radiologyfinalnotes by Udc4XK1S

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									Titel:                                                                                   5/4/02
URL: 7123f218-abef-4b6d-a2a1-142375a7f45a.doc                                            15:40:53
                              Oral Radiology Winter 2002
                                    Student Notes

                           8/30/01 – The Radiology of Caries
                                1/8 – Dental Anomolies
                1/10 - Radiology of Trauma to the Jaws & Related Bones

                        2/5 – Radiology of the Paranasal Sinuses
               2/21 – Variations in the Size, Shape, and Number of Teeth
                          2/26 – Radiology of Apical Problems
                               2/26 – Resorption of Teeth
                  *2/28 – Radiology of Jaws and Periosteal Reactions
                  †3/5 – Radiology of Oral and Perioral Cysts I and II
                             3/8 – Radiology of Odontomas
                    3/14 – Radiology of Benign Neoplasms I and II
                   3/26 - Radiology of Malignant Neoplasms I and II
                     4/2 – Radiology of Dysplastic Diseases I and II
               4/4 - Radiology of Endocrine Diseases of the Jaw I and II
                   †4/12 – Imaging of the Temporomandibular Joint

                         *No student notes -- can anyone help?
         †Rough Draft Notes by Barry (some info missing) -- can anyone help?
Are there any other lectures from last fall that I could include? Please send them to me if
                                         there are.

86:135 Oral Pathology and Radiology
Lecture Notes 8-30-01

Power point presentation can be retrieved from website
ruprecht.radiology.uiowa.edu
(also monthly quiz available there)

The Radiology of Caries

Proximal Caries
The early prox. lesion is what we are usually trying to look for when we make
radiographs. The first radiographic evidence of prox. caries is a dimple (radiolucency) in
the outer surface of the enamel. Early lesion appears as radiolucency, dimple, not
extending more than halfway through the enamel. Expect them to appear above the level
of bone and most or all soft tissue, at or apical to the contact pt. Radiographic image of
caries is almost always smaller than the clinical lesion. When entire surface of the enamel
is involved the lesion appears linear or triangular with the apex toward the dentin. Next
the lesion spreads along the amelodentinal jnctn (DEJ). Realize we are seeing this in 2
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dimensions but know that the lesion spreads also in facial lingual direction and even
tends to be larger in facial lingual direction than it is in the direction we are seeing it.
Then spreads toward pulp. First regularly like a second triangle w/apex toward the pulp
b/c that’s the way the tubules are running. Then spreads more irregularly. If one tooth is
involved prox. then the adjacent tooth is soon involved as well. (Note, Not the carious
lesion from one tooth spreading to the other tooth. It could be the result of a different
microbial colony. What would be common to both areas is the oral hygiene. Probably
will be distal lesion of the one tooth that will be larger relative to the mesial lesion of the
other tooth, but remember it is always variable.
Occlusal Caries
Radiographs are not made to locate them but may be made to determine the extent of the
lesion. Pit and fissure caries appear radiographically only when the lesion is larger. Bulk
of enamel can mask small lesions in occlusal pits, etc. Early on even if may see the lesion
clinically you still may not be able to see it radiographically. Only as it becomes larger
will there be a hint of something that you can detect radiographically. Then will see
spread of that same type of radiolucent appearance that you saw as lesion went through
enamel on the proximal surface. Expect to see earliest signs of occlusal lesion in occlusal
pits then spread along DEJ at the same time as they spread towards the pulp. With the
radiograph we are looking for some idea of the extent of the lesion so we have an idea of
how close it has gotten to the pulp. But remember we are looking at a 2 dimensional
image of a somewhat complex 3 dimensional object. Cannot always accurately tell if
there has been a pulp exposure.
Facial and Lingual Caries
Are not well seen radiographically b/c edges are not projected in profile (or at best only
one is) Wont see sharp definition betwn the two all the way around the lesion.
Some edges are beveled which makes them difficult to see radiographically. Will be able
to detect lesion clinically well before able to detect radiographically. Wont be able to tell
depth of lesion, extent of lesion you should be able to see clinically.

SLOB Rule - allows you to localize where something is
Make a radiograph of a lesion. Make a second radiograph of the same lesion only this
time move the source of the x radiation. The image of the lesion on the second radiograph
will appear to have moved in relation to the image on the first radiograph. If the lesion
moves in the same direction as the source of the radiation was moved then the lesion is
towards the lingual surface. If the lesion moves in the opposite direction than the
radiation was moved then the lesion is towards the buccal surface. If the lesion does not
appear to have moved then the lesion is in the middle. Same lingual opposite buccal.
Recurrent Caries
Those lesions that occur alongside existing restorations. May not be radiographically
visible if the lesion is not on an edge that is depicted (facial or lingual) or if the central
ray is not aimed tangentally to the involved edge.
Differential Interpretation
               1. Recurrent caries
               2. mach band - brain enhances contrast for us, not a change in the tooth
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             3. Poorly seated restoration
             4. Intermediate band - metallic ions from amalgam leach out and go into
                 dentinal tubules, if enough accumulate can appear radiopaque on
                 radiograph. Doesn’t just enter surface of dentin but migrates into it
                 leaving a band of normal dentin between it and the restoration. This
                 normal dentin may then appear somewhat radiolucent by comparison
                 when viewed between the radiopaque restoration and the radiopaque
                 metallic ions. Radiolucent band is the intermediate band which may
                 sometimes be mistaken for caries.
Cervical caries
Along cervical area of tooth. Not a common finding on individuals who have normal
periodontal health. Has to have been recession in order for it to occur.

Differential Interpretation
              1. cervical caries
              2. adumbration (cervical burnout) Often seen on canines. Ex. If a portion of
                  the tooth is not covered by bone or a large bulk of enamel like adjacent
                  parts of the same tooth are then that “bare” portion may appear
                  radiolucent compared to the adjacent tooth surfaces.
              3. erosion (chemical wearing away of the tooth surface) not seen much on
                  cervical area, seen more on coronal aspect, specifically lingual surfaces
                  of max. ant. teeth if due to bulimia.
              4. abrasion (physical wearing away of the tooth surface) excessive tooth
                  brushing - seen as radiolucent line on cervical area of tooth. Similarly to
                  facial caries it will tend to have one edge that is well defined and one
                  that is not.
Radiolucent restorations cause some problems radiographically especially with the newer
“glue on” restorations where we dont use the same amout of mechanical retention so
can’t look at the outline form to determine if iatrogenic.
Usually outline form may indicate an iatrogenic cause (restoration)
Presence of a radiopaque base may also indicate iatrogenic cause (restoration)




Jan 8 2002
Radiology-Ruprecht DENTAL ANOMOLIES

I apologize if this was not expedient enough-my favorite computer battery croaked! I will
forewarn you, as much as this may make Dr. Ruprecht and possibly some of you cringe--
I will probably type the term “x-ray” in place of radiograph-sorry.

There is a much broader range of dental anomalies seen in children versus adults.
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Make yourself aware of the general morphology, relative positions, dental anatomy and
eruption sequence to determine normalcy of development.
Differences in stages of mineralization of developing teeth affect the radioopacity on
radiographs (less mineralization, less material to attenuate the beam=less opacity). To
compensate for this, relative adjustments are made to the exposure time when ‘making’
the xray according to the age of the patient and their stage of development/mineralization.

With children you’ll see teeth in all stages of development so Dr Ruprechts advice,‘use
your head’:
The Follicle:
         This may look like a cyst when it still lacks mineralization. So to determine if it is
pathologic or normal - ask yourself some questions: What is the age of the patient? What
is the location of it? Should there be a tooth developing there?
HERE COMES MY FAVORITE LINE: “Common things occur commonly and rare
things occur rarely and if it’s common to have a tooth there and that’s what you see then
that’s what you expect that it’s going to be.” (did you get that?)
Next in normal development: Initial mineralization @ the amelodentinal junction…crown
development… crown completion… circumferential root formation begins… with a
blunderbust apex until it’s completion. Recognize these normal paths of development.
You are trying to determine absence of normal/common development.
Common anomalies:
Premature Closure of the Root Canal at the tip - root appears short but the apex is closed
         therefore you know development is complete. Cause unknown(poss. Genetics).
Variance in #’s of canals - on xray you’ll see an abrupt narrowing of the canal as you
         move to the apex which is indicative of multiple canals.
Nonresorption of deciduous roots - you may need to extract the primary tooth to allow
         for permanent eruption. (Extractions of deciduous teeth need to be evaluated
         carefully for space maintenance).
He spent a lot of time on this next one:
Ectopic eruption - teeth erupting where they shouldn’t. This can cause premature
         resorption of the wrong deciduous root or the root of a permanent tooth and/or not
         resorb the deciduous roots they’re supposed to. Teeth that erupt ectopically are
         not always but may end up impacted.
         COMMONLY FOUND: Mesial eruption of the perm 1st molar into the distal
         of the deciduous 2nd molar…becoming ‘locked-in’. You NEED to intervene-
         it’s easy to fix and won’t remedy itself.
         ****Remember his “Separating Wire” trick, especially for 3rd yr!! Here’s how it
         works: you place a brass separating wire between the two teeth, loop it around the
         contact and twist tie it. Make ¼ to ½ turns biweekly, then in a few weeks it’s all
         over. 95% of the time this is all you need to do. Try this first. If it doesn’t work
         you might have to cut the distal of the primary but don’t damage the permanent
         tooth! You don’t want to extract the primary tooth because of space maintenance
         issues.

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Transposition - a form of ectopic eruption. Here two teeth exchange positions-usually
        between the canine and the lateral. When erupting, the canine drops in early
        and ends up between the central and the lateral. It can also happen between the
        canine and the 1st premolar. If the canine drops late it can end up between the 1st
        and 2nd premolar.
Migration - This usually occurs with the mandibular 2nd premolar and next commonly
        the 1st premolar. Teeth usually follow ‘mesial drift’ with the exception of the 2nd
        premolar. This can happen during eruption or if there is a space the 2nd premolar
        may bodily upright and move distally. He says it wouldn’t be uncommon to find
        a 2nd premolar right up against the border of the ramus. (he said so)
Transmigration - same as above but it crosses the midline, it’s rare.
Retained deciduous root fragment(root fragment NOT tip-it’s not the apex!) - very
        common. When resorption of the furcation occurs faster than the outer surface
        leaving a fragment…it often looks like a thin, vertical, linear radioopaque strip.
Amputation of tooth roots -Permanent teeth erupting into permanent teeth. Commonly,
        the misguided mesial eruption of the 2nd molar can amputate the distal root of the
        1st molar.
Follicles - a 2mm crypt (lucent follicular area) except for the canine which is often
        larger but still following the anatomy of the tooth is normal. If you see a large,
        rounded follicular area it is most likely a dentigerous cyst. Look for the absence
        of normal anatomy.
Ankylosis - the tooth doesn’t look fully erupted. It’s not submergence (the brick in the
        bathtub theory). Don’t worry about the missing PDL… he’s here to tell us …blah,
        blah, blah.... it’s damn unlikely…it’s not rocketscience… beating the hell out of
        something… the fact is if it’s below the line of occlusion it’s ankylosis.
        Commonly found with deciduous molars and usually symmetrical.
Nondevelopment of teeth - Most common in maxillary permanent laterals then in1st
        premolar. Be aware of the need for space maintainers in this case. Permanent
        maxillary central incisors are NOT normally congenitally missing but they may
        be blocked out by supernumerary teeth.
Supernumerary teeth - more than normal number of teeth-often max. lateral incisor,
        then mandibular premolars. Aka: supplemental if they look like adjacent teeth.
Relationship of primary to permanent teeth - Although very rare, the pulpal necrosis of a
        primary tooth can affect the development of the succeeding permanent tooth-
        Turner’s enamel hypoplasia of primary teeth.
Variation in bone pattern - In adults- there is NO linearity in bone pattern! This may
        suggest osteomyelitis or possibly Pagets disease. In children it’s possible to
        have minor, superficial, horizontal linearity especially in the mandible
        because of their developmental stage.

