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Oral Pathology Exam 6 > Bone Pathology I > Flashcards

Bone Pathology I Flashcards

1
Q

What are the categories of Osteodystrophy

A
  1. Genetic Diseases
  2. Metabolic Diseases
  3. Others or unknown causes
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2
Q

What Osteodystrophic diseases are considered genetic diseases

A 
Osteogenesis imperfecta
Osteoporosis
Cleidocranial Dysplasia
Cherubism
Hypophosphatasia
Vitamin D-resistant rickets
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3
Q

What Osteodystrophic diseases are considered metabolic diseases

A

Rickets
Steomalacia
Hyperparathyroidism
Renal osteodystrophy

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4
Q

What Osteodystrophic diseases are classified as either others or unknown causes

A 
Paget's disease of bone
Fibrous dysplasia
Aneurysmal bone cyst
Idiopathic osteosclerosis
Focal osteoporotic bone marrow defect
Bisphosphonate-associated osteonecrosis of jaw
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5
Q

Most common inherited bone disease

A

Osteogenesis imperfecta

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6
Q

Pathology of Osteogenesis imperfecta

A

Mutations in collagen type I

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7
Q

Symptoms and presentation of Osteogenesis imperfecta

A 
Bone fragility and deformity
Joint hyper extensibility
Hearing loss
Blue sclera
\+-opalescent teeth (dentinogenesis imperfecta)
  • Abnormal collagen result in bones with a thin cortex and osteoporosis which are soft and prone to fracture.
  • Bones characterized by bowing, angulation and deformity
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8
Q

Describe the different forms and inheritability of Osteogenesis imperfecta

A

Type I-IV
Autosomal dominant or recessive
- Severity varies

Rare form with florid cemento-osseus dysplasia

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9
Q

Management of Osteogenesis imperfecta

A

Physiotherapy
Orthopedic therapy
Bisphosphonates, IV or oral, for more severe patients but long term outcome in pediatric patients unknown

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10
Q

What is Osteopetrosis (Marble bone disease)

A

Defect in osteoclast function

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11
Q

Describe the genetic inheritance of infantile osteopetrosis

A

Autosomal recessive

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12
Q

Characteristics of infantile osteopetrosis

A

Severe
Sclerotic skeleton
Marrow failure (anemia, hepatosplenomegaly, osteomyelitis)
Facial deformity
Neurological deficit (paralysis, blindness, deafness)

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13
Q

Describe the genetic inheritance of Adult osteopetrosis

A

Autosomal dominant

- Mild, 40% asymptomatic

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14
Q

Dental considerations for Osteopetrosis

A

Jaws affected
Although bones denser, they are more fragile
Fractures
Fracture and osteomyelitis after both extraction

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15
Q

Management of Infantile osteopetrosis

A

Prognosis poor

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16
Q

Management of Adult osteopetrosis

A

Variable prognosis, some long term survival

  • Bone marrow transplantation
  • Other experimental protocols
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17
Q

What is Cleidocranial Dysplasia

A

Defect of differentiation of osteoblasts and a subset of chondrocytes caused by mutations

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18
Q

Describe the genetic inheritance of Cleidocranial dysplasia

A

Autosomal dominant or somatic mutation

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19
Q

Clinical characteristics or features of Cleidocranial Dysplasia

A 
Short stature
Frontal bossing
Patent fontanels
Late closure of cranial sutures
Absence or hypoplasia of the clavicles
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20
Q

Dental characteristics of Cleidocranial Dysplasia

A

Retention of deciduous teeth
Delayed eruption of permanent teeth
Supernumerary teeth
+- narrow high arched plate

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21
Q

Prognosis and management of Cleidocranial Dysplasia

A
  • Prognosis good and no treatment for the developmental bone disorder
  • Dental treatment planning based on clinical findings
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22
Q

What is the genetic inheritability of Cherubism

A

Autosomal dominant or spontaneous mutation

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23
Q

Clinical characteristics of Cherubism

A

Bilateral post. mandibular painless swelling
Maxillary swelling push the orbital base upward
Upturned eyes
Rounded eyes

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24
Q

When is cherubism most common?

