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Lab 1 Developmental Changes (2008 Script)
Lab 1 Developmental Changes (2008 Script)
We talked about Cleidocranial Dysplasia & we will talk about Crouzon Syndrome & Treacher Collins Syndrome. And after that we will go back to Dentin 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 was delayed 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.
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 lower eyelid (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 )
Hereditary condition Affecting both dentitions (primary & permanent) Dentin Dysplasia type I Dentin Dysplasia type II
Defect in coronal & radicular dentin Rare Radiographically , like DD type I in deciduous dentitions in the permanent dentitions , the pulp chambers are abnormally large , flame shape , pulpal calcifications (pulp stones )
More common
the teeth in dentinogenesis imperfect) in the permanent dentitions the color is normal Short root
Ectodermal dysplasia
No eyelashes or eyebrows The hair thin and scanty & easily lost Lips are protruded Some protuberance of the
frontal bone
Hypodontia.
Supernumerary tooth Because it looks like the adjacent teeth it is called supplemental as it has the same morphology.
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.
is it a supernumerary?
What is the cause?? It could be trauma. After complete mineralization?? No, before as it could fracture. And here trauma is one of the causes, the other one is idiopathic
Taurodontism.
The pulp chamber increased in dimension occluso-apically. So the furcation will go more toward the apex more apical. And the canals will be short.
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, which developmental abnormality? Look at the difference in the radioopacity within the crown. There is a thing more radio-opaque than dentin, so there is enamel in the dentin,
so this is called dense in dente which is invaginating within the crown or reaching the apex.
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 if partial necrosis & then periapical 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)
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 .
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 chalkywhite 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 to
Dr. ^_^)
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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 the cervical margin ) their clinical significance relates to that they could form periodontal pocket (periodontal attachment loss) , which might lead to periodontal disease and paradental cyst
Turner tooth
These are permanent teeth , newly erupting There is color change Localized Hypoplasia or hypomineralization of enamel
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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 the permanent or deciduous dentition, the cause is an infection occurs during tooth development at a certain time.
Dental Fluorosis Fluoride ions entering the structure of enamel instead of hydroxyl group lead to changing in structure of hydroxyapatite enamel crystals.
It is a chemical insult and abnormality structure and it 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
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Pinpoint sized pits scattered across surface of teeth Generalized , affected all the teeth in the arch
The hardness is well (not chipped away ) Hypoplastic ( reduction in thickness , shape and formation of enamel )
Size is abnormal
imperfecta localized
Horizontal rows of pits, linear depression or one large area of hypoplastic enamel
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(generalized )
Hypocalcification
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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 : obliterated pulp canals
Rapid loss of enamel followed by rapid loss of dentin but the teeth is caries resistant
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Dentin Dysplasia I Normal appearance of dentition Disorder in radicular dentin Obliteration of the pulp chambers
Periapical
Radiolucency
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Hypophosphatasia
Congential lip pits : Small gap or canal , it is a blind canal , and sometimes minor salivary glands open inside it
Paramedian lip pit : surrounding the mid line of the lower lip , its associated with vander woude syndrome
Double lip : Excess tissue projecting form the inner side of upper lip , it's associated with Asher
thyroid gland )
Ankyloglossia :
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
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
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 )
Clinical significance : it may form Lymphoepithelial cyst Another common location for lymphoid tissue intraorally 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 :
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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)
Decrease in the size of one side of the face (degeneration) The cause : Problem in sympathetic innervations
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The worst is to have opening and communication between Nasal and oral cavities
Glandular tissue(submandibular salivary gland) form concavity in lingual cortex of the mandible
Locations :
Third molar area Mandibular canal The inferior border of the mandible
No treatment is required
In areas of extraction teeth and in severe anemia cases (to compensate the deficiency ) hematopoietic marrow instead of trabecular bone which is the normal for the area
Clediocranial dysplasia :
Multiple of supernumaerary teeth , retain the primary denteion into adulthood Numerous formed teeth
embedded
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
Mandibular retrusion
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Done by : HeRoN
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