January 10, 2002

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                    Radiology of Trauma to the Jaws & Related Bones

Dislocation of the TMJ
-difficult to determine radiographically
-you may be able to determine that the condyle is not where it is supposed to be, but the
patient might not be able to bring the condyle back to where it is supposed to be in the
first place so in order to determine this radiographically you must know the patient’s
range of motion

Fractures of Bone
-look for the discontinuity through the cortex, the bone, and the cortex on the other side
of the bone- a continuous radiolucent line indicates a simple closed fracture
-facial fractures are rarely compound (open), but they can occur

Types of Fractures:
1. Impacted Fracture
    -the bone fractures and then the two pieces of bone have been driven together
    -not common

2. Comminuted Fracture
    -shattering of the bone
    -the result of a sharp blow
    -usually due to a gunshot in facial bones

3. Greenstick Fracture
    -may occur in young individuals in the mandible, but are not overly common
    -occurs on the opposite side of a blow to the face and doesn’t go all the way through
    the bone

4. Torus Fracture
    -incomplete fracture on the side of the blow

5. Avulsion Fracture
    -a fragment of the bone is torn away by the muscle or ligament

6. Compression Fracture
    -most common in the vertebral column
    -one vertebra is crushed between two others
    -usually occurs when someone jumps from a great height and lands hard or if the
    vertebral column has already been weakened by a pathologic process and a blow is
    experienced

7. Depression Fracture
    -one bone is driven into another
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8. Butterfly Fragment
    -see this often in the mandible
    -a triangular butterfly fragment is seen
    -two fracture planes


9. Segment Fracture
    -common in the mandible
    -have two fractures leaving a segment of bone (usually one in the 3rd molar area and
    the other near the canine on the other side of the mandible)
    -usually due to a lateral blow to the jaw (i.e. fights, car accidents)


10. Pathologic Fracture
    -underlying pathologic problem weakens the bone (i.e. neoplasm, inflammatory
    process)

-fractures can be combinations of these types

Alignment
-refers to how the long axis of one bone fragment relates the other fragment after a
fracture has occurred
-if the long axes are parallel then it is referred to as good alignment, if they are not
parallel then this is poor alignment and is called angulation

Apposition
-refers to how the ends of fracture segments come together
-partial apposition means that the fracture segments are not end to end, but they can still
have good alignment
-overlapping or bayonet apposition
-distraction means that the two fragments of the bone are pulled apart
-rotation means that the fragments are well aligned and apposed, but one segment is
rotated; this doesn’t occur too often in the lower part of the face

Favorable vs. Unfavorable
-if normal muscle action pulls the fractured fragments together this is favorable and if
they are pulled apart then this is unfavorable
-the movement can be either horizontal or vertical based on the pull of the muscle
-these terms are not used that often

Fracture Healing
Three Phases

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       1. Inflammatory Phase
       2. Reparative Phase
       3. Remodeling Phase
       -these phases are not necessarily as clearly defined and separated as this

1. Inflammatory Phase
    -the immediate reaction after a fracture has occurred
    -begins with bleeding
    -a response to a disruption of the tissues and the necrosis of surrounding tissue
    -first get a hematoma which mobilizes the bone fragments
    -the periosteum is stripped due to the bleeding and the trauma causing the fracture
    -necrotic marrow and bone due to the disruption of the vasculature

2. Reparative Phase
    -the body is trying to put the two parts of the bone back together
    -normal cells (i.e. osteoblasts) or other connective tissue cells that become functional
    and cartilage formation is seen
    -osteoblasts come from the periosteum and form bone resulting in a callus (seen as a
    bump of bone on the outside of the fracture)
    -granulation tissue grows into the hematoma and begins to organize and begins to
    replace the hematoma with tissues that will form bone
    -callus forms on the inside and the outside of the fracture

3. Remodeling Phase
    -callus is replaced
    -in most cases the bone is remodeled so that you would not be able to tell that there
    was a fracture


Radiographs used to evaluate fractures
1. Plane Films
2. Tomographs
3. CT

1. Plane Films
    -Look For:
    Discontinuity
    Jog (Partial Apposition)- occlusal plane(must compare to normal occlusal plane)
    Two Lines (fracture plane)
    Widened PDL
    Increased Radiopacity
    Decreased Radiopacity- look for bones pulled apart
    Callus
    -segmental fractures are common in the mandible, they are common in relatively
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   minor accidents (not car accidents, etc.)
   -a segmental fracture extending from the 3rd molar area on one side of the mandible
   to the canine on the other side is common- make sure to look for this

-the lateral pterygoid is the major muscle pulling on the head of the condyle and this runs
obliquely so it pulls the head medially and anteriorly

2. Tomographs
    -Look For:
    Discontinuity
    Jog
    Two Lines (fracture plane)
    Widened PDL
    Can see discontinuity in the maxillary sinus

-Blowout Fracture: front of the orbit is hit by something larger than the orbit itself
(i.e. being hit by a ball), this affects the weakest part of the orbit (the floor)

3. CT
    Axial
    Coronal
    2D Reconstruction
    3D Reformation-used in surgical planning




Radiololgy

2/5/02 1:03 pm
Imaging of the paranasal sinuses.

First lecture mostl with imaging, second mostly with interpretation.

Paranasal sinuses: The maxillary sinuses...
Development of the max sinus. Enlarges throughout life. You get a hollowing out of the
maxilla.

Radiographs common in dentistry that showe the max sinus:
1. periapical -- look for thin radiopaque border.
2. occlusal -- will see a radiolucent area superimposed onto the palate.
3. pantomograph -- max sinus will be portrayed about where you'd expect, but they are
distorted.
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Radiographs less common in general dentistry that show max sinus:
4. Occipomental (waters) view -- Head is tilted back 37-45 degrees. Come in horizontal
through that area. Waters can also show mastoid air cells. Can see fluid level in sinus.
These are generally done with mouth open -- then you can see posterior aspect sphenoid
sinus.

5. Posterioanterior view -- Problem -- you'll project posterior sapect of the cranium onto
your view. not ideal.No good single images to show all paranasal sinuses.

2526. Lateral Skull view -- one side can superimpose upon another. (note: max sinueses
are variable in size between right and left)

7. Submentovertex (axial, basal) view -- patient head tilted way back, or have them
laying on a table if in hospital setting. Jaws will look like a horseshoe/arch.

8. Tomography in same views -- you will see a series of blurred images. this can actually
be a helpful way to follow outline of the sinus. Gotta know what you can and can't do
with this type of image.

Not at all common in dentistry:
9. Computerized tomography (CT) a. axial, b. coronal. In these tomographic slices, you
don't need to worry at all about superimposition. you can set it to see soft tissue images,
and the "bone windows" are what we want to look at -- they are pretty much the gold
standard nowadays.

10. 2-D CT reconstruction -- a data block, where you can decide exactly where you want
your slice to come from. Not good for integrity of osseus borders, but good to see soft
tissue thickening. Can do oronal or sagital slices.

11. 3-D CT reconstruction. Same concept as with 2-D. Choose soft or hard tissue by
having computer remove images above or below a certain attenuation coefficient. Can
rotate them on screen, real time.

12. Magnetic resonance imaging (MRI). Align protons with an electromagnetic frequency
-- not x radiation. An important imaging modality. T-1 weighted images give a bright
signal from fat...

"That's all, folks." (That's it for imaging)

Next lecture:
the sinuses: max, frontal, ethmoid, sphenoid.

Max Sinus -- starts as a small invagination between ____. enlarges throughout life.
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Extends out into palatal recess, alveolar recess, zygomatic recess. Not just the body or
bulk of the maxilla that has the sinus. A sinus can extend into any component of a host
bone. Common plain film views of maz sinus: waters view, caldwe=ll view, basal view,
lateral view, (pantomograph). These four constitue a "plain film sinus series."

Waters -- primarily for max sinus. can also see frontal sinus or ethmoid air cells. Waters
view has a big W. Max sinus in waters looks like a pear or ligt bulb. Mastoid pretty tough
to see with waters, due to petrous superimposition. Open mouth waters allows pretty
good view of sphenoid sinus. Can even see ethmoid air cells in the medial aspect of the
orbit, but only to a degree. Can also see the infraorbital canal, which you should think of
as being on the ceiling of max sinus. "Head of the elephant picking up a peanut."
Zygomatic bone is the elephant's trunk. Peanut is the mandibular condyle. Can see
mandible, but not very good view with all the superimposition of maxillary structures.
Infraorbital canal looks like a suspended air duct in a wareouse. Can see nasal
septum, lacrimal fossa, supraorbital rim, lateral orbital proess - all this can be good for
fracture views. Can see odontoid process in closed mouth view. Zygomaticofronto suture:
don't confuse with a fracture line.

Caldwell View: Primarily for frontal sinus. Forehead and nose are put against film. 15
degrees from canthomeatal line. Clear view of nasal septum, supraorbital rim, ethmoid air
cells, orbital process, infraorbital rim (good stuff, cause mostly free of superimposition),
sphenoid sinus os not well seen. Sam e with max sinus and mastoid air cells.
Zygomaticofronto suuture. Can see greater wing of the sphenoid (blk of posterior wall of
orbit). Good shot of superior orbital fissure. Note that frontal sinuses are not symettrical.
Petrous ridge is superimposed over maxillar sinus

Basal View -- good for ethmoiid air cells primarily, but gets max okay. downlong axis of
skull. Good view of dens, or odontoid process. Also of foramen ovale, foramen
spinosum, condyle. Straight line, looks like capitol I, behind 3rd molar. The I is from the
orbit. Then there is an S for the sinus. I + S = ENT $ (!). Then there is a C for the middle
cranial fossa. We look for these things to identilfy trauma, neoplasms. On seeing
neoplasia - conrast peoblems can oftenoccur.

Lateral View -- we will align midsaggial plane parallel to film, but in hospital they don;t
use it with bilateral symmetry. You go 2.5 anteroir ans 2 cm superior to EAM (centered
on sella turcica). Big problem - one side ends up superimposed on the other. Spenoid
sinus, ethmoid air cells, frontal sinus, max sinus. In the midline you have nasal fossa and
conchae. Understand that you get distortion -- the ray is coming in an upwards direction.
Make sure you are aware of that so our expectations are approprotae. You don;t always
see max sinus on PA views. Then often ou will see it on superior aspect of roots (apices).
Max sinus can even invaginate between roots. In that case, lamina dura is all you got.
Picture: crest of alveolar process and lamina dura of max sinus is one and the same! The
max sinuses are superficially symetrical, but they aren;t to a significant degree. Max
sinus will become larger after teeth are extracted: disuse atrophy. Max sinus can be
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mistaken for a big space occupying lesion in edentulous patients. Max sinus may be one
large cavity, or several partially connected compartments: loculi. Like office cubicles. So
some are unilocular, and some are multilocular

variations of normal:

Antral projection/exostoses -- stalagmite like profection on sinus: a "bump of bone."
Can look like root fragment, but isn't necessarily.

Pathosis:
Mucous retention pseudocyst -- dome. intact border is key. Note that ou won't see an
osseus border when you see this intact border. An extrememly common finding. A dime a
dozen. Generally just an incidental finding. Commonly seen in fall and spring, when
people go from air conditioning to heating. The are not more common in those with hx of
allergy, oddly enough. Allergic sinusitis is what you would see in that case. They will
rupture and go away by themselves in most cases. Will be on floor or wall of max sinus.
If it's on the roof it could be a polyp. Sometimes they will sag -- they are full of fluid, and
they are affected by gravity. Basically the mucous retention pseudocyst is in the max
sinus.

odontogenic cyst -- starts from outside max sinus, but encroaches on the osseaous boder.
It is outside max sinus. Plus the cyst itself has an osseus border. Again, it is not IN the
maxillary sinus. It displaces it. It will cause resorption of the bone, and the
mucoperiostium. radiographicallly - can inject iodine, which is very radiopaque. But that
shows the lumen only.

Pathosis -- other thinkgs:
signs of inflamation:
mucous membrane thickening. signs of:
- membrane thickening mucousistis: a localized thickening from perio disease or PA
pathosis. Same thing as sinusitis -- just a difference between generalized and localized.
periostitis -- (really ossifying periostitis). Sometimes called a halo effect, or halo shadow.

air fluid level -- gotta have a central ray going horizontal to be seen. Why have fluid?
Bleeding. Sinusitis. Levage remnats. Pus. You can have fluid in every sinus. Often from
an allergic rxn. DON'T USE PANTOMOGRAPHS TO SEE FLUID LEVELS -- you
won't be coming in parallel to fluid level interface.

Changes in the bony wall - Muscous retention pseudocyst is not a mucocele, with regard
to sinus. A mucocele of the sinus does indeed need tx, becasue the osteum is blocked.
Osseus thickening will also occur.

Next time: signs of trauma.

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Radiology of Paranasal Sinuses
2-5-02

The maxillary sinus starts out around birth as an outpouching of the middle meatus and
enlarges throughout life (rapidly early on, slower later on). Hollowing out of the maxilla,
you may encounter when making radiographs.

Common radiographs in dentistry:

   Periapical radiographs: radiolucent area is max sinus, it will be superior to or
       superimposed on the roots of the posterior max teeth. Has a thin radiopaque
       border.
   Occlusal radiographs: might see max sinus, on both sides.
   Pantomographs: occupy an area that covers the lower and mid-face region of the jaw,
       but will be a distorted view.

Less common in dentistry:

   Occipitomental (Waters) View: designed specifically for the max sinus, problem is
      that the base of the skull superimposes over them. So the head is tilted back to 37-
      45 degrees, so this projects the max sinuses over an area of the skull that doesn’t
      have a heavy osseous component. Also to be seen on the Waters View would be
      the mastoid air cells. There are 2 variations, closed-mouth and open-mouth. With
      the open-mouth view you see the posterior-inferior aspect of the sphenoid sinus.
      If there is a problem with one sinus there may be a problem with others.
   Posteroanterior (PA) Skull View: There is a problem with this one, will project the
      posterior aspect of the cranium over the max sinuses.
   Lateral Skull View: This view has a different problem, you will have one max sinus
      superimposed on another. Can’t tell which is which. So you would be able to tell
      which sinus the problem is in or if it’s in the nasal fossae.
   Submentovertex (Axial, Basal) View: Coming from below the chin up to the vertex or
      in the opp. Direction. Also called axial or basal views. These are done with the
      patient having the head either tilted back or laying on their back with head
      hyperextended over table edge. Jaws look like a horseshoe. Can see max sinuses.
   Tomography in same views: Can make these in most of these same directions. Source
      of radiation and the film linked and they move throughout the exposure and
      wherever you have the focal point set that is the plane that’s going to be in focus.
      Series of images, sharply defined.

Not common in dentistry:
   Computerized Tomograph (CT): The images are clear and independent, no
      superimposition. True slices! Axial and Coronal views.
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   2DCT reconstruction: Slices taken from CT and they are stacked digitally on a
     computer as a block. This way you can view slices axially or coronally.
   3DCT reformation: Here you also have a digital block and you have the computer
     remove parts you DON’T want. Ex: the specific attenuation coefficient of
     mineralized structures.
   Magnetic Resonance Imaging (MRI): No radiation is used, all soft tissue. Sinus will
     show up black because its bone and air (not soft tissue).

