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Oral Pathology, Stephen > ch 14 Bone Pathology > Flashcards

ch 14 Bone Pathology Flashcards

1
Q

Most common type of inherited bone disorder

A

Osteogenesis imperfect

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2
Q

Osteogenesis imperfecta is an impairment of what tissue maturation

A

type I collagen

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3
Q

What parts of the body are affected by OI

A

bone Dentin

Sclera Ligaments Skin

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4
Q

What is the bone character in O.I.

A

thin cortex, fine trabeculations, diffuse osteoporosis

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5
Q

How will bone heal in O.I.

A

heal, but with abundant callus

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6
Q

What are the radiographic hallmarks of O.I.

A

osteopenia Bowing
Angulation/deformed long bones Multiple fractures
Wormian skull bones

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7
Q

What are wormian bones

A

10 or more sutural bones that are 6X4mm in diameter or larger and mosaic patterned, but not specific to O.I.

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8
Q

O.I. can appear dentally identical to what other disorder

A

Dentinogenesis imperfect

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9
Q

How will the dentition look in both Osteogenesis Imperfecta and Dentinogenesis Imperfecta

A

blue to brown opalescent teeth

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10
Q

What should you call teeth that have the characteristic brown or blue opalescence? Should it be D.I. or O.I outright

A

No, just opalescent teeth until determined if only D.I.

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11
Q

What is the characteristic malocclusion in O.I. and why

A

1.) Class III due to maxillary hypoplasia

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12
Q

What is the most common, mildest form of O.I.

A

Type I

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13
Q

What is the most severe form of O.I.

A

Type II

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14
Q

Other physical characteristics of O.I.

A

Blue sclera
Hypoacusis(hearing loss)
Long bone & spine deformaties Joint hyperextensibility

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15
Q

Most severe form of O.I. noted in patients beyond

the perinatal period and has moderately severe to severe bone fragility

A

Type III

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16
Q

Type III O.I. patients die from cardiopulmonary complications from what

A

kyphoscoliosis = abnormal spin curvature in coronal and sagittal plane

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17
Q

O.I. type associated with mild to moderate bone fragility

A

Type IV

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18
Q

What happens to bone throughout life in O.I.

A

Cortical bone is attenuated
Reduced bone matrix production
Bone immature throughout life
Woven bone never transforms to lamellar

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19
Q

What is the primary goal of O.I. treatment

A

No cure, goal to improve symptoms (bisphosphonates later in life)

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20
Q

rare hereditary skeletal disorder characterized by marked increase in bone density

A

Osteopetrosis

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21
Q

Osteopetrosis cause

A

defect in osteoclast function

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22
Q

What causes the thickening of cortical bone and sclerosis of cancellous bone

A

defective osteoclast function + continued osteoblast function + endochondral bone formation

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23
Q

2 types of osteopetrosis

A

Infantile/Malignant Adult/Benign

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24
Q

Character of Infantile/Malignant Osteopetrosis

A

diffusely sclerotic skeleton Marrow failure
Frequent fracture (accusations of child abuse)
Cranial nerve compression (blind/deaf/facial paralysis)

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25
Q

Facial character of Infantile/Malignant Osteopetrosis

A

broad face Hypertelorism
Snub nose
Frontal bossing

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26
Q

Tooth eruption in Infantile/Malignant Osteopetrosis

A

Delayed

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27
Q

Common complication of tooth extraction in Infantile/Malignant Osteopetrosis

A

osteomyelitis

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28
Q

What are common in Infantile/Malignant Osteopetrosis even though bone is dense

A

pathologic fractures

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29
Q

How will bone look radiographically in Osteopetrosis

A

increased radiographic density with loss of distinction between cortical and cancellous bone

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30
Q

O.I with opalescent teeth normally show what

A

severe attrition

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31
Q

Which part of skeleton has significant sclerosis in Adult/Benign Osteopetrosis

A

axial skeleton, long bones not as sclerotic

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32
Q

When is Adult/Benign Osteopetrosis diagnosed and how

A

dental radiographs by increased radiopacity of medullary portions of bone

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33
Q

How do patients that are symptomatic with Adult/Benign Osteopetrosis present

A

with pain

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34
Q

Most common treatment with best prognosis for Infantile Osteopetrosis

A

bone marrow transplant

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35
Q

Secondary treatment for Osteopetrosis that decreases bone mass, decrease infection prevalence, and lower frequency of cranial nerve compression

A

Interferon gamma 1b with calcitriol

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36
Q

Cleidocranial dysplasia affects what type of bone formation

A

endochondral ossification

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37
Q

Most prominent abnormalities of Cleidocranial dysplasia affect what bones

A

clavicles and skull

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38
Q

Absent/hypoplastic clavicles with underdeveloped neck muscles allowing shoulders to be approximated in front of the chest is characteristic of

