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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
dif app of dif opacities associated with apices: COD condensing osteitis idiopathic osteosclerosis cementoblastoma hypercementosis
unlabled one: idio osteoscler
26
Osteogenesis imperfecta  Group of? characterized by?  Worldwide prevalence?
 “Brittle bone disease”  Group of heritable disorders characterized by osteopenia and bone fragility  Worldwide prevalence of 6-7 per 100,000 population
27
Osteogenesis Imperfecta inheritence? mutation to? results? categories?
 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
OI clinical findings  Bone injury?  deformity in which bones commonly?  Growth?  sclerae?  Hearing?  Joints?
 Bone fractures  Long bone, spine deformity  Growth impairment  Blue sclerae  Hearing loss  Joint hyperextensibility or contractures
29
OI radiograph findings (systemic)
 Osteopenia  Bowing deformity of long bones  Multiple fractures  Wormian bones (skull)  Small sutural bones arranged in a mosaic pattern
30
OI dental alterations  Clinically and radiographically identical to?  tooth color?  wear on teeth?  Tooth roots?  malocclusions?
 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
Osteogenesis Imperfecta  Diagnosis requires?  Treatment
 Diagnosis requires correlation of the clinical features, radiographic and/or prenatal ultrasound findings, family hx  Treatment: physiotherapy, rehabilitation, orthopedic surgery, IV bisphosphonates
32
Osteopetrosis  bone density?  Failure of?  result?
 Markedly increased bone density  Failure of osteoclast function or differentiation  Decreased bone resorption →sclerotic bone
33
AD Adult Osteopetrosis  commonality? severity? what part of skeleton affected?  Bone pain?  dental implications?
 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
AD adult osteopetrosis radiogrpahs
Diffuse radiopacity of medullary bone
35
osteopetrosis, no clear cortex and medulla for mandible
36
Osteopetrosis  Treatment:  Adult osteopetrosis:s  Infantile osteopetrosis:
 Adult osteopetrosis: management of disease complications  Infantile osteopetrosis: Poor prognosis, Most patients die during 1st decade
37
Cleidocranial Dysplasia disorder of? abnormalities where?  Mutation?  May also have role in?  Worldwide prevalence?
 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
Cleidocranial Dysplasia  Clinical Features:  Clavicles?  stature?  skull?  Ocular?  nose?
 Clavicles: hypoplastic, 10% cases absent  Approximate shoulders anteriorly  Short stature  Enlarged skull  Ocular hypertelorism  Broad-based nose
39
Cleidocranial Dysplasia  Radiographic features (skull)
 Skull radiographs: sutures and fontanels show delayed closure  Wormian bones
40
Cleidocranial Dysplasia dental findings
 Over-retained deciduous teeth  Numerous unerupted permanent and supernumerary teeth
41
Cleidocranial Dysplasia tx
 Removal of primary and supernumerary teeth  Orthognathic surgery
42
likely diagnosis?
clediocran dys
43
Paget disease of bone  mechanism  result?  demo?  factors involved in pathgenesis
 Abnormal, anarchic resorption and deposition of bone  Skeletal weakening  Anglo-Saxon ancestry, highest rates in UK  Genetic and environmental factors involved
44
Paget disease of bone  Clinical features:  demo  % present with bone pain  Arises where?  common locations?
 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
Paget disease of bone  Clinical features:  Affected bones app?  Bowing?  Skull involvement?
 Affected bones: thickened, enlarged, weakened →increased risk of fracture  Bowing deformity  Skull involvement: progressive increase in head circumference
46
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?
 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
Paget disease of bone  Radiographic findings: early and late stages  Generalized what can be observed at the teeth?
 Early stages: decreased radiodensity, course trabecular pattern  Later stages: patchy areas of bone sclerosis: “cotton wool” appearance  Generalized hypercementosis may be observed
48
paget dx of bone, cotton wool pattern= late stage
49
Paget disease of bone  Diagnosis: lab values?
 Correlation of clinical and radiographic findings  Lab testing: elevated serum alkaline phosphatase levels
50
Paget disease of bone  Dental complications:  extractions?  hemorrhage?  wound healing?  Edentulous patients?
 Difficult extractions (hypercementosis/ankylosis)  Extensive hemorrhage –vascular lytic phase  Poor wound healing, osteomyelitis – avascular sclerotic phase  Edentulous patients- provide new dentures periodically
51
Paget disease of bone  Disease progression?  Malignant transformation?
 Disease is chronic and slowly progressive  Malignant transformation: osteosarcoma <1%
52
Paget disease of bone tx
 Bisphosphonate therapy – reduce bone turnover, decrease bone pain  Orthotics, canes, orthopedic surgery
53
Antral Pseudocyst  Common finding on?  Develops due to?  Results in?
 Common finding on panoramic  Develops due to an accumulation of inflammatory exudate  Results in a sessile elevation
54
Antral Pseudocyst  Radiographic findings:
 Uniform, dome shaped faintly opaque lesion
55
Antral Pseudocyst  Treatment:
 No treatment if asymptomatic  Symptomatic cases – endoscopic surgery
56
antral pseudocyst
57
antral pseudocyst

PATH II (32 decks)

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