The sinuses:
Maxillary, frontal, ethmoid, sphenoid


Max sinuses: located between inferior and middle conchae, enlarge throughout life. They
each may have up to 3 different recesses:
Palatal recess: the sinus extends into the palate
Alveolar recess: this is usually seen on radiographs
Zygomatic recess: the sinus extends into the zygomatic bone

Plain film sinus series

   Waters: Primarily for max sinus, Sec for frontal and ethmoid air cells
     Can see a “W” on the radiograph. May also see:
     Petrous ridge over max sinus
     Sphenoid sinuses at center
     Ethmoid air cells medial to orbit
     Frontal sinus over superior orbit
     Infraorbital canal in roof of max sinus
     PSA in lateral wall of max sinuses
     Floor of nose and septum at center
     Lacrimal fossa

   Caldwell: Primarily for frontal, Sec for ethmoid
      15 degrees to canthomeatal line
      May be hard to see the max sinus b/c the petrous ridge is over it

   Basal: up the long axis, 90 degrees to canthomeatal. Can see:
      Foramen ovale: a radiolucency
      Foramen spinosum: behind ovale
      Check for “SIC”
      S: posteriorlateral borders of max sinus (ENT$)
      I: lateral border of orbit
      C: middle cranial fossa
      Petrous ridge, sphenoid sinuses, ethmoid air cells

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   Lateral: Primarily for sphenoid, Sec for frontal, max, ethmoid
      2.5 cm anterior to and 2 cm superior to the external auditory meatus (centered on
      the sella turcica

   Pantomograph: distorted because you are coming upwards and rotating around.

Variations from the norm:

   Mucous cyst: this is a dome shaped radiopacity in the max sinus, it has an intact
      border. This is very common, especially in the fall and spring. Not associated with
      sinusitis/allergies.
   Mucous retention pseudocyst: this is INSIDE the max sinus.
   Odontogenic (Radicular) cyst: this is OUTSIDE the max sinus, and has grown
      upward and displaced the osseous border of the max sinus.

Sign of Inflammation:

   Mucous membrane thickening:
       Generalized: sinusitis
       Localized: mucositis (pulpal necrosis or periodontal disease)
       Periostitis: the Halo effect, around the apex
   Air-fluid level: can only be seen if central ray is directed HORIZONTAL.
   Radiopacity of sinus: due to soft tissue, fluid, or both.
   Changes in bony wall: sclerosis (thickening), outward displacement (mucocele or
       block ostium).

Just remember that mucocele and mucous retention pseudocyst are different in Ruprect’s
mind. A mucocele is an outward displacement of the sinus and a mucous retention
pseudocyst is just inside the sinus.



(Hi, I’m idiot who didn’t schedule anyone to do radiology notes on Thursday and am now
paying the piper. These notes are from last year with some additions since it is impossible
to do those lectures in there full entirety in the time allotted. I’m sorry that this is all I
can do for you.) MMM

Variations in Size Shape and Number of Teeth

Size:
Microdontia- tooth size is smaller than a tooth that would normally be in that area. Tooth
is called a microdont.
Macro/Megadontia- Tooth is larger than normal. Larger than other surrounding
structures. Tooth is called a macrodont.
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Number>Increase
Gemination-Means twin in latin. Represents a tooth, which unsuccessfully attempted to
split into two teeth. The normal number of teeth exists in the dentition when the tooth in
question is counted as one tooth.

Supernumerary teeth- greater than the normal number of teeth. Described and named
according to their location. They are most common in the maxilla
    i. Mesodens/Mesiodens- located in the anterior region (canine to canine)
    ii. Peridens- Found in the premolar region. Most commonly shaped like a premolar.
             *least common * most common in the mandible.
    iii. Distodens (paramolar)- found near the back of arch. Usually distal to molars.
             Vary in shape and size. Usually occur bilaterally.


    -most common shape for supernumerary teeth is “canioform”
    -most common in the permanent dentition
    -supernumerary teeth most commonly occur in the maxillary midline
    -may erupt into the floor of the nose or into the maxillary sinus
    -block the eruption of permanent teeth ( maxillary central incisors)
    -A supernumerary tooth is called a supplemental tooth when it appears identical to a
    neighboring tooth. The furthest tooth form the normal location is the supplemental
    tooth if you need to extract one.

    Neonatal Teeth- present at or near the time of birth.
      i- Keratin Pearls- Not really teeth. Large, hard lumps of keratin located on
              gingival. Present a problem for breast feeding mothers.
      ii- Premature deciduous teeth- premature eruption of primary teeth*(most
              common and usually in the maxillary anterior region) Once again a
              problem for those who lactate.
      iii- Supernumerary teeth- Very unlikely to occur.


       Number>decrease
       Fusion- represents two teeth with a common pulp, which fused during
       development in which the follicles grow together resulting in one tooth with the
       characteristics of two teeth. When the tooth in question is counted as one tooth
       there are fewer than the normal number of teeth in the dentition.
       Individual teeth, which have undergone fusion or gemination, may look the same
       or may be differentiated by counting the number of teeth in the dentition. They
       are the most common in the deciduous dentition.

       Concresence- teeth that are joined by cementum.
       - Due to fusion of two teeth in close proximity
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       - Due to excess cementum production
       - May not be seen radiographically-be aware during extractions.
       - Most common in the molars.

Nondevelopment teeth(third molars are the most deranged looking)
Oligodontia- Fewer than normal number of teeth.
Anodontia- No teeth
-most common missing teeth: 1.maxillary lateral incisors 2.mandibular 2nd premolars and
then the mandibular central incisors.
-Least common missing are the maxillary central incisors.
****remember that we are not including third molars.


Shape
Remember that what may be considered normal for one may be different for another
Extra cusps- a list of terms for similar entities
       i-Extra cusp
       ii- Enlarged cingulum
       iii-Carabelli cusp- palatal surface of max 1st molar of European descent

       iv- Dens evaginatus-means “tooth bulging out” common in the premolars
       v- Talon cusp- Extreme version of the enlarged cingulum
       vi- Enameloma- displaced extra cusp during development
       vii- Tricone- means “three horns” A type of extra cusped tooth that, from the
               occlusal, looks like an equilateral triangle with a cusp at each vertex.
               Radiographically, this looks like a talon cusp.


       Non- Develpement

              1. maxillary lateral incisors 12.79%
              2. max/man 2nd premolars 12.64%
              3. mandibular central incisors 10.32%


Bob Alert!!!!!!Board Question!!!!! Continued next page
Hypohydrolytic/anhydrolytic ectodermal dysplasia
      - oligodontia
      - decrease seat glands
      - thin hair
      - problems with nails



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       Multiple roots-
       More roots than normal, very common, ie. Mandibular molar with 3 roots.
       Pulp comes to an abrupt end on radiograph: root canal bifurcates here


       Invagination of the tooth
           1) dens invaginatus- invagination from lingual pit on an anterior tooth or
               occlusal pit in a posterior on normally shaped teeth ( stick your finger in
               the Pillsbury dough boy) “Not where Chris would though!”
       - most common in maxillary later incisors
       - potential source of caries, but relatively small incidence of apical problems
       - often bilateral
       - usually can’t detect clinically; they usually have small openings
       - treatment option are sealants


           2) dens in dente * invagination of incisal edge (anteriors)
       -remember that this is a ridiculous term?( because Dr. R doesn’t make mistakes)

       -thick or thin enamel lined invagination
       - tooth is not normal shaped( usually a peg lateral)
       - originates from the incisal surface, not from an occlusal or lingual pit
       - most common in maxillary lateral incisor

          3)dilated odontome-(radix in radice) purely ridiculous!!!!!

       - invagination from the radicular end occurring during soft tissue formation
       - least likely to look like a normal tooth



       Enamel Abnormalities

       -amelogenesis imperfecta- genetically inherited 1:14,000. This is an
       undergrowth of enamel that can be described as less enamel but what is there is
       actually hard.

       -Enamel Hypoplasia-
       -this is an acquired abnormality (hypoplastic enamel)

       -due to serious infectious disease during childhood during tooth development,
       often with severe, elevated temperature occurring at a specific time
-temporal line can form; can tell exactly what age the child was when sick
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      - manifests as abnormality in enamel at that time of tooth development
      - can be localized as well (tooth tumor) if there was trauma specific to that tooth
          or pulpal necrosis and abcess of the deciduous tooth that affected the
          permanent tooth(inflammatory process)
      - causative diseases may include measles, mumps, or chicken pox
      - drugs tetracyclines and other antibiotics


      Dental Abnormalities

      1) dentinogenesis imperfecta
          -autosomal dominant, 1 in 8,000 births
      - decrease in amount of dentin and the dentin is softer(higher water %)
      - Radiographically we see a bulbous crown, cervical constriction, spike shaped
          root, wide pulp and root canals, later on pulp chambers and canals will
          become small and may not even be visible
      - When multiple roots: look like an octopus lifted by head with dangling legs
      - Enamel may fracture off and increased wear will occur “ shell teeth”

      Classic appearance 1. bulbous crown 2. spike roots 3. cervical constriction

      2) Dentinal dysplasia
      - strictly a radiographic finding
      - teeth look normal clinically, but light does not travel through teeth normally,
           they look dull
      - anterior teeth- can see a demilune(crescent moon ie. shape of Ben P’s head) or
           cheveron: short spiky roots
      - posterior teeth; thin canals with “W” shaped root
      - histopathologically; globular dentin in pulp, relatively small root canals
      - areas of rarefying osteitis
      -


         Cemental Abnormalities

           1) Hypercementosis-
      - increase in the cementum around roots
      - bulbous, or thickened root, but other wise normal architecture
      - cementum is slightly more radiolucent than dentin so you see an outline or the
           original root structure
      - no treatment required, may have problems with extracting that tooth, and
           orthodontically
      - etiology= unknown, or possibly due to pagets disease of bone
      - can affect a variable number of teeth
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Peroapical cemental dysplasia
      - mandibular anterior teeth
      - replacement of bone or osteocementum “ blob on root”
      - originates on separate from roots, but may become continuous with them in
          time”assymetrical”


Multiple Dental Tissues

 1) Regional odontodysplasia
     -hypoplasia of all components of tooth
     -less radiopaque than normal “ghost teeth”
     -“runny” looking teeth can involve deciduous and permanent teeth
       - can cross midline-involving several teeth in a row ( regionally)
       - unknown cause
 2) Dilacerated
       - an extreme bend in the root
       - can occur anywhere


 3) Taurodontism
      - not much cervical constriction
      - enlarged pulp chamber
      - apical positioning of bifurcation
      - tends to involve multiple teeth ( Ask to see Mike F’s hereditary example)


       Just a reminder! Most of us are doing a very good job of keeping up with student
       notes. Remember that you are responsible for giving the recorder to the next
       person, and also for bringing a tape for the lecture. For all you that have not been
       paying attention to note service, I know who you are, and I will eventually corner
       you in some dark alley!!!! No joke.

       P.S.
       Lets finish paying class dues soon

       See you on the flip side,
       MMM

       2/21/02 1:06 pm -- Barry's notes
Variations in size, shape, and number of teeth.

Smaler teeth: Microdontia
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Larger: Macrodontia, sometimes megalodintia.

Micordontia:
Peg laterals fit into this description.
This stuff isn't rocket science.

Macrodontia:
"one big honkin' tooth... if you had two of those, you'd have a beaver."

Number of teeth problems:
Fewer: hypodontia, or oligodontia
More: hyperdontia. Extra teeth are generally called supernumerary teeth.

When it looks like a tooth is on its way to beoming two teeth: gemination (akin to
siamese twins).
Supernumerary teeth -- another group of cells decides t set up shop and create a nother
tooth.
Neonatal teeth.

Gemination: also called twinning, or schizzo_____. Example -- two fused jelly beans --
was trying to become it didn't make it. Gemination hapens everywhere. Part of the tooth
has doubled off, but the split hasn't been made complete, like siamese twins. With
gemination you can radiographically see clefts -- two separate root canals. So gemination
is not just a simple macrodont.

Suernumerary teeth -- when you do actually have extra teeth. Most common site:
midline. They don't always erupt -- the might be facing in the wrong direction. May
sometimes go through floor of nose. So to further the analogy, supernumerary are like
normal, identical twins. If, for examples, you have two identical teeth, like two max
laterals, then the extra tooth is also known as a supplemental tooth. So which one do you
extract? It can be somewhat arbitrary. Mesiodens. Mesiodens in the maxilla (midline
region) is way way more common that=n in mandible. They often look like like a tiny
canine. Some people use mesiodens if it is only in the midline or if only it hsa erupted,
but Dr. Ruprech doesn't like that. He feels a mesiodens is anything from cacnine to
canine.
*Note: if a patient presents with lack of maxillary central incisors, keep in mind that they
are the least likely to be developmentally missing. So you can usually put money on it
that they are not actually developmentally absent, but they are actually being blocked
from eruption, usually by a supernumerary tooth. You can predict this with about 95%
percent accuracy, wthout even seeing radiograph. Peridens is another term for
supernumary. They are usually supplemental. They are more common in the mandible,
sometimes called perimolar, but they aren't just molars. If supnumerary is usually distal,
it is called a distodens. Again, if supernumeraries look like they belong there, they are
supplemental.
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Natal/Neonatal Teeth
Teeth or toothlike structures that occur in the newborn. There are keratin pearls that may
occur on anterior ridge, that can look somewhat like bumps of teeth. Premature eruption
of deciduous teeth is the most likely thing. These can be a problem if the mother is
breastfeeding.