A

cleidocranial dyplasia

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39
Q

Physiologic appearance of pt with Cleidocranial dysplasia

A

short stature
Large head
Prominent frontal and parietal bossing Hypertelorism
Broad nasal base and depressed nose bridge

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40
Q

Skull bone character in Cleidocranial dysplasia

A

delayed or never closed fontanels with sutures featuring wormian bones

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41
Q

Palate character in Cleidocranial dysplasia patient

A

narrow, high arched palate

Increased prevalence cleft palate

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42
Q

Teeth character of Cleidocranial dysplasia

A

prolonged deciduous retention, permanent eruption failure, numerous unerupted supernumand permanent teeth with dilacerated roots or abnormal crowns

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43
Q

What do Cleidocranial dysplasia teeth lack that may be associated with eruption failure

A

Lack of secondary cementum

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44
Q

Cleidocranial dysplasia mandible character on radiograph

A

coarse trabeculation
Narrow ascending rami
Narrow pointed coronoid process

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45
Q

Cleidocranial dysplasia maxilla character on radiograph

A

Thin zygomatic arch

Hypoplastic maxillary sinus

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46
Q

Profile of Cleidocranial dysplasia patient as they age

A

short lower face height
Acute gonial angle
Anterior incline of mandible
Prognathic

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47
Q

Treatment of choice for Cleidocranial dysplasia dentally

A

removal of primary and supernum teeth followed by exposure of permanent teeth to be extruded orthodontically

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48
Q

An area of hematopoietic marrow that is sufficient in size to produce an area of radiolucency that may be confused with an intraosseous neoplasm (i.e. it is not a pathologic process)

A

Focal Osteoporotic Marrow Defect

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49
Q

Demographics of Focal Osteoporotic Marrow Defect

A

Post menopausal females, posterior mandible, endentulous areas

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50
Q

Is there expansion in the mandible from Focal Osteoporotic Marrow Defect

A

No

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51
Q

How treat Focal Osteoporotic Marrow Defect

A

incisional biopsy for diagnosis, if it is FOMD, then no further treatment required

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52
Q

Focal area of increased radiodensity that is of unknown cause and cannot be attributed to any inflammatory, dysplastic, neoplastic, or systemic disorder

A

Focal Idiopathic Osteosclerosis

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53
Q

What must do to the tooth if see a radiopaque lesion at the root apex

A

Test Tooth vitality

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54
Q

If teeth are nonvital with testing then what should be the diagnosis of the radiopacity at the root apex

A

condensing osteitis or focal chronic sclerosis osteomyelitis

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55
Q

When does Focal Idiopathic Osteosclerosis begin and end

A

begins 1st to 2nd decade and ceases with bone maturity ~ 4th decade

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56
Q

Where does Focal Idiopathic Osteosclerosis normally appear

A

90% mandible, most common near 1st molar, but also common in 2nd PM and 2nd Molar

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57
Q

What should be included in the differential diagnosis if more than one area of osteosclerosis is noted

A

multiple osteomas associated with Gardner’s syndrome

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58
Q

Radiographic character of Focal Idiopathic Osteosclerosis (size, shape, rim)

A

radiopaque 3mm-2cm, well-defined round to irregular with no rim

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59
Q

Is root resorption common in Focal Idiopathic Osteosclerosis

A

No

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60
Q

Radiographic character of Focal Idiopathic Osteosclerosis

A

dense lamellar bone with scant fibrofatty marrow

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61
Q

Treatment for Focal Idiopathic Osteosclerosis

A

serial radiographs until growth stops, then no treatment required

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62
Q

What would be an indication for biopsy with focal idiopathic osteosclerosis

A

if cortical expansion occurs (indicates a neoplasm)

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63
Q

Abnormal and anarchic resportion and deposition of bone resulting in distortion and weakening of the affected bones

A

Paget’s Disease (Osteitis Deformans)

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64
Q

Paget’s disease demographics

A

more common in Britain, after 4th decade, Males > women, Whites > blacks

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65
Q

Most commonly affected bones in Paget’s

A

lumbar vertebrae
Pelvis
Skull
Femur

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66
Q

Can Paget’s jump a joint space to a previously unaffected bone

A

No

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67
Q

Can just the mandible be affected in Paget’s

A

No, maxilla must be involvd if mandible involved

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68
Q

Paget affected bone character

A

thickened, enlarged, weakened

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69
Q

Characteristic stance of Paget’s disease and why

A

weight bearing bones bow, resulting in Simian stance

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70
Q

Paget’s disease head circumference

A

Large head circumference

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71
Q

Term for extreme cases of maxillary expansion in Paget’s disease

A

leotiasis ossea (gross expansion of midface)

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72
Q

Phase I of Paget’s Disease is osteolytic or osteoblastic

A

Osteolytic

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73
Q

What is osteoporosis circumscripta

A

waves or fronts of progressive demineralization occur in skull in Paget’s disease

