Bone Pathology II - Metabolic endocrine disorders Flashcards
1
Q
name metabolic endocrine disorders?
A
- Osteoporosis
- Primary hyperparathyroidism
- Secondary hyperparathyroidism
- Rickets and osteomalacia
- Acromegaly
2
Q
osteoporosis?
A
reduction in bone density
Excessive bone loss or reduced deposition
bone is a dynamic tissue
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.
4
Q
risk factors of osteoporosis?
A
alcohol abuse and steroid therapy.
5
Q
diseases associated with osteoporosis?
A
Cushing syndrome,
thyrotoxicosis and primary hyperparathyroidism.
6
Q
radiographic appearance of osteoporosis?
A
- Increased radiolucency.
- Thinned cortex.
- Increased marrow spaces in the cancellous
bone. - Thin trabiculae.
- Jaws may become involved.
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
8
Q
who is more likely to have primary hyperparathyroidism?
A
middle-aged women
9
Q
cause of primary hyperparathyridism?
A
carcinoma
hyperplasia
adenoma
10
Q
what does primary hyperparathyroidism result in?
A
hypercalcaemia (blood)
hypercalciuria (urine)
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.
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.
13
Q
what does Primary Hyperparathyroidism look similar to under the microscope?
A
cherubism
multinucleated giant cells
14
Q
why is primary hyperparathyroidism called brown tumour?
A
lost of blood
have haemosidorin - breakdown product of blood
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.
16
Q
Why does secondary hyperparathyroidism occur? (3)
A
- Response to chronic hypoclacaemia.
- Chronic renal failure.
- Rickets and osteomalacia
17
Q
secondary hyperparathyroidism in children?
A
rickets
18
Q
secondary hyperparathyroidism in adults?
A
osteomalacia
19
Q
why does osteomalacia/rickets occur?
A
deficiency or resistance to vit D
20
Q
risk factors to vit D deficiency?
A
- Lack of exposure to sunlight, dietary causes.
21
Q
does rickets and osteomalacia affect ca absorption?
A
yes
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.
23
Q
histopathology of rickets/ osteomalacia?
A
- Trabiculae contain wide
areas of uncalcified
osteoid.
curved bones
24
Q
dental abnormalities related to rickets/osteomalacia?
A
- Enamel hypoplasia.
- Increased width of
predentine. - Large amounts of interglobular dentine.
- Delayed tooth eruption.
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.