Fusion
When in development, two teeth grow together. A double tooth is the result. you get a
double tooth, but it is the oposite phenomenon as gemination. So in this case you count
the fused tooth as two teeth. In gemination you count it as one tooth. Neither fusion nor
gemination are particularly rare. Can see more often in deciduous teeth. But it vertainly
can happen in permanent dentition.

Concrescence
two teeth joined strictly in their cementum. Usually a positioal phenomenon.
Hyercementosis. two teeth in very close proximity become comon in their cementum. If
you extract one, you'll probably get the other.

Oligodontia
Missing teeth. the most common to be missing is the maxillary lateral incisor (some
studies say this is THE most commonly missing. It usually tops the list of
developmentally missing tooth). The next most common is max or mandibular second
premolars. Next in line is the mandu=ibular central incisor. After that a lot of things are
possible. Don't memorize. but knoe the first three, and the very least most commonly
missing: the max central.
Anodontia -- Don't say partial anodontia (that's like saying yes, we have no bananas). For
oligodontia you will see on deciduous radiographs that nothing is coming to follow the
primarys, once they leave.

Shape changes:
It must be remembered that abnormal for one racial group may be normal for another.

Extra cusps:
1. Extra cusp
2.. Enlarged cingulum
3. carabelli cusp -- max first molars.
4. Dens evaginatus - extra cusp from another than occlusal aspect. Grows outwards. More
common in Mongloid race.
5. Talon cusp -- like what is on a bird of prey -- such as Herkey
6. Enameloma -- really a displaced cusp. Root sheath of Hertwid determines tooth shape.
7. tricone. Kind of related to enlarged cingulum or talon cusp. But in this case it has
invaginations that look kind of like 3 corner hats.

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Extra roots:
Extra roots (or extra rooth canals) in this context means more than the number number
are traditionally considered to eb the correct number. When pulp chamber looks like it
came to an abrupt end (well before it reached the apex), then it has probably bifurcated.

Invagination
An inpouching. Like poking finger into pillsbury doughboy's stomach.
- Dens in vaginatus
- Dens in dente (not a tooth within a tooth. Don't say it that or I'll thump you)
- Dilated odontoma (radix in radice)

Dens invaginatus
Invaginations (or enlarged and deeper) of the lingual or an occlusal pit in an otherwise
norlammy shaped tooth. It is usually lined by enamel. the invaginations can look like the
pull tab on a soda pop can on a rasiograph. It is not a statistically significant cause of
pulpal invasion.

Dens in dente
Invagination (or enlarged and deeper) of the lingual pit

Dilated odontoma
Invagination (and dilation) from theroot surface of a tooth. "An even stupider term than
dens in dente." Bazzare. can be a coonservative invagination from the radicular end, or it
can really balloon out.

Enamel Abnormalities
Amelogenesis imperfecta
Enamel hyoplasia (aquired)

Amelogenesis imperfecta
congenital. Hypoplastic, hyomaturatio, hypomineralization. there are the three subsets.
Radiographically you see underveloped enamel (hypoplastic).

Enamel hypolasia
Aquired, not congenital. Any of teh group of developmental abnormalities tha.... some
things that casue high fever for a long time can make this happen -- measles, mumps,
chicken pox, rickettic disease. In this case you'll get a distinct line across the teeth that
can be traced to a specific, traumatic time, creating a temporal line. You can also have
more of a localized form, called a turners tooth, which is decribed as the result of an
anflammatory problem around the aex of the decisuous precursor. More likely to be from
trauma. The inflamation type is very rare. Then you will get a localized temporal line.
[pic: tetracycline staining. tetracycline is very broad band ab].

Dentin Abnormalities
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- dentinogenesis imperfecta
- Dentin dysplasia

Dentinogenesis imperffecta
A decreased mineralized (increased water) component in dentin that makes it softer. Pulp
chambers and root canals become obliterated qickly. Amelogenesis imperfecta is 1 in
14,000. Dentinogenesis imperfecta is aboit 1 in 8,000. So they are not rare at all. It often
goes hand in hand with OI -- the genes for these travel together on the same allele.
Classic presentation on radiographs: bulbous crowns, due to cervical constriction. Spikey
roots. On multirooted teeth, the roots converge instead of diverge (think octopus with
smoothed out tentacles). The Di that is associated with OI has strikingly large pulp
chambers. DI and OI are not from the same gene, but the genes travel on the same allele.
Know the calssic look of DI for boards. 1 in 8000. You may see this in your office.

Dentin dyplasia
Clinically, the teeth look normal. radiographically, you have either thistle shaped teeth, or
chevrons/demilunes. This comes from globular dentin. W shaped roots in posterio teeth .
Lots of periapical radioluscent areas. Not sure what these represent -- Dr. ruprecht thinks
its just plain ole rarifying osteitis.

Cementum Abnormalities
Hypercementosis
Periaical cemento-osseus dysplasia

Hypercementosis
extra deposition of cementum. It is slighltly more radiolucent than dentin. Cause:
idiopathic. We don't know. Paget's disease of bone often has hypercementosis.

PACOD
You get cementoosseaus tissue that lays down in the region of bone, and sometimes it
connects to root. We'll have a full lecture on this later.

Multiple dental tissues
Regional odonodysplasia (ghost teeth).
- Dilacerations
- Taurodontism
Regional Odontodysplasia
abnormal growth of teeth. Hypoplastic, hypomineralized, but just in one region. Pic:
uneruted anteriors. It used to be said that it doesn't cross the midline. But it most certainly
does. Contiguous teeth will be involved.

Dilacerations
bending of teeth. All teeth have some of this. But it is notable when it gets in the way of
tx (oral surg, endo, ortho, etc). Picture: a full s-shape of the tooth. Another pic: almost a
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90 degree bend.

Taurodontolism
Not much of a cervical constriction. Large pulp chamber, but that it=s a secondary
finding. An apical positioning of the furcation area. These teeth were thought to be
similar to those found in ungulates (cows?). In Saudi Arabia -- found 11.2% of this in the
general population. So it is not an unusual thing.



2/26/02
Radiology of Apical Problems:

*Not all periapical/inflammatory problems will manifest radiographically.
Most of the time the problem is inflammatory, but do not make this an assumption!
Inflammatory problems manifest radiographically after about 8-14 days and after 30-60%
Ca+ loss through deossification.
Unless the inner surface of the cortex is involved, the bone pattern will not appear to
change. So most of what is seen as a change in the bone pattern radiographically is due to
the trabecular bone being removed from the endosteal surface.
An acute periapical abscess may be diagnosed clinically before it shows any radiographic
changes in the early stages!! ***Therefore, in the early stages of an acute periapical
abscess, clinical diagnosis is more important than radiological interpretation.***
There may be acute exacerbation of chronic inflammation, a preexisting chronic problem.
Therefore, the acute problem may be superimposed on a chronic inflammatory problem.
Just because the pain came on acutely doesn’t mean that problem just started.
Once radiographic change is detected, it is due to a chronic problem, not an acute one.

Early changes in the apex:
   1. widening of the PDL space
   2. pushing up of the tooth because of the inflammatory exudate
   3. loss of the dental lamina dura and trabecular bone (if it was just the lamina dura
       being lost - wouldn’t be able to see it radiographically)
   4. rarefying osteitis

Rareifying Osteitis: a radiographic term meaning that it appears the bone is being
resorbed by an inflammatory process. There is no distinguishable border seen.
Rareifying Osteitis cannot be distinguished from a cyst, abscess, or granuloma
radiographically.
This apical problem can be a result of a pulpal or periodontal problem. However, the
apical problem (radiolucent area) is not always indicative of disease. When it’s a
developing tooth, you will be able to follow the lamina dura down the side of the tooth to
the apex. Loss of normal tooth architecture and loss of lamina dura is indicative of
rarefying osteitis. Generally speaking, on a multi-rooted tooth, if there is a carious lesion
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on the distal, you will see the change first on the mesial root; if the carious lesion is on
the mesial - you will see the change first on the distal root.
Granulomas generally cause resorption of the tooth it is associated with. A cyst and
abscess will not resorb the root of the tooth they are involved with. A cyst tends to resorb
the roots of the neighboring teeth.
Sclerosing osteitis - due to a chronic low-grade inflammatory response or is often found
around the outside of a rarefying osteitis. A low-grade inflammatory response tends to
stimulate the production of bone as opposed to the resorption of bone. May, then, have an
area of bone removal (rarefying) surrounded by an area of deposition of bone
(sclerosing). Can have either one or both.
You don’t always have to have rarefying osteitis to have inflammation.
Hypercementosis = “lumpy root” with two lines surrounding it radiographically
representing the PDL space and lamina dura - this is not seen this with inflammation.
Idiopathic hypercementosis - This is a problem only if it interferes with another
procedure. The extra cementum is slightly more radiolucent than dentin.
If there are multiple areas of hypercementosis, you should consider Padget’s Disease of
bone.
If you have hypercementosis without a normal architecture - this is a result of
inflammation.
Remodeling of bone: (i.e. post-extraction healing)…May have bone that looks like the
surrounding bone or may have sclerotic healing (a deposition of more bone in the area
than would expect to find) - may be amorphous or “root-like.”
Normal healing = wouldn’t be able to tell where the socket was.
Radiolucent healing = the amount of bone laid down in this area is less than the
surrounding bone and may or may not be defined by the remnant of the lamina dura. This
is NOT abnormal!
“Root-like” healing - tends to be more sclerotic - there may be a blood vessel running up
the middle - therefore, it may mimic the appearance of a root that’s been retained.
Retained roots, however, do not tend to be even with the crest of the alveolar process -
usually a little bit above or below the crest of the alveolar process. This is one way to
differentiate between the two.
Sclerotic healing is also possible -
the BIG POINT is that you can have post-extraction healing variations, which are
considered completely normal.
Disuse atrophy - subsequent to tooth extraction - this is localized to the area of disuse. It
is commonly seen from the outer surface of the bone that is the border of the maxillary
sinus. Therefore, maxillary sinus enlarges because the bone is becoming smaller.
Disuse Osteoporosis - Less bone per unit volume. Looks more radiolucent.
Fibrous Scar - you must have osteoblasts from periosteum for laying down bone. When
there are no blasts, then fibroblasts lay down fibrous tissue - leaves a rolled edge
rounding off of bone.
Enostosis - dense bony island - area in the bone where there is more sclerotic bone or
may be a bump coming out of the endostial surface of the cortex.
Inostosis - root resorption within the root itself - can have both internal and external
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resorption
Exostosis - bump on the outside of bone.



2/26/02
Resorption of Teeth

Subdivided into external and internal resorption
***Resorption only occurs where there are vital cells (odontoblasts)!!!
Won’t have resorption in the presence of an abscess - granulomas are most likely to cause
resorption - get resorption around the periphery of a cyst
General characteristics of tooth resorption:
Root is blunted and squares-off (unlike natural teeth that come to a point)
Root canal does NOT come to a point
Root canal extends to tooth’s apex radiographically - under normal circumstances, you
can’t follow the root canal all the way to the apex!!!


External Resorption
-from the outer surface of the tooth
-seen as blunting
-see root canal all the way to the apex (normally lose the root canal radiographically)
-straight forward if the external resorption is from the mesial or distal
-if the external resorption is from the facial or lingual, it is harder to distinguish - but will
see the outline of the pulp with a dark area superimposed over it
-most common in the apex area - “chews off” the end of the root
-need to distinguish between internal and external resorption because treatment is
different:
Internal Resorption - tx. is endo
External Resorption - tx. is empiracle

CLASSIFIED BY LOCATION:
Apex -
        (most common area of occurrence) - don’t mistake this with a tooth that’s still
        developing (blunder-bust apex)
Mesial and Distal surfaces
-idiopathic external resorption
-inostosis - bone grows into “chewed-up appearing” areas of tooth root, where
        root resorption occurs (alveolar bone grows in the same shape around the root as
        the shape of the resorbed root)
Facial surfaces
-appears radiographically as an area of increased radiolucency within the image of
the tooth - this can be superimposed over the root canal
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       ***If resorption is on facial or lingual surface - expect to be able to see the root
       canal pattern through it.
Resorption of un-erupted teeth
-almost always occurs at the coronal
-“moth-eaten” irregular pattern all the way around
**can have combinations of these

CLASSIFIED BY ETIOLOGY:
  a. Physiological: Deciduous teeth are programmed to undergo external resorption in
      the presence or absence of a permanent successor. This usually occurs from the
      apical area. You can follow the root canal to the tooth’s apex
      *don’t confuse short roots (blunder-bust apex) of teeth that aren’t fully developed
      with resorption.
  b. Pathological - Non-Deciduous teeth - caused by:
          - Idiopathic (of unknown cause) - may affect one or more teeth
          - Ortho. - movement of teeth thru bone can cause blunting of tooth apices.
              This may represent excessive use of force. Identical external resorption
              patterns are seen in people who have never had ortho. Other normal
              architecture is seen (Lamina Dura, etc.)
          - Space-Occupying Lesions - slowly growing. Causes teeth to be displaced or
              resorbed. Resorption is due to pressure phenomenon.
          - Cysts - usually the neighboring teeth are the ones that undergo ext.
              resorption, not the tooth associated with the cyst. Resorption is due to
              pressure phenomenon. These are usually slow growing.
          - Giant cell Lesions - blunting of the apex. Often these have large amounts of
              root resorption associated with them. They lose their normal architecture.
          - Endocrine Diseases - Hyperparathyroidism causes bone NOT ROOT
              resorption except via Brown Tumor (this actually causes resorption due to
              PRESSURE phenomenon)
          - Chronic Inflammation - seen in conjunction with rarefying osteitis and root
              blunting. The root often appears more shortened (when compared with
              adjacent teeth due to the inflammation process pushing the tooth cervical

