lab 1 developmental changes ( 2008 script )
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Developmental changes
We talked about Cleidocranial Dysplasia & we will talk
about Crouzon Syndrome & Treacher Collins Syndrome.
And after that we will go back toDentin Dysplasia type I &
II, to make everything clear then we will start the lab.
Crouzon syndrome :
A genetic disorder
Characterized by the premature closure of Cranial
Sutures (Craniosynostosis )
The opposite of Cleidocranial Dysplasia, that wasdelayed closure & opened fontanelles
Radiographically : marking of the veins on the skull
because closure is early & there is no space for the
veins to enlarge within , so there will be beaten
metal pattern of the inner aspect of the skull.
Increased interpupilla distance, so exophthalmos as
there is no space for the eyes
Maxillary retrusion (malocclusion)
Patients exhibit vision and hearing deficits
Hypoplastic maxilla and short upper lip.. when the
maxilla is hypoplastic , there is no space for the
palate to grow so the palate will be ( V ) shaped or
arch shape , sometimes there is cleft palate.
Treacher Collins syndrome:
A genetic disorder
Characterized by abnormal development of
structures derived from the first and second
branchial arches
Eyelid is dropping down , there is a notched lowereyelid (coloboma).
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Mandibular retrusion as there is condylar and
coronoid hypoplasias (short condyle and coronoid)
which lead the mandible to be pushed back to the
fossa, so retruded mandible,
The ears have many changes, hypoplasia, aplasia,
alteration, etc. (deafness)
Macrostomia resulting from unilateral or
bilateral facial clefting (rare cases )
Dentine dysplasia (DD):
Hereditary condition
Affecting both dentitions (primary & permanent)
Dentin Dysplasia typeI
Dentin Dysplasia type II
Defect in radiculardentin
Defect in coronal &radicular dentin
More common Rare
Radiographically, thereis obliteration in thepulp chambers &canals
Radiographically , likeDD type I in deciduousdentitionsin the permanentdentitions , the pulpchambers areabnormally large ,
flame shape , pulpalcalcifications (pulpstones )
There is premature lossof both deciduous &permanent teeth
The color of the teeth
within the normalrange
In the deciduous
dentition there ischanging in color (like
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the teeth indentinogenesisimperfect)in the permanentdentitions the color is
normal
Short root Normal root length
Periapicalradioluscency
Horizontal pulpchampers
Now the lab part :
Microdontia :
It is a change in size of teeth not
in the structure
Common.
Ectodermal dysplasia
No eyelashes or eyebrows
The hair thin and scanty &easily lost
Lips are protruded
Some protuberance of the
frontal bone
Decrease in sweating so intolerance for heat
(hypohidrotic)
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Anodontia or hypodontia and Microdontia
Hypodontia.
Supernumerary tooth
Because it looks like the
adjacent teeth it is called
supplemental as it has the
same morphology.
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Mesiodense, specific term giving
for a supernumerary tooth
between the maxillary central
incisors. This supernumerary tooth
may erupt in the floor of the nose;
it maybe horizontal or it may erupt
in between the central I .
Here we have multiple
supernumerary teeth.
Mesiodense may be
impacted to erupt in the
floor of the nose, or it
erupts between the two
central incisors or it may
be impacted.
What are the syndromes that have supernumerary
teeth?
Gardner syndrome
C leidocranial dysplasia syndrome.
Natal or neonatal tooth
is it a supernumerary?
No
it should be extracted?
No.
When it should be extracted?
If it causes trauma, & interferes with feeding, & here wecan see ulcer on the tongue.
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Dilaceration, sharp angel in the root.
What is the cause?? It could be trauma.
After complete mineralization?? No, before as it couldfracture.
And here trauma is one of the causes, the other one is
idiopathic
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Taurodontism.
The pulp chamber increased in
dimension occluso-apically. So thefurcation will go more toward the
apex more apical. And the canals
will be short.
Dense in Dente(Dens Invaginatus
).
invagination of enamel within the crown &
sometimes it reaches the root & sometimes
the apex; sometimes it may change the
whole morphology of the tooth, not only
causing a pit or invagination, this will be
called dilated odontoma, because it will
dilate the crown & change its morphology.
& in the odontomes contain enamel pulp &
dentine so if you have enamel within the
crown so it looks like odontome. Dense in dente, may be
wide & may be a small pit, or more severe reaching the
pulp, may be to the root & may be more & more severe
reaching the apex & cause dilated odontome, here
extraction and RCT will not be easy.
If we said there is a periapical lesion
here, periapical inflammation, whichdevelopmental abnormality?
Look at the difference in the radio-
opacity within the crown.
There is a thing more radio-opaque than
dentin, so there is enamel in the dentin,
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so this is called dense in dente which is invaginating
within the crown or reaching the apex.
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What is the cause of radio-apical radioluscency when
there is a pit within the crown?
The food will accumulate in the pit, so food impaction with
the bacteria which is found there, the bacteria will
produce acids, & this acid will cause demineralization of
the enamel, lead to caries, so caries within this pit will
make hole, so there is caries within the depth of the pit, &
it will open the pulp & the bacteria will reach the pulp,
then the bacteria will cause pulpal inflammation &
necrosis, then all the products will go in the periapical
area causing inflammation.
Pulpal inflammation & involvement & necrosis even ifpartial necrosis & thenperiapical peridontitis.
Dense Evaginatus
Change in shape, it is a
supernumerary cusp, at
premolars (upper & lower,
more commonly in the
lower but in this pic it is in
the upper)
Significant: it may interfere
with occlusion
If we decide to trim this cusp, can we trim it?
No, as there is pulp horn & if I trim it I will
expose the pulp causing severe pain to the
patient & there may be pulp necrosis & periapical
radioluscency, so if I have to trim this evaginatus
we have to do root canal treatment .
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Talon cusp
Extension of the cingulum, to variable distances & it
may reach the incisal edge
look at the radio-opacity, always enamel whiter
than dentin, if you want to decide which
abnormality is here look at the radio-density or
radio-opacity, & you will see that this is chalky-
white much whiter than the surrounding tissue,
so you can decide that this is enamel & it tipper
in that way so it is a cusp.
talon cusp contains a pulp horn & we have to take
care of it.
Fusion
Usually if I count the big tooth
there will be a missing tooth in the
dental arch
In fusion we should have at least
union in camentum? No.
We should have union in the pulp? No.
(3ala zemt al Dr.)
The union should be at least in
dentin (in crown or root), but could
be in dentin & pulp for example but
not in cementum. (Again, according toDr. ^_^)
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If the fusion in cementum it is called
concrescence.
Gemination
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Enamel pearl
Occur in the bifurcation area
It may contain dentin
There is no clinical significance with
it
Cervical enamel
projection (extensions of the
coronal enamel beyond thecervical margin ) their clinical
significance relates to that they
could formperiodontal pocket(periodontal
attachment loss) , which might lead to
periodontal disease andparadental cyst
Turner tooth
These are permanent teeth , newly
erupting
There is color change
Localized
Hypoplasia or hypomineralization of
enamel
What do you think the cause is ?
Inflammation or
trauma during tooth
development
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Chronological hypoplasia
Chronological >> time related
These are permanent teeth , the deciduous teeth should be
affected too ? No , because it is time related it either thepermanent or deciduous
dentition, the cause is an
infection occurs during
tooth development at a
certain time.
Dental Fluorosis
Fluoride ionsentering the
structure of enamel
instead ofhydroxyl
group lead to changing in structure ofhydroxyapatite
enamel crystals.
It is a chemical insult and abnormality structure andit is a hypoplastic enamel
Excessive fluoride can cause chalky- white spots, and
in severe cases, brown stains or pitting of enamel
especially the anterior teeth because of light
exposure as in this case
It is high mineralized and largely resistant to dental
caries
Is it soft tissue ?
