystic formation
o Secondarily affected granuloma can become abscess
• Cyst cannot become granuloma
o Secondarily affected cyst can become abscess
ADDITIONAL NOTES
•
•
•
•
•
The goal of infection is to find drainage, to be drained out. If left untreated, the virulence of
bacteria will increase, causing more complex and severe damage (tissue destruction –
consequence in defense mechanism; i.e., cyst / granuloma / blood clot (thrombus)).
Infection will find its path of least resistance; it depends on:
o Local Factors
▪ Thickness of the bone (e.g., in maxilla, buccal/facial is thinner compared to
palatal bone)
▪ Anatomic location of the root
▪ Presence of Connective Tissue (CT) Barriers (i.e., muscle attachment)
o Systemic Factors
▪ Host response
▪ Virulence of Bacteria
If infection penetrates and destructs the cortical bone / plate and exits in:
o ENCLOSED AREA (kulob) – ABSCESS (A lesion, localized infection of soft tissue, localized collection of pus) –
Confined in area with CT BARRIERS (i.e., muscle attachments)
o FASCIAL SPACES (kalat) – CELLULITIS (Not localized, widespread infection in fascial spaces) – E.g., posterior tooth
infection (either MX / MD) spreading to buccal space
▪ -itis – acute, its onset signifies the entry of bacteria, INFLAMMATION ONLY, NOT INFECTION (E.g., Cellulitis)
▪ If infection spread in buccal space – Buccal Space Cellulitis (swelling of buccal space)
▪ Sublingual space and submandibular space are connected, divided by mylohyoid muscle
▪ If infection spread in sublingual and submandibular space – Ludwig’s Angina
LUDWIG’S ANGINA - very common among young patients, cellulitis spreading in the floor of the mouth and neck
o ENT first before dental department
o Infection in Ludwig’s Angina spreads very fast as it spreads directly into the submandibular space (not through
lymphatics); the roots of lower teeth are close to mylohyoid muscle which are located within submandibular space
CAVERNOUS SINUS THROMBOSIS – defense mechanism forms blood clot (thrombus) containing bacteria (in
response to infection) and reaches / trapped / occluded in the cavernous sinus (venous drainage of the brain, not a
sinus)
o During soft tissue infection, body forms blood clot to contain and prevent the spread of bacteria, circulating in
the body
DR. F.M.TAN
RMRM
OP1
DR. F.M.TAN
RMRM
OP1
DR. F.M.TAN
OSTEOMYELITIS, CONDENSING OSTEITIS
Disease
Etiology / Description
OSTEOMYELITIS
Etiology:
• Extension of periapical
abscess
• Physical Injury such as
fracture or surgery
• Bacteremia
• Trauma
Description:
• Acute and chronic
inflammatory process
in the medullary cortical
surfaces of bone that
extends away from initial
site of involvement
CONDENSING
OSTEITIS
(Focal Sclerosing
Osteomyelitis)
Etiology:
• Low grade focal bone
irritation (e.g., pulpitis)
Description:
• Periapical lesion that is
seen at the apex of a
tooth with long standing
pulpitis
Pathophysiology / Tissue
Damage
Pathophysiology:
• The periapical area infection is
left untreated, causing the
spread of infection into the
adjacent cortical bone
• The infection spreads in the
medullary bone instead of
making drainage (drainage will
occur after)
• Some parts of medullary
bone are not destroyed
Tissue Damage:
• Bone destruction, resorption
Clinical Signs
and Symptoms
•
•
•
•
•
•
Radiographic Features
Histopathologic
Feature
• Opaque-lucent
• Resorption of the lesion or
demineralized bone over
time diffuse radiolucent • Purulent
Pain
exudate
changes begin to appear
Pyrexia
• Bony
Painful lymph- • Islands / remnants of bone
trabeculae
(Sequestra
–
undestroyed
adenopathy
showing
bone)
Leukocytosis
reduced
Paresthesia of
osteoblastic
the lower lip
activity
Draining Sinus
• Sequestrum
Management
• Antibiotics
and
Drainage
• Sequestrect
omy
Pathophysiology:
• Radiopaque mass usually at
• Asymptomatic
• The periapical area infection is
the apex of the premolar or
found on routine
• Lymphocytes
left untreated, causing bone
molars
dental
and
plasma
calcification
examination
cells
• Root Canal
Tissue Damage:
• Mild, persistent,
•
Sequestrum
treatment
• Bone calcification instead of
and dull pain in
• Fibrosis
resorption
the affected area.
replacing fatty
• Associated with carious • No
systemic
manners
tooth
(if
not,
can
be
symptoms
like
cementoblastoma)
fever or chills.