All types of Pathological External Resorptions:
-occur when teeth have been in an un-erupted stage for a long time
-occurs at the coronal end of the tooth
-crown looks “chewed-out”
-occurs in the presence of chronic inflammation (morphologic appearance of the root is
the same, but the surrounding bony architecture is different and looks like rarefying
osteitis)
-when the crown is lost, the roots migrate toward the occlusal surface and the roots will
appear to shorten due to resorption, too.
-normally, you should not be able to follow the root canal to the apex of a root. If you
can, suspect that it might be pathological external resorption.
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External-Internal Resorption
-“chews” its way through the mineralized structure of the root - tends to leave the root
canal chamber intact - the walls of the root canal are not affected.
-irregular border is seen (see chewing out around the outside of the intact root canal)
-it spares the root canal until late in the process
-idiopathic

Internal Resorption
-localized
-is always pathological
-probably due to inflamm. of bone
-starts at the pulp and works its way out
-results in localized enlargement (widening) of root canal (seen radiographically)
-usually associated with large carious lesions or restorations
-progress rapidly
-root canal border is continuous with the outer border of the resorptive process
-can NOT see distinct outline of the root canal that is separate from the resorption like
you see in external resorption!!! The root canal is continuous with the outer border of the
resorptive process!
-if you see rarefying osteitis, the tooth is non-vital!
-tx: endo will usually cure this

Internal-Internal Resorption
-also chews up the internal part of the tooth, but starts from the pulp
-tx. is also endo
-this is a type of internal resorption, but has an irregular pattern of resorption



3/5/02
The Radiology of Oral and Perioral Cysts

Cyst: a pathologic cavity that is epithelium lined and fluid filled
-grows equally in all directions, anatomy modifies the shape of the cyst
-a sac of fluid like a balloon on the end of a water tap
-as they come up against anatomical structures, they distort
-enlarge along the long axis of the bone (mandible) because they resorb trabecular
bone easier than cortical
-have a thin cortex surrounding radiolucent middle
-have a rounded (hydraulic) appearance and are not painful
fenestration: a rapidly growing cyst resorbs bone at a greater rate then it deposits bone;
        this leads to a lack of continuity of the bone
theories of why cysts enlarge:
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        1) As epithelial cells grow, they push against each other and cause enlargement
             (physical)
        2) Goblet cells produce fluid which creates osmotic pressure and pulls fluid in
             from the outside which increases pressure and causes enlargement
        3) Epithelial cells sloughed off into the lumen, macromolecules draw fluid in
             creating hydraulic pressure
        4) Cysts with more bone resorbing cells grow faster (cells in wall that produce
             prostaglandins)
                 -dentigerous cysts and deratocysts contain a semisolid keratin-little
                 osmotic pressure
Odontogenic Cysts
Radicular cysts (dental cysts)
-0.5% of odontogenic cysts, histopahologically but not radiographically
-most common cyst
-associated with necrotic pulp/caries
-associated with the root of a tooth (hence radicular)
        - treatment is RCT
        - tend to not cause resorption of the tooth with the necrotic pulp, but it does tend
             to cause resorption of the surrounding teeth
        - an inflammatory cyst
        - cysts the encroach on the maxillary sinus will be more radioopaque than the
             surrounding air in the sinus, but radiolucent relative to most other structures
        - difficult to diagnose radiographically
Dentigerous Cysts (Follicular cyst)
        - 24% of odontogenic cyst, histopathologically but not radiographically
        - easy to diagnose radiographically
        - 2nd most common cyst
        - occur between the reduced enamel epithelium and the enamel of the crown of
             unerupted teeth
        - surround all or part of the crown, but do not extend apically beyond the crown
        a lateral dentigerous cyst only covers a side of the tooth
        - displaces the tooth that it is associated with and other teeth
        - contain prostaglandins which cause more bone resorption that is associated with
             radicular cysts
        - not an inflammatory cyst
        - benign
        - in the posterior mandible, they tend to look more scalloped instead of hydraulic

Eruption Cyst/ Hematoma
       - may not be a cyst, but often considered a type of dentigerous cyst
       - bleeding present
       - rupture upon eruption, so they are self limiting
       - clinically, a hard lesion because bone or tooth is present in the cyst

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Keratocyst (Odontogenic Keratocyst)
        - more serious than the other cysts
        - act like cysts and neoplasms
        - may or may not have keratin
        - rapid growth, and basal cell layer is 4-6 cells thick
        - have extensions/ outpouchings/ daughter/ satellite cysts, therefore, high
             recurrence rate after removal as these are left behind
        - most commonly found in the 3rd molar area, or in an area with no teeth
        - less hydraulic appearing than other cysts
        - can be solitary or multiple (multiple are associated with Gorlin-Goltz syndrome)
        - anatomically associated with teeth; grape-like appearance
Nevoid Basal Cell Carcinoma Syndrome (Gorlin-Goltz Syndrome)
        - multiple keratocysts
        - associated with bifid ribs, cleft palate, calcification of the falx cerebri, fusion of
             digits, short 4th and 5th knuckle
        - may make max sinus appear radioopaque because of keratocyst encroaching on
             the sinus
Residual Cysts
        - not associated with a tooth because the tooth it was associated with was
             extracted to treat the cyst
        - epithelium is left after the extraction and is the source of this cyst
        - often time the original was a dentigerous cyst
Paradental Cyst
        - associated with the mandibular 1st molar of young patients, buccal to the tooth
        - often infected so not a well defined cortex
Lateral Periodontal Cyst
        - found in premolar
        - a developmental cyst, and only anatomically associated with teeth
Bytryoid Cyst
        - “bunch of grapes”
        - premolar region
Glandular Odontogenic Cyst
        - very uncommon
        - most common in the anterior mandible
        - salivary glands or through metaplasia

Nonodontogenic Cysts - less common
Incisive Canal Cyst (nasopalatine)
-found inside the nasopalatine canal, so are not inside the bone
        - radiographically, will not see bone all the way around because the canal is
             tubular
        - lined with respiratory epithelium
        - not associated with teeth, the cyst is posterior to the teeth (radiographically

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             superimposed)
        - normally the canal is less then 10 mm, if it is greater than 10, start thinking
             about a possibility of cyst
        - not heart shaped - this image is a superimposition of the anterior nasal spine
        - appear larger in edentulous patients
        - pathognomonic = calcifications within the cells
Median Mandibular Cyst
-midline region of mandible (very uncommon)
Mucous Retention Pseudocysts
        - arise from mucous membrane lining in the sinus
        - accumulation of mucous from blockage
        - does not encroach max sinus because it is inside the sinus - found most
             commonly on the floor of max sinus
        - appear as a non-radioopaque to radioopaque dome-shaped bulge in the sinus
             with no osseous border
        - asymptomatic
        - droop in association with pull of gravity
Simple Bone Cyst (not a true cyst)
        - cavity within the bone; extremely delicate cortex
        - tends not to displace teeth; generally no effect on the lamina dura
        - invaginates between the teeth
        - most common in mandible
        - will usually resolve in jaws, but not in the long bones
        - can resorb bone but not roots
Salivary Gland Inclusion Defect
        - small caves in the bone from finger-like projections of salivary glands where
             bone has grown around
        - normal anatomic variants
Periostitis
-inflammatory periosteal infection
Fibrous Lesion
        - no source of osteoblasts so fibrin used to heal area of surgery
- well defined , rolled edge “bundt pan”



Eric Adams
3/8/02
The Radiology of Odontomas
For a good radiographic review look at text pgs.395-400 in the Oral Radiology: principles
and interpretation

   Hamartoma- a benign disorderly arrangement of tissue composed of mature cells,
     which are normal to the area.
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   Odontoma- a representation of hamartomas that contain dental tissue
         Radiographic appearance: important
                 Radiopaque mass radiolucent line radiopaque line
          Variations:
                  Compound Odontoma: several radiopaque masses that look like teeth
                  Complex Odontoma: extremely large disorderly radiopaque mass with
                      no discernible pattern
                  Ameloblastic Odontoma:
                          ameloblastic fibro-odontoma
                          odonto ameloblastoma: mineralized dental tissue components
                              (not a hamartoma)
   Ameloblastic Fibro-odontoma
          benign mixed component tumor of neoplastic epithelium and mesenchymal
              tissue (same as the ameloblastic fibroma)
          radiolucent stage fibroma
          radiopaque stage fibro-odontoma
          for radiological purposes these are developing odontomas
          multiple nodules are found in Gardner Syndrome
                  a.k.a. Familial Intestinal Polyposis
   Compound Odontoma
          malformation in which all dental tissues are represented in a disorderly
              fashion
          individually the tissues are well formed, teeth look like teeth
   Complex Odontoma
          malformation in which all tissues are represented, however they do not
              represent morphologically normal teeth
          are associated with unerupted teeth
   Dentinoma- rare neoplasm of odontogenic epithelium with immature connective
      tissue, characterized by dysplastic dentin (Dr. R doesn’t think they exist)
   Supernumerary vs. Supplemental vs. Odontoma
          A supernumerary is identified by having only one tooth in a given crypt, while
              and odontoma has 2 or more dentoid structures in a crypt
          Supplemental: is a extra tooth with similar features as a neighbor, most
              commonly found in the mandibular pre-molars than the maxillary laterals;
              named by location
   Enameloma
          Enamel pearl misplaced cusp located on the root or in the furcation
          Entity is not separate, rather continuous with root even having its own pulp
              horn
          Radiographically marked changes are noticed with angle variations
   Evaginated Odontoma- misplaced cusp on the occlusal surface of a premolar
   Dilated Odontome:
          Dens in Dente- infolding of the outer surface into the interior of a tooth,

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              commonly found in permanent maxillary lateral incisors
           Dens Invaginatus- an outfolding of the enamel organ, resulting in an enamel-
              covered tubercle near the middle of the occlusal surface of a pre-molar.




Radiology - 3/14/02


Radiology of Benign Neoplasms
    I. Features of benign neoplasms
            - Well-defined - can determine where it is
            - Corticated - defined line
            - Space occupying
            - Displacement of teeth
            - Directional resorption of teeth
            - Displacement of anatomical structures
Displacement of teeth, directional resorption of teeth, and displacement of anatomical
structures can all occur at the same time.
Benign neoplasms can also show:
            - Displacement of periosteum - resorption on inner surface, apposition on
                outer surface creates thin cortex
            - Internal structure: trabeculae and calcification
            - Unilocular/multilocular
How to differentiate b/t cysts, benign neoplasms, and malignant neoplasms:
Cysts - corticated, more hydraulic, unilocular
Benign neoplasms - corticated, less hydraulic, less unilocular
Malignant neoplasms - loss of cortex, rapid growth

    II. Odontogenic benign neoplasms: can be classified as epithelial, epithelial w/
            induction/mixed (epithelial and mesenchymal), and mesenchymal
Epithelial
Ameloblastoma = occurs b/t ages 20-50 yrs (predominately 30’s and 40’s),
mandible:maxilla ratio is 85:15, 60% occur in the mandibular molar-ramus area, 15% in
the mandibular premolar area, 10% in mandibular anterior areas, 10% occur in the
maxillary molar area, 3% in the maxillary premolar area, and 2% in the maxillary anterior
area. Can be unilocular, however most are multilocular showing coarse septa and
appearing like a soap bubble or a honeycomb. Can cause displacement or resorption of
teeth, extends beyond radiographic limits, superior aspect is often lost. Recurrent
ameloblastomas are radiolucent areas in a circular pattern
Squamous odontogenic tumor = occurs b/t ages 10-60 yrs (mean of 40),
mandible:maxilla ratio is 1:1, occurs in alveolar process area, possibly from rests of
Malassez, these appear radiolucent, well-circumscribed, semilunar, and are associated
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with roots of teeth. They are locally invasive, recur w/o conservative treatment, excision
is treatment of choice.
Adenomatoid odontogenic tumor = occurs b/t ages 10-20 yrs (mean of 18), occurs in
the anterior maxilla or mandible, appears radiolucent or w/ radiopaque foci, may mimic
dentigerous cysts
Calcifying epithelial odontogenic tumor (Pindborg tumor) = occurs b/t ages 10-90
(mean of 40), maxilla:mandible ratio is 1:2, occurs in the molar-ramus area, usually
associated with impacted teeth, can be unilocular or multilocular, appears radiolucent or
with radiopaque foci.
Clear cell odontogenic tumor = rare, occurs around 60 yrs of age, most often in females,
can occur in both mandible and maxilla, appear radiolucent, poorly circumscribed, and
locally aggressive
[Melanotic neuroectodermal tumor of infancy] = rare, young, usually in first year of
life, occurs in anterior maxilla, moderately well circumscribed, around apical areas of
root

Epithelial w/ induction/Mixed (epithelial and mesenchymal)
Ameloblastic fibroma - primitive myxoid connective tissue, resemblance to dental pulp,
strands of odontogenic epithelium two cells wide
Ameloblastic fibro-odontoma - primitive myxoid connective tissue, resemblance to
dental pulp, strands of odtonogenic epithelium two cells wide, cells differentiate to
produce enamel and dentin, prominent enamel matrix often seen before final maturation
of hard tissue, enamel and dentin in the form of compound or complex odontoma
(compound or complex odontoma) - prominent enamel matrix often seen before final
maturation of hard tissue, enamel and dentin in the form of compound or complex
odontoma
Ameloblastic fibroma ameloblastic fibro-odontoma Compound/complex odontoma
Odonto-ameloblastoma - rare, occurs in young, usually in first decade, contains an
ameloblastoma component and an odontoma component

