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RADIO INTERPRETATION > generalized opacities > Flashcards

generalized opacities Flashcards

1
Q

generalized opacities we discuss

A
  1. Fibrous dysplasia – Polyostotic
  2. Florid cemento-osseous dysplasia
  3. Paget’s disease
  4. Osteopetrosis
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2
Q

polyostotic FD dx mechanism

A
  • Is a localized change in normal bone metabolism that
    results in the replacement of all the components of
    cancellous bone by fibrous tissue containing varying
    amounts of abnormal-appearing bone.
    ▪ Affects more than one bon
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3
Q

polyostotic FD usually found in what demo?

A

Usually found in children younger than 10

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4
Q

polyostotic FD associated syndromes

A

Jaffe-Lichtenstein Syndrome or Jaffe type
McCune-Albright Syndrome

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5
Q

Jaffe-Lichtenstein Syndrome or Jaffe type

A
  • Polyostotic FD with cutaneous pigmentation (café au lait spots)
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6
Q

McCune-Albright Syndrome

A
  • Polyostotic FD with cutaneous pigmentation (café au lait spots) and endocrinopathies
  • Affects almost exclusively women
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7
Q

what structure could be compressed in poly FD? implication?

A

pterygomax fissure= nn symptoms

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8
Q

florid COD dx mech

A
  • FCOD is a widespread form of Periapical cemento- osseous dysplasia (PCOD)
  • If PCOD is identified in three or four quadrants or is
    extensive throughout one jaw, it usually is FCOD.
  • Normal cancellous bone is replaced with dense,
    acellular amorphous bone in a background of fibrous connective tissue.
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9
Q

FCOD vascularity?

A

Poor vascular supply (susceptibility to infection and poor healing)

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10
Q

likely?

A

FCOD could also argue multiple osteomas/DBI

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11
Q

what can be seen with FCOD radio images periphery?

A

RL rim, similar to COD

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12
Q

FCOD clinical features
* Demo?
* Predilection for?
* symptoms?
* Extensive lesions often have?
* infection?
* Teeth vitality?

A
  • Most patients are female and middle-aged, although the age range is broad.
  • Predilection for African Americans and Asians.
  • Often FOD produces no symptoms (incidental finding).
  • Extensive lesions often have an associated bony swelling.
  • If the lesions become secondarily infected, features of osteomyelitis may develop
  • Teeth in the involved bone are vital.
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13
Q
A

FCOD

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14
Q

FCOD imaging features:
internal structure

A
  • Can vary from radiolucent - mixed - almost totally radiopaque.
  • The radiopaque regions can vary from small oval and circular regions to large, irregular and amorphous
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15
Q

does FCOD need teeth?

A

no

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16
Q

what is likely? dif?

A

FCOD
dif: osteomas, DBIs, osteoblastoma

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17
Q

FCOD effects on surr strucutres
Large lesions displacement of?
* The roots of associated teeth?

A

Large lesions can displace the inferior IAC inferiorly, the floor of the maxillary sinus superiorly and enlarge the alveolar bone.
* The roots of associated teeth may have hypercementosis.

18
Q

dif dx of FCOD?

A
  • Osteomyelitis (may appear similar to the sequestrum seen in osteomyelitis): This is not to be confused with a situation where FOD has become secondarily infected, resulting in osteomyelitis. The foci of amorphous bone that are secondarily infected have a wider and more profound radiolucent border.
19
Q

FCOD management

A
  • Under normal circumstances, FOD does not require treatment.
  • No age limit is apparent for the cessation of growth of FOD.
  • Because of the propensity to develop secondary infections in FOD, oral hygiene is important in order to avoid odontogenic infections.
20
Q

pagest dx mechanism

A
  • Is a skeletal disorder involving osteoclasts resulting
    in abnormal resorption and apposition of poor- quality bone in one or more bones.
  • May involve many bones, but it is not a generalized
    skeletal disease.
  • It is initiated by an intense wave of osteoclastic activity, with resorption of normal bone resulting in
    irregularly shaped resorption cavities. After a period of time, osteoblastic activity startsv
21
Q
A

pagets

22
Q

pagets clinical features
* Affects what ages?
* At age 65 years, gender?
* Affected bones app?
* teeth affected?
* Jaw pain?
* nn symptoms?
* Patients have severely elevated levels of ?

A
  • Affects later middle and old age (3.5% of individuals older than 40 years of age)
  • At age 65 years, the incidence of involvement in men is approximately twice that
    of women.
  • Affected bone is enlarged and commonly deformed because of the poor quality of bone formation, resulting in bowing of the legs, curvature of the spine, and enlargement of the skull. The jaws also enlarge when affected.
  • Separation and movement of teeth may occur, causing malocclusion. Dentures may fit poorly.
  • Jaw pain is uncommon.
  • Patients may also have ill-defined neurologic pain as the result of bone impingement on foramina and nerve canals.
  • Patients have severely elevated levels of serum alkaline phosphatase
23
Q
A

pagets

24
Q

pagets imaging features:
location
* Often in what bones?
* jaw? which arch more common?