SUPERFICIAL INFECTION
CELLULITIS
Etiology:
• Bacterial infection
Description:
• Acute
inflammatory
process that diffusely
spread throughout the
tissue
rather
than
localized
Pathophysiology:
• From an untreated infection,
the infection penetrates and
destructs the cortical plate
and exits in fascial spaces
(not localized spread)
Tissue Damage:
• Bone destruction, tissue
destruction
•
•
•
•
Pain and tenderness
Redness and inflammation
Fever
Abscess with pus
• CT Scan shows
a cobble stone
appearance
• Zone
of
liquefaction
composed of
proteinaceou • Antibiotics
s exudate
IV
• Main bacteria • Surgical
Streptococcu
drainage
s
and
Staphylococc
us
RMRM
OP1
DR. F.M.TAN
DEEP FACIAL INFECTION
CAVERNOUS
SINUS
THROMBOSIS
LUDWIG’S
ANGINA
Etiology:
Pathophysiology:
• Bacterial infection has • From an untreated infection,
spread to the blood
the defense mechanism of the
stream
body is to form a blood clot
Description:
(thrombus)
• Very
rare
life- • The thrombus (containing
threatening condition
bacteria)
circulates
and
that can affect adults and
became occluded in the
children, a blood clot
cavernous sinus.
blocks a vein that runs Tissue Damage:
through
a
hollow • Swelling / redness in the
space underneath the
areas which are lined with the
brain behind the eye
venous drainage of the brain
socket. The veins carry
(cavernous sinus)
blood from the face and
head back to the heart.
Pathophysiology:
• From the untreated infection
(e.g., apical abscess), the
Etiology:
infection spreads directly
• Trauma to the floor of
into
the
submandibular
the mouth
space and up to the floor of
• Upper
respiratory
the mouth and neck.
infection
Tissue Damage:
• Oral lacerations
• Neck / face swelling
• Endotracheal
intubation.
• Tongue piercing
Description:
• Soft tissue infection
of the floor of the
mouth
which
is
bilateral and involves
the
submandibular
and
sublingual
spaces
• Unilateral
periorbital
edema
• Headache,
• Photophobia
• Paralysis
of
cranial nerve
• Proptosis
(bulging
of
eyes)
• CT scan reveals a bulging
lateral margin of cavernous
sinus
• Staphylococc
us
and • Broad
Staphylococc
spectrum
al
antibiotics
IV
• Zone
of
liquefaction
• Surgical
composed of
Drainage
proteinaceou
s Exudate
• Radiopaque
•
•
•
•
•
•
•
•
•
•
Fever
Tachypnea
Swelling
Pain in the floor
of the mouth
Hoarseness of
voice
Difficulty
swallowing
(dysphagia)
Difficulty
speaking
Drooling
Respiratory
disease
(advanced stage)
Pus
drainage
from the floor of
the mouth or
throat.
• Antibiotics
• Corticostero
• Staphylococc
ids
us
and
• Endotrachea
Staphylococc
l intubation
al
• Tracheosto
my
RMRM
[ADDITIONAL NOTES FROM CANVAS]
OP1
DR. F.M.TAN
CYSTS OF THE ORAL REGION
ODONTOGENIC CYST
Odontogenic Cysts are those cysts which derives from epithelium associated during the development of the dental apparatus. The tooth involved may be vital or non-vital and
the pain may or may not be present. Asymmetrical appearance of the jaw may be evident as the cysts grows.
Disease
Etiology / Description
Clinical Features
Radiographic Features
Histopathologic Feature
Management
• Radiolucency at the
end of root of a nonEtiology:
• Surgical
vital tooth
• Asymptomatic
• An epithelial jaw cyst, caused by
incision
inflammatory
activation
of
• Will not response to
coupled
RADICULAR
• Lined with nonepithelial
any standard pulp
with
CYST
keratinized
Description:
testing procedures
removal
(Apical or
epithelium
of cause
• Often found on tooth with deep
• Invisible on intraoral
Periapical Cyst)
will cure
carious lesion, deep restoration
clinical examination
the cyst
and inadequate root canal filling
•
DENTIGROUS
CYST
(Follicular Cyst)
Description:
• A common epithelial lined jaw
cyst
• Surrounding the crown of an
unerupted or impacted tooth
• Common
in
mandibular
3rd molar and maxillary cuspid
• May cause root resorption on
adjacent tooth
• Hollowing out in an unerupted
mandibular 3rd molar of the
entire ramus extending up to the
coronoid process and condyle
•
•
Solitary well defined
radiolucent
that
surrounds the crown
of an unerupted teeth
or
supernumerary
teeth
•
Facial asymmetry –
enlargement of jaw
Displacement of tooth
Radiographic Variations
1. Central Variety – cysts
surrounding the crown
of tooth and the crown
projects into the cyst
2. Lateral
Variety
–
usually associated with
mesioangular
impaction, cysts grow
Complete
surgical
removal
RMRM
OP1
•
PRIMORDIAL
CYST
Description:
