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WEEK 24:
Bone 2- bone development, growth, and repair:
| Question | Answer |
|---|---|
| types of bone formation/ development in the embryo (2) | intramembranous and endochondral |
| both intramembranous and endochondral involve | replacing a connective tissue template |
| intramembranous bone development | involves sheets of mesenchymal cells which differentiate into osteoblasts in centres of ossification and merge to form trabecular bone that is remodelled. Remaining mesenchyme cells make bone marrow and periosteum. |
| endochondral bone development | cartilage template where blood supply to bone shaft causes osteoblast differentiation in primary centre of ossification. At birth, blood supply goes to epiphysis starting secondary centres of ossification. Cartilage growth plate remains so bone lengthen |
| bone growth in the epiphyseal end | proliferation |
| bone growth in diaphyseal end | chondrocytes mature and die and are replaced by bone |
| bone growth in long bones | bone grows in length via epiphyseal growth plate |
| when do long bones fuse | adulthood |
| other bones (apart from long bones) grow by | coordinated appositional growth at periosteum and resorption at inner surface, where long bones gain circumference by this method |
| humerus appearance | proximal epiphysis gestation occurs week 36 months- 4 years and distal epiphysis occurs 6 months- 10 years |
| humerus fusion | proximal epiphysis 12-20 years and distal epiphysis 11-19 years |
| femur appearance | proximal epiphysis 1-12 years and distal epiphysis gestation week 36-40 |
| femur fusion | proximal epiphysis 11-19 years and distal epiphysis 14-19 years |
| when does proximal epiphysis gestation occur in humerus | week 36 - years |
| when does distal epiphysis gestation occur in humerus | 6 months - 10 years |
| when does proximal epiphysis fusion occur in humerus | 12-20 years |
| when does distal epiphysis fusion occur in humerus | 11-19 years |
| proximal epiphysis gestation in femur occurs | 1-12 years |
| distal epiphysis gestation in femur occurs | 36-40 years |
| proximal epiphysis fusion in femur occurs | 11-19 years |
| distal epiphysis fusion in femur occurs | 14-19 years |
| describe the ossification of carpal bones | predictable sequence starting with capitate and ending with pisiform |
| describe calcification in carpal bones at birth | no calcification |
| when does the capitate and hamate ossify | 4 months |
| when does the triquetral ossify | 3 years |
| when does the lunate ossify | 4 years |
| when does the scaphoid, trapezium and trapezoid ossify | 6 years |
| when does the pisiform ossify | 11 years |
| achondroplasia | congenital bone disease (dwarfism) caused by mutation on the fibroblast growth factor receptor 3 activation which inhibits chondrocyte proliferation affecting growth plates |
| activation of the fibroblast growth factor receptor 3 (FGFR3) does what | inhibits chondrocyte proliferation affecting growth pates |
| features of achondroplasia | lordosis, bowed legs and stunted extremities (especially proximal) |
| bone contributes to calcium homeostasis under the influence of (3) | PTH, calcitonin, and vitamin D |
| what does calcitonin do | calcitonin (thyroid C cells) decreases blood calcium |
| what happens in a bone fracture and repair | periosteum broken -> haematoma (blood clot) -> replaced by vascular collagenous (granulation) tissue -> becomes more fibrous (fibrous granulation tissue) -> replaced by hyaline cartilage (form provisional callus) -> cells make bony callus -> lamellar bone |
| what happens first when bone is fractured | periosteum is breached and haematoma/ blood clot forms |
| haemtoma (blood clot) in bone fracture is replaced by | vascular collagenous tissue (granulation tissue) which becomes increasingly fibrous (fibrous granulation tissue) |
| vascular collagenous tissue (granulation tissue) becomes increasingly fibrous becoming | fibrous granulation tissue |
| fibrous granulation tissue is replaced by | hyaline cartilage (making firm flexible provisional callus) |
| osteoprogenitor cells from perio and endosteum differentiate into | osteoblasts which lay down new woven bone making bony callus |
| when does bony callus form | when osteoprogenitor cells from perio and endosteum differentiate into osteoblasts which lay down new woven bone |
| bony union | site completely bridged by bone |
| final stage of bone fracture and repair | the bony callus/ bony union is slowly remodelled to form orientated lamellar bone |
| metabolic bone disease result from | imbalance between bone formation and resorption |
| simple flowchart of bone fracture and repair | haematoma (blood clot) -> granulation tissue -> fibrous granulation tissue -> provisional callus -> bony callus -> bony union -> lamellar bone |
| four main diseases caused by metabolic bone disease | osteoporosis, rickets and osteomalacia, paget's disease, and hyperparathyroidism |
| osteoporosis | increased bone erosion and loss of bone mass due to imbalance of osteoblasts and osteoclasts leading to thinner trabeculae initially and then thinned cortical bone where bone tissue is normal. Fracture risk |
| osteomalacia | lack of vitamin D leads to inadequate mineralisation of bone making it weak and soft where osteoid is normal, leading to bowing of bones and bone pain |
| pagets disease | overactive osteoclasts which destroy bone and result in osteoblasts responding by laying down immature woven bone rapidly - this increases bone mass but it is weak. High energy demands of disease lead to metabolic consequences |
| hyperparathyroidism | increase osteoclast activity as a result of increased levels of PTH due to renal disease/ tumour leading to the destruction of cortical and trabecular bone. There is inadequate compensation by osteoblasts leading to loss of bone mass and fracture risk |
| osteoid | organic unmineralised matrix of bone |
| causes of osteoporosis (5) | old age, post menopausal decrease in oestrogen, disuse and reduced activity, prolonged steroid use (especially in rheumatoid arthiritis), and some endocrine disease (Cushing's syndrome) |
| diagnosis of osteoporosis (3) | asymptomatic pre-fracture, serum ALP + Ca + Pi levels are unreliable, 30-40% reduction in bone mass |
| how does osteoporosis need to be seen | radiologically with no marked numbers of osteoclasts on histology/ need sensitive DEXA scan |
| clinical outcomes of osteoporosis (3) | pathological fractures due to falls in elderly, back pain and kyphosis due to compression fractures, hip replacements due to fractured neck of femur |
| treatment of osteoporosis (4) | prevention (diet and exercise), bisphosphonates, oestrogen receptor agonists, and PTH |
| what disease is in mature bones | osteomalacia |
| what disease is seen in growing bones | rickets |
| describe osteomalacia and rickets | normal osteoid architecture of bone but failure of correct mineralisation of osteoid leading to soft bones (cortical and trabecular) |
| cause of osteomalacia and rickets | lack of vitamin D as vitamin regulates calcium metabolism |
| how does renal failure lead to osteomalacia and rickets | dietary/sunlight/malabsorption affect conversion of vitD in kidney |
| symptoms of osteomalacia and rickets | bone pain (pelvis, back, legs), and if untreated- bowing of legs |
| early signs in children of osteomalacia and rickets | swelling of epiphysis of bones (wrist) and along costochondral cartilage of ribs |
| diagnosis of osteomalacia and rickets uses | x ray and labs showing low serum vitamin D |
| treatment of osteomalacia and rickets (2) | supplementation and advice on prevention |
| explain the defects in calcium metabolism leading to hyperparathyroidism | normally increased PTH secretion means osteoclasts are stimulated to resorb bone and calcium is released into plasma and feedback to reduce PTH secretion- but there is failure of feedback |
| types of hyperparathyroidism | primary and secondary |
| primary hyperparathyroidism | tumour causing elevated serum calcium |
| secondary hyperparathyroidism | low serum calcium caused by renal disease (excessive loss via abnormal kidneys) causing hyperplasia of parathyroid glands |
| pagets disease | excessive bone resorption by osteoclasts followed by haphazard bone formation and laying down immature woven bone (not related to stress but poor architecture) resulting in potential increase in bone mass that is structurally weak |
| explain metabolic demand in pagets disease | high due to excessive bone turnover |
| bone pain in pagets disease | 80% in axial skeleton and proximal femur, and consequences of nerve impingement (headaches, back pain) |
| pagets disease has an increased risk of | osteosarcoma (bone cancer), nerve compression, or pathological fracture and, high metabolic demand can cause heart failure |
| pagets disease affects up to | 10% of population in europe and US (mostly mild cases) |
| examples of structures made from intramembranous bone formation | flat bones, skull, maxilla, and mandible |
| examples of structures made from endochondral bone formation | long bones and base of skull |
| primary centre of ossification in endochondral bone formation | blood supply to shaft of bone (causing osteoblast differentiation) |
| secondary centre of ossification in endochondral bone formation | at birth, blood supply to epiphysis |
| cartilage growth plate remains from endochondral bone formation to | allow bone to lengthen |
Created by:
kablooey
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