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BDS3 Oral Pathology > Bone Pathology II - Metabolic endocrine disorders > Flashcards

Bone Pathology II - Metabolic endocrine disorders Flashcards

1
Q

name metabolic endocrine disorders?

A
  • Osteoporosis
  • Primary hyperparathyroidism
  • Secondary hyperparathyroidism
  • Rickets and osteomalacia
  • Acromegaly
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2
Q

osteoporosis?

A

reduction in bone density

Excessive bone loss or reduced deposition

bone is a dynamic tissue

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3
Q

who is more likely to have osteoporosis?

A
  • Post menopausal women (1-2% of bone mineral a
    year).
  • Rate of mineral loss is twice as fast in women
    compared to men.
  • Increased bone loss in Cushing syndrome,
    thyrotoxicosis and primary hyperparathyroidism.
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4
Q

risk factors of osteoporosis?

A

alcohol abuse and steroid therapy.

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5
Q

diseases associated with osteoporosis?

A

Cushing syndrome,
thyrotoxicosis and primary hyperparathyroidism.

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6
Q

radiographic appearance of osteoporosis?

A
  • Increased radiolucency.
  • Thinned cortex.
  • Increased marrow spaces in the cancellous
    bone.
  • Thin trabiculae.
  • Jaws may become involved.
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7
Q

parathyroid hormone role?

A

Your parathyroid gland releases parathyroid hormone (PTH) when your body detects low calcium levels in your blood.

increase bone resorption by activation of osteoclasts

increased vitamin D - increase amount of calcium the gut can absorb

increased ca absorption in the kidneys and intestine

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8
Q

who is more likely to have primary hyperparathyroidism?

A

middle-aged women

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9
Q

cause of primary hyperparathyridism?

A

carcinoma

hyperplasia

adenoma

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10
Q

what does primary hyperparathyroidism result in?

A

hypercalcaemia (blood)

hypercalciuria (urine)

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11
Q

what does increased calcium result in?

A
  • Hypercalcaemia and
    hypercalciuria…
  • Pathologic metastatic
    calcifications.
  • Urinary calculi and
    calcification of blood vessel
    walls and lungs.
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12
Q

histopathology of primary hyperparathyroidism?

A

bone resorption due to osteoclast activation to release calcium

  • Focal areas of bone resorption.
  • Brown tumours: multinucleate osteoclast-like giant cells in a highly cellular vascular fibroblastic connective tissue stroma.
  • Haemosiderin Pigment.
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13
Q

what does Primary Hyperparathyroidism look similar to under the microscope?

A

cherubism

multinucleated giant cells

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14
Q

why is primary hyperparathyroidism called brown tumour?

A

lost of blood

have haemosidorin - breakdown product of blood

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15
Q

radiographic appearance of primary hyperparathyroidism?

A
  • No changes.
  • Osteoporosis.
  • Partial loss of the lamina dura.
  • Brown tumours: sharply defined radiolucencies.
  • More frequent in the mandible.
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16
Q

Why does secondary hyperparathyroidism occur? (3)

A
  • Response to chronic hypoclacaemia.
  • Chronic renal failure.
  • Rickets and osteomalacia
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17
Q

secondary hyperparathyroidism in children?

A

rickets

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18
Q

secondary hyperparathyroidism in adults?

A

osteomalacia

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19
Q

why does osteomalacia/rickets occur?

A

deficiency or resistance to vit D

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20
Q

risk factors to vit D deficiency?

A
  • Lack of exposure to sunlight, dietary causes.
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21
Q

does rickets and osteomalacia affect ca absorption?

A

yes

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22
Q

how does rickets and osteomalacia affect ca absorption?

A
  • Impaired calcium absorptiopn (wholemeal grains containing phyates). absorption in the gut
  • Renal failure, calcium malabsorption.
  • Failure of calcification of osteoid and cartilage.
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23
Q

histopathology of rickets/ osteomalacia?

A
  • Trabiculae contain wide
    areas of uncalcified
    osteoid.

curved bones

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24
Q

dental abnormalities related to rickets/osteomalacia?

A
  • Enamel hypoplasia.
  • Increased width of
    predentine.
  • Large amounts of interglobular dentine.
  • Delayed tooth eruption.
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25
Q

acromegaly?

A

gigantism in adulthood

  • Excessive secretion of growth hormone after the
    closure of epiphyses.
  • Growth of jaws, hands and feet bones.
  • Growth of some soft tissues.
26
Q

acromegaly affects the jaw?

A
  • Activation of the condylar growth centre in the
    mandible.
  • Mandible becomes enlarged and protrusive with
    spacing of present teeth.
  • Nose and lips become thickened and enlarged

MALOCCLUSION

27
Q

PAGET’S DISEASE OF BONE?

A
  • Disorganized formation and remodelling of bone.
  • Disfunction of osteoclasts.
28
Q

three stages of paget’s disease of bone?

A
  • Osteolytic phase. - bone resorbed
  • Mixed osteolysis and osteogenesis. - still bone resorption and bone deposition
  • Osteoblastic (sclerotic) phase. - bone formation, stay in deformed shape
29
Q

what starts the osteolytic phase of pagets disease?

A

overactivation of osteoclasts

30
Q

epidemiology of pagets disease?

A
  • Over 40 years.
  • Differences in the geographical incidence.
  • Monostotic or polystotic.
  • Weight bearing bones.
  • Sacrum, lumbar, thoracic and cervical vertebrae,
    followed by the skull and femur.
  • Maxillary lesions more common than mandibular.
31
Q

clinical presentation of Paget’s disease?