Mesenchymal
Odontogenic fibroma - central odontogenic fibroma and peripheral odontogenic fibroma
Central odontogenic fibroma - rare, occurs in all age groups, appears radiolucent,
usually unilocular
Peripheral odontogenic fibroma - arises in the periphery, ossification w/i area d/t
periosteum, has sun ray appearance, don’t confuse w/ osteosarcoma
Odontogenic myxoma - occurs b/t 10-50 yrs (15-35 most common, mean of 30),
maxilla:mandible ratio is 1:1, may be infiltrative and aggressive, has a “tennis racket”
appearance (neither coarse or fine septa), shows cortical expansion, shows root
displacement rather than resorption
Benign cementoblastoma - occurs in the second or third decade of life, usually before
age 25, it is continuous with the root which is resorbed, pulp vitality is unrelated, appears
as a radiopaque mass, surrounded by a radiolucent line, surrounded by a radiopaque line
Cementifying fibroma - occurs in all age groups (mainly around 40), appears
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radiolucent, mixed, or radiopaque, it is usually unilocular

    III. Non-odontogenic benign neoplasms
Giant cell lesion -
         Central giant cell lesion (central giant cell granuloma) - occurs b/f 21 yrs of
age, unknown nature, occurs anterior to first permanent molars, painless, appears
radiolucent w/ “salt and pepper” calcification, contains thin wispy septa, resorption of
teeth is very common
         Peripheral giant cell lesion (peripheral giant cell granuloma) - occurs and
arises in the periphery
         Giant cell tumor (true giant cell tumor) - occurs after 21 yrs of age, rare
occurance in the jaws, occurs posterior to first permanent molars, painful, considered by
some to be a variant of GCG, radiographic appearance similar to GRG
Hemangioma (Haemangioma) - Intraosseus and Extraosseus hemangiomas
Intraosseus - some may be true neoplasms, most are probably developmental,
uncommon, no phleboliths, there’s an altered bone pattern, appearance of “moth-eaten”
bone pattern, contains hypoplastic teeth
Extraosseus - may be some true neoplasms, most are probably developmental, common
occurance, contains phleboliths (bull’s eye appearance, means stone in vein), may have
hypo- or hyperplasia of neighboring bone
Neurofibroma - solitary or multiple (neurofibromatosis), radiolucent, well-defined,
corticated, unilocular or multilocular, hypo- or hyperplasia of neighboring bone
Fibroma - appears radiolucent, unilocular, corticated, may look like a cyst
Osteoma - cortical osteoma, cancellous osteoma, osteoid osteoma, osteoma cutis
Cortical and cancellous osteoma - almost exclusively in the skull and facial bones, most
common in the paranasal sinuses (frontal>ethmoid>maxillary>sphenoid), uncommon in
the jaws, many so-called osteoma probably reactive or “burned-out” fibrous dysplasia
Cortical osteoma (Ivory osteoma) - osseous neoplasm of cortical bone, many so-called
osteoma probably reactive or “burned-out” fibrous dysplasia
Cancellous osteoma - osseous neoplasm of cancellous bone, uncommon in the jaws,
many so-called osteoma probably reactive or “burned out” fibrous dysplasia
Gardner Syndrome - autosomal dominant, multiple osteomas (one of first features),
polyposis of colon (polyps become malignant), epidermoid and sebaceous cysts, desmoid
skin tumors, associated with impacted supernumerary and permanent teeth, and
odontomas
Osteoid osteoma - osseous neoplasm of bone, uncommon in the jaws, may be painful,
bull’s eye appearance, subperiosteal, radiopaque nidus, radiolucent band, sclerotic border
Osteoma cutis - non-neoplasm of bone, found in facial region, calcification in scar tissue
Osteoblastoma - uncommon primary lesion of bone, occasionally located in maxilla or
mandible, more common in mandible than maxilla, may grow rapid and cause pain,
tender to palpation, “radiolucent”
Chondroma - we’re going to talk about this at a later date


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3/26/02
Tanner Clark
Radiology

Malignant Neoplasms

    - Two categories of malignant neoplasms: Carcinoma and Sarcoma
    - Carcinoma: Malignant neoplasm made up of epithelial cells or cells derived from epithelial
        tissue.
    - Sarcomas: Malignant neoplasms made up of connective tissue cells, but some are of
        epithelial origin.

-Looking at the number of new cancer cases per year:
Melanoma of the skin 3%, males and females
-Number of cancer deaths per year:
Melanoma of the skin 2% males and 1% females
-New cases:
Oral cases 3% males and 2% females
-Deaths:
Oral cases: 2 % males and 1% females
-Leukemia and lymphomas:
New cases: 7 % males and 4 % females
Deaths: 6% males and 8 % females

We are responsible for understanding a general idea of basic features of malig neoplasms. We
will be talking about some specific ones, but that’s only so that we have them for examples of
things.

Malignant Neoplasms (Basic Features):
-Poorly defined
-Non-corticated
-Space occupying
-Generally there’s no resorption of teeth, but if there is it’s non-directional/diffuse destruction in
it’s early phase.
-Destroy anatomical structures

Poorly defined: Because of the nature of the disease, it grows out into the surrounding tissues.
There is gross destruction, followed by not so gross destruction, followed by the inapparent
grossly destruction is such that it will expand out gradually into the surrounding areas (he was
mumbling so this made no sense at all). So there is no sharp edge to them.

Non-corticated: Goes with poorly defined. Benign neoplasms, cysts, and benign space occupying
lesions are corticated.

Space occupying: They obviously occupy space, because they exist. But the way they occupy
space is diffusely. Eventually there will be frank destruction in an area. They also can be space
occupying around teeth. They occupy the space around teeth, but don’t displace the teeth.
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Usually there is non-resorption of teeth: Generally speaking the benign neoplasms cause
resorption and the malignant neoplasms do not. Resorption usually indicates a slow growing
lesion. Malignant neoplasms tend to grow around teeth. IF there is resorption by a malignant
neoplasm (which is not common) then it will be a non-directional resorption of teeth. So the
resorption can be anywhere around the roots of the teeth.

Destroy anatomical structures: They will cause destruction of the osseous anatomical
structures.

Effects of the lesion when it enlarges: Malignant neoplasms cause destruction of periosteum and
the benign neoplasms displace periosteum.
-As the malignant neoplasm enlarges, it does so at the expense of the trabcular bone rather than
the cortical bone, because it is an easier path for it. Once it breaks throught the cortical bone it
will destroy periosteum which will displace the cortical bone around the lesion.
-As the lesion enlarges there may be a stripping off of the periosteum at the edges of the lesion
(seen more with sarcomas) these are called Codman’s triangles. Codman’s can occur with non-
malignancies as well, such as in osteomyelitis, because of the stripping of the periosteum causing
it to lay down bone.
-You can also have a carrying out of parts of the periosteum together with blood vessels. Bone
then gets laid down along the blood vessels and you get a sun-ray/burst appearance. There can be
the sun-rays and Codman’s triangles together as well.
-May have internal structure of trabeculae and calcification. This is seen more in sarcomas b/c
they are connective tissue lesions, but secondary carcinomas can also have this.
-They may have unilocular or mulitlocular appearance.

Carcinomas

Ulceration: common finding, can sometimes be seen radiographically. Generally not tumor mass
meaning no large swelling, and also less elevated than sarcomas.

Primary: that is where it originated
-Look for a destruction of bone w/out any apparent reaction around the outside.
-Frank destruction of bone. Looks like a “melting away” or “chewing out” of the bone.

-Can also have primary intraosseous carcinomas in the jaws, especially b/c there is epithelium in
the jaws.
-If you suspect primary intraosseous lesion it is likely that this is a metastatic lesion, especially if
it’s starting in multiple areas. As these separate areas grow, they grow together and you can’t tell
if it was primary or secondary based solely on that criteria

Primary Squamous Carcinoma: (90% of the cancers in the oral cavity)
-Can be intraosseous, they grow and get frank destruction with eventually breaking through of the
cortex with NO reaction around the outside.
-Has ulceration and flows around the teeth. The teeth look like they are standing in space,
“melting away of bone”
-This can look like periodontal bone loss, but perio disease this bad would most likely be
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generalized.
-It could look like an extraction site, but get Hx from the patient to help you Dx.

Skip Lesions
-Is a term that may be used whe describing some malignant lesions. Skip lesions are when yousee
two lesions next to each other that seem to be separated. You have one lesion that is growing and
it is growing through the bone. It looks like the lesion skipped from one site to another and is two
separate lesions. However, the lesions are in continuity, there is just minimal destruction b/w
what looks like two lesions, so they look separate, but are not.


Glandular carcinomas:
-Cancers that have an origin of tissue that is glandular. The high grade lesions are very aggressive
and destructive.
-The low grade lesions may have an appearance that looks more multilocular, moderately well-
defined. They are well-rounded, not “melted away” appearance. Keep them in mind when
deciding if you’re dealing with a keratocyst, ameloblastoma, or salivary gland tumors.

Carcinomas involving the sinuses are dangerous. Look at the sinuses on the radiographs.
-These are frankly destructive. There is little rxn from the outside.
-These are carcinomas that grow into bone and flow around some areas. The areas that are left
behind look like a dagger stuck into the heart of the lesion. It tells you that this is invading from
all directions.

Secondary Carcinomas: Are metastatic, “seeded appearance”
-They have broken off and via the lymphatics, blood stream, or neural spread have set up and
independent colony someplace else.
-Look like a multicentric area, looks like seeds will thrown everywhere - “seeded appearance.” It
doesn’t look as if it just started in one area. As they grow, they grow together and will eventually
look just like a primary intraosseous lesion.
-Metastatic lesions generally don’t have a bone rxn around it, but some can and you can get the
sun-ray appearance.

Sarcomas (ct. tissue cells, but does have some epithelial origin)

Basic Features:
-Mass, that is a tumor, is often found
-Destruction
-Bone production is more possible with sarcomas than with carcinomas (some metastatic lesions
have bone production)

Myeloma
-Most common malignant neoplasm of bone.
-Metastatic in that it is widespread with no primary lesion
-Painful, lytic lesions, punched out with well-defined margins.

Solitary plasma cytoma: neoplasms of plasma cells
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Multiple myeloma:
-A disease that is metastatic, it is generally widespread and painful.
-Classic appearance: in skull - multiple punched out lesions. Rounded and well defined margins.
Can get same appearance from metastatic carcinoma, but it is much more common with
myeloma. In jaws - looks like series of metastatic lesions starting to grow together into one
lesion.
-If you see multiple punched out lesions on an exam it will be multiple myeloma, but it may not
be on a patient.
-Not all multiple myeloma has punched out lesions, especially later on. These lesions are diffuse
and begin to grow together.

Osteosarcoma:
-Rare in the jaws (more in the distal femur, prox. tibia area which is the knee)
-Ages 20-30 most common, but can be seen throughout life.
-Maxillary facial region more in 40-60 year olds, more in males than females.
-More in mandible (younger age group) than maxilla (older age group)
-Garrington’s sign: widening of periodontal ligament space. (actually a skip lesion, the second
lesion is in the PSL space.)
-Ragged, ill-defined, radiolucent or mixed radiolucent/radioopaque
-Often destruction of cortex, sun-ray appearance is common
-Codman’s triangles can be seen

Chondrosarcoma
-Low-grade chondrosarcoma is very hard to differentiate from chondroma radiographically or
histopathologically. Do surgery and follow them.
-Slow growing. Radiographically it looks well defined (moderately radiolucent b/c the cartilage is
radiolucent). Can have bone deposition within them as well.
-Tends to be destructive and space occupying
-Flocculent calcification: fluffy precipitate, like a cotton ball. This happens in its early stages.
-Garrington’s disease may be present = widened PDL
-Most common in Ant. Maxilla or Post. Mandible, because cartilage was or is there
-In maxilla often involves the septal area.
-In mandible often involves symphysis, coronoid process and condyle.

Leukemia
-Loss of teeth b/c of destruction of bone (due to overgrowth of marrow)
-Loss of lamina dura and loss of trabeculae
-May simulate periapical inflammation and patient usually has blue gums clinically

Langerhans Cell Disease (Histocytosis)
-Disease or group of diseases with proliferation of Langerhans cells
-The lesions may be solitary or multiple
-Disseminated to viscerous skin and bone so localized or generalized.

Letterer-Siwe/Acute Disseminated Form:
-Not likely to see radiographically b/c it tends to be rapidly progressive in young individual and is
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fatal. See it in infants and young children.
-May be malignant neoplasm, may be more than one entity.

Hand-Schuller Christian Syndrome/Chronic Disseminated Form:
-The disease is just a chronic form of disseminated Langerhans Cell Disease.
-The syndrome has specific features: 1) Exopthalmos 2) Diabetes Insipidus 3) Bone Lesions -
sharply defined bone loss with teeth standing in space, but the space is well defined with a sharp
border around it.
-Geographic skull -- looks like a globe. The lesions are in all 4 quadrants.

Eosinophilic Granuloma/Chronic Localized Form
-Older age group. Usually unifocal and well-defined.

Differential DX for these include: 1) Juvenile periodontitis 2) Diabetic periodontitis 3)
Hypophosphatasia 4) Leukemia 5) Cyclic neutropenia 6) Agranulocytosis

---------------------------
Radiology of Malignant Neoplasms I and II – Barry's Notes
Sarcoms - malignant neoplams that ______.
Myeloma, osteosarcoma, chondrosarcoma, leukemia

Sarcoma -- more likely to fina a mass or tumor. Bone production is possible.