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74
Q

What is the cause of the increased cranial circumference in Paget’s disease

A

expansion of diploic table of skull

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75
Q

Phase II of Paget’s Disease is osteolytic or osteoblastic

A

osteoblastic

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76
Q

Descriptive term of the radiographic appearance of Phase II Paget’s Disease with patchy areas of sclerotic bone

A

cotton wool appearance

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77
Q

Character of Phase III Paget’s Disease

A

mixed osteolytic/osteoblastic, but no coordination between the two

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78
Q

What is pathognomonic for Paget’s Disease

A

Generalized hypercementosis

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79
Q

What type of root resorption is seen in Paget’s Disease

A

external root resorption

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80
Q

Change in teeth due to Osteoblastic (Phase II) of Paget’s disease

A

diastema

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81
Q

What other pathology is included in the differential when diagnosing Paget’s Disease

A

cement-osseous dysplasia

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82
Q

Consideration of Pagetoid bone

A

hypervascular, therefore poor hemostasis, sensitive to inflammation, high output cardiac failure (?)

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83
Q

Malignant bone tumor associated with Paget’s disease (because it is rare to find in someone older than 40)

A

Osteosarcoma

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84
Q

What is required for diagnosis of Paget’s disease

A

clinical, radiographs, lab tests (high alkaline phosphatase among other things)

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85
Q

What should patient be sent for once diagnosed with Paget’s disease

A

Bone scintography to detect skeletal involvement

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86
Q

What is histologically characteristic of Paget’s disease

A

numerous basophilic reversal lines forming mosaic or jigsaw pattern

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87
Q

What replaces marrow in Pagetoid bone

A

highly vascular fibrous connective tissue

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88
Q

Common treatment for the bone pain common in Paget’s disease

A

NSAID

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89
Q

What can result due to compression of cranial nerves during Phase II (osteoblastic) Paget’s

A

deafness, blindness

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90
Q

What can be prescribed to reduce bone resorption

A

parathyroid hormone antagonist (calcitonin or bisphosphonates)

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91
Q

What pagetoid bone is an osteosarcoma likely to occur in

A

pelvis or lower extremities

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92
Q

What tumors normally develop in Pagetoid bone in the craniofacial skeleton

A

benign and malignant giant cell tumors

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93
Q

Character of anterior Mandibular Central Giant Cell Granuloma

A

anterior can cross midline

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94
Q

Central Giant Cell Granuloma commonly found before what age and in what gender

A

before age 30, females

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95
Q

majority presentation of Central Giant Cell Granuloma

A

asymptomatic, but have swelling

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96
Q

Are central giant cell granulomas aggressive, fast growing, perforate cortical plate, and do they cause root resorption

A

No, nonaggressive slow growing with no cortical expansion and no root resoprtion (Nonaggressive Central Giant Cell Granuloma)

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97
Q

Can Central giant cell granulomas be aggressive and grow quickly causing perforation of the cortical plant and root resorption

A

Yes (Aggressive Central Giant Cell Granuloma)

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98
Q

Central Giant Cell Granulomas can be what flavor (unilocular or multilocular)

A

Either unilocular or multilocular

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99
Q

Central Giant Cell Granulomas are radiopaque or radiolucent

A

radiolucent with well-defined rim, but rim is not corticated (does not have a definite white line)

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100
Q

What is a differential diagnosis for a multilocular radiolucent lesion of the jaw

A

Central Giant Cell Granuloma

Ameloblastoma

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101
Q

Unilocular radiolucent lesion of the jaw differential diagnosis

A

Central Giant Cell Granuloma
Periapical Granuloma
Cyst

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102
Q

Giant Cell Granulomas are histopathologically identical to what tumor associated with hyperparathyroidism

A

brown tumors

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103
Q

Common histology in all Central Giant Cell Granulomas

A

multinucleated giant cells in background of ovoid to spindle mesenchymal cells & round Macrophages

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104
Q

Before preceeding with treatment of Central Giant Cell Granuloma, what disease must be first ruled out

A

hyperparathyroidism (because brown tumor of hyperparathyroidism is histologically identical to Central Giant Cell Granuloma)

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105
Q

What disease should be investigated in a child that has multiple foci of apparent central giant cell granuloma and why

A

Cherubism. Because Central Giant Cell Granuloma normally occurs as 1 lesion while Cherubism is bilateral lesions presenting commonly at age 2-5

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106
Q

Treatment of nonaggressive Central Giant Cell Granuloma

A

Curettage (has 15%-20% recurrence)

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107
Q

3 alternatives to surgery for Aggressive Central Giant Cell Granuloma

A

Corticosteroids
Calcitonin
Interferon alpha-2a

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108
Q

Where do giant cell tumors normally occur in the body

A

epiphysis of long tubular bones

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109
Q

Rare developmental condition of painless bilateral expansion of the posterior mandible involving the angles and ascending rami

