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PATH II > Bone lecture 1 > Flashcards

Bone lecture 1 Flashcards

1
Q

basic bne anatomy

A
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2
Q

Focal Osteoporotic Defect

A

 Area of hematopoietic marrow which produces a defect

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3
Q

Focal Osteoporotic Defect potential pathogenesis

A

 Aberrant bone regeneration after tooth extraction
 Persistence of fetal marrow
 Marrow hyperplasia in response to increased demand for erythrocytes

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4
Q

Focal Osteoporotic Defect common demo

A

75% adult females

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5
Q

Focal Osteoporotic Defect
 Clinical and Radiographic features:
 location?
 symptoms/expansion?
 radio app?

A

 70% posterior mandible, MC in edentulous areas
 Asymptomatic, nonexpansile
 Well-defined or ill-defined radiolucency

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6
Q

Focal Osteoporotic Defect
Histopathologic features:

A

 Cellular hematopoietic/fatty marrow

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7
Q

what bony lesion could this be? cystic lesion?

A

focal osteoporotic defect
borytiod cyst
OKC
odontogenic fibroma

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8
Q
A

focal osteoporotic defect
normal marrow with increased fat

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9
Q

dif dx (2)

A

focal osteo defect
traumatic bone cyst

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10
Q

Focal Osteoporotic Defect
 Treatment:

A

 Incisional biopsy indicated to establish diagnosis
 No further treatment needed after diagnosis established

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11
Q
A

focal osteo defect

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12
Q

Traumatic bone cyst

A

 Bone cavity that is empty or fluid-filled
 NOT a true cyst – no epithelial lining (pseudocyst)

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13
Q

traumatic bone cyst etilogy

A

 Trauma-hemorrhage theory

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14
Q

where can simple bone cysts occur

A

 Reported in most bones of the body

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15
Q

Traumatic bone cyst
 location?
 age?
 Pain and paresthesia?
 May exhibit?

A

 MC in mandible
 MC in young patients, peak in the second decade
 Pain and paresthesia infrequent
 May exhibit painless jaw swelling

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16
Q

Traumatic bone cyst
 Radiographic features:

A

 Well-defined, unilocular RL
 Occasionally ill-defined, multi-locular
 Range from 1-10 cm
 RL defect often scallops upward between roots of teeth
 Root resorption, cortical expansion infrequent

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17
Q

does root resorb occur with traumatic bone cysts

A

usually not

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18
Q

Traumatic bone cyst
 Treatment:
 Cavity contents
 resolution
 recurrence

A

 Surgical exploration and biopsy
 Cavity often empty, may contain serosanguinous fluid
 New bone formation, resolve after 1-2 years
 Low recurrence

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19
Q

Idiopathic osteosclerosis
(Dense bone island, Bone scar)
 Most arise when?

A

 Focally increased bone density of unknown cause
 Most arise in late 1st decade or early 2nd decade

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20
Q

Idiopathic osteosclerosis
 Clinical features:
 growth?
 symptoms/expansion?
 % location? fav tooth?

A

 May remain static or slowly increase in size
 Asymptomatic and nonexpansile
 90% occur in mandible, 1st molar MC

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21
Q

Idiopathic osteosclerosis
 Radiographic features:

A

 Well-defined radiopacity, 0.2 cm to 2.0 cm
 Nonexpansile

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22
Q

Idiopathic osteosclerosis
 Diagnosis:
 how can we rule against a neoplastic process?

A

 History, clinical features and radiographic findings
 Lack of cortical expansion and continued growth rule against a neoplastic process

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23
Q

Idiopathic osteosclerosis tx

A

 Periodic radiographs during adolescence

24
Q
A

idiopathic osteosclerosis

25
Q

dif app of dif opacities associated with apices:
COD
condensing osteitis
idiopathic osteosclerosis
cementoblastoma
hypercementosis

A

unlabled one: idio osteoscler

26
Q

Osteogenesis imperfecta
 Group of? characterized by?
 Worldwide prevalence?

A

 “Brittle bone disease”
 Group of heritable disorders characterized by osteopenia and bone fragility
 Worldwide prevalence of 6-7 per 100,000 population

27
Q

Osteogenesis Imperfecta
inheritence?
mutation to?
results?
categories?

A

 90% AD inheritance pattern
 Type I collagen gene mutations: COL1A1 and COL1A2
 Type I collagen: bone, dentin, sclerae, ligaments, skin
 Mutations result in abnormal type I collagen, low tensile strength
 Disease characterized as mild, moderate, severe

28
Q

OI clinical findings
 Bone injury?
 deformity in which bones commonly?
 Growth?
 sclerae?
 Hearing?
 Joints?

A

 Bone fractures
 Long bone, spine deformity
 Growth impairment
 Blue sclerae
 Hearing loss
 Joint hyperextensibility or contractures

29
Q

OI radiograph findings (systemic)

A

 Osteopenia
 Bowing deformity of long bones
 Multiple fractures
 Wormian bones (skull)
 Small sutural bones arranged in a mosaic pattern

30
Q

OI dental alterations
 Clinically and radiographically identical to?
 tooth color?
 wear on teeth?
 Tooth roots?
 malocclusions?

A

 Clinically and radiographically identical to dentinogenesis imperfecta
 Blue, yellow, brown translucence (primary and permanent)
 Severe attrition, loss of VDO
 Tooth roots narrow
 Class III malocclusion due to maxillary hypoplasia, crossbite, open bite

31
Q

Osteogenesis Imperfecta
 Diagnosis requires?
 Treatment

A

 Diagnosis requires correlation of the clinical features, radiographic and/or prenatal ultrasound findings, family hx
 Treatment: physiotherapy, rehabilitation, orthopedic surgery, IV bisphosphonates

32
Q

Osteopetrosis
 bone density?
 Failure of?
 result?