Myeloma:
Most people think osteosarcoma is most common malignant neoplsm of none, but that's
wrong. Myeloma is.
- Multiple myeloma (all metastatic, really)
- Solitary Plasmacytoma

Can see multiple punched out lesions. This is not the only thing that causes this
appearance, althuogh it usually means m. myeloma. You will see multiple lesions around
the skull. On board exams, call it multiple myeloma, baby, casue that's what they're fishin
for. So multiple myeloma causes a diffuse destruction of bone (pelvis picture)

Pic: bone destruction but then some production, creating a lump on frontal bone.

M myeloma can be in the jaw, mandible, and it won't look a lot different than other
metastatic lesions. You get loss of anatomical structures.

Osteosaroma:
Popular for boards, even though it isn't very common in dentistry. Dr. Ruprecht has seen
only three in fifteen years of being here. Subsets:
- parosteal osteosarcoma
- _______________

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Osteosarcoma is rare in the jaws (distal femur, proximal tibia -- 20s, 30s, ______. M>F.
Mand>Max. Mandible younger than maxilla. Garrington sign: widened periodontal
space. Localized, like a skip lesion. Not like an entire poket. Ragged, ill-defined
radiolucent area. May be mixed radiopaque/lucent area, but most tend toward lucent.
Destruction of cortex, sun ray spicule appearance. Codmans triangles.

story - woman sensed displacement with molar (our proprioceptive receptors in PDL are
exuisitely sensitive). Dx: dentigerous cyst. Would you accept that? No. D.C. has round,
cortical border, radiolucent, well defined. So the radiographs DO NOT correlate!
Pathologist was wrong. Remember -- you are in charge of the Dx, Path results must
correspond with everything else you know about the case (and about lesions :-))
radiographs of this case had a garrington's sign. The oclual radiograph showed sunray
spicules. This was a 26 year old female. Could have killed her.

Chondroma vs. Chondrosarcoma... it may be difficult if not impossible to tell
chondromas from chondrosarcomas, radiographically or histopathologically, in all cases.
In the end you may not know by anything except for whether the patient live s through it.
Sad but true.

Chondrosarcoma is:
- moderately radiolucent (after all, cartillage is lucent)
- destructive, space occupying
- flocculet calcification
- Garrington sign
- anterior maxilla (lot of cartillage there -- nose), posterior mandible (used to be cartillage
in development)
- maxilla: mandible 1:1
Others -- see lecture slides.
radiograph: septal chondrosarcoma, expands alar cartillage laterally. Another pic:
flocculent calcification in the TMJ.

Leukemia: monocytic, ______ dang it. see slides.
- lossof teeth, lamina dura, and trabelulae. Can look like advanced periodontal bone loss.
- can be generalized bone destruction involving more than one jaw. Might see cyanotic
gingiva.

Langerhan's cell disease. See slides. A whole ton of classifications.

Letterer-Siwe syndrome (part of langerhans) -- acute disseminated fform.

and-Schuller- Christian syndrome (langerhans subset): exopthalmos, diabetes insipidis,
bone lesions with teeth standing in space, but space is well defined. Geographic skull --
well defined radiolucent areas make skull looks like a globe with continents on it.

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Juvenile periodontitis, diabetic perio, hypophosphatasia, leukemia, cyclic neutropenia and
others -- all these are the differential.




Tamim Sifri
Radiology
April 4, 2002

   The Radiology of Dysplatic Diseases
DYSPLASTIC DISEASE:
        Refers to abnormal or altered growth. AKA Fibro-osseous disease or Fibro-
        calcific disease. We lump dyplastic with fibro-osseous disease b/c may be
        morphologically the same. Etiology may be different.

A. FIBROUS DYSPLASIA
   most common in younger patients (residual disease in older individuals)
   in general there’s no sex predilection (may favor the ladies)
   osteosarcomatous change unusual although it’s possible-most as a result of radiation
       therapy
   Two Types: Monostotic Fibrous Dysplasia (70%) and Polystotic Fibrous
       Dysplasia (30%)
   Remember variability is the norm when discussing fibrous dysplasia. Also, diagnosis
   of dysplastic disease processes is almost exclusively radiographic.

    1. Monostotic:
        involves one bone
        no extraskeletal involvement except perhaps skin pigmentation
        most frequent sites: ribs, femur, tibia, maxilla, mandible
        max:mand 2:1 (this may depend on the population being surveyed)
        bone lesion usually ends with somatic growth but not always; explains why we
            see these in pre-pubertal folks.

        Fibrous dysplasia in the jaws
        Not common (compare with Cherubism);
        more common in the max than the mand;
        more posterior than anterior;
        unilateral involvement;
        crainofacial involvement leads to blindness, anosmia (loss of sensation of smell),
            or deafness because of nerve impingement

        Radiologic features of Monostotic:
        relative radiolucency depends upon age;

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       usually unilocular but may have septa; won't look like a cyst
       radiopaque appearances: Lesions can be radiolucent- but usually
           radioopaque (again with the variability)
               1. ground glass on extraoral views, (grey w/o a trabecular pattern)
               2. orange peels on intraoral views, (little detail, definition)
               3. thumb-print on intraoral views
       The lesion is continuous with surrounding bone,
       situated within the bone-not appositional (he emphasized this several times),
       the cortex is thinned, it may be displaced, but usually continuous. The alterations
           in bone pattern may or may not displace teeth. It displaces anatomical
           structures. The lesion is not well defined. You may have an idea of where
           pathology starts/stops- but it is generally tough to pinpoint. No cortical border
           (as you would see with a cyst or benign neoplasm)
       There’s a “loss” of lamina dura- The lamina dura is not really lost- rather the
           surrounding bone is changing and thus the contrast between surounding bone
           and lamina dura is lost.

       Histopathological appearance: Bone with active osteoblasts and osteoclasts;
       Chinese lettering appearance (unless you actually can write Chinese)

       Tx for fibrous dysplasia: Do not even think of doing a biopsy on this.
       Remember, diagnosis is primarily radiographic. If you disturb it when it’s active
       you may make it worse. It will stop on its own most of the time. At the end of
       somatic growth you can recontour it. He mentioned something about
       treating/diagnosing with nuclear medicine.


2. Polystotic Fibrous Dysplasia
       involves multiple bones
       most frequently involved bones: femur, skull, tibia
       increased skin pigmentations(café-au-lait spots)
       often monomelic (involving one limb)
       The skin and bone lesions are usually unilateral;
       may cause fractures and severe deformities;
       bone lesion growth usually ends with somatic growth.
       Jaffe type: less severe type
       Albright type: more severe type; various endocrine disturbances affecting
           females > males. Most common endocrine disorder is percocious puberty.
       Radiographic appearances:
       More widely distributed. May have dramatic change in shape in jaw or skull.
       Lesions always remain within the cortex; there’s an alteration in the bone pattern
           but the cortex is intact….
       In general: when the lesion is in long bones, it’s radiolucent; when the lesion is in
           facial area, it’s radiopaque.
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       Recap: Polysotic dysplasia may be radioopaque, radiolucent or bothe=

Cherubism (Familial Fibrous Dysplasia)
           Named for the little baby-angel dudes/dudolas flying around jesus and
           disciples and stuff. Do cherubs have a gender designation- or are they asexual
           or what? If someone could get back to me on this, it would be great. At any
           rate, they have round, chubby little faces.
      rare, inherited (autosomal dominant), limited to the jaws, develops early in
           childhood
      bilateral involvement of the mandible; sometimes followed by bilateral
           involvement of the maxilla; unilateral cases (which are rare) have been
           reported (but Dr. R. thinks this is bunk)
      Radiologic features: Radiolucent- not radiopaque
      bilateral radiolucent cyst-like lesions; begin the 3rd molar ramus area; extends
           posteriorly and anteriorly; occasionally it will affect the condyle; maxilla
           involvement is usually after the mandible; Early stages: appears corticated;
           Late stages: less corticated
      Enlargement of the jaws; cortex remains intact;
      it can encroach upon maxillary sinuses;
      displacement of developing teeth and early exfoliation of deciduous teeth. Think
           of our blob of growing dough anaology with raisons (where the
           raisons=teeth). As the dough grows, the raisons will just be all over the place.
      Histopathologically: giant cells can be found in the bone and there’s not as much
           bone present.
      Differential Interpretation: nevoid basal cell carcinoma syndrome, bilateral
           dentigerous cysts (also radiolucent), multiple keratocysts

Ramon Syndrome (type of cherubism)
     relatively uncommon; inherited autosomal recessive

Paget Disease of Bone (Be sure to specify bone, as there is also Pagents Disease of the
   Breast (!)
       AKA Osteitis Deformans (bad name), Osteodystrophy Deformans
       Common in Central Europe, United Kingdom, Australia, New Zealand
       Less common in United States and Scandinavia
       Seen in older folks (40+)- see widespread, often striking changes in bone. May
           see bowing of legs, encroachment of foramina and enclosed nerves, artieries,
           veins.
       If you outgrow your hat, dentures, you may have Paget's (don't even try to pull
           a French pronunciation, as the disease was named after a British chap, Dr.
           Paget)
       2,500,000 cases in the US but only 5% are serious enough to require specific
           treatment. It’s often found incidentally on autopsy

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       A specific isoenzyme of alkaline phosphatase is high in these patients. In all of
          the fibro-osseous lesions, there is elevated serum alkaline phosphatase
          because there is active bone turnover. However, in Paget Disease of bone
          there is a certain isoenzyme present.
       The concentration of hydroxyproline in the urine is increased. Hydroxyproline
          is found in collagen so it’s not surprising to see it show up in a disease with
          active bone turnover.
       Calcitonin from the parafollicular cells of the thyroid gland is important in
          treatment
       There’s a 3-5% chance of Pagetoid bone undergoing change into osteosarcoma
          (*****this is important*****)

       Radiographic appearance of Pagets:
       bones become bowed and the skull enlarges; changes in the skull and pelvis are
           important because these two locations are almost always involved
       bone has a cotton-wool appearance; both radiopaque and radiolucent (sorry
           this is confusing- blame the lesion, not me). Characteristic of Pagets is a
           sharp (possibly undulating) border between radiopaque/radiolucent in the
           skull.
       osteoporosis cicumscripta (radiolucent and sharply defined) tends to sweep
           across the skull. Not actual osteoporosis.
       linear pattern in the bone (rarely seen)
       the sinuses do not decrease in size (unlike fibrous dysplasia where it can decrease
           the size of the sinuses)
       Radiopaque appearances: ground glass on extraoral views and orange peel on
           intraoral views
       Hypercementosis (***Important feature***): occurs in three situations: chronic
           inflammation, idiopathic, and Paget disease of bone. With Paget disease, the
           hypercementosis looks like the hypercementosis in idiopathic disease.
       Also have periapical cemento-osseous dysplasia and osteosarcomatous change
           possible
       There’s a thickening of the outer and inner table of the skull; it has a cotton-wool
           appearance; there are radiolucent areas; teeth get displaced; there’s a loss of
           cortication in certain areas not b/c the structure is lost but b/c of changes in the
           bone pattern result in the loss of contrast.
       BOARD QUESTION: If you see a radiograph with sharp transitions btw
           radiolucent/radiopaque areas PLUS hypercementosis, you should be able to
           come up with a diagnosis of Paget's.

Periapical Cemento-Osseous Dysplasia:
       Know this disease! It is only found in the jaws- though it is uncommon in Iowa
           (due to demographics). For all of the beautiful black women in my life, my
           apologies- as this is the population at greatest risk.
       Can be seen in Paget disease
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         It occurs in a specific distribution of the population: Age: 40; Sex: 94% female;
             Racial predilication: 76% negroid, 23% caucasoid, 1% mongoloid; Lesion:
             33% solitary (one tooth), 66% multiple (2+ teeth); Location: 91%
             mandible,64% anterior mandible
             Radiographic appearance:
                 Stage I: radiolucent
                 Stage II: mixed radioloucent/radiopaque
                 Stage III: radiopaque {radiopaque mass surrounded by radiolucent line
                 surrounded by a radiopaque line}
             Anterior mandible; one or more teeth, no root resorption or displacement,
             teeth are generally not loosened; the lamina dura is lost or intact;
             asymmetrical hypercementosis (with some radiolucent areas). Has nothing
             to do with pulp vitality.
             Replacement of bone around the apex of a tooth with fibrous tissue may be
             confused with rarefying osteitis so you need to check the tooth vitality and do
             the appropriate treatment: Nonvital: root canal therapy; Vital: leave it alone

Florrid Cemento-Osseous Dysplasia
       Florrid- means more widespread. Similar distribution as above.
       Specific distribution: Age: 40; Sex: 94% female; Racial predilication: 76%
            negroid, 23% caucasoid, 1% mongoloid
       in at least 2 quadrants symmetrically (it can be in all four quadrants)
       Stage I: radiolucent, Stage II: mixed radioloucent/radiopaque; Stage III:
            radiopaque
       it’s a larger version of PCOD

Focal Cemento-Dysplasia
       Specific distribution: Age: 40; Sex: 94% female; Racial predilication: 76%
          negroid, 23% caucasoid, 1% mongoloid; in
       one quadrant
       Stage I: radiolucent, Stage II: mixed radioloucent/radiopaque; Stage III:
          radiopaque

Periapical, Florid, and Focal cemento-osseous dysplasia are all probably the same disease
just at different ends of the spectrum

Miscellaneous
       Alveolo-Osseous Induction Effect, Sclerosising Osteitis, Osteosclerosis, Enostosis
       we don’t know how to classify these…that’s all he said about these.




