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30 Cards in this Set
- Front
- Back
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What is the term for the temporary group of cells that remodel cancellous and cortical bone?
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"Basic multicellular unit" - BMU
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What are the two types of of remodelling and where do they occur?
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osteonal remodelling - cortical bone
hemiosteonal remodelling - cancellous bone |
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What are the two major physiological roles of bone remodelling?
Why is this a constant/continuous occurrence? |
1. repair microcracks (plus preventative maintenance)
2. calcium homeostasis This is constant because calcium balance is very critical to human survival, we do NOT have time to wait for the bone remodelling process to initiate and produce enough calcium to fix low calcium crises. Therefore always remodel and just change speed in one or more areas to adjust for calcium imbalance. |
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Describe the stages involved in cortical bone remodelling.
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0. Activation
1. resorption at "cutting cone" (osteoblasts get called in and dig a tunnel) **blood vessels in this tunnel are essential as they supply nutrients to cells and constantly bring in new osteoclast precursors (from mesenchymal cells) since they die by apoptosis after a week and it takes months to remodel portion of bone) 2. reversal until "closing cone" (as cell type changes to osteoblast the tunnel narrows, resorption stops) 3. formation (the more bone (osteoid that gets calcified) that is formed by osteoblasts, the narrower the tunnel becomes until only an haversian canal is left) -- CREATING CONCENTRIC LAMELLAE/OSTEONS THAT COMPOSES CORTICAL BONE 4. resting (no growth or resorption) with bone lining cells on top |
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How does cancellous bone remodelling look compared to cortical and what are the stages.
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It is half of the tear drop shape as this bone has holes.
1. resorption 2. reversal 3. formation 4. resting |
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Use one important descriptor of how bone is formed throughout the body. What does this tell us about how bone remodelling is controlled?
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asynchronous (occurring at various stages throughout the body) This tells us that remodelling is under LOCAL control.
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What are three triggers for bone formation?
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1. microfracture
2. increase load 3. low calcium |
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Describe how bone remodelling is similar to the inflammation response.
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#1 THEY ARE BOTH UNDER THE CONTROL OF CYTOKINES
injury: tissue damage or microfracture reaction: WBC, macrophage OR osteoclast come to resolve the immediate issue repair: mesenchymal cells OR osteoblasts replace lost tissue (fibrous scar formation OR bone formation) |
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Describe how aspirin interferes with bone formation.
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Aspirin reduces prostaglandins to reduce signalling of (pain or inflammation or fever?) but also impairs signalling required for bone formation and repair. (CYTOKINE SIGNALLING)
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Describe TWO WAYS OF how the coupling process works with respect to bone formation when bone resorption occurs TO MAKE SURE THERE IS A BALANCE BETWEEN LOSS AND GAIN OF BONE. (eg. how do we know how much to lay down?)
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1. As bone is resorbed by osteoclasts recruited by cytokines due to micro fracture or otherwise, growth factors are released from bone matrix (put there by osteoblasts when bone laid down) to recruit osteoclasts! (more resorbtion = more GF released = more osteoblasts called in = more bone made)
2. As osteocytes resorb bone, bone becomes weakened and bends. Osteocytes in bone sense this stress and signal (to surface) to recruit osteoblasts to lay down bone |
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Define osteoporosis.
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A systemic skeletal disease characterized by low bone mass and micro architectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture. (BONE ATTACK > deadly)
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Describe the alterations in bone remodelling with osteoporosis.
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Less estrogen, less activation of GH, less cell proliferation so less bone formation, thinner, brittle bones
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Describe the changes in bone remodelling in Paget's disease (second most common bone disease).
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Localized increase in osteoclastic resorption PLUS compensatory increase in bone formation. But, because its occurring so fast, bone is formed in a disorganized fashion. Unknown cause. HIGH TURNOVER! |
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Hyperparathyroidism How common is this and what type of disease is it (not bone)? What is the cause? Describe the changes in bone remodelling in hyperparathyroidism. |
Third most common endocrine disorder
Cause: benign tumor |
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Describe the diurnal variation in bone remodelling activity and WHY.
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There is MORE bone RESORPTION at NIGHT because bone is resorbed by OSTEOCLASTS and osteoclasts are activated by PTH and PTH is released in response to low calcium. At night calcium is low because we are not eating.
1. sleep therefore not eating 2. low calcium 3. activate PTH 4. activate osteoclasts 5. resorb bone to increase calcium |
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Bone is a mosaic of bone that was formed at different times (different ages of bone) BUT NORMALLY, healthy bone will be laid down to maintain the same:
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structure, mass, density, and shape of original bone
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What happens when there is an estrogen deficiency?
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bone resorption takes over because estrogen normally increases GH which increases cell devision and therefore bone formation. This weakens the bone, changes the structure and makes the person more prone to fractures
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Why is bone loss permanent?
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Because you cannot form bone from nothing. You need bone to resorb for the remodelling process.
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Why is OP such a serious disease?
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Because it actually kills people. After first OP, death is likely within 5 years...?
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List 3 most common OP fractures.
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1. hip
2. spine 3. wrist |
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Describe bone mass over the life span and how it corresponds with fracture risk .
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You build bone until approximately 30 and then bone mass begins to fall and as it falls your fracture risk increases
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Why are men at lower risk for OP?
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Because of increased testosterone, men more bone mass by 30 so takes longer to fall to risky levels
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How is OP diagnosed?
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x-ray to assess bone density
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What is the treatment for OP? How does it work? What are the risks? What is another option for treatment?
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Bisphosphonates (slow osteoclasts to decrease bone resorption). Because less bone is being resorbed, less FG are being released therefore there is less building of bone as well as osteoblasts are not recruited as much. Also, INTERMITTENT parathyroid hormone.
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How can we prevent OP?
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Build max bone mass as high as possible by:
weight bearing exercise increasing vitamin D increasing calcium |
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What are the signs and symptoms of Paget's disease?
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1. bone pain
2. increased bone size and vascularity 3. bone deformity (since rushed remodelling) 4. increased susceptibility to fracture 5. "hat doesn't fit anymore" since skull deforms 6. feel heat on head due to increased vascularity to skull to support constant, fast remodelling |
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What is the treatment for Paget's disease?
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bisphophonates & calcitonin (peptide hormone that you snort)
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What is the problem with calcitonin as a treatment for Paget's disease?
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you become desensitized over time.
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What are the signs and symptoms of hyperparathyroidism?
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hypercalcemia
polyuria, kidney stones (calcium deposits) muscle weakness/fatigue bone cysts (increased bone turnover creates lump) subperiosteal resorption |
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What is the treatment for hyperparathyroidism?
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If large tumour > surgery If mild issue > bisphosphonates
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