A

Cherubism

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110
Q

Cherubism: genetic or random mutation

A

can be autosomal dominant genetic transfer or spontaneouls mutation

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111
Q

Cherubism usually manifests at what age range

A

2-5 years

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112
Q

Besides the chubby cheeks, what is the other physiologic feature that leads to the naming of Cherubism

A

“eyes upturned to heaven) appearance due to infraorbital rim and orbital floor involvement tilting eye up while pulling lower lid down exposing more sclera below iris

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113
Q

When will the lesion regress

A

stabilize and slowly regress at puberty

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114
Q

What is the diagnostic (pathognomonic) radiography for Cherubism

A

multilocular expansile radiolucency with a bilateral symmetrical presentation

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115
Q

Side effects of the bilateral symmetrical jaw expansion of cherubism

A

displaced teeth, delayed eruption, impaired mastication and speech

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116
Q

What is contraindicated for Cherubism treatment and why

A

No radiation therapy, rick of post irradiation sarcoma

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117
Q

Benign empty or fluid-filled cavity within bone that is devoid of epithelial lining

A

simple bone cyst

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118
Q

Where do Simple Bone Cysts commonly occur in the body

A

long bone

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119
Q

Where do simple bone cysts commonly occur in the head and in what age range

A

mandible, between 10-20 years

120
Q

What is the radiographic appearance of Simple bone cyst (radiolucent or opaque, uniloc or multiloc)

A

unilocular well-defined radiolucency

121
Q

What is highly suggestive of simple bone cysts radiographically

A

superior border of cyst scallops up and down between adjacent tooth roots

122
Q

Are teeth adjacent to Simple bone cysts vital or non-vital

A

vital

123
Q

Is there root resorption with simple bone cyst

A

no root resorption

124
Q

Does a simple bone cyst have an epithelial lining

A

no, may have a thin vascular connective tissue membrane adjacent to the bone

125
Q

Treatment for Simple bone cyst

A

curettage and enucleation with submission of any recovered tissue to pathology

126
Q

How will the walls of the simple bone cyst appear on surgical exploration

A

smooth and shiny

127
Q

What will happen to simple bone cyst after curettage and enucleation

A

bony fill within 6 months

128
Q

Intraosseous accumulation of variable-sized, blood-filled spaces surrounded by cellular fibrous connective tissue that is often admixed with trabeculae of reactive woven bone

A

Aneurysmal bone cyst

129
Q

Aneurysmal bone cysts commonly located

A

shaft of long bone

Vertebral column

130
Q

Patient age normal for aneurysmal bone cyst in long bones and vertebral column

A

<30

131
Q

Patient age for aneurysmal bone cyst in jaw

A

children and young adults, mean age 20

132
Q

Aneurysmal bone cyst in head normally occur in what region of what bone

A

posterior segments of mandible (mandibular molar region)

133
Q

Most common clinical symptom of aneurysmal bone cyst

A

rapid facial swelling

134
Q

What is the radiographic appearance of an aneurysmal bone cyst

A

unilocular or multilocular, radiolucent, marked cortical expansion and thinning

135
Q

Treatment of aneurysmal bone cyst

A

enucleation and curettage, can look like a blood soaked sponge

136
Q

What does the aneurysmal bone cyst do to the surrounding bone

A

blow out or balloon

137
Q

Does the aneurysmal bone cyst have an epithelial lining

A

No, just spaces filled with clotted blood surrounded by fibroblastic tissue with gian cells and trabeculae of osteoid

138
Q

Odontogenic neoplasm of cementoblasts

A

cementoblastoma

139
Q

Most common area for cementoblastoma

A

mandibular molar and mandibular premolar region

140
Q

What age is cementoblastoma commonly found

A

late teens to 30’s

141
Q

What has occurred in a cementoblastoma that does not allow you to follow the root outline to the apex

A

root resorption has occurred and lesion is fused with tooth

142
Q

What is fused onto the root surface

A

sheets or thick trabeculae of mineralized cementum or osteocementum

143
Q

what is the cell type that lines the trabeculated sheets attached to the tooth root in cementoblastoma

A

blast cells

144
Q

Radiographic appearance of cementoblastoma

A

radiopaque mass fused to one or more tooth roots surrounded by thin radiolucent rim

145
Q

Treatment of Cementoblastoma

A

surgical extraction of tooth and attached mass, does not recur

146
Q

Primary malignant tumor of bone composed of small undifferentiated round cells of questionable etiology

A

Ewing’s sarcoma

147
Q

What is thought to be the origin of the round cells of Ewing’s sarcoma

A

neuroectodermal

148
Q

what are the top three most common osseous malignancies (in order)

A
  1. Osteosarcoma
  2. Chondrosarcoma
  3. Ewing’s Sarcoma
149
Q

Demographics of Ewing’s sarcoma

A

20’s, white, male

150
Q

Most common symptom of Ewing’s sarcoma

A

pain and swelling

151
Q

What does the tumor or Ewing’s sarcoma do to the cortical bone and what results

A

perforates cortical bone and soft tissue mass lies over the affected bone

152
Q

Majorityu of the cases contain what in the cytoplasm of the Ewing’s sarcoma tumor cells