A

Average 7 y/o (14 months - 12 y/o)

Progress until puberty then slowly regress

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25
Q

Radiographic features of Cherubism

A
  • Radiolucency
  • Usually multilocular
  • Bilateral of posterior mandible
  • Often from mandibular notch on one side to contralateral side
  • Usually with maxillary involvement also
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26
Q

Histopathology of Cherubism

A

Giant cell granulomas

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27
Q

What is the natural history of Cherubism

A

stabilization around puberty and often regression

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28
Q

What is hypophosphatasia

A

Mutations of non-specific alkaline phosphatase (liver-, bone-, or kidney-type)

29
Q

What is the genetic inheritability of Hypophosphatasia

A

Variable degrees of expression

- Autosomal dominant or recessive

30
Q

Clinical characteristics of Hypophosphatasia

A
  • Reduces levels of ALP in liver, bone, kidney, intestine and serum
  • Increased levels of blood and urinary phosphor-ethanolamine
  • Bone abnormalities similar to rickets

Dental: Premature loss of primary (or permanent) teeth due to lack of cementum

31
Q

What is the genetic inheritability of Vitamin D-resistant Rickets (Hereditary hypophosphatemia)

A

X-linked dominant trait
severity varies

Caused by mutations

32
Q

Clinical characteristics of Vitamin D-resistant Rickets

A
  • Decreased reabsorption of phosphate from renal tubules
  • Decreased intestinal absorption of calcium
  • Hypophosphatemia
  • Shortened lower body segment?

Dental:

  • Large pulp horns extending to DEJ
  • Cleft in dentin
  • Periodical abscess
33
Q

Vit D deficiency during infancy = ?

A

Rickets

34
Q

Vit D deficiency during adulthood = ?

A

Osteomalacia

35
Q

Describe the clinical characteristics of Rickets

A

Growth retardation
Prominence of the costochondral junctions
Bowing of the legs

36
Q

Describe the clinical characteristics of Osteomalacia

A

Weak bone
Fractures
Diffuse skeletal pain

37
Q

Describe Primary Hyperparathyroidism

A

Parathyroid adenoma (80-90%) or hyperplasia

38
Q

Demographics of Primary Hyperparathyroidism

A

> 60 y/o

Increase in females

39
Q

Pathology of Primary Hyperparathyroidism

A

Increase in PTH = Increase bone resorption = increase serum Ca

40
Q

Describe Secondary Hyperparathyroidism

A

Secondary to chronic renal disease

  • Vitamin D Activation in kidney decreases
  • Absorption of calcium in intestine decreases
  • Serum calcium decreases = PTH increases
41
Q

Clinical characteristics of Hyperparathyroidism

A
  • Stones, bone and abdominal groans
  • Kidney stones, calcifications in b.v.
  • Subperiosteal resorption of the phalanges of the fingers
  • Loss of lamina dura
  • Ground glass trabecular pattern
  • Brown tumor (radiolucency)
  • Renal osteodystrophy (secondary hyperpara)
  • Duodenal ulcers
  • Histo of brown tumor: indistinguishable from central giant cell granuloma
42
Q

What is Renal Osteodystrophy

A

Complication of secondary hyperparathyroidism in end-stage renal stage

  • Enlargement of the jaws
  • Radiography: Ground glass pattern
  • Histology: fibre-osseous lesion
43
Q

Describe Paget’s disease of bone

A

Accelerated resorption and deposition of bone

- ultimately osteoblasts win and bones become sclerotic, larger and brittle

44
Q

Demographics of Paget’s disease of bone

A

Geographic variance in prevalence
White
Male predominant
Older than 40 yrs

45
Q

Clinical characteristics of Paget’s disease of bone

A

Monostotic but increased Polyostotic

  • Bone pain
  • Deformity
  • Weakened bone
  • Can be asymptomatic
46
Q

Etiology of Paget’s disease of bone

A

Paramyxovirus infection;

Genetic factor

47
Q

Radiographic features of Paget’s disease of bone

A

Well defined RL –> Mixed RL/RO –> Cotton wool-like RO

Generalized hypercementosis

48
Q

How to diagnose Paget’s disease of bone

A
  • Clinical
  • Radiographic
  • Laboratory (increase alk phosphatase; usually normal Ca, increase urinary hydroxyproline)
  • Scintigraphical findings
49
Q