A
  • Often in the pelvis, femur, skull, and vertebrae and infrequently in the jaws.
  • It affects the maxilla about twice as often as the mandible.
  • Although this disease is bilateral, occasionally it affects only one maxilla, or the involvement may be significantly greater on one side
25
Q

what can happen to roots with pagets

A

generalized hypercementosis

26
Q
A

pagets

27
Q

pagets dx int structure

A
  • Generally, the appearance of the internal structure depends on the developmental stage of the disease: three radiographic stages although these often overlap in the clinical setting:
    1. Early radiolucent resorptive stage.
    2. A granular or ground-glass appearance.
    3. A denser, more radiopaque appositional late stage.
    These stages are less apparent in the jaws
28
Q

pagets dx possible radiographic patterns of int structure

A
  • Linear: The trabeculae may be long and may align
    themselves in a linear pattern, which is more common
    in the mandible.
  • Granular: Similar to that of fibrous dysplasia.
  • Cotton-wool appearance.
29
Q

pagets dx effects on surr structures:
* affected bone?
* The outer cortex?
* The lamina dura?
* roots?
* The teeth?

A
  • Always enlarges an affected bone (3x, 4x)
  • The outer cortex may be thinned but remains intact.
  • The lamina dura may become less evident and may be altered into the abnormal bone pattern.
  • Exuberant and irregular hypercementosis
  • The teeth may become spaced or displaced in the enlarging jaw
30
Q

pagets dx management
* Usually managed how?
* correct deformities?
* Extraction sites?
* Higher incidence of?
* % of cases develop osteosarcoma?

A
  • Usually managed medically (bisphosphonates).
  • Surgery may be required to correct deformities
  • Extraction sites heal slowly.
  • Higher incidence of osteomyelitis
  • 10% of cases develop osteosarcomas
31
Q
A

pagets

32
Q

what is likely?

A

pagets

33
Q

osteopetrosis dx mechanism

A

▪ Is an inherited disorder of bone that results from a defect in the differentiation and function of osteoclasts → Abnormal formation of bone and abnormal bone turnover thereafter.
▪ The failure of bone to remodel causes the bones to become densely mineralized, fragile, and susceptible to fracture and infection

34
Q

osteopetrosis cranial nn’s/ hematopoesis

A

Hematopoiesis is retarded and cranial nerves may be compressed

35
Q

osteopetrosis vs paget’s

A

petrosis is generalized

36
Q

clinical forms osteopetrosis
▪ Infantile malignant:
▪ Intermediate:
▪ Benign or Adult type:

A

▪ Infantile malignant: Autosomal recessive. Apparent short after birth. Fatal within the first few years of life
▪ Intermediate: Autosomal recessive or dominant. Occurs in the first decades of life and can allow a normal life expectancy. Severity is variable
▪ Benign or Adult type: Autosomal dominant. Full life expectancy. Mild symptoms in late childhood to adulthood.

37
Q

infantile osteopetrosis
▪ foramina?
▪ marrow?
▪ dental eruption?

A

▪ Progressive deposition of bone results in narrowing of bony canals and foramina → sensorineural and sensorimotor deficits including hydrocephalus, blindness, deafness, vestibular nerve dysfunction, and facial nerve paralysis, etc
▪ Diminished marrow spaces→ Affects hematopoietic development of blood cells
▪ Delayed dental eruption

38
Q

▪ Adult osteopetrosis
▪ May be entirely?
▪ It may be discovered when?
▪ marrow spaces?
▪ higher risk of?

A

▪ May be entirely asymptomatic or have mild signs and
symptoms.
▪ It may be discovered at any time from childhood into
adulthood as an incidental finding, or it may manifest as a bone fracture.
▪ Diminished marrow spaces secondary to the deposition of bone → Affects hematopoietic development of blood cells → anemia, leukopenia, and thrombocytopenia.
▪ The increased bone density and relatively poor vascularity: Higher risk of osteomyelit

39
Q

osteopetrosis imaging features: Effects on the teeth and jaws.

A

▪ Because this condition is systemic, the changes affect all bones (it is bilateral and symmetrical)
▪ The bone may be so dense that teeth roots and other
structures within the bone may not be apparent
▪ The lamina dura and cortical boundaries are thickened or blended into the surrounding dense bone
▪ Effects on teeth: missing teeth, malformed roots and crowns, poorly calcified teeth and delayed eruption as a result of the increased bone density.

40
Q

osteopetrosis management
▪ Bone marrow transplantation?
▪ When osteomyelitis develops?

A

▪ Bone marrow transplantation to attempt to stimulate the formation of functional osteoclasts.
▪ When osteomyelitis develops it is difficult to treat, and a combination of antibiotics and hyperbaric oxygen therapy is used. Prevention of odontogenic inflammatory disease is key.

41
Q

this is seen bilaterally

A

osteopetrosis

RADIO INTERPRETATION (18 decks)

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