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Oral Pathology > Bone Pathology > Flashcards

Bone Pathology Flashcards

1
Q

mode of transmission of osteogenesis imperfecta

A

genetic transmission
90% autosomal dominant

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2
Q

what genes are implicated in osteogenesis imperfecta?

A

COL1A1 or COL1A2

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3
Q

describe the condition of bones in osteogenesis imperfecta

A

defective collagen
abnormal bone mineralization
low tensile strength
very fragile (fractures easily)

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4
Q

dental findings of osteogenesis imperfecta

A
  1. dentinogenesis imperfecta
  2. bulbous crowns
  3. constriction at cervical margins of teeth
  4. absence of pulp chambers
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5
Q

ocular findings of osteogenesis imperfecta

A

blue sclera

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6
Q

sclera (definition)

A

outermost layer of eyeball

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7
Q

choroid (definition)

A

lies deep to sclera
is pigmented (melanin)

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8
Q

why are eyes blue in osteogenesis imperfecta?

A

melanin helps to absorb excess light and limits uncontrolled reflection and confusing images (pigment shows through the thin sclera as blue)

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9
Q

management of osteogenesis imperfecta

A
  1. minimize factors that cause fractures
  2. rehabilitation, orthopedic surgery
  3. IV bisphosphonates (prevent osteoclastic destruction of bones)
  4. over dentures
  5. bone is of poor quality for implants
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10
Q

what is the basic defect in osteopetrosis?

A

rare, defect in osteoclast function (bone turnover is lacking)

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11
Q

major disease patterns in osteopetrosis

A

infantile (birth, early infancy) = autosomal recessive
adult = milder disease, autosomal dominant

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12
Q

changes in bone in osteopetrosis

A
  1. persistance of bone formation leads to diffuse sclerosis of skeleton
  2. marrow space filled in by dense bone
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13
Q

what results when the marrow space is filled with dense bone in osteopetrosi?

A
  1. loss of hematopoietic marrow
  2. pancytopenia (all 3 cell types depleted)
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14
Q

pancytopenia (osteopetrosis)

A
  1. anemia (normocytic) with compensatory hepatosplenomegaly
  2. infections (due to leukocytopenia)
  3. bleeding tendencies (due to thrombocytopenia)
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15
Q

systemic implications of osteopetrosis

A
  1. increase in bone density with absence of medullary bone
  2. increase width of cranium
  3. proptosis due to deposition in orbital cavity
  4. blindness (optic canal compressed)
  5. deafness (compression fo CN 8)
  6. facial palsy (compression of stylomastoid foramen)
  7. hypertrophy of bones (relative microsomia)
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16
Q

blindness in osteopetrosis is due to…

A

optic nerve compression

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17
Q

deafness in osteopetrosis is due to…

A

CN 8 compression

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18
Q

facial palsy in osteopetrosis is due to…

A

compression of stylomastoid foramen

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19
Q

oral complications of osteopetrosis

A
  1. impacted teeth in recessive form of disease
  2. poor oral health, dental decay, infections following dental extractions
  3. mandibular osteomyelitis with multiple draining sinus tracts
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20
Q

management of osteopetrosis

A

1.bone marrow transplant
2. support measures to minimize infection / fracture risks
3. aggressive treatment of osteomyelitis (antibiotics, hyperbaric O2)
4. interferon gamma-1b with calcitriol and restricted calcium intake

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21
Q

interferon gamma-1b in the treatment of osteopetrosis has shown to…

A

reduce bone mass
decrease prevalence of infections
lower nerve compression frequency

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22
Q

what gene mutation results in cleidocranial displasia?

