Metabolic bone disease: Histopathology Flashcards
What is the composition of bone
85% hydroxyapatite-stores calcium, sodium, magnesium
35%-organic-cells + protein matrix (osteoblasts/clasts/cytes)/collagen
Bone greography
End part-epiphysis
Kuckle looking part-condyles-betwee have trochlea
articular cartilage Under-subchondral bone
Epiphesys join diaphysis at metaphysis (where the growth plate is)-epiphyseal line separates
Diaphysis-shaft-outside is compact bone (coritcal bone) +periosteum out of that
then medullar bone cavity inside (trabecular)
WHat are the 5 anatomical types of bone? How can each be classified?
anatomical definition Flat/Long/Short/Cuboid/irregular (pelivs) /sesamoid
Macroscopic structure-trabecullar/cancellous (spongy)+cortical (compact)
Microscopic structure-Woven bone (immature) and lamellar bone (mature)
What is the difference between cortical and cancellous bone?
Cortical-long bones-80% of skeleton-appendicular-90% clacified-structural-not very metabolic active
Organised with parallel osteons (concentric lamellae around central aversion canals (blood vessels))-also circumferential lamellae (all around the bone) and interstitial lamellae
Has many osteocytes canaliculi network
More inwards find trabecular bone-not organised
Cancellous-vertebear and pelivus-20% of skeleton-lot lower calcification-very metabolic active-renewal often
What is the main difference between woven and lamellar bone?
Mature lamellar bone-organised as the osteons etc
Woven bones-not organised-usually found in growing/early skeleton
BUT can also be present in places with high turnover/rapid growths/breaks
What are the 3 cell types of bones?
Osteocytes-90% of bone cells-live very long and act as brain
Osteoblasts-produce osteoid to make new bone
Osteoclasts-multinucleated cells that resorb bone
Describe the bone remodelling cycle
Osteocytes control the osteoclast production by producing M-CSF and RANKL-
When an osteocytes dies-release RANKL-making osteoclasts differentiate and come to lesion-resorb to the right place (where damage)-and that is then stoppedand osteoblasts come in, lay osteoid down for new bone to be formed
Why would you perform a bone biopsy? How? Where?
Need direct histopathological evidence to:
confirm diagnosis, find cause of bone pain
Abnormalities on Xray, bone tumour, determine the cause of unexplained infection and therapy perfomance-
Easy to do but slight infection risk
Closed biopsy-noral-Jamshidi needle-core into bone
Open-sclerotic/abnormal bones-then open surgery needed
if non general-Usually taken from illiac crest -a 5cm core where you can see all 3 types of bone easy
What are the different thing you do once you have a bone sample?
H&E stain -normal-seperate bone/cartilage/cells/etc (nuclei blue and ECM-pink)
more specific-Masson stain (mineralised vs not (orange))
Tetracycline/Calcein (measure rate of bone turnover-create fluorescent line at exterior of bone-then inject again few days later-second line-and then measure how much grew between the two lines)
What is the definition of metabolic bone disease
Disease that cause reduce bone mass and stength
Due to imbalance of various chemcials in the body
altered bone cell activity-rate of mientalisation and changes in bone structure
What is osteoporosis? Main causes? What types are there?
Defined as bine mineral density-T-score under 2.5 (BMD more than 2SD away from average)
primary: No external causes: ages/post-menopause
Secondary-external causes-drugs/systemic disease, etc
Usually happens because higher resorbtion than creation
but can happen to be High turnover (both very high but one higher than other) or low turnover (both low-but still imbalance)
What bones type tends to be affected by osteoporosis? How does it look histologically?
usually trabecular bone because more metabolicatlly active-weaken the structure
Will look thinner, less of it, and find some pieces just floating around
looking as the amount of unminralised bone around-can tell if high turnover vs low turnover
What is osteomalacia? What types are there? How does it look histopathologically?
Defective mineralisation of normally synthesised bone matrix (osteoid) (rickets in children(
2 types-deficiency is Vitamin D OR deficiency in PO4
(vit D important-increase Ca absorb in intestine and Kidney)
Masson stain-HUGE orange areas-unmineralised bone
easy tos ee
Bone pain/tenderness
Factures, weakness, deformity
In children-widening of the bones-arced legs because of deformation
Also causes fractures in Loosers zones (high tension areas)-fracture 90 degrees from the lamellar organisation
What is hyperparathyroidism? Different types? Main symptoms? Histophathology
Excess PTH-
Cause release of Ca from stores of bone/increase intestine intake-all to rise serum Ca (and normally Ca then downregulates PTH-if not then bad)
Cause increase Ca+PO4 excretion in urine
Cause hypercalceamia and hypophosphatemia
primary-parathyroid adenoma / chief cell hyperplasia
Secondary-chronic renal disease (inability to excrete PO4 or make VitD)
Symptoms: Stones (kidney, etc), Bones (now rarer-happens later in disease), ABdominal groans (acute pancreatitis) and psychic moans (psychosis)
Fibrosa cystica-large cysts replace bone-fibrious tissue with very large cells in them-called brown cell tumour
What is Renal osteodystriphy?
Comprise all the skeletal changes resulting from CKD-
Fibrosa cystica, Osteomalacia, sclerosi, growth retardation, osteoporosis
Inability to excrete PO4 and make Vit D
