Radiology Sheet #2 By Suhaib Attieh

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Radiology Sheet #2 By Suhaib Attieh

Post by Sura on 12/10/2012, 6:07 pm

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تاريخ التسجيل : 2010-09-29

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Re: Radiology Sheet #2 By Suhaib Attieh

Post by Shadi Jarrar on 9/11/2012, 4:50 pm

بسم الله الرحمن الرحيم
Radiology sheet no. 2
Suhaib Attieh
We will in radiology course talk about subject in the first lecture, and do a conference about it in the next one. In the conference we’ll discuss cases, those will be provided by the doctor. Today we’ll talk about the developmental and congenital anomalies and next lecture will be the conference about the cases.

Developmental and Congenital Anomalies

· Anomaly: a deviation from the normal. Could be congenital or acquired. Congenital is something that you are born with and acquired is something that you are not, it is subjected to an environmental effect by nature.

· Dental anomalies: dental anomalies could be:

1) In number.

2) Size.

3) Eruption.

4) Morphology.

In number:

We could have:

1. Too many “hyperdontia” : could be found anywhere in the oral cavity, third premolar, forth molar, mesiodens, they’re all supernumerary teeth.

- Isolated instances are not a big deal, and management could be by following up or extraction.

- The problem is when there’s a suspected systemic disease!! Two main systemic diseases could be associated with multiple supernumerary teeth are the cliedocranial dysplasia and Gardner’s syndrome.

- The importance of Gardner’s syndrome is its highly premalignant polyps! 100% chance to turn into malignancy. So when a kid come to your clinic with a little bit more teeth as a chief complaint and you diagnose a more morbid disease this might save his life!!

- Some cases are easily diagnosed, but others are very difficult to be diagnosed in a two dimensional x-ray and needs the third dimension which is gotten by the new techniques like CT scan or the cone beam.

2. Too little “hypodontia” : is the condition at which the patient has missing teeth as a result of their failure to develop.

- Oligodontia: when there’s an extreme hypodontia, missing more than six teeth excluding third molars.

- Anodontia: congenital absence of all primary or permanent teeth.

- In cases of anodontia or extreme oligodontia we suspect in a systemic disease that is the “ectodermal dysplasia”.

- The connection between the ectodermal dysplasia and the extreme missing teeth condition is the ectoderm. Ectoderm gives origin to enamel organ, skin, hair, nails and sweat glands.

- Oligodontia could be seen with down syndrome patients, cleft lip and palate, Hemifacial microsomia and radiation patients.

- Hemifacial microsomia is a congenital disorder that affects the development of the lower half of the face, most commonly the ears, the mouth and themandible. It can occur on one side of the face or both. If severe it can lead to difficulties in breathing, obstructing the trachea and requiring atracheotomy. It is the second most common facial birth defect after clefts, with an incidence in the range of 1 in 3500 to 4500 [1]. Hemifacial microsomia shares many similarities with Treacher Collins syndrome.

- So these connected systemic diseases are probably as important as the management of the dental issue.

In the size:

- Could be true or relative. For example patient with generalized diastemas, the jaw might be larger than normal “relative micro dontia” or the teeth are smaller than normal “true micro dontia”. So you take an impression and you measure the dimensions of the teeth and then you diagnose your problem and manage treatment upon that.

- Could be localized or generalized.

We could have:

1. Too big “macro dontia”: seen sometimes with vascular anomalies “hemangioma”. Hemangioma gives more vascularization, more oxygen so more nutrients, that gives larger teeth in that area.

Also could be seen with hypertrophy of the face and gigantism.

2. Too small “micro dontia” : we see it a lot as peg-shaped laterals.

But sometimes could be seen in association with congenital heart diseases, Down syndrome and progeria.

- Progeria (also known as "Hutchinson–Gilford Progeria Syndrome",[1] "Hutchinson–Gilford syndrome",[2] and "Progeria syndrome"[2]) is an extremely rare genetic disease wherein symptoms resembling aspects of aging are manifested at an early age.

Multiple missing vitamins. Rapid aging in the childhood and failure to growth. The patients grow physiologically but not in size.

