Bones Flashcards
Fatigue in bones
With increasing loading and unloading cycles there is a change in modulus of elasticity, meaning that there is increases strain for same amount of stress (more compliant). With even more increases in loading the bone does not even return to starting point meaning some deformation is permanent.
The same concept is evident when strain is kept constant, the amount of stress to deform the bone to a certain point decreases as loading cycles increases.
Both show the bone accumulating damage (macrostrains)
Inorganic and organic components of bone
Bones act as a calcium reservoir which the body can withdraw from
Organic - mostly collagen (flexibility)
Inorganic - Calcium and phosphate (brittleness and strength)
Cortical vs trabecular bone internal organisation
Cortical - Very high stiffness, important as it requires more stress to causes strain (acts as lever for muscle)
Trabecular bone - more of a shock absorber as it is easier to deform elastically. Low resistance to stress but high resistance to strain.
Bone organisation
ECM - bone matrix (hardened), large proteins and proteins that bind material (calcium bind proteins), collagen fibres and water
Cellular - osteoblast (secret non mineralised matrix on surface of bone called osteoid), osteoclast, osteocytes
Periosteum - connective tissue membrane outside of bone
Endosteum - lines internal surface
Osteon - in compact bone these are long cylindrical structures with central canals filled with vessels.
Bone remodelling
Bone tissue is form and then remodelled throughout life, most prominent in teenage years in the growth spurt where temporary bone needs to be placed down quite fast.
What controls bone resorption
Two main hormones:
- Parathyroid hormone (PTH)
- Enhanced release of Ca2 from bone
- Indirectly stimulates osteoclast activity to cause bone resorption
- Calcitonin
- Inhibits Ca2 absorption in the intestines and inhibits renal tubular cell resorption from urine (promoting excretion)
- Inhabits osteoclast activity and promotes bone retention
Changing bone morphology
Growth - Intramembranous ossification (within membrane) or endochondral (within cartilage)
Modelling - Formation of new bone or resorption of bone, changes shape
Remodelling - Resorption and formation occur togther!!, linked in one event at the same location. Periodically replaces bone.
Chondrogenesis and endochondral ossification
Chondrogenesis is formation of cartilage (hyaline used in bone growth). Chondroblast make cartilage. Periosteal bud will invade into cartilage and bring blood vessels and osteoprogenitor cells to form a ossification centre. Cartilage is replaced by bone.
Large bones will repeat this process multiple times resulting in several ossification centres. First one to form (middle) is primary while others are secondary. Cartilage left between these forms growth plats which are regions of highly active growth that will be replaced by bone in adults.
What happens in a growth plate
Allow bone to grow in length, joint can remain functional while bone is growing. Bone already exists and want to add more, cartilage is avascular meaning diffusion to site of growth is needed (growth plate cant be too long or this cannot occur causing death)
Intramembranous ossification
- Connective tissue contains mesenchymal cells that develop into osteoblast
- They lay down areas of woven bone, remodelled into lamellar and trabecular bone
- Cortical bone forms around outside
Clavicle, skull vault and facial bones are formed by this method
Cells involved in bone growth
Matrix of bone comprises mostly of collagen 1
Mesenchymal stem cells - Differentiate into osteoprogenitor cells on periosteal and endosteal surfaces
Osteoprogenitor cells - Give rise to osteoblasts
Bone lining cells - derived from osteoblasts, regulate movement of calcium into and out of bone, may activate osteoclasts, help maintain osteocytes. Seen on periosteal and endosteal surfaces
Osteoblast - can either become trapped in osteoid and turn into osteocytes or remain on surface of bone as bone lining cells
Osteocytes - monitor and maintain bone matric. When they are resorptive they secret MMPs (matrix metalloproteinase enzyme). This degrees bine matrix around cell in a process called osteocytic osteolysis. This may function in calcium and phosphate ion homeostasis
Osteoclasts - eating cells, eat bone matric to resorb bone.
Bone numbers in children vs adults
Initially children have more bones than adults. Mostly due to growth plates which separate ossification centers and are counted as separate bone.