Complications of Paget’s disease of bone

A

Fracture

Malignant transformation

50
Q

What is Fibrous dysplasia

A
  • A postzygotic mutation
  • Bones become replaced with fibrous tissue and immature bone

Gene encodes stimulatory G protein alpha subunit, activates adenylyl cyclase –> cAMP, Affects differentiation of preosteoblasts, prolonged activation stimulates endocrine receptors

51
Q

Anatomic distribution of Fibrous Dysplasia

A

80-85% Monostotic
Polyostotic
Craniofacial
Polyostotic with café au lait spots (Jaffe-Lichtenstein syn. )
Polyostotic with café au lait spots (McCune-Albright Syn.)

52
Q

Clinical features and demographics of Fibrous Dysplasia

A
  • 1-2 decades
  • equal in males and females
  • Long bone: pain and fracture
  • Craniofacial: expansion and disfigurement, crosses suture lines
  • Craniofacial involved about 1/3
  • CFFD may compress vital structures
  • Optic nerve compression may result in blindness
53
Q

McCune-Albright Syndrome

A

Somatic mosaicism accounts for clinical diversity

  • Hyperendocrine function: > gonads, thyroid
  • Sexual precocity, > girls
  • Café au last spots within first two years, irregular margins
  • Polyostotic, > long bones, CFFD in 1/4
  • CFFD morbidity assoc with > GH
54
Q

Radiographic features of Fibrous Dysplasia

A
  • Early lesions radiolucent –> mixed –> ground glass opacity
  • Margins blend
  • cortical expansion
  • cortical reaction absent
55
Q

Demographic and locations of Central Giant Cell Granuloma

A

Female > Male
Before 30 years of age
70% in mandible
Anterior jaws and classically crosses the midline

56
Q

Clinical features of Central giant Cell granuloma

A

Nonaggressive
- Asymptomatic, Slow growth, no cortical perforation or root resorption

Aggressive
- Pain, rapid growth, cortical perforation and root resorption

57
Q

Radiographic features of Central giant Cell Granuloma

A

Unilocular to multilocular radiolucency
Margins tend to be noncorticated
+- Cortical perforation or expansion
+- Root resorption

58
Q

What is an Aneurysmal Bone Cyst

A

An intraosseous accumulation of variable-sized, blood-filled spaces surrounded by cellular fibrous tissue with giant cells

59
Q

Demographics of Aneurysmal Bone Cysts

A

Most common in long bones or vertebrae
2% in jaws
Children and young adults

60
Q

Clinical features of Aneurysmal bone cyst

A

Rapid swelling, pain

Unilocular or multi-locular RL

61
Q

Radiographic findings of Aneurysmal bone cyst

A

Radiolucent, unilocular but > multilocular
Cortex often expanded and thinned or perforated
Borders can be well defined or diffuse

62
Q

Demographics of Idiopathic Osteosclerosis

A

Blacks, Chinese, Japanese
No gender predilection
90% in Md, > 1st molar
80% contact tooth root

63
Q

Clinical features of Idiopathic Osteosclerosis

A

Characteristically no pain or expansion
Rarely root resorption
Easily confused with condensing osteitis but tooth is VITAL

64
Q

Radiographic findings of Idiopathic Osteosclerosis

A

Well defined radiopacity, may be asymmetric
Typically without a radiolucent halo but blends
80% contact a tooth root
Occasionally show root resorption
Diagnosis can usually be made on clinical and radiographic features

65
Q

What is Focal Osteoporotic Bone Marrow defect

A

An asymptomatic radiolucent lesion

66
Q

Demographics of Focal Osteoporotic Bone Marrow defect

A

Middle aged females
- theory: secondary to low grade anemia

70% in posterior mandible
Often at site of previous extraction

67
Q

Radiographic findings of Focal Osteoporotic Bone Marrow defect

A

radiolucency often with fine internal trabeculation

68
Q

Diagnosis of Focal Osteoporotic Bone Marrow defect

A

Incisional biopsy may be necessary to establish diagnosis

Oral Pathology Exam 6 (5 decks)

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