A

RUNX2 gene

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23
Q

transmission of cleidocranial dysplasia

A

uncommon autosomal dominant condition
40% spontaneous mutations

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24
Q

clinical findings of cleidocranial dysplasia

A
  1. affects skull, jaws, CLAVICLES
  2. large skulls with prominent forehead (frontal and parietal bossing)
  3. hypertelorism
  4. depressed bridge and wide base of nose
  5. high narrow or cleft palate
  6. hypopalstic maxilla
  7. primary dentition retained as permanent teeth do not erupt
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25
Q

radiographic findings of cleidocranial dysplasia

A

can see retained primary teeth with unerupted perm teeth or super teeth

edentulous patient with impacted teeth

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26
Q

management of cleidocranial dysplasia

A
  1. surgical and ortho care to correct skeeltal relations
  2. remove supernuemrary teeth and bring permanent teeth into proper relatoin
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27
Q

prognosis of cleidocranial dysplasia

A

good
normal life span

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28
Q

clinical features of osteoporotic bone marrow defect

A
  1. middle aged to older females
  2. incidental finding - no swelling or pain
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29
Q

radiographic features of osteoporotic bone marrow defect

A

asymptomatic ill-defined radiolucency in BODY OF MANDiBLE AT OLD EXTRACTION SITE

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30
Q

wht tissue is encountered if osteoporotic bone marrow is biopsied?

A
  1. may resemble metastatic disease (biopsy sometimes necessary)
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31
Q

when is a biopsy for osteoporotic bone marrow necessary?

A

when the patient gives history (current or past) of cancer

need to rule out

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32
Q

what is seen microscopically for osteoporotic bone marrow?

A

fatty and hematopoietic marrow

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33
Q

treatment of osteoporotic bone marrow defect?

A

pack with bone chips and bring back bone quality - follow up after

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34
Q

radiographic findings of idiopathic osteosclerosis

A
  1. ENOSTOSIS / DENSE BONE ISLAND
  2. asymptomatic lesion discovered on routine radiographs (PDL space continuous)
  3. RADIOPAQUE, NO EXPANSION
  4. PREMOLAR - MOLAR REGION MOST COMMON
  5. margins may be sharp or blended with adjacent bone
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35
Q

treatment of idiopathic osteosclerosis?

A

don’t need to biopsy
will show dense vital bone

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36
Q

what are the clinical features of condensing osteitis

A
  1. localized bone sclerosis associated with apices of teeth with pulpitis (large carious lesion or deep coronal restoration)
  2. associated with area of inflammation is critical or diagnosis (pulpitis and osteitis: inflammation)
  3. will have pain
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37
Q

what are the radiographic features of condensing osteitis

A
  1. seen in tooth with pulpitis
  2. bone responts with calcification (fights back by forming more bone) - follows contour of the tooth with sclerosis
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38
Q

how are the bone changes with condensing osteitis affected by either extraction or root canal treatment of the tooth?

A
  1. can reverse completely or partially
  2. removed the source of the focus of infection, normal routine bone remodeling will make that bone go away
  3. 85% of cases regress totally or partially upon removal of focus of infection
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39
Q

describe the clinical features of paget’s disease of bone

A
  1. osteitis deformans
  2. abnormal resorption and deposition of bone
  3. distortion and weakening of bone
  4. unknown etiology
  5. older patients, male predilection
  6. many asymptomatic, but bone pain may be present
  7. most cases polyostotic
  8. affected bone thickened but weak
  9. involvement of femurs, simian stance develops due to BOWING OF LEGS
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40
Q

radiographic features of paget’s disease

A

cotton wool appearance of skull with areas of osteoporosis circumscripta

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41
Q

histopathological features of paget’s disease

A

irregular trabeculae with resetting and reversal lines - “mosaic” pattern

dark lines are reversal lines

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42
Q

jawbone / teeth findings of paget’s disease

A

10-15% of affected patients
maxilla ? mandible
HYPERCEMENTOSIS OF TEETH

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43
Q

what serum marker is elevated in paget’s disease of bone?

