ToB - bones Flashcards
describe the process of bone remodelling
osteoclast line front of cone (wide)
osteoclasts release H+ ions and lysosomal enzymes breaking down the bone
the empty surface left are then covered by osteoblasts which synthesise new bone by laying down osteoid
resulting in cone shape
describe bone repair
blood clot haematoma formed in which granulation tissue arises
procallus of granulation tissue forms
replaced by fibrocartilaginous callus in which bony trabeculae are developing
cancellous bone replaced by compact (cortical) bone
further bone remodelling
What happens in haematoma formation in bone fracture and repair?
blood vessel in bone and periosteum break
haematoma forms
bone cells at the fracture edge die
swelling and inflammation occur
phagocytic cells and osteoclasts remove dead and damaged tissue
macrophages eventually remove blood clot
what happens in fracture repair stage?
new blood vessels infiltrate
procallus of granulation tissue (tissue rich in capillaries and fibroblasts) develops
fibroblasts produce collagen fibres other differentiate into chondroblasts that form hyaline cartilage
this splints the broken bone - fibrocartilaginous callus
what happens in bony callus formation?
new bony trabeculae appear
develop into hard callus of cancellous bone
endochondral ossification replaces all cartilage (temporary for structure)
from 2 days to 2 months until a very firm union is formed
what happens in bone remodelling?
bone remodelled into compact bone
bulging removed by osteoclasts
what is intramembranous ossification? where does it occur? which type of cells? (appositional growth)
occurs mainly in flat bones e.g. skull bones, pelvis & clavicle to thicken bones
originally, there is membrane of primitive mesenchymal tissue
mesenchymal cells differentiate into osteoblasts which synthesis matrix
what happens in endochondral ossification?
replacement of hyaline cartilage template with bone
the way which most (long) bones develop
the growth plates in the femur disappear after cessation of growth
describe the process of bone development from hyaline cartilage (embryo)
- formation of bone collar around hyaline cartilage model
- primary ossification centre forms in the diaphysis of the bone
- nutrient artery enters via the primary ossification centre supplying osteoblasts laying down osteoid
- the primary ossification centre ossifies (medulla cavity)
- secondary ossification centres appear (epiphysis) and have their own blood vessels
- secondary ossifications calcify leaving only growth plates (hyaline) and articular cartilage (ends of long bones)
where is growth hormone synthesised and stored?
anterior pituitary
what happens before puberty? excess and insufficient GH?
excess GH causes gigantism through promotion of epiphyseal growth plate
insufficient can affect the epiphyseal cartilage and cause pituitary dwarfism
what happens in an adult if there is excess GH? what is it called?
increase bone width by promoting periosteal growth (around bone) called acromegaly
which hormones induce secondary sexual characteristics? what do they give rise to
androgens (males) and oestrogens (females)
give rise to pubertal growth spurt
what is precocious sexual maturity? where does the hormone come from and what does it lead to?
sex hormone producing tumours
retards bone growth because of premature fusion of epiphyses
what happens if there is a deficient sex hormone?
lead to tall stature
epiphyseal plates keep growing longer, prolonged bone growth
what happens in osteoporotic bone and osteomalacial bone?
osteoporotic: decreased bone mass
osteomalacial: lack of vit D –> lack of Ca2+ –> bone not mineralised
what is osteogenesis imperfecta?
autosomal dominant
disorder of CT (type I collagen)
often leads to fractures (especially as infant begins to sit and walk)
bones thin and abnormally curved
sclerae thin and blue (type 1)
affects hearing (cartilage in pinna of ear, eustachian tube, external acoustic meatus)
growth retardation - short
describe the process of vitamin D hydroxylation
vit D: some is dietary but most from lack of UV
vit D hydroxylated in kidneys then liver (vit D –> calciferol –> calcitriol (active)
forms 1,25 dihydroxyvitamin D3
this increases Ca2+ absorption by the small bowel
promotes mineralisation of bone
lack of vit D = lack of mineralisation of bone = bones don’t harden
what is rickets and osteomalacia?
caused by vit D deficiency
rickets in children
in rickets bones do not harden as there is insufficient calcium deposition, so bones become soft and malformed (especially skull and ribs)
lack of vit D –> non-mineralisation of spongy bone –> fracture
what is osteomalacia?
osteomalacia in adults - vit D deficiency
osteomalacia causes less severe symptoms e.g. back pain & muscle weakness
large amount of non-mineralised bone on trabecular surface, leads to fractures
what is osteoporosis? what is used to treat? how does the treatment work?
loss of bone density, increased risk of fracture
common in elderly and post menopausal (due to effect of oestrogen withdrawal)
bisphosphonate used to treat, which inhibit osteoclastic activity
what is achondroplasia? what causes it? - underlying defect, what does it lead to?
achondroplastic dwarfs have a normal lifespan and mental ability
decreased endochondral ossification (lengthening of bone)
chondrocyte mitosis inhibited within the growth plate cartilage
less cell hypertrophy (enlargement)
decreased cartilage matrix production (from chondrocytes)
limbs are short
80% due to a new mutation
homozygous is fatal e.g. dd or DD
what is cancellous / spongy bone?
no haversian or volkmann's canals osteocytes lying between lamellae interconnecting trabeculae (causes mesh) osteocytes within, osteoblasts (deposit osteoid) & osteoclasts on the surface to remodel
describe compact bone, what is in it? how do they exist?
the Haversian and Volkmann’s canals carry blood vessels, lymph vessels and nerves through bone
Haversian canals travel in the centre of osteons, IN LINE with interstitial lamellae
Volkmann’s connect Haversian canals across the lamellae