A
  • Bony deformities of
    the weight bearing
    bones, skull and facial
    bones.
  • Mild in most cases.
  • Bone pain.
  • Sensory or motor
    disturbances due to
    cranial nerve
    compression.
  • Maxillary enlargement
    leads to thickening of the
    alveolar ridge and
    flattening of the palate.
  • Incompetence of the
    lips.
  • Derangement of
    occlusion.
  • Dentures - pt say dont fit anymore die to enlargement of alveolar tissue
  • Hypercementosis.
  • Root resorption.
  • Post extraction
    haemorrhage.
  • Avascular bone (prone to infection)
32
Q

Paget’s disease more common in the maxilla or mandible?

A

maxilla

33
Q

bones most commonly affected by Paget’s disease?

A

Bony deformities of
the weight bearing
bones, skull and facial
bones.

34
Q

palate shape in paget’s disease?

A

flat

35
Q

paget’s disease cause complication in extraction?

A

sclerotic disease - excess bone formation

leads to…

  • Hypercementosis
    leading to ankylosis of teeth

bone formed fuses with cementum

difficult to extract

reduced blood supply - lead to infections

if pt taking bisphosphonates even more bone resorption

36
Q

radiographic appearance of paget’s disease?

A
  • Varies with the stage of the disease.
  • Appearance ranges from radiolucent to mixed to
    radiopaque.
  • Cotton wool appearance.

3 phases

  1. radiolucent
  2. mixed radiolucency/radiopacity - cotton wool
  3. hypercementosis and sclerosis
37
Q

what is shown here?

A

cotton wool appearance

mixed phase in paget’s disease

38
Q

what is shown here?

A

paget’s disease

bone sclerosis has occured

Thickening of the cortical plates of the skull.

  • Loss of the lamina dura, hypercementosis and
    ankylosis.
39
Q

histopathology of osteolytic phase of paget’s disease?

A
  • Osteoclastic resorption.
  • Resorbed areas are filled with cellular and
    vascular fibrous marrow.
40
Q

what phase of pagets disease could have excessive bleeding?

A

stage 1

osteolytic phase

41
Q

histopathology of mixed phase in paget’s disease?

A
  • Osteoclastic activity continues.
  • Formation of bone within the fibrous marrow.
  • Remodelling and further bone formation.
  • Reversal lines (mosaic appearance).
42
Q

histopathology of sclerotic phase in paget’s disease?

A
  • Trabiculae join to form dense sclerotic
    masses of mosaic bone.

masses of bone fused together - sclerotic bone now

43
Q

what is shown?

A

mixed phase in paget’s disease

mosaic appearance

reversal lines

44
Q

how to diagnose paget’s disease?

A
  • Clinical presentation
  • Radiography
  • Blood chemistry:

The serum calcium and phosphorus levels
are usually within normal limits but the serum
bone alkaline phosphatase level is often
raised, sometimes markedly so in patients with
widespread active disease.

45
Q

management of paget’s disease?

A
  • Once diagnosed, Paget’s disease of bone can
    be controlled using bisphosphonate drugs.
  • Medication- related osteonecrosis of the jaw
    (MRONJ) may follow invasive dental procedures
    in patients with Paget’s disease.
46
Q

wy do you need to be aware of pt with paget’s disease?

A

MRONJ

management is often bisphosphonates

47
Q

epidemiology of central giant cell granuloma?

A
  • Second and third decades.
  • Female predominance.
  • Mandible more frequently
    than maxilla.
  • Anterior parts of the jaws.
48
Q

cause of central giant cell granuloma?

A

unknown

could be a disturbance in bone remodelling

reaction to haemodynamic
disturbance in bone marrow associated with trauma or
haemorrhage?

49
Q

Is Central Giant Cell Granuloma a tumour?

A

no, it is a granuloma

50
Q

features of Central Giant Cell Granuloma?

A
  • Second and third decades.
  • Female predominance.
  • Mandible more frequently
    than maxilla.
  • Anterior parts of the jaws.
51
Q

Is Central Giant Cell Granuloma rapid or slow growth?

A

rapid - can be alarming to pt

can perforate bone in oral mucosa
- appear as red or brown swelling

52
Q

Clinical presentation of Central Giant Cell Granuloma?

A
  • Swelling of bone, rapid growth.
  • Could present as a brown or red swelling that perforates
    the cortex in the alveolus.
  • Could be symptomless.
53
Q

what disease is shown?

A

Central Giant Cell Granuloma

54
Q

radiographic appearance of central giant cell granuloma?

A
  • Well defined radiolucency.
  • Thinning, expansion and sometimes
    perforation of the cortex.
  • Might be multilocular.
  • Displacement of teeth.
  • Resorption of roots.
55
Q

disease shown?

A

Central Giant Cell Granuloma

56
Q

disease shown?

A

Central Giant Cell Granuloma

57
Q

name the giant cell

A
58
Q

what disease is shown?

A

Central Giant Cell Granuloma

59
Q

histopathology of Central Giant Cell Granuloma?

A
  • A large number of
    multinucleate osteoclast like
    giant cells. Arranged in
    aggregates or scattered.
  • Vascular stroma.
  • Small spindle shaped cells
    (precursors of giant cells,
    fibroblasts and endothelial
    cells).
  • Extravasated RBCs and
    haemosiderin.
  • Trabiculae of osteoid or bone.
60
Q

management of Central Giant Cell Granuloma?

A
  • Intra- osseous giant cell granulomas respond well to
    injection of steroids, sometimes after curettage.
  • Impossible to distinguish histologically from a focal lesion
    of hyperparathyroidism, which must be excluded by
    biochemical investigations (serum calcium and alkaline
    phosphatase) when a giant cell lesion is diagnosed on
    biopsy.

BDS3 Oral Pathology (31 decks)

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