A

markedly elevated serum alkaline phosphatase

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44
Q

treatment of paget’s disease

A

no good therapy

bisphosphonates reduce bone turnover with normalization of serum alkaline phosphatase levels, decrease bone pain and improve quality of life

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45
Q

complications of paget’s disease

A
  1. chronic and progressive
  2. patients to be monitored for development of giant cell tumor of bone as well as malignant bone tumors, especially osteosarcoma
  3. hypercementosis and complicates tooth extraction
  4. unfavorable results with dental implants
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46
Q

demographics affected by central giant cell granuloma

A

2nd-4th decade of life
2:1 female predilection

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47
Q

clinical features of central giant cell granuloma

A
  1. benign lesion of jaws
  2. unilocular when small; larger lesions often multilocular and expansile
  3. central - intraosseous process (inside jaw)
  4. try pulp testing first, ask any trauma, teeth would test vital
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48
Q

radiographic features of central giant cell granuloma

A
  1. mandible, often crossing the midline
  2. thin wispy trabeculae perpendicular to outer cortex
  3. multilocular radiolucency of the mandible, crossing the midline (buccal expansion)
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49
Q

histopathologicla features of central giant cell granuloma

A

vascular CT with copious amounts of erythrocytes and multinucleated giant cells

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50
Q

management of central giant cell granuloma

A

aggressive currettage
intralesional steroid injections
calcitonin

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51
Q

possible complication in older patients with central giant cell granuloma

A

possiblity of brown tumor of hyperparathyroidism that should be explored

52
Q

what is a brown tumor of hyperparathyroidism?

A
  1. take out all the calcium from the bone and put into the blood
  2. osteitis fibrosa cystica
  3. histology identical to the central giant cell granuloma with many erythrocytes
  4. hemoglobin converts into hemosiderin pigement (looks brown in color due to pigment)
53
Q

jawbone findings in brown tumor of hyperparathyroidism

A
  1. ground glass appearance, loss of lamina dura, brown tumor
  2. trabeculae thin out (bone looks homogenous, opaque ground glass)
54
Q

demographics affected by cherubism

A

childhood
autosomal dominant condition?

55
Q

clinical findings of cherubism

A
  1. painless, bilateral expansion of jaws, especially in the mandible
  2. “chubby” due to bone expansion, upward turn of eyes
56
Q

radiographic features of cherubism

A
  1. bilateral multilocular radiolucencies of posterior mandible
  2. less frequently, maxillary involvement
  3. some unilateral cases described
  4. often significant anterior placement of teeth
57
Q

management of cherubism

A
  1. lesions regress after puberty
  2. by 4th decade, facial features almost normal
  3. residual deformity may be surgically removed
58
Q

etiology of traumatic (simple) bone cyst

A
  1. hemorrhagic bone cavity
  2. idiopathic condition seen in 1st and 2nd decase
  3. questionable relation to trauma
59
Q

demographics affected by traumatic bone cyst

A

male predilection; posteiror mandible

60
Q

radiogrpahic features of traumatic (simple) bone cyst

A

well circumscribed radiolucency with scalloping between roots

lamina dura still intact, lack of expansion, intact cortex

61
Q

intraoperative findings of traumatic bone cyst

A
  1. empty cavity is found within bone (often inferior dental canal may be noted at the bottom of the cavity)
  2. difficult to obtain lesional tissue (scant amount of serous fluid)
62
Q

management of traumatic bone cyst

A
  1. empirically, the recommendation has been to enter the lesion, establish the diagnosis, then induce bleeding
  2. supposedly the hemorrhage organizes and the lesion heals
63
Q

fibrous dysplasia (definition)

A

developmental, tumor like lesion

hard bony growth

64
Q

etiology of fibrous dysplasia

A

post zygomatic mutation of tumor suppressor (GNAS) gene

65
Q

can the post-zygotic mutation of fibrous dysplasia be passed onto children?

A

no

66
Q

types of fibrous dysplasia

A

monostatic form
polyostotic fibrous dysplasia

67
Q

monostatic form of fibrous dysplasia

A

most cases are late post zygotic and result in this form

68
Q

polyostotic fibrous dysplasia

A

early post-zygotic mutation causes this form

69
Q

demographics affected by fibrous dysplasia

A

first or second decade
no sex predilection

70
Q

are most cases of fibrous dysplasia monostatic or polostotic?

A

monostatic

71
Q

jawbone manifestations of fibrous dysplasia

A

jaws are among the most commonly affected bones

72
Q

maxilla or mandible more affected by fibrous dysplasia?