- To get a true diagnosis, we have to rule out:

a) Positioning errors, as it might affect the dimensions on the radio-graph!! Positioning errors gives wrong dimensions of teeth on the radio-graph.

b) Radiation effects.


1. Impaction: simply is failure to erupt. Could be as easy as impacted third molar, or as hard as the case of multiple impactions.

Usually multiple impactions comes with multiple supernumereries and they all are co-related to cliedocranial dysplasia.

In some cases impactions are clear and sharp enough to be easily detected in a two dimensional radio-graph, in other cases it needs a third dimensional technique.

2. Transposition: teeth switch places.

3. Ankylosis: most of the time is a clinical diagnosis, clinical decision and it’s very difficult to give an accurate diagnosis through radio-graph. The idea of ankylosis is that the tooth is no more having periodontal ligaments, the root and bone become a one unit. Also it’s not a must to have all the root surfaces ankylosed to the bone to have a clinical ankylosis, one side on one root ankylosed to the bone is enough to give a rise to clinical ankylosis “infra-occlusion, or sub-merged tooth”.

- So, good clinical examination is needed to detect ankylosis. Signs like infra-occlusion and metallic sound upon percussion are much more helpful and powerful in the diagnosis than a radio-graph.

4. Ectopia: tooth is erupting in abnormal position. Example like palately impacted canine, labially erupting canine. Many things could be the cause, trauma, teeth\jaw size discrepancies, genatics, but no single thing have shown a clear evidence that it cause ectopic tooth.


1. Fusion: union of two normally separated tooth germs.

2. Gemination: complete division of tooth bod twins.

- We can differentiate between fusion and gemenation by counting the teeth. If we have one more tooth, then it is gemenation, and if we have one less, then it’s fusion.

3. Concrescence: fusion on the cementum level. It’s difficult to be diagnosed radio-graphically, as it needs the third dimension. But if we suspect a concrescence by the radio-graph “no periodontal ligament space for example”and we want to extract the tooth, we manage by surgical extraction to do sectioning.

Concrescence could be congenital “true” or acquired “truma and hyper-cementosis that lead to concrescence”. But t the end it’s the same clinical problem.

4. Taurodontism: large trunk, small short roots, bull-shaped teeth.

- Sometimes seen in patients with Down’s syndrome and patients with Amilogenisis Imperfecta. But if we have one taurodontic tooth in one quadrant that doesn’t mean much, it just means that this tooth will have an interesting endo!!.

5. Dilacerations: it’s a trauma thing.

6. Dens in dente: “dens invaginatus”

- Invagenation: inward folding of the enamel organ or inward folding of the hertwig sheet, have two types: Coronal type and radicular type.

- In the coronal type, the folding is lined by enamel and in the radicular type it’s lined with cementum. So that it’s called tooth within tooth.

- Dens in dente is a challenging in the dental care and in the endo treatment. Endo treatment is questionable, so prophylactic endo could be done for such patients.

7. Dens evagenatus: the problem is that the pulp follows the evagenation, and after attrition of the evagenation, pulp exposure occurs. So prophylactic endo is necessary.

8. Enamel pearls: it’s an extra enamel spot on the bifurcation area, its importance is that it worsens the prognosis of perio treatment.

9. Talon cusp: is an extra cusp on the lateral incisors mostly and could be on the central. It looks like the talon of some birds!! Usually not associated with any systemic disease, but sometimes could be associated with cleft lip patients.

10. Turner’s hypoplasia: local hypoplasia of a permanent tooth due to infection or mechanical trauma of the primary tooth. Localized infection or trauma simply causes Turner’s tooth, radiation might cause generalized hypoplasia.

11. Hutchinson’s teeth: one of the dental signs of congenital syphilis. Screw incisors, mulberry molars.

· Anomalies in the tooth structure:

1. AI “amilogenesis imperfecta”: hereditary ectodermal disturbance,

Multiple types:

a) Hypoplastic type: teeth are smaller in size. When you look at a radio-graph, you won’t see the normal thickness of enamel but instead you’ll see just a line of enamel “one thin line of enamel” but still it is denser than dentine. Again, it’s small in amount but it has a good density and can be differentiated from dentine. “Enamel is of good quality but in lesser amount”.