• Arises from a tooth germ that
extend pushing a tooth adjacent
into a cyst
• Least
common
type
of
odontogenic cyst
• Found in place of a tooth rather
than clinically associated with one
•
•
•
•
Associated
with
a
missing tooth
Mandible
involved
more frequent than the
maxilla
Enlargement of jaw
Asymptomatic
and
may cause migration
of erupted teeth
All teeth in the area
are vital
DR. F.M.TAN
laterally along the root
surface and partially
surrounds the crown
3. Circumferential – cysts
surround the crown
and extends for some
distance along the root
• Well
determined
radiolucency in place
of normal tooth
• Situated below the neck
of teeth or root of
adjacent teeth or near
the crests of the ridge
•
•
ODONTOGENIC
KERATOCYST
(Keratocyst or
Keratinizing cyst)
Description:
• A jaw cyst of Dentigerous or
Primordial origin
• Common in the mandible
• Mandibular 3rd molar is the
common site
Multilocular
Appearing
as
a
radiolucent around the
crown of an unerupted
tooth (dentigerous) or
in a missing tooth
(primordial) \
•
Lined
with
keratinizing
epithelium
•
Keratinized
epithelium
Actively
proliferating
epithelium
Keratinize filter
central cavity
Thin cyst wall –
epithelium and CT
Flat epithelium –
CT interfere
Epithelium
pouches – cul de
sacs,
scattered
cyst
•
•
•
•
•
•
Surgical
removal
with
thorough
curettage
of
the
bone
•
Excision,
but they
tend
to
recur
RMRM
OP1
DR. F.M.TAN
•
•
•
LATERAL
PERIODONTAL
CYST
Description:
• Rare of unknown etiology
• Found on interdental alveolar
process between adjacent teeth
•
Associated tooth is
vital
Anterior region of
mandible
is
commonly affected
No clinical signs and
symptoms may be only
determined
during
routinely radiographic
examination of teeth
•
Solitary small (1 cm in
diameter)
circumscribed
radiolucency in the
lateral surface of a tooth
root
Cystic
border
is
surrounded by a thin
layer of sclerotic bone
•
•
RCT with
enucleati
on
or
extractio
n
Does not
recur
after
removal
NON-ODONTOGENIC CYST
Non-Odontogenic Cysts develop from epithelium trapped during the development of the oral cavity.
These cysts are not associated the dentition but may somehow affect the position of it as the cysts expands.
• Fissural cysts are not related to teeth
• Fusions of upper jaw bones and from epithelial trapped during development of the oral cavity and face
• It does not arise in the mandible and is formed by the fusion of separate structures
• Upward down pearDescription:
shaped radiolucency
• Arises from epithelial remnants
• Non-keratinizing
between the maxillary
left during fusion of the globular • Enlargement and migration
• Lines
with
canine and lateral
of adjacent teeth
and maxillary process of the
stratified
incisor
GLOBULLOMAXIL
embryonic face
• Asymptomatic
squamous
non
LARY CYST
• Neck of the pear is
• Seen between the root of • Teeth are vital
keratinizing
between the coronal
maxillary lateral incisor and
epithelium
pars of these teeth
canine
• Root of canine and
central incisor are
•
Enucleati
on
–
removal
of cyst
RMRM
OP1
DR. F.M.TAN
spread apart by the
radiolucency
•
•
Description:
• May arise from proliferation of
epithelium trapped during the
NASOLABIAL
development of middle face
CYST
(lacrimal duct)
(Nasoalveolar Cyst)
• Rare soft tissue cyst appearing
as a facial swelling
•
MEDIAN
PALATAL CYST
Description:
• Situated in the midline of the
palate
•
•
Asymptomatic
Lesion is confined
solely to the soft
tissue and are
Swelling
in
the
midline of the palate
Covering mucosa is
intact
May cause problems
during
mastication
and speech
•
Not
visible
in
radiographs, it can only
be seen by using
intravenous dyes such
as Barium
•
Circumscribed area in
the midline of the hard
palate
Mistaken
to
nasopalatine
cyst
because of its site, which
is in the anterior position
•
•
Excision
in
the
labial
vestibule
to avoid
facial
scar
•
Surgical
excision
RMRM
OP1
DR. F.M.TAN
•
Description:
• Most common of all nonodontogenic cyst
NASOPALATINE
CYST
• Incisive Canal – located in the
(Incisive
Canal
incisive papilla
Cyst)
• Cyst of Palatine Papilla – located
within the nasopalatine canal
•
•
•
•
Asymptomatic
Elevation
in
the
anterior part of the
palate
Covering mucosa is
normal
Teeth in the area are
vital
•
Heart
shaped
radiolucency located
midline just lingual to
the maxillary central
incisor
Superimposition of the
nasal spine on the
radiolucent area
•
•
•
Excision
Enucleati
on
Removal