A

maxill

73
Q

cranial bone manifestations of fibrous dysplasia

A
  1. maxillary lesions may involve adjacent facial bones, including sphenoid, zygoma, occipital
  2. known as craniofacial fibrous dysplasia
  3. more severe presentation
  4. marked facial deformity
74
Q

radiographic appearance of fibrous dysplasia

A

ground glass
poorly defined, blended margins
lamina dura lost over time

75
Q

loss of lamina dura in hyperparathyroidism vs fibrous dysplasia

A

early generalized loss of lamina dura is characteristic of hyperparathyroidism

lamina dura is lost over time in fibrous dysplasia

76
Q

histopathology of fibrous dysplasia

A

irregularly shaped trabeculae of immature bone (“chinese letter”)

trabeculae somewhat evenly spaced

77
Q

polyostotic fibrous dysplasia

A

many bones involved

78
Q

jaffe type of polyostotic fibrous dysplasia

A

two or more bones affected
cafe-au-lait spots

79
Q

mccune type of polyostotic fibrous dysplaisa

A

2+ bones affected
cafe-au-lait spots
exocrine disturbances manifest as precocious puberty
intramuscular myxomas (mazabraud syndrome)

80
Q

treatment of fibrous dysplasia

A
  1. small lesions may not need treatment or may be recovered by en bloc resection
  2. significant cosmetic or functional deformity may require an attempt at surgical reduction (debulking)
  3. sometimes the disease stabilizes iwth skeletal maturation
81
Q

potential complications of fibrous dysplasia

A
  1. 25-50% of surgically treated lesions show regrowth, particularly in younger patients
  2. malignant transofrmation is rare and reported in lesions that have received radiaiton therapy
82
Q

most important thing to remember in treatment of fibrous dysplasia

A

never radiate anything that is a benign lesion

83
Q

what is the most important thing to remember about cemento-osseous dysplasia

A

never perform endodontic treatment on these patients!

84
Q

ethnic predilection of cemento-osseous dysplasia

A

african american females
southeast asia

85
Q

variants of cemento-osseous dysplasia

A

periapical (most common, mild)
focal (moderate)
florid (severe)

86
Q

radiogrpahic features of cemento-osseous dysplasia

A
  1. usually detected on routine radiographs
  2. mandibualr anteiror region
  3. initially, radiolucencies at apicies of several teeth, with gradual central opacity developing
  4. radiopacity is completely in bone (not part of root)
87
Q

nature of cemento-osseous dysplasia disease

A

osteolytic –> osteoblastic –> maturative

88
Q

treatment of cemento-osseous dysplasia

A

none necessary! do nothing at all!

89
Q

focal cementoosseous dysplasia is usually detected on

A

routine radiographcs

90
Q

focal cemento-osseous dysplasia - location

A

body of mandible

91
Q

difference between focal cemento-osseous dysplasia and odontoma / central ossifying fibroma

A

when treating odontoma or central ossifying fibroma, has thick capsule surrouding. easy to separate from surroudnign bone

nto case for florid type cemento-osseous dysplasia (not well defined)

92
Q

treatment for focal cemento-osseous dysplasia

A

no treatment required

93
Q

complications associated with florid type fo cemento-osseous dysplasia

A
  1. more severe expression fo the cemento-osseous dysplasias
  2. affects multiple quadrants of jaws
  3. radiolucencies with multiple cotton wool radiopacities in at least 2 quadrants of the jaws
  4. lesions become mroe radiodense with time
94
Q

central ossifying fibroma

A

uncommon benign neoplasm that probably arises from periodontal ligament fibrobalsts

95
Q

demographics of central ossifying fibroma

A

mandibular premolar / molar region
female
3rd to 4th decade

96
Q

clinical features of central ossifying fibroma

A

actual tumor!
swelling may be present if lesion is large

97
Q

radiographic features of central ossifying fibroma

A
  1. well circumscribed radiolucency with vairable amount of central opacity
  2. range from almost purely radiolucent or very radiodense with a defined lucent border
98
Q

management of central ossifying fibroma

A

treatment consists of enucleation - lesions tend to shell out as one mass

99
Q

what diseases may the central ossifying firboma like tumor be associated with?