We can see the hypoplastic type of the AI and we can manage it as it is the mildest type.

b) Hypomaturation type: normal thickness of enamel but of poor quality. In the radio-graph there’s no dentino-enamel junction as in the normal cases, so you can’t differentiate between enamel and dentine “gray color for both enamel and dentine on the radio-graph”.

The problem is that the enamel is so weak, so it chips away from the dentine.

c) Hypocalcification type: it’s even harder, although enamel is of normal thickness once the tooth erupts, but because of the lack of calcification, it’s actually even less mineralized than dentine, it can’t tolerate the oral environment and chips away immediately.

Pitting and irregularities are seen on the surface.

d) Hypomaturation\hypocalcification type: just in case that the clinician couldn’t specify the type. In other words, the enamel structure isn’t extremely damaged to the degree of hypocalcification, and not hypomaturation we put it in this mixed type.

2. DI “dentinogenesis imperfect”: is a dentine problem.

Typical appearance: bulbous crowns, constricted necks and short roots with obliterated pulps.

Three different types:

a) Type I: associated with osteogenesis imperfecta.

b) Type II: no associated osteogenesis imperfecta.

c) Type III: Brandywine Type Dentinogenesis Imperfecta, Brandywine is a small town in Maryland. This type of DI has never been seen in anywhere else in the world!! And it has a different appearance from the typical appearance of DI “it has a wide pulp”.

Radio-graphically speaking, we can’t differentiate between type I and type II DI “as both of them have the typical appearance”, but we look for other signs like; sclera color, long bones density to decide if there’s osteogenesis imperfect or not.

There’s a huge difference between AI and DI in the radiographic appearance. DI has constricted, bulbous teeth with short roots and obliterated pulps in appearance. Clinically, teeth in DI have opalescent appearance. In contrast with AI where enamel will be lost or is already of very minimal amount, DI has abnormal dentine that will fill the pulp “pulp obliteration”. Finally, if we find enamel in the radiograph, that certainly mean it’s not AI.

3. Dentinal dysplasia:

Two types:

a) Type I “radicular type”: rootless teeth, very minimal root formation.

b) Type II “coronal type”: roots are ok, but still we have pulpal problems; flame shaped pulp, many pulpal stones and spontaneous apical diseases “apical radio-lucencies”. The problem is that we have irregularities in dentine that allow the bacteria to pass to the pulp without causing caries or trauma. Many of these teeth will have apical disease and will become non-vital, so these teeth need very good follow up to intervene with RCT when needed.

4. Regional odontodysplasia: problems in all the tissues that form the tooth. It’s usually regional so that why it’s called regional.

Also called ghost teeth because neither enamel nor dentin is well-developed, so you see something look like teeth, but you don’t know why it look like that.

· Non-odontogenic anomalies


v Hypertrophy: increase in the size.

v Hyperplasia: increase in the number.

v Hypoplasia: under development or incomplete development.

Many of the head abnormalities are correlated to the skull sutures, when they close and how they close.

v Synostosis: problem in the fusion, premature fusion.

(Synostosis means fusion of two bones, it can be normal in puberty, fusion of the epifyse, or abnormal. When synostosis is abnormal it is a type ofdysostosis.

Examples of synostoses include: craniosynostosis- being an abnormal fusion of two or more cranial bones, radio-ulnar synostosis- being the abnormal fusion of the radius and ulna bones of the forearm, tarsal coalition - being a failure to separately form all seven bones of the tarsus (the hind part of the foot) resulting in an amalgmation of two bones and syndactyly - being the abnormal fusion of neighboring digits.)WiKi

v Wormian bone: another sign of abnormal fusion. It’s small, irregular pieces of bone found inside the suture.

As we have more than one suture in the skull, abnormality in the fusion of any of them will cause head abnormality, with differences regarding what is the affected suture. Examples:

v Brachycephalic: short and broad head.

(In humans, the disorder results from premature fusion of the coronal sutures (seecraniosynostosis) or from external deformation (see plagiocephaly). The coronal suture is the fibrous joint that unites the frontal bone with the twoparietal bones of the skull. The parietal bones form the top and sides of the skull. This feature can be seen in Down syndrome)WiKi.

v Hypertelorism: the eyes are away from each other.