4/4/02
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URL: 7123f218-abef-4b6d-a2a1-142375a7f45a.doc                                             15:40:53
The Radiology of Endocrine Diseases
Disturbances of Osteoid Mineralization
***The underlying principle is that calcium homeostasis in the blood is important for
muscle function.
-bone is a storehouse of calcium for proper homeostasis in the blood
-bone may be sacrificed for calcium for muscles
-low calcium levels in the blood threaten muscle function and stimulate parathyroid
hormone

Vitamin D acts on gut and bones
-1,25 DHCC (the most active form of Vitamin D) pulls calcium across the gut into the
blood
-25 HCC takes calcium out of bone and into blood
-there is a deossification or an unbuilding of bone

Parathyroid hormone acts on bone, gut, and kidney
-calcium to blood from gut
-calcium to blood from bone
-calcium to blood from kidney (through the distal convoluted tubule) and phosphate is
released in the urine
-loss of phosphate also results in an ossification problem
-decreased blood levels of calcium threaten muscle function and active parathyroid
hormone release
-calcium deficiency can lead to tetany and improper muscle function

-problems with parathyroid hormone or Vitamin D decrease blood calcium levels

Hyperparathyroidism (primary/idiopathic)
-due to idiopathic hyperplasia of parathyroid glands
-leads to an increase in parathyroid hormone and causes a generalized demineralization
(this demineralization may or may not be as great as that of parathyroid adenoma)
-How to diagnose hyperparathyroidism:
-calcium increase above 12.5mg/dL (normal 10)
-phosphate decrease below 3mg/dL (normal 5)
-serum alkyaline phosphatase (SAP)
-calcium decrease from skeleton leads to osteoporosis and weakening of the bones
-in addition multiple giant cell lesions called “brown tumors” (these can resorb teeth)
occur late in the disease
-when calcium in blood is greater than kidney threshold, hypercalcuria can lead to
precipitation resulting in kidney stones
-deossification of the skeleton occurs leading to these radiographic appearances:
-loss of trabeculation
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-widening of medullary canals
-loss of lamina dura (but know that this occurs in only about 5% of all cases)
-after damage to kidneys (by kidney stones) occurs calcium decreases and phosphate
increases (reverse of before) due to attempted bone repair
-secondary hyperparathyroidism is similar to primary described above except another
condition causes calcium decrease first

Rickets
-occurs due to inadequate synthesis, inadequate compensating intake, or renal loss of
calcitrol (Vitamin D3)
-can also occur in a calcium or phosphate poor diet
-a disease of the growing skeleton (young people)

7 dihydrocholesteron (provitamin D3) Vitamin D3 (cholecalciferol) 25
hydroxycholecalciferol (#1 with adequate Vitamin D3 or #2 with inadequate Vitamin D3)

#1 24,25 dihydroxycholecalciferol (this is inactive Vitamin D3)
#2 1,25 dihydroxycholecalciferol (active form which acts on the gut to pull calcium
across)

-if calcium supply from gut is inadequate, the body must choose between the blood or
bone (bone loses)
-leads to poor mineralization of growing bone and epiphyseal plate cartilage
-calcium decrease leads to increase in parathyroid hormone secretion
-blood chemistry:
-calcium decrease
         -phosphate decrease (because parathyroid hormone is acting on distal convoluted
         tubules to get calcium)
         -SAP increase
-radiographic appearances:
-radiolucent epiphyses
-get flaring of bones at ends (especially if they are weight bearing)
-craniotabes and frontal bossing
-usually no jaw lesions (maybe some generalized demineralization)
-enamel hypoplasia- can see temporal line at stage of occurance
-“theoretic” loss of lamina dura

Osteomalacia
-Vitamin D problem of adult skeleton due to lack of sunlight
-most common in young females with children who are losing calcium through feeding
and nursing
-do not confuse with osteoporosis (osteomalacia is soft bones with adequate matrix and
without proper mineralization; osteoporosis is brittle bones with inadequate matrix and
with proper mineralization)
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-blood chemistry is same as Rickets
-radiographic appearances:
-generalized radiolucencies and softening of bone
-looser zones (rare in jaws) “pseudofractures”
-maybe lamina dura loss
-no changes in teeth

Renal Osteodystrophy (renal rickets)
-a disease of a developing skeleton
-kidney dysfunction
-leads to dwarfism
-poor skeletal mineralization but increases density and thickness of skull and jaws
(diagnostic feature)
-blood chemistry:
-calcium normal or maybe decreased
-phosphate increased because it is not being pulled out of the kidney
-radiographic appearance:
-generalized radiolucency of long bones
        -increased radiopacity of skull and jaws with granularity (does not appear to be
        ossified) this is similar but more striking than with primary hyperparathyroidism
        -slight demineralization of cortex or mandible and lamina dura (“loss” due to loss
        of contrast)
        -brown tumors are not usually present with this
        -subperiosteal resorption
-Tx is transplant
-Renal Osteomalacia is an adult disease with same problems as above

Hypophosphatemia
-Vitamin D refractory rickets (phosphate diabetes)
-at least 6 subsets
-calcium is decreased or normal
-decreased phosphate in blood due to loss in kidney
-poor bone mineralization due to due to decrease in phosphate
-bicarbonates are lost to compensate for protons and calcium ions are pulled to combat it
-parathyroid hormone is released (hyperparathyroidism is caused)
-deossification/ossification problem
-radiographic appearance:
-growing skeleton problem- cortices are less radiopaque and thinner
-bent bones (as in any rickets disease)
-enlarged pulp chambers, long pulp horns

Hypophosphatasia
-decreased phosphatase, a deficiency of serum alkaline phosphatase
-results in deficient ossification due to decrease in osteoid formation
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Titel:                                                                                   5/4/02
URL: 7123f218-abef-4b6d-a2a1-142375a7f45a.doc                                            15:40:53
-poor cementum production
-may produce cranial stenosis due to a production problem
-teeth can be lost prematurely due to a bone and cementum problem
-long bones will have mineralization problems but not calcium problems
-blood chemistry:
-decreased SAP
-phosphorethanolamine is produced (this is the lab test for hypophosphatasia)
-radiographic observations:
        -cranial stenosis (premature closing of suture in cranium/calvarium area)- will not
        see sutures, and will have a “beat on copper” appearance
        -decrease in anterior-posterior diameter of orbits because of pressure from brain
        -deformation of skull depending on which sutures closed at what time
        -slope of anterior cranial fossa
        -premature loss of teeth and poor ossification in the alveolar process

Hyperphosphatasia
-too much SAP
-radiographic appearance:
-often have a large head with enlarged and overhanging frontal bone
-thick cortices, referred to as “juvenile Paget’s disease”
-pagetoid skull in children
-missing lamina dura may occur

Hypoparathyroidism
-inadequate secretion of parathyroid hormone
-primary (idiopathic) or secondary (due to surgical removal of the glands)
-calcium decrease in blood can lead to tetany, carpopedal cramps, and/or generalized
convulsions
-long standing hypoparathyroidism can lead to dwarfism, poor dental development, and
early loss of teeth
-generalized decreased amount of bone being laid down
-radiographic appearance:
-increased radiopacity in long bones
-normal skeletal appearance
-poorly developed teeth
Pseudohypoparathyroidism
-many subsets
-enough parathyroid hormone (administration of it will not help)
-the end organs are unresponsive
-short stature, moon face, stubby misshapen hands
-problem is in the metacarpals and can be seen when making a fist
-may be areas of subcutaneous calcified objects, cataracts, enamel hypoplasia
-blood:
-decreased calcium
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Titel:                                                                                    5/4/02
URL: 7123f218-abef-4b6d-a2a1-142375a7f45a.doc                                             15:40:53
-increased phosphate
-radiographic appearance:
-poorly developed teeth
-short metacarpals
-subcutaneous calcification

Pseudopseudohypoparathyroidism
-same as pseudohypoparathyroidism except calcium and phosphate levels are normal

Acromegaly
-“large extremities”
-abnormal secretion of growth hormone from eosinophilic cells of the anterior pituitary
-due to hyperplasia or adenoma (most common)
-leads to excessive growth of mesenchymal tissues
-in adults the disease manifests wherever there is remaining growing cartilage (noses,
mandible, hands, feet, tongue, sinus walls, and ears enlarge)
-called gigantism if it occurs in adolescence



Radiology 4/5/02 2:09 pm

Imaging of the TMJ

Pantomographs -- designed for giving images of teeth. Gotta remember that. You are not
coing thorugh horizontally with a beam. Dentists forget this. It is a fan shaped beam with
the central ray aiming upwards. So you will get a depictio of a distorted relationship. So
can they help? Yes, esp in seeing assymetry (but patient must be centered).
- It can be okay for gross diseae
- Disad
- does not show TMJ's
- shows the condyles, but only in a distorted manner.
- doesn;t show gelenoid fossa or articul ar eminence.
- not good for positional changes?)

So at best you are going to see the condyle. but thay may be distorted, too. You aren't
really seein gsuperior surface - ou are only seeing superior aspectof themedial surface. So
yes. you see the condyle, but not actaulally in the shape it woul appear.

Lateral Skull View
Advantages:
- NONE. They aren't gonna show the TMJ
disadvantages:
- cant't see TMJ
                                       Page 52 from 56
Titel:                                                                                      5/4/02
URL: 7123f218-abef-4b6d-a2a1-142375a7f45a.doc                                               15:40:53

PA (posteroanterior view)
heavy osseaous structures superimposed over the tmj area.
Advantages:
- NONE.
Disadvantages:


Waters (Occipitomental):
Advantages:
- can see the condyle in a distorted PA direction
- cann see realtionship of condyle to glenoid fossa
Disadvantages:
- Cannot see the TJ in detail

Axial (Basal) View
Does get used in soe TMJ investigations.
Advantages
Disadvantages
(get from someone)

Parma (transpharyngeal) View
Takes PID off the dental machine. bring it up really close, so that one side is magnified
so much that the superimposition doesn't become a problem. Mouth has to be already
open
Advantages:
- can see a distorted view of the condyle in a lateral direction
okay for gross disease
- good for ????
Disad:
- cannot see relationship of condyle to glenoid fossa

Transcranial Views:
Were used for a considerable period of time. you can't send the beam straight through or
you will just get superimpositio. You start the pid a little higher and aim down about 23*,
then ou come slightly from the back.

Advantages:
- can se distorted condyle in glenoid fossa.
- can see gross disease.
Disadvantages:
- cannot see accurate - only good for gross disease, can't see early disease.

You're pretty much way out on a limb when you use these. Dr. Ruprecht doesn't like
                                        Page 53 from 56
Titel:                                                                                  5/4/02
URL: 7123f218-abef-4b6d-a2a1-142375a7f45a.doc                                           15:40:53
these - they don't gove good info. So what if you get an image. Probably could with a
flashlight. .. got rid of them 15 yrs ago,when Dr. R. came.

TranscranialTomographic views
Advantages:
- can see relationship of condyle to glenoid fossa
- can see earlier gross disease
- cannot see early disease easily
- cannot see disk


transorbital View
An AP view, taken from behind head. 30* from anterior, 15* from midsaggital, to put
condyle through orbital area. Patient opens. this is

Advantages
- god for AP view of condyle
-??
-??

dis:
- cant see condyle in glenoid fossa - patient is open.

transmaxillary sins view
advantages
- good modified AP view
- okay for gross disease
- maybe okay for mandibular fractre
but:
- not in glenoid

Town view (sp?)
designed to be a foramen magnum view. good for condylar neck fractures
advantages- god AP, gross disease, factures
dis
- can;t see con in glenoid
- must be able to open wide to tanslate

Computer Tomographic Views
These cost more, more radiation. (But none of the others really work very well anyway,
so this is the way to really get a good image)
Advantages
- can see components of tmj
- good for osseaous disease,
                                        Page 54 from 56
Titel:                                                                                  5/4/02
URL: 7123f218-abef-4b6d-a2a1-142375a7f45a.doc                                           15:40:53
- - ??
dis
- can't

Arthography and Arthrotomography
We do very few of theseat the hospital 6 a year at best. MRI is gold standard for looking
at disk, what it is doing.

ad
- can oultile componens of TMJ
- can see relationships of components
- can see perforations of disk
dis:
- invasive
- painful
- some have allergies to iodone/contrast medium


MRI
MRI's aren't bsed on x radiaition. they work on magnetic field. Any proton spins like a
top. It wobbles in a amgnetic field. The wobble to varying degrees depending upon
strength of fiels. Proton flips on side like a amagnet. You get a pulse every time proton
moves over past a measurable point. Coil. Voltage gets read at coputer . Body divides as
a seried of voxel vox segments... there are slices.... volume elements

ad:
- can see componenets of tmj
- can see relationship of components (can't literally see bone -- to much ossaus
- good for soft tissue
dis:
- not good for osseaous
- thich slices
- cannot use for claustrophobics. Some people can't take it. "those who have stopped in at
McDonalds too often can't fit in there.
- Cannot do is ferrous metals present. Metals will interfere with signals. PLus if ferrous
metals are in soft tissues, the magnetic dtrengthof MR will rip it around the body (eye
example, metalworkers)

T1 weighted image. T1. fat will give a bright signal

Nuclear Medicine (Scinttigraphic) Views
You inject a radionucleide bound to a base that will go to specific tissues..
this is a fiel dunto itself
advantages;
                                        Page 55 from 56
Titel:                                                                                    5/4/02
URL: 7123f218-abef-4b6d-a2a1-142375a7f45a.doc                                             15:40:53
- good for activity (reodelling, inflammation) of bone
dis:
- not good for morphology.

There you are -- that's a fast overview for the imaging pf the TMJ

bottom line -- "most things not initially invented for tmj shuldn't be used for it. And they
are basicaly crap. "




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