Week 2 Flashcards
What type of nodes are there in imaging methods for bone?
2D projection: x-ray, DEXA.
2D cross-sectional: invasive (microtome) & non-invasive ( CT, MRI)
3D: invasive (microtome) & non-invasive ((whole body) CT, MRI) –> combination of multiple cross-sections.
Characterisations of
- X-ray/ CT
- DEXA
- MRI
- Sectioning (histology)
Characterisations of
1. X-ray/ CT: differences in X-ray attenuate of tissues. Surrounding tissues also absorb radiation (not quantitative for bone).
- DEXA: differences in absorptiometry of bone only.
- MRI: differences in water concentration.
- Sectioning (histology): differences in color after staining.
How can you quantify cancellous bone microstructure?
- Amount of bone tissue
- Directionality trabeculae
- Geometry & connectivity trabeculae
What are the parameters & equations to determine the amount of bone? Amount of bone: Volume fraction: Porosity: Volumetric bone density:
Amount of bone:
areal bone mineral density (aBMD) [g/cm2] / bone mineral content (BMC) [g]
Volume fraction: bone volume (BV) / total volume (TV)
Porosity: 1- BV/TV
Volumetric bone density (BMD)= total mass [kg/m3] / total volume [g/cm3].
What are the parameters & equations to determine the directionality of bone?
Directionality:
Mean intercept length (MIL) = total length (L) / #transitions to bone (I(w)).
What are the parameters & equations to determine the geometry & connectivity trabeculae bone:
Tb.N, Tb.Th, Tb. Sp, Conn.D =
Structure Model Index (SMI)=
Geometry constrituive elements: Trabecular number: Tb.N Trabecular thickness: Tb.Th Trabecular separation: Tb. Sp Connectivity density: Conn.D
Other 3D parameters:
Structure Model Index (SMI)= equation with tissue volume and tissue surface. The number/gain (-3 till 3) determines the shape.
Mechanobiology=
Mechanotransduction=
Mechanobiology= focuses on the way that physical forces and changes in cell or tissue mechanics contribute to development, physiology or disease.
Mechanotransduction= any of various mechanisms by which cells convert mechanical stimuli into electrochemical activity.
Bone modeling=
Remodeling=
Bone modeling= bone resorption and formation occur independently at different sites to sculpt one (i.e. during growth and/or response to mechanical loading).
Remodeling= process of bone renewal throughout life during which small packets of bone are removed and subsequently replaced within the basic multi-cellular unit (BMU).
How does bone responds to mechanical load?
Steps: mechanical load > fluid flow in canaliculi > mechanosensing by osteocytes > bone remodeling by osteoclasts & osteoblasts.
Force transmission on tissue level: Physical forces acts on bone on the tissue level.
Force transmission on cell level: (static) mechanical properties of the matrix surrounding the cells & mechanical forces acting on the cell.
Reaction on tissue level: bone mass + alignment –> structural change.
Reaction on cell level: electrochemical and biological responses –> change in cellular acitivity.
What is the difference between bone remodeling on trabecular bone and cortical bone?
Trabecular bone remodeling: osteoclasts create Howship’s lacunae that are refilled by osteoblasts.
Corticol bone remodelling: the osteoclasts erode bone tissue and are followed by osteoclasts that repopulate/refill the gap with new bone. So a tunnel in the bone is made for a bloodvessel and cells/ nutrients work from within.
Low/high strain results in formation/ resorption of bone.
Low strain: resorption.
High strain: formation.
Why is it necessary to have osteocyte viability & osteocyte apoptosis?
Osteocyte viability: maintenance of bone homeostasis/ integrity.
Osteocyte apoptosis: essential for damage repair and normal skeletal replacement. Apoptotic osteocytes are often in contact with osteoclasts. These osteoclasts resorb apoptotic osteocytes. Osteoblasts misses a signal from osteocytes and start making bone.
How does wall shear stress influence osteogenesis?
<0.11 mPa: too low stimuli
0.11-0.55 mPa: osteogenesis (no mineralization)
0.55-10 mPa: osteogenesis (mineralization)
>10 mPa: too high stimuli