Lecture 18 - Bone Function & Repair Flashcards
What are the mechanical, synthetic and metabolic functions of bone?
Mechanical = protect important organs, provide overall framework for human body and form basis of levers involved in movement.
Synthetic = Haemopoiesis (holds and protects red bone marrow)
Metabolic = mineral storage (Ca2+ and PO4), fat storage, acid-base homeostasis
What are the 2 types of ossification, what types of growth do they display + what kind of bones are grown from these types?
1) Endochondral ossification - formation of long bones from a cartilage template, continued lengthening by ossification at epiphyseal growth plates (appositional growth) - growth at edges
2) Intra-membranous ossification - formation of flat bone from clusters of mesenchymal stem cells in the centre of bone (interstitial growth) - growth from the middle out
What are the main differences between endochondral and intra-membranous ossification?
Intramembranous takes place within condensation of mesenchymal tissue, endochrondral by replacement of hyaline cartilage template.
Intramembranous ossification contributes to bone thickening of long bones, at their periosteal surfaces (appositional growth) - rather than lengthening.
Intramembranous ossification growth occurs from in to out, the central point is the primary ossification centre.
Intramemranous ossification of long bones produce immature bone that undergoes remodelling into mature bone.
What is the difference between immature and mature bone?
- Immature bone has osteocytes in random arrangements
- Mature bone has osteocytes arranged in lamellae of osteons.
- Resorption canals in mature bone run parallel with osteons’ long axis.
Which one of compact or cancellous bone contains Haversian’s and Volkmann’s canals?
What do these structures do?
- compact/cortical bone HAVE them
- cancellous/spongy bone do NOT HAVE them
- They carry blood vessels, lymph vessels and nerves - to Osteon units of compact/cortical bone.
Why does bone have great tensile and compressive strength?
Lamallae within cortical bone are able to slip relative to each other to resist fracture - although excessive load can still cause fractures.
What are the main factors affecting bone stability?
- Mostly activity of osteoblasts (bone deposition) and osteoclasts (bone resorption), however osteocytes have some ocsteoblast/clast activity too.
- Other important factors include nutrition - Vit D, Vit C and Vik K and B12.
Describe the 4 stages of bone repair after a fracture occurs.
1) Blood clot (haematoma) is formed in which granulation tissue arises, causing swelling and inflammation, eventually removed by macrophage. Tissue dies due to lack of oxygen.
2) Fibrocartilaginous callus is formed, first a procallus of granulation tissue is replaced by a fibrocalliganous (soft) callus in which bony trabeculae are developing.
3) Bonus callus formation - endochondral (replaces cartilage with cancellous bone) and intramemranous ossification (produces new cancellous bone in any gaps) give rise to a bony (hard) callus of spongy/cancellous bone.
4) Cancellous bone replaced by compact cortical bone until remodelling is complete
What is the genetic basis of Osteogenesis imperfecta?
What are the clinical features?
Who does it mainly affect?
- Mutation in COL1A (collagen type 1) gene, leading to incorrect production of collagen 1 fibres.
- Weak bones, increased risk of fracture, shortened stature, blue sclera
- Neonates + children
What is rickets caused by?
What are the clinical symptoms?
- Vit D deficiency, leading to poor Ca2+ mobilisation and ineffective mineralisation
- Leads to soft bones, shortened heigh, bow legs, pain while walking
NB: Rickets in adults is called Osteomalacia.
What are the 2 main divisions of osteoporosis?
What is each one due to?
1) Primary - can be type 1, which occurs in postmenopausal women, due to increased osteoclast number (as there is a loss of oestrogen which keeps osteoclast number under control) or type 2, which occurs in the elderly, due to loss of osteoblast function (due to loss of oestrogen/androgen)
2) Secondary - result of drug therapy (corticosteroids), is a major risk factor for bone fracture in elderly.
NB: Osteoporosis is the incomplete filling of osteoclast resorption bays - therefore remodelling of trabeculae by osteoclasts resorption and osteoblast deposition doesn’t occur properly.
What are 3 modifiable risk factors for osteoperosis?
1) Insufficient Ca2+ intake
2) Exercise - immobilisation of bone leads to accelerated bone loss, physical activity is required
3) Cigarette smoking
What is Achondroplasia caused by?
What does it consequently affect?
What does it result in?
- Inherited mutation in the FGF3 receptor gene
- FGF promotes collagen formation from cartilage, therefore endochondral ossification affected (but not intramembranous).
- Results in short stature, but normal sized head and torso (long bones cannot lengthen properly, e.g.: femur!)