(Hypertelorism is an abnormally increased distance between two organs or bodily parts, usually referring to an increased distance between the orbits (eyes)--orbital hypertelorism) WiKi.

v Oxycephaly: cone-shaped appearance of the head.

v Trigonocephaly: triangular-shaped appearance of the head.

And all of that is dependent on what suture is defected, and which suture is closing earlier than the others.

1. Stafne’s bone defect: also called pseudocyst as it look like a cyst in a radiograph, but actually it’s outside the bone. It’s a salivary gland hyperplasia that pushes the bone and makes a cavity in the bone to hide in. Mostly in the mandibular salivary gland, but the lingual and the parotid glands can make one too. So actually we have to differentiate between intra-bony and extra-bony disease. The thickness of the wall of the radio-lucent lesion helps in the diagnosis –thick wall indicates many layers of cortical bone, which means the lesion is extra-bony-. Stafne’s bone defect has a thick wall, as it’s an extra bony lesion.

Diagnosis of Stafne’s bone defect is important, as it has no treatment. So if we diagnose stafne’s defect we won’t do a surgery to remove it!! But we have to take care when we are in that area not to cause injury to the gland.

2. Bone exostosis: also simple thing that doesn’t need a management. Tori fall under the definition of bone exostosis.

3. Enostosis: the opposite of exostosis. Mostly in the mandible, in the premolar area. It should be differentiated from sclerosing ostiitis “endo in the tooth that lead to sclerosis”, and to differentiate we look at the lamina dura and the periodontal ligament space and do vitality test.

The diagnosis of endostosis is important not to do RCT to the tooth near the lesion.

4. TMJ abnormalities:

5. Cleft palate is a congenital abnormality we could have. We usually detect it when we are looking for an impacted tooth, or when we are following up a patient.

6. Maxillary sinus anomalies:

Larger or smaller

Pneumatization: when the sinus grow to fill the adjacent space. Most of the pneumatized sinuses come with extracted teeth. Some people say that pneumatization will cause changes in the voice, but there’s no clinical presentation, only a radiographic changes that detected incidentally.

Agenesis (In medicine, agenesis (/ˈɛnəsəs/[1]) refers to the failure of an organ to develop during embryonic growth and development due to the absence of primordial tissue. Many forms of agenesis are referred to by individual names, depending on the organ affected) Wiki.

7. CCD “clidocranial dysplasia”: Characteristic facial features may include a wide, short skull (brachycephaly); a prominent forehead; wide-set eyes (hypertelorism); a flat nose; and a small upper jaw. Dental characteristics like multiple supernumeraries, impactions and associated dentigerous cyst. Also not to forget about the absence of the clavicles. All of that forms the typical presentation of CCD.

8. CFD “craniofacial dysplasia”: also called Crouzan’s syndrome. The problem mostly in the upper face. “cranio-facial” skull and mid face, so there’s frontal prominence, hypertelorism “eyes are away from each other”, hypoplastic mid face and beaten metal appearance of the skull on the radiograph. When the sutures decide to close prematurely and the brain still needs to grow, so it pushes the inner tablet of the skull and eventually make these markings “beaten metal appearance”.

9. MFD “mandibulofacial dysplasia”: also called Treacher-collins. Patients have colobomas, problems with the external ear, problems with hair and macrostomia. On radiographs we see hypoplasia of the zygoma and mid face and we see facial clefts as well.

Skull is ok, but the problem is in the mid face and the mandible “mandibulo-facial”.

Coloboma: A coloboma (from the Greek koloboma, meaning defect,[1]) is a hole in one of the structures of the eye, such as the iris, retina, choroid or optic disc. The hole is present from birth and can be caused when a gap called the choroid fissure between two structures in the eye, which is present during early stages of prenatal development, fails to close up completely before a child is born. The classical description in medical literature is of a key-hole shaped defect. A coloboma can occur in one or both eyes. WiKi.

Macrostomia: Macrostomia refers to a mouth that is unusually wide.[1]

Best of luck J
Shadi Jarrar
مشرف عام

عدد المساهمات : 997
النشاط : 12
تاريخ التسجيل : 2009-08-28
العمر : 26
الموقع : Amman-Jordan

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