A

glycogen

153
Q

Treatment for Ewing’s sarcoma

A

chemotherapy, multidrup chemotherapy to address micrometastasis, surgery. No radiation due to post irradiation sarcoma risk

154
Q

Most common form of cancer involving bone

A

Metastatic Carcinoma

155
Q

Carcinomas of what organs or tissues give rise to the majority of gnathic metases

A

Breast, Lung, Prostate, Colon, Thyroid, Renal

156
Q

How do the primary carcinomas metastasize to the jaw

A

hematogenous route

157
Q

Majority of metastatic tumors of the jaw are what type and occure where and in what age

A

intraosseous, posterior body of mandible, condyle, anterior maxilla, 5th – 7th decade

158
Q

In general, metastatic tumors of the jaw are found in areas of what (think of the route of transmission)

A

areas of red marrow

159
Q

Symptoms found in metastatic tumors of the jaw

A

pain, swelling, mass, tooth mobility, paresthesia, numb chin syndrome

160
Q

In general, the metastatic lesion in the jaw appears how radiographically

A

radiolucent with moth eaten appearance and possible PDL widening

161
Q

Metastatic process in jaw particular to breast and prostate cancer as primary site

A

osteoblastic

162
Q

If the metastasis is osteoblastic, how will it appear radiographically

A

radiopaque or mixed density

163
Q

In the 25% of the metastases to the oral cavity that don’t go to bone, where do they go

A

soft tissue: gingival or dorsal tongue

164
Q

2 things a metastatic tumor to the Oral cavity can be confused for

A

pyogenic granuloma
PGCG
Fibroma

165
Q

Why is the prognosis dismal if it is a metastatic tumor or the jaw

A

because metastasis automatically places pt in Stage IV, survival generally 1 yr

166
Q

diverse group of processes that are characterized by replacement of normal bone by fibrous tissue containing a newly formed mineralized product

A

Fibro-osseous lesions

167
Q

Developmental tumorlike condition characterized by replacement of normal bone by an excessive proliferation of cellular fibrous connective tissue intermixed with irregular bony trabeculae

A

Fibrous dysplasia

168
Q

What is the character of the abnormal fibro- osseous tissue

A

poorly formed

Functionally inadequate

169
Q

By what process does the abnormal fibro-osseous tissue arise in Fibrous dysplasia

A

Metaplasia

170
Q

when Fibrous dysplasia is confined to 1 bone

A

Monostotic (80% all cases)

171
Q

Most common symptom of Monostatic fibrous dysplasia

A

painless swelling at site

172
Q

Part of oral cavity most affected by Fibrous dysplasia

A

Maxilla

173
Q

Fibrous dysplasia that involves 2 or more bones

A

polyostotic

174
Q

Polyostotic fibrous dysplasia associated with café au lait pigmentation

A

Jaffe-Lichtenstein Syndrome

175
Q

Maxillary fibrous dysplasia normally involves more bones than just the maxilla, so it is commonly called

A

Craniofacial fibrous dysplasia

176
Q

Polyostotic fibrous dysplasia with café-au lait and multiple endocrinopathies (e.g. sexual precocity, pituitary adenoma, hyperthyroidism)

A

McCune-Albright Syndrome

177
Q

This fibrous dysplasia syndrome also has affectation or effeacement of various neural foramina at base of skull in CT

A

McCune-Albright Syndrome

178
Q

What is the character of the café au lait pigmentation in McCune Albright syndrome

A

uniform pigment with irregular border

179
Q

What is the radiographic character of Fibrous dysplasia

A

highly variable from radiolucent to radiopaque

180
Q

2 radiographic clues for Fibrous dysplasia

A

1) cortical persistence of inferior border mandible with bone enlargement
2) Superior displacement of IAN canal

181
Q

What is the most common radiographic appearance of Fibrous dysplasia and what does it indicate

A

ground glass pattern(end of slide or decanter stopper). Indicates lesion is hard & will be difficult to remove surgically

182
Q

2 pathognomonic radiographic returns for Fibrous dysplasia

A

peau d’orange

Fingerprint

183
Q

Fibrous dysplasia lesions in youth versus adult

A

Youth: Hypervascular
Adult: avascular

184
Q

Concern with surgery in youth fibrous dysplasia

A

Hemostasis due to hypervascularity

185
Q

Concern with adult fibrous dysplasia

A

avascular bone so more susceptible to infection

186
Q

Only fibrous dysplasia type that has risk of malignant transformation

A

polyostotic

187
Q

dysplastic condition at apices of anterior mandible teeth

A

periapical cement-osseous dysplasia

188
Q

What demographic does periapical cement- osseous dysplasia have a marked predilection for

A

middle aged African American females

189
Q

What is the status of the teeth associated with Periapical Cemento-Osseous dysplasia