A

 Markedly increased bone density
 Failure of osteoclast function or differentiation
 Decreased bone resorption →sclerotic bone

33
Q

AD Adult Osteopetrosis
 commonality? severity?
what part of skeleton affected?
 Bone pain?
 dental implications?

A

 Most Common type, less severe manifestations
 Sclerosis affects axial skeleton, minimal involvement in long bones
 Bone pain frequent
 Increased risk of fracture and osteomyelitis following tooth extraction

34
Q

AD adult osteopetrosis radiogrpahs

A

Diffuse radiopacity of medullary bone

35
Q
A

osteopetrosis, no clear cortex and medulla for mandible

36
Q

Osteopetrosis
 Treatment:
 Adult osteopetrosis:s
 Infantile osteopetrosis:

A

 Adult osteopetrosis: management of disease complications
 Infantile osteopetrosis: Poor prognosis, Most patients die during 1st decade

37
Q

Cleidocranial Dysplasia
disorder of? abnormalities where?
 Mutation?
 May also have role in?
 Worldwide prevalence?

A

 Bone disorder, dental and clavicular abnormalities
 Mutations in RUNX2 gene: Osteoblastic differentiation, chondrocyte maturation
 May also have role in odontogenesis
 Worldwide prevalence: 1:1,000,000

38
Q

Cleidocranial Dysplasia
 Clinical Features:
 Clavicles?
 stature?
 skull?
 Ocular?
 nose?

A

 Clavicles: hypoplastic, 10% cases absent
 Approximate shoulders anteriorly
 Short stature
 Enlarged skull
 Ocular hypertelorism
 Broad-based nose

39
Q

Cleidocranial Dysplasia
 Radiographic features (skull)

A

 Skull radiographs: sutures and fontanels show delayed closure
 Wormian bones

40
Q

Cleidocranial Dysplasia dental findings

A

 Over-retained deciduous teeth
 Numerous unerupted permanent and supernumerary teeth

41
Q

Cleidocranial Dysplasia tx

A

 Removal of primary and supernumerary teeth
 Orthognathic surgery

42
Q

likely diagnosis?

A

clediocran dys

43
Q

Paget disease of bone
 mechanism
 result?
 demo?
 factors involved in pathgenesis

A

 Abnormal, anarchic resorption and deposition of bone
 Skeletal weakening
 Anglo-Saxon ancestry, highest rates in UK
 Genetic and environmental factors involved

44
Q

Paget disease of bone
 Clinical features:
 demo
 % present with bone pain
 Arises where?
 common locations?

A

 Older patients, rare in patients <40 years
 Male predilection
 40% present with bone pain
 Arises in one or more bones simultaneously
 Pelvis, femur, lumbar vertebrae, skull and tibia

45
Q

Paget disease of bone
 Clinical features:
 Affected bones app?
 Bowing?
 Skull involvement?

A

 Affected bones: thickened, enlarged, weakened →increased risk of fracture
 Bowing deformity
 Skull involvement: progressive increase in head circumference

46
Q

Paget disease of bone
 DENTAL Clinical features:
 Jaw involvement %
 Maxilla: mandible ratio
 Enlargement of?
 what vital structures can be obstructed/obliterated
 Severe cases?
 Alveolar ridges ca become?
 Dentures?

A

 Jaw involvement (17% patients)

 Maxilla: mandible (2:1):
 Enlargement of middle third of face
 Nasal obstruction, obliterated sinuses
 Severe cases: leontiasis ossea

 Alveolar ridges grossly enlarged: spacing between teeth
 Denture too small!

47
Q

Paget disease of bone
 Radiographic findings: early and late stages
 Generalized what can be observed at the teeth?

A

 Early stages: decreased radiodensity, course trabecular pattern

 Later stages: patchy areas of bone sclerosis: “cotton wool” appearance

 Generalized hypercementosis may be observed

48
Q
A

paget dx of bone, cotton wool pattern= late stage

49
Q

Paget disease of bone
 Diagnosis:
lab values?

A

 Correlation of clinical and radiographic findings
 Lab testing: elevated serum alkaline phosphatase levels

50
Q

Paget disease of bone
 Dental complications:
 extractions?
 hemorrhage?
 wound healing?
 Edentulous patients?

A

 Difficult extractions (hypercementosis/ankylosis)
 Extensive hemorrhage –vascular lytic phase
 Poor wound healing, osteomyelitis – avascular sclerotic phase
 Edentulous patients- provide new dentures periodically

51
Q

Paget disease of bone
 Disease progression?
 Malignant transformation?

A

 Disease is chronic and slowly progressive
 Malignant transformation: osteosarcoma <1%

52
Q

Paget disease of bone tx

A

 Bisphosphonate therapy – reduce bone turnover, decrease bone pain
 Orthotics, canes, orthopedic surgery

53
Q

Antral Pseudocyst
 Common finding on?
 Develops due to?
 Results in?

A

 Common finding on panoramic
 Develops due to an accumulation of inflammatory exudate
 Results in a sessile elevation

54
Q

Antral Pseudocyst
 Radiographic findings:

A

 Uniform, dome shaped faintly opaque lesion

55
Q

Antral Pseudocyst
 Treatment:

A

 No treatment if asymptomatic
 Symptomatic cases – endoscopic surgery

56
Q
A

antral pseudocyst

57
Q
A

antral pseudocyst

PATH II (32 decks)

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