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