A

vital(key for endo)

190
Q

Stage I periapical cement-osseous dysplasia radiographic appearance

A

periapical radiolucency (do vitality testing so don’t do unnecessary endo)

191
Q

Stage II periapical cement-osseous dysplasia radiographic appearance

A

mixed radiolucent/radiopaque lesion as woven and lamellar bone and cementum mineralize

192
Q

Stage III periapical cement-osseous dysplasia radiographic appearance

A

large radiopaque mass due to masses coalescing to form acellular disorganized cement-osseous material

193
Q

Is there any treatment indicated for periapical cement-osseous dysplasia

A

No, don’t want to biopsy or extract because exposing to oral environment could superimpose osteomyelitis on dysplastic bone

194
Q

a subset of Periapical Cemento-osseous dysplasia that has extensive periapical cement-osseous dysplasia in multiple posterior quadrants

A

Florid Cemento-osseous dysplasia

195
Q

Does Florid cemento-osseous dysplasia have 3 developmental stages like Periapical cement-osseous dysplasia

A

Yes

196
Q

What is the danger with Periapical or Florid cement-osseous dysplasia

A

Exposing it to oral environment which can cause osteomyelitis

197
Q

What is the characteristic Florid Cemento-osseous dysplasia histologically

A

ginger root curvilinear trabeculae

198
Q

Benign, well-circumscribed, slow-growing neoplasm of craniofacial bones, predominantly in the mandibular molar and premolar region, with a predilection for Females in their 3rd – 4th decade

A

cement-ossifying fibroma

199
Q

What radiographic feature is key for cement- ossifying fibroma

A

well-circumscribed, sharply defined border

200
Q

How does cement-ossifying fibroma grow

A

equidirection expansion with centrifugal growth pattern that can thin cortical bone

201
Q

What is composition of Cemento-ossifying fibroma

A

uniform fibroblasts and small irregular masses resembling cementum

202
Q

What is a differentiating characteristic between cement-ossifying firbrom and fibrous dysplasia

A

cement-ossifying fibroma does not arrest at skeletal maturity like fibrous dysplasia does

203
Q

Cemento-ossifying fibroma treatment

A

complete enucleation with larger possibly requiring surgical resection and bone grafting

204
Q

Ossifying fibrom that is rapidly growing, well- circumscribed lacking continuity with adjacent bone

A

Juvenile aggressive ossifying fibroma

205
Q

Major pattern of Juvenile/Aggressive Ossifying Fibroma that occurs in the craniofacial skeleton

A

psammomatoid

206
Q

What part of the craniofacial skeleton does Juvenile/Aggressive Ossifying Fibroma occur most often

A

maxilla, psammomatoid. 70/5 in orbital, frontal bones and paranasal sinuses

207
Q

Symptoms of Juvenile/Aggressive Ossifying Fibroma

A

nasal obstruction, pain, sinusitis, headache, proptosis (eye bulging)

208
Q

Juvenile/Aggressive Ossifying Fibroma histology

A

psammomatoid bodies embedded in cellular stroma of stellate cells w/ hyperchromatic nuclei, no mitotic bodies. Osteoid and woven bone when mature

209
Q

Treatment and recurrence of Juvenile/Aggressive Ossifying Fibroma

A

surgical excision and curettage, 30-58% recurrence but no malignant transformation

210
Q

Most common osseous tumor of the jaw

A

Osteoma (benign neoplasm of bone)

211
Q

Does an osteoma occur in immature or mature bone

A

mature lamellar bone

212
Q

Do palatal tori, mandibular tori, and buccal exostoses represent osteomas

A

No

213
Q

2 ways osteomas can arise

A

1) on bone surface = periosteal/peripheral/exophytic osteoma

2) In medullary bone = endosteal or central osteoma

214
Q

Most common osteoma location

A

body of mandible or condyle

215
Q

When osteoma found in the body of the mandible, where will it most likely occur

A

posterior to premolars, lingual side

216
Q

How would one differentiate between and osteoma in the condyle and condylar hyperplasia

A

condylar osteoma would be lobulated, condylar hyperplasia the condyle retains its shape

217
Q

How will an osteoma look histologically

A

lots of dense bone w/ little marrow and prominent osteoblastic activity

218
Q

What is the demographic for osteomas

A

6th decade, females

219
Q

How do osteomas appear radiographically

A

well circumscribed sclerotic mass attached by a broad base to underlying bone. Radiopaque

220
Q

Can an osteoma cause root resorption

A

yes

221
Q

Where are the two most common sinus locations for maxillary osteomas

A

Frontal osteoma, 80%. # 2 is ethmoid sinus

222
Q

what is the problem with sinus osteomas

A

they are aggressive, cause obstructions and recur after initial attempts to remove

