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
acromegaly?
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
acromegaly affects the jaw?
* 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
PAGET'S DISEASE OF BONE?
* Disorganized formation and remodelling of bone. * Disfunction of osteoclasts.
28
three stages of paget's disease of bone?
* Osteolytic phase. - bone resorbed * Mixed osteolysis and osteogenesis. - still bone resorption and bone deposition * Osteoblastic (sclerotic) phase. - bone formation, stay in deformed shape
29
what starts the osteolytic phase of pagets disease?
overactivation of osteoclasts
30
epidemiology of pagets disease?
* 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
clinical presentation of Paget's disease?
* 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
Paget's disease more common in the maxilla or mandible?
maxilla
33
bones most commonly affected by Paget's disease?
Bony deformities of the weight bearing bones, skull and facial bones.
34
palate shape in paget's disease?
flat
35
paget's disease cause complication in extraction?
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
radiographic appearance of paget's disease?
* 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
what is shown here?
cotton wool appearance mixed phase in paget's disease
38
what is shown here?
paget's disease bone sclerosis has occured Thickening of the cortical plates of the skull. * Loss of the lamina dura, hypercementosis and ankylosis.
39
histopathology of osteolytic phase of paget's disease?
* Osteoclastic resorption. * Resorbed areas are filled with cellular and vascular fibrous marrow.
40
what phase of pagets disease could have excessive bleeding?
stage 1 osteolytic phase
41
histopathology of mixed phase in paget's disease?
* Osteoclastic activity continues. * Formation of bone within the fibrous marrow. * Remodelling and further bone formation. * Reversal lines (mosaic appearance).
42
histopathology of sclerotic phase in paget's disease?
* Trabiculae join to form dense sclerotic masses of mosaic bone. masses of bone fused together - sclerotic bone now
43
what is shown?
mixed phase in paget's disease mosaic appearance reversal lines
44
how to diagnose paget's disease?
* 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
management of paget's disease?
* 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
wy do you need to be aware of pt with paget's disease?
MRONJ management is often bisphosphonates
47
epidemiology of central giant cell granuloma?
* Second and third decades. * Female predominance. * Mandible more frequently than maxilla. * Anterior parts of the jaws.
48
cause of central giant cell granuloma?
unknown could be a disturbance in bone remodelling reaction to haemodynamic disturbance in bone marrow associated with trauma or haemorrhage?
49
Is Central Giant Cell Granuloma a tumour?
no, it is a granuloma
50
features of Central Giant Cell Granuloma?
* Second and third decades. * Female predominance. * Mandible more frequently than maxilla. * Anterior parts of the jaws.
51
Is Central Giant Cell Granuloma rapid or slow growth?
rapid - can be alarming to pt can perforate bone in oral mucosa - appear as red or brown swelling
52
Clinical presentation of Central Giant Cell Granuloma?
* Swelling of bone, rapid growth. * Could present as a brown or red swelling that perforates the cortex in the alveolus. * Could be symptomless.
53
what disease is shown?
Central Giant Cell Granuloma
54
radiographic appearance of central giant cell granuloma?
* Well defined radiolucency. * Thinning, expansion and sometimes perforation of the cortex. * Might be multilocular. * Displacement of teeth. * Resorption of roots.
55
disease shown?
Central Giant Cell Granuloma
56
disease shown?
Central Giant Cell Granuloma
57
name the giant cell
58
what disease is shown?
Central Giant Cell Granuloma
59
histopathology of Central Giant Cell Granuloma?
* 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
management of Central Giant Cell Granuloma?
* 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.