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What is the organic component of bone?
What is the inorganic component of bone?
What other part of the body is composed of the inorganic component of bone?
How are the organic and inorganic components of bone structured?
What is a Haversian canal?
Which two types of stem cells are the origins of bone cells?
List five differences between haemopoietic and mesenchymal stem cells.
List the six tissue types that can be formed from a mesenchymal stem cell.
What is the name for an immature bone cell?
What is the name for a mature bone cell?
What type of immature cell is involved in Ca2+ and vitamin D usage?
Which cell type involved in bone remodelling is derived from the haemopoietic stem cell lineage? Exactly what lineage are they from?
With regard to haemopoietic stem cells, what is the difference between a multipotent progenitor and a committed progenitor?
When are osteoclasts considered mature?
In what way are osteoblasts related to osteoclasts?
What is the difference in function in the osteoblast and the osteocyte?
What is the network of collagen also known as?
Once trapped in the collagen, how do osteocytes communicate with one another?
Which is larger: an osteoblast or an osteoclast?
Describe a distinctive feature of an osteoclast.
Why is an osteoclast multinucleate, unlike an osteoblast which has a single nucleus?
What is the secreted collagen in bone referred to as before mineralisation?
Once osteocytes are trapped in lacunae, what is their primary function?
What is the name for the groove/cavity that contains osteoclasts during bone resorption?
How is an osteocyte lacuna formed?
Numerous extrinsic factors including hormones and growth factors activate osteoblast-specific signalling proteins and transcription factors required for osteoblast differentiation. What is the major transcription factor involved?
How does Cbfa1/Runx2 result in osteogenesis?
Which proteins can upregulate Cbfa1/Runx2 expression?
Is Cbfa1/Runx2 sufficient to induce osteogenesis alone?
What are the three main pathways for osteoblast regulation known as?
Does the formation and resorption of bone occur normally, or pathologically?
Macrophage colony stimulating factor (M-CSF) is pro-osteoclastic. What could this mean during infection?
How does oestrogen protect against osteoclastic activity?
What does RANKL binding to RANK on a pre-osteoclast signal it to do?
Where is RANKL derived from?
Other than RANKL binding to RANK, what else is necessary for fusion of multiple pre-osteoclasts? Is this factor sufficient on its own to cause this?
Put the following in the correct order: 1) PTH binds to receptors on osteoblasts. 2) Bone is resorbed. 3) Serum calcium decrease. 4) PTH released. 5) Osteoblasts express RANKL on surface. 6) Calcium released. 7) RANK/RANKL interaction causes osteoclast maturation and activation. 8) Serum calcium increase. 9) RANKL binds to RANK.
How is osteoprotegerin production modulated?
What is the mechanism by which osteoclasts resorb bone?
Which chemical factors influence bone growth?
Why does damaged cartilage heal slowly?