No , except in very severe cases
Amelogenesis imperfecta
hypoplastic, rough pattern
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Pinpoint sized pits scattered across surface of teeth
Generalized , affected all the teeth in the arch
Deciduous dentition involved
The hardness is well (not chipped away )
Hypoplastic ( reduction in thickness , shape and
formation of enamel )
Size is abnormal
Amelogenesis
imperfecta
rough pattern
Thin, hard, rough enamel
Deciduous dentition
involved
A
mel ogenes
is
imperfecta
localized
Horizontal rows of pits, linear depression or one large
area of hypoplastic enamel
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At the time of eruption it looks normal
Very soft enamel (chipped away )
Exposed dentin ( easily stained ) , will lost because it
soft and cannot with-stand occlusal forces
Radiographically : lake of opaque line of enamel ,
because calcification is less than normal so it looks
like dentin or even less
Dentinogenesis imperfect
Lost of tooth structure
Both dentition are affected
(here Deciduous dentition)
Radiographically : obliteratedpulp canals
Bulbous crowns and
the neck -Cervical line
constructed
Rapid loss of enamel followed by
rapid loss of dentin but the teeth is caries resistant
Color changes , because the hue
of abnormal dentin
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Dentin Dysplasia I
Normal appearance
of dentition
Disorder in radiculardentin
Obliteration of the
pulp chambers
Periapical
Radiolucency
Horizontal radiolucent line of the pulp
Short root
Premature lost of
teeth
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Dentin Dysplasia, Type II
Wider pulp chamber and Flame
shape appearance of the pulp
Normal root length
Pulpal calcification ( pulp
stones )
Hypophosphatasia
Premature loss of
teeth (deficiency in
alkaline phosphatase
enzyme )
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C ongential lip pits :
Small gap or canal , it
is a blind canal , and
sometimes minor salivary
glands open inside it
Commissural lip pit
Paramedian lip pit :
surrounding the mid line of the
lower lip , its associated withvander woude syndrome
Double lip :
Excess tissue
projecting form the inner
side of upper lip , it's
associated with Asher
syndrome
what are the other components of asher
syndrome ?
Dropping in the eye lid
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Nontoxic Goiter(enlargement of
thyroid gland )
A nkyloglossia :
Abnormal tissue attached
between the tonge and the floor
of the mouth , so here will be
abnormal tongue mobility .in the
most severe case: gingival
recession , abnormal swallowing
and talking
Treatment : surgically removalof lingual frenum
forduce granules :
Yellowish spots contains collection of
sebaceous glands
Location : buccal mucosa
There is no clinical significance ,except that they may accumulate
sebaceous secretions and form a
small cysts
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leukoedema
Accumulation of fluids within the epithelial cells
(intracellular ) of buccal mucosa
How can we make sure that it is leukoedema ?
Stretch the buccal mucosa , if it is leukodemea
the whitish appearance will disappear or decrease
White Sponge Nevus :
Doesn't disapper upon stretching , usually
it involves other mucosal surfaces nasal
cavity is involved , other family members
may be affected
The cause : mutation in a pair of
keratin k4&k13
Thyroid nodule
At the bottom of the
tongue at foramen
cecum
Can we remove it ?
No , we must first make sure that patient
has another thyroid gland , because if he dosent
have another one and we remove it , he will
have a shock because he will need replacement
of thyorid hormones ( t3 & t4 )
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Oral Tonsil
This is the floor of the
mouth , and this is the
lingual frenum ,and the
nodules on sides of lingual
frenum are the oral tonsils
which contain lymphoid
tissue (mucosal
associated lymphoid tissue )
They are a part ofwaldeyer ring which contains
Palatine tonsils (faucial )
Lingual tonsils
Pharyngeal tonsils (adenoid)
Clinical significance : it may form Lymphoepithelial
cyst
Another common location for lymphoid tissueintraorally is in association with the foliate papilla at
the lateral border of the tongue posteriorly , if it is
enlarged we call it foliate papillitis
Hemifacial
hypertrophy:
Unilateral
enlargement of
Facial tissues
(bone , muscle, tongue..)
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May exhibit an increased incidence of certain
Visceral Tumors
if only the tongue was enlarged is it
Hemifacial hypertrophy ? No
It may be a tumor ( lymphangioma ,
hemangioma or neurofibroma)
Down syndrome : symmetrical
enlargment of tongue
Romberg syndrome (hemifacialatrophy ) :
Decrease in the size of one side of the
face (degeneration)
The cause :
Problem in sympathetic
innervations
Infection
Trauma
Systemic Sclerosis
Cleft lip an
palate :
This is mildest form
of it
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In areas of extraction teeth and in severe anemia
cases (to compensate the deficiency )
hematopoietic marrow instead oftrabecular bone
which is the normal for the area
Clediocranial dysplasia
:
Multiple of
supernumaerary teeth ,
retain the primary
denteion into adulthood
Numerous formed teethembedded
Defective cementum
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Crozon syndrome :
Mutation in fibroblast
growth factor 2 ( FGF2)
Maxillary hypoplasia
Short upper lip
Widely spaced eyes(hypertelorism )
P
rotruding eyeballs
Exophthalmos
Treacher collins
syndrome
Mandibular retrusion
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Ear is abnormal downward
Sloping lower eyelid
Done by :
HeRoN
"Sometimes the Wrong train can take us to the right
place"
(Paulo Coelho)