During early childhood and through to mid adult hood increases demands of force application on skeletons are matched with ability to adapt. Later in life as exercise decreases also a reduction in skeletons ability to met this demand.
What is bone modelling
Allows bone to change in proportion and shape
Bone remodelling
Resorption and formation are linked together
Activation -> resorption ->formation progression (ARF)
Osteoclasts are recruited and activated (dig a trench like hole), dissolved the bone matrix to resorb the bone. After a short time osteoblast are recruited and lay down new osteoid (formation).
This process occurs on the surface
Haversian systems
Remodelling process that doesn’t occur on the surface Microdamage can accumulate in the cortical bone of the shaft.
Follows the same ARF progression
1. Osteoclasts form a cutting cone (bore out a tunnel through existing bone)
2. After short period of time osteoblasts will in from outwards inward (closing cone). Between cutting and closing cones there is reversal zone where resorption and bone formation are coupled together
3. Note that the endosteal cells line the final central canal
This process normally always occur along long axis of bone and take about 4 months from start of cutting to closing cone has secondary osteons
Intracortical remodelling (trabecular)
Formed from struts of bone, similar to surface remodelling in the sense that a trench is dug via osteoclast and osteoblasts fill it with new osteoid.
2 main reason for bone remodelling
Calcium demands - if not enough from diet than can get from Skelton
Micro damage - Targeted intracortical remodelling can target microdamage to ensure it is replaced
Bone adaptation
Tensile loading can cause thickening to areas on the bone that resist that loading. While shear loading can causes increase in diameter but same thickness of cortical bone (increase J).
Bone adaptation
Mechanotransduction is the reason this can occur.
Bone cells react to changes in their environment, particularly strain. They cannon monitor stress directly because they cannot collectively monitor the area over which stress is being applied, but they can individually monitor the stretch in themselves.
Machotransduction occurs in 4 phases when bone is concerned:
- Mechanocoupling - force applied generates a strain affecting the cells within bone
- Biochemical coupling - biochemical response in cells
- Transmission of signal from sensory cell to effector - transmission from cells that sense strain to those that can act
- Effector cell response - cell generates response to strain
Bone loss
When loading if removed then bone is lost.
Osteoblast activity and number is decreased while osteoclast number remained unchanged with major loading change such as astronauts.
Bone gain
Bone mineral content only increased slightly while bone strength and energy required to fracture the bone increased drastically. Also bone was laid down on the side of the bone under tension
Same amount of loading is more effective over shorter periods separated by rest periods rather than all at once when new bone formation is considered.
Rest is important as the cells that detect loading become desensitised after a period of repeated loading. Rest allows them to recover their sensitivity so they can induce formation.
Acute bone failure
Risk of fractures with age - women rise before males due to onset of menopause (post menopause bone mineral density drops due to lower oestrogen)
Remember the pre discussed trade off on bone strength and how expensive they are for the body. Net result is we have bone that are strong enough to withstand forces in daily life as well as some additional loading on top.
Can quantify this as a safety factor. Shows that bones are build not just for everyday life but they have an extra capacity for excess loading.
Fatigue loading - bone failure
Repeated loading and stress lower than failure stress can cause micro damage. Concept of fatigue.
Bone is loaded repeated within the elastic region meaning deformation was not permanent after unloading. Eventually there is a slow and progressive loss of stiffness and the bone will eventually fail.
Protecting bone against micro damage
Cortical bone
Repair - intercortical remodelling, too much simultaneous repair can weaken the bone
Structural - organisation of bone into lamella (layers) within osteons can resist crack propagation, arrangement of collagen fibrils in the bone matrix
Trabecular bone
Will accumulate damage with repeated compression and the horizontal and vertical vertebra can split (can be repaired through remodelling)
Ageing of skeleton
Bone mineral density decreases with ageing after about 20 years. Women also have a second sudden decrease after menopause. Bone mass also follows a similar trend.
Remodelling causes this, with each cycle of remodelling more bone is lost then is laid down again. In women the remodelling loss is sped up by loss of oestrogen after menopause.