223
Q

how treat an osteoma

A

surgical removal to secure diagnosis and treat cosmetic or functional defects

224
Q

What is osteoma is small, asymptomatic, and located endosteal, how treat

A

observed periodically

225
Q

Autosomal inherited trait with 100% penetrance or the result of spontaneous mutation on Chromosome 5 characterized gnathically by multiple osteomas and multiple supernumerary teeth

A

Gardner syndrome

226
Q

What is another systemic manifestation of Gardner syndrome

A

colorectal polyps that will become malignant

227
Q

What does Chromosome 5 have to do with Gardner syndrome

A

it is the adenomatous polyposis coli (APC) tumor suppressor gene (think colon polyps)

228
Q

What will all patients with Gardner Syndrome develop in their life, 50% by age 30

A

aggressive colon adenocarcinoma

229
Q

2 prophylactic treatments in Gardners

A

prophylactic colectomy

Screen other family members

230
Q

when do the multiple osteomas of Gardners syndrome usually present

A

during puberty and precede colon polyps

231
Q

Can the multiple osteomas of Gardners be treated

A

yes, for cosmetic reasons, but long term prognosis depends on bowel adenocarcinomas

232
Q

Benign tumors composed of mature hyaline cartilage

A

Chondroma

233
Q

Where are chondromas normally located

A

short tubular bones of hands and feet

234
Q

) If a chondroma is going to occur in the head and neck, what is the embryonic origin of its location

A

where embryonic cartilaginous remnants located

235
Q

Where are the embryonic cartilaginous remnants that are conducive to chondromas located in the head and neck

A
  • Mandible: premolar area(Meckel’s cartilage), condyle, coronoid process, symphysis
  • Maxilla: nasal septum, ehtmoid sinus
236
Q

When are chondromas normally diagnosed

A

Before age 60

237
Q

How do chondromas look radiographically

A

localized irregular radiolucent defect with punctuate or stippled calcifications

238
Q

What will chondromas do to small bones

A

expansion and cortical thinning

239
Q

If chondroma in the jaw, is there root resorption

A

yes

240
Q

What is the dilemma with chondromas in the jaw

A

Some believe they are chondrosarcomas meaning they are malignant

241
Q

What indicates a chondroma versus a chondrosarcoma in the jaw

A

Chondroma will have absence of pain, lack of disturbed cortex and surrounding bone architecture and no cytologic atypia

242
Q

What does an osteochondroma consist of

A

cancellous bone surrounded by compact bone with a cartilaginous cap

243
Q

If patient has multiple osteochondromas what will be the physical character of their bone and what are they at risk for

A

deformed bone

Propensity to develop chondrosarcoma

244
Q

What will an osteochondroma look radiographically

A

radiopaque extraosseous projection

245
Q

where do osteochondromas occure most frequently

A

condyle and coronoid process

246
Q

Benign bone tumor arising from osteoblasts that is rare in the jaw

A

Osteoid osteoma

247
Q

Demographic for Osteoid Osteoma

A

Males (3:1), 2nd decade

248
Q

Pathonomonic clinical symptoms for Osteoid Ostemoa

A
  • pain of increasing severity
  • Worse at night
  • Relieved w/in 20-30 min of aspirin/NSAID dose
249
Q

How does and osteoid osteoma appear radiographically

A

well demarcated radiopaque nidus, round to ovoid wit h a peripheral radiolucent rim surrounded by zone of reactive host sclerosis

250
Q

Is the sclerosis surrounding an Osteoid Osteoma a part of the lesion or a host response

A

host response that resolves once nidus is gone

251
Q

When the nidus is well ossified, how can the Osteoid Osteoma look radiographically

A

targetoid or bulls-eye appearance (what is other pathology that has targetoid appearance?)

252
Q

What is the histopathology of Osteoid Osteoma

A

irregular randomly ordered trabeculae of osteoid and woven bone

253
Q

What is the character of the nidus in Osteoid Osteoma

A

well vascularized, clearly separate from reactive bone

254
Q

what is the growth potential of Osteoid Osteoma

A

limited growth, nidus < 2 cmdiameter

255
Q

What is responsible for reactive host sclerosis, inflammatory changes in soft tissue and pain in Osteoid Osteoma

A

large amounts of prostaglandin E2 and prostacyclin

256
Q

Treatment of Osteoid Osteoma

A

surgical excision of nidus and surrounding bone and curettage

257
Q

Also a benign bone tumor arising from osteoblasts that occurs in Males(3:1) in 2nd decade

A

Osteoblastoma

258
Q

Differences of osteoblastoma from Osteoid Osteoma

A

Osteoblastoma will grow >2cm, does not have nocturnal pain relieved by aspirin/NSAID, lacks secondary peripheral sclerosis

259
Q

Where will an osteoblastoma appear in mandible radiographically

A

in vicinity of tooth root with a central opacity surrounded by peripheral radiolucent halo

260
Q

How treat osteoblastoma

A

surgical en bloc excision (as a unit, all together). Nidus is well demarcated and can be removed easily from surrounding bone

