fractures through the ages Flashcards
why do bones have trabeculae *
so that they have structural support but are not too heavy
thicker the trabeculae = better the bone density
as the structure deteriorates - get more fragile = fractures
descibe the composition of bones *
cells and matrix
matrix has organic and inorganic parts
- organic mucopolysaccharides, non-collagenous proteins and collagen - main component is type 1 collagen
- inorganic - ca and phosphorus (hydroxyapetite) - bone has 99% of the body’s Ca it is a resevoir
cells
- osteoprogenitors - can differentiate into the other cell types
- osteocytes - trapped in the trabeculae and oversee homeostasis
- osteoblasts - make bone so lower Ca in blood and make bone thicker
- osteoclasts break down bone and let it into the periphery
describe normal bone turnover *
each year 5% of the bones are remodelled so dont get stress cracks and fractures
this is monitored by osteocytes
osteoclasts dominate when bone turnover goes wrong = osteoporosis
describe the diagnosis of osteoporosis *
DEXA scan
measure BMD to figure out if people are going to get fractures
not a good measure because it doesnt look at the quality of the trabeculae
done by firing 2 different X rays of different energy lengths through the lumbar, hip and distal radius (areas that tend to get fragility fractures)
get T score - compare bone mass to someone the same ethnicity and gender at 25 and see how many SD the person’s bone mass is from that
- 1-2.5 SD less is osteopenia
- >2.5 less is osteoporosis - bone mass is significantly reduced so should have treatment to prevent fractures
what are the groups that are at risk of osteoporosis *
post menopausal women
amputee group - because of Wolff’s law - they put no load through their bones (easier to load through cut tibia than cut femer) and have lost muscle insertions so they dissolve - this is mechanostat theory - muscle pulls bone and in amputees you ave lost this so not getting the stimulus so not getting bone being layed down, also artificial leg takes the load through the pelvis rather than the femer
what should the treatment be for amputees with osteoporosis *
to load the joint and be active - they have a localised loading response
describe the mechanism of bisphosphonates *
kill osteoclasts either by toxic ATP analogue, or interfering with cholesterol pathway
they stop the imbalance between osteoclasts and osteoblasts
what are the problems with bisphosphonates *
the T1/2 is 7yrs
they stop the remodelling of bone so microcracks are not repaired and you get atypical fractures eg through shafts - have normal thick cortices but dead bone
repairing of fractures is difficult because there are no osteoblasts
in repair you can form meshes that you expect the bone to grow into - if they are on bisphosphonates they cant do this
describe the mechanism of denosumab *
osteoclasts have RANK on them
RANKL is secreted by the osteoblasts - stimulate the progenitor osteoclasts to differentiate into osteoclasts
denosumab is a monoclonal Ab that binds to RANKL so osteoclasts are not active
they have a short half life
are expensive
what are the complications of hip fractures *
high mortality risk and financial cost
not just because of fracture - can be sign of decline in medical state - elderly people who have other medical conditions
describe the developmental origin of peak bone mass *
children lay down bone prepubesently - therefore should give high impact exercise prepuberty and encourage children to drink full fat milk
if you dont fill Ca store to max in childhood, you are at risk later in life
max bone mass depends on diet, exercise, natural aging process and the ability to absorb certain things, vit D
people with osteoporosis are told to drink Ca so that there is more free Ca available for other functions - it wont be put into bone
osteoporosis happen in menopause, andropause, prostate problems and other things where there is an imbalance of hormones
should older people stop stairs *
no - need to continue doing deep flexion - stimulate the neck of femer growth
describe ca homeostasis *
vit D and PTH increase ca level in blood
calcitonin decrease ca levels
PTH/vit D stimulate osteoclasts and Ca resorption in PCT and phosphorus excretion
calcitonin causes excretion of Ca
can take in Ca from gut from fish and some veg
describe production of active vit D *
UV turns cholesterol into Vit D3
then hydroxylsed in liver = 25-hydroxycholecalciferol
then hydroxylsed in liver = 1,25-hydroxycholecalciferol
describe the fracture healing process *
- wk1 blood pools in to fracture - haev haemotoma of blood - clot, pro-healing inflammatory molecules are present - macrophages, leukocytes, IL1-6, BMBs, granulation tissue forms, progenitor cells invade
- wk2-3 blood is replaced by soft callus type of cartilage - stabalises the bone and stops it moving
- wk4-16 have hard callus - callus is calcified to bone - this is wovern bone - strong but disorganised so not as strong as normal bone
- wk17 and beyond - wolff’s law means the compression at the edge of the woven bone is reinforced and the bit in the middle is resorbed by osteoclasts