A

hyperparathyroidism
gnathodiaphyseal dysplasia
familial gigantiform cementoma

100
Q

demographics of trabecular variant of juvenile ossifying fibroma

A

11years

101
Q

demogrpahics of psammamatoid variant of juvenile ossifying fibroma

A

22 years

102
Q

common site of juvenile ossifying fibromas

A

predominantly maxillary tumors
70% of psammamatoid variant arises in bones of the orbit, frontal, and paranasal sinuses

103
Q

clinical features of juvenile ossifying fibroma

A
  1. progressive enlargement
  2. symptoms associated with impingement on adjacent structures
  3. most aggressive tumors in infants and young hcildren
104
Q

management of juvenile ossifying fibroma

A
  1. small lesions = local excision with thorough currettage
  2. large lesions = wide resection
105
Q

histopathology of two variants of juvenile ossifying fibroma

A

trabecular = fine trabeculae
psammamatoid = small sand grains, calcificaitons

106
Q

osteoma

A

benign osseous tumor, usually affecting membranous bone

107
Q

location of osteoma

A

parnaasal sinus involvement is common
jaw lesions are usually associated with condylar area

108
Q

clinical features of osteoma

A

painless, slow enlarging

109
Q

relationship of osteoma with gardner sydnrome

A

autosomal trait
one of the must intestinal polyposis syndrome
characterized by osteomas of the facial bone
epidrmoid cysts and desmoid tumors

110
Q

inheritance of gardner sydnrome

A

autosomal dominant trait (uncommon)

111
Q

clinical features of gardner sydnrome

A
  1. one of the multiple intestinal polyposis sydnromes
  2. characterized by osteoms of the facial bone
  3. epidermoid cysts and desmoid tumors
112
Q

radiographic features of gardner syndrome

A
  1. radiographically, the osteoma of gardner sydnrome could resemble florid cemento-osseous dysplasia or osteitis deformans
  2. may see impacted supernumerary teeth or less commonly odontomas
113
Q

complications of gardner sydnrome

A
  1. the most significant aspect of the sydnrome is the development of precancerous polyps of the colon
  2. 50% of patients develop adenocarcinoma of the colon by 30 years of age
  3. also develop multiple epidermoid cysts on the scalp
114
Q

prophylaxis of gardner syndrome

A
  1. prophylactic colectomy
  2. removal of costmetically problematic cysts and osteomas
  3. genetic counseling
115
Q

incidence of osteosarcoma

A

most common primary bone malignancy - twice as common as chondrosarcoma

only 900 new cases int he US annually

116
Q

age predilection in jaw bones vs long bones

A

osteosarcoma of long bone = mean 18 years
osteosarcoma of jaws = mean 28 years

117
Q

clinical features of osteosarcoma

A

pain
swelling
loss of teeth
paresthesia

118
Q

radiogrpahic features of osteosarcoma

A
  1. mixed radiopaque / radiolucent lesions with ill defined borders
  2. widened PDL of teeth
  3. spiking root resorption
  4. sun brts pattern of periosteal expansion
119
Q

management of osteosarcoma

A

radical surgery
preceded by neoadjuvant chemoterapy in high grade tumors

120
Q

two other examples of primary jawbone malignancy

A

chondrosarcoma
ewing sarcoma

121
Q

chondrosarcoma

A

adult males
10% in jaw bones

122
Q

ewing sarcoma

A

children and adolescents
commonest primary bone malignancy in kids

123
Q

metastatic tumros are often called

A

seocndaries

124
Q

incidence rates of metatistic tumors

A

mandible = 61%
maxilla = 24%
soft tissue = 15%

125
Q

role of baston’s plexus in spread of tumor

A
  1. odler and elderly
  2. mobility of spread, paresthesia (NUMB CHIN)
  3. irregular widening of PDl, moth eaten apperance (could easily be misdiagnosed as periodontal disease)
126
Q

majority of metastatic tumors in jaw come from

A

breast
lunk
kidney
colon
prostate

Oral Pathology (14 decks)

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