261
Q

Histology of Osteoblastoma (same as Osteoid Osteoma)

A

interlacing network of bone trabeculae evenly distributed in loose fibroblastic stroma with prominent vasculature and osteoblastic rimming

262
Q

Aggressive Osteoblastoma character

A

occur in older patients (>30) larger than normal osteoblastoma (>4cm) severe pain, locally destructive w/ high recurrence after surgery

263
Q

The most common primary malignancy of bone (excluding hematopoietic tumors)

A

osteosarcoma

264
Q

What must an osteosarcoma be able to do

A

produce osteoid and immature bone

265
Q

What is demographic for osteosarcoma

A

males, during periods of highest growth. 10-20 years and >50 years

266
Q

What bones does osteosarcoma arise in normally

A

skeletal areas with highest growth rate: distal femur, proximal tibia, proximal humerus

267
Q

At what age does an osteosarcoma in the mandible or maxilla normally occur

A

3rd and 4th decade

268
Q

What disease and treatment can predispose for osteosarcoma

A

Paget’s disease

Previous irradiation

269
Q

Osteosarcoma clinical symptoms

A

pain (weeks to months) of increasing intensity, swelling, skin warm to touch

270
Q

Weight loss associated with osteosarcoma indicates metastasis to what area

A

Lungs

271
Q

What are the radiographic features of jaw osteosarcoma

A

ill defined border/indistinct, spiking of teeth due to root resorption, sunburst/sunray appearance, Codman’s triangle

272
Q

What causes the sunburst/sunray appearance on an osteosarcoma

A

osteophytic bone production on surface of lesion

273
Q

What is an important early radiographic sign of a jaw osteoma

A

symmetrical widening of PDL around 1 or several teeth

274
Q

What will be elevated in patient with osteosarcoma

A

alkaline phosphotase

275
Q

Treatment for osteosarcoma

A

Neodjuvant (preop) chemo and radiation
Surgical excision
Adjuvant (postop) chemo

276
Q

What is Codman’s Triangle

A

Tumor growing on bone surface can elevate periosteum and cause periosteal reaction of open triangle showing radiographically

277
Q

What will happen to the teeth along with the external root resorption in osteosarcoma jaw lesions

A

mobility

278
Q

Essential microscopic criterion for osteosarcoma

A

direct production of tumor osteoid by malignant mesenchymal cells

279
Q

Secondary Osteosarcoma can arise from where

A 
Paget’s disease 
Fibrous dysplasia
Ionizing radiation >3000 Gys 
Bone infarcts
Chronic osteomyelitis 
Metallic prosthetic implants
280
Q

What are the clinical symptoms associated with sarcomatous transformation

A

sudden onset of pain
Rapid worsening of previous pain
Increased deformity

281
Q

Character of Secondary Osteosarcomas

A

high grade
Aggressive
Poor prognosis

282
Q

Malignant tumor characterized by the formation of cartilage, but not bone, by tumor cells. Can arise de novo or within a preexisting benign chondroma

A

chondrosarcoma

283
Q

Second most frequent bone sarcoma

A

chondrosarcoma

284
Q

where do chondrosarcomas occur gnathically

A

Maxillary anterior alveolus, orbit, nose, condyle or skull base

285
Q

Can there be a periosteal reaction with chondrosarcoma

A

yes

286
Q

Cortical disruption with significant extension into soft tissues signifies what type of chondrosarcoma

A

advanced lesion

287
Q

What can be seen with the teeth in chondrosarcoma that was seen with osteosarcoma

A

widening of PDL with root divergence or resorption

288
Q

Most common type of chondrosarcoma

A

Mesenchymal

289
Q

How are chondrosarcomas graded

A

by histologic features

290
Q

Chondrosarcoma with lobular architecture, rarely metastasizes

A

Grade I

291
Q

Chondrosarcoma with myxoid stromaand mitotic figures, 10% metastasis rate

A

Grade II

292
Q

Chondrosarcoma with markedly cellular, spindleform, abundant mitosis, 71% metastasis rate

A

Grade III

293
Q

treatment for chrondrosarcoma and where contraindicated

A

Wide local or radical surgical excision. May not be possible in base of skull

294
Q

Is radiotherapy or chemotherapy useful in chondrosarcoma treatment

A

No

295
Q

When is prognosis for Chrondosarcoma worse

A

Jaws. Maxilla worse prognosis than mandible

296
Q

What can a chondrosarcoma be confused for

A

Chondroblastic osteosarcom which would have some bone in it (radiograph would have some more opacity and greater change of periosteal reaction)

297
Q

Why is it important to differentiate between a chondrosarcoma and a chondroblastic osteosarcoma

A

because treatment and prognosis is different. Osteosarcomas are slower growing with a reduced metastasis rate which increases their prognosis. As well osteosarcomas have other therapy options beyond surgical excision.

Oral Pathology, Stephen (13 decks)

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