lab 1 Developmental Changes ( 2008 script )

8/3/2019 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)

Documents

lab 1 Developmental Changes ( 2008 script )