Bone as a biomaterial

Material science as applied to bone

  • Trabecular and cancellous bone act as biomaterials, and have measurable characteristics.
  • The dynamic nature of bone in response to stress and with aging mean that these characteristics are not static and identical through life, however the relative behaviour between bone types remains similar and predictable
  • Bone is one of the only tissues capable of regeneration back to its original state, without scarring, however this is dependent on the callus being exposed to an appropriate environment.

Youngs modulus

Youngs modulus, (E = stress / strain, in N/mm^2 or Pa), has been measured for cortical and cancellous bone. While there are vast differences in results depending on testing methods (dried / fresh, microstructural / macrostructural, compression / tension / flexion, and measurement techniques), the relative behaviours remain relatively consistent.

The range of quantified Youngs Moduli in the literature for cancellous bone is very wide, being 1-23 GPa. This is a result of the above factors, as well as variation between donor sites being assessed, age of donor material, and underlying health. What has been shown consistently is that the Youngs modulus of cancellous bone is lower than that of cortical bone, with cancellous deforming more for a given force.

Having implants with a similar Youngs modulus to the bone in which it is implanted means that there will be less variation in deformation under load, and in turn less separation and movement at interfaces. Examples of modulus

Dynamic nature of bone

Wolff’s law
Wolff’s law is a statement reflecting the dynamic, adaptive nature of bone. From Julius Wolff (1836-1902), it states that in a healthy individual, bone will adapt to the loads under which it is placed. This is achieved through mechanotransduction, where osteocytes detect mechanical load and initiate biochemical signalling to promote structural responses.

Mechanical load may be tensile, compressive or bending forces, but a key feature for promotion of response is that a load is cyclic. The various mechanisms of mechanotransduction are rapidly desensitised to mechanical loading. The efficacy of mechanotransduction is age-related, with mouse models demonstrating reduced response with age.

The biochemical systems of mechanotransduction are primarily produced within osteocytes. These have been demonstrated in laboratory settings to respond to fluid flow shear forces, reflecting fluid flow through canaliculi when exposed to load. Some of the systems known to exist include:
– Integrin signalling: integrins, trans-membrane molecules linking the extracellular matrix to the cytoskeleton, are able to change their structure in response to external forces, and then trigger tyrosine kinase responses. These kinases then influence and promote deposition of type 1 collagen and bone matrix.
– Calcium ion signalling: fluid flow or stretch triggers intracellular calcium release through calcium channels. The channels involved include stretch-activated channels, and L-type calcium channels such as those that can be inhibited by anti-hypertensive Ca-channel blockers nifedipine and verapamil.
– Prostaglandin signalling: fluid flow shear forces on osteocyte cell surfaces trigger the release of PGE2 from osteocytes, which in turn inhibits bone resorption by individual osteoclasts. PGE2 acts through the EP2 receptor to promote boen formation, and an increase in its expression is seen after fracture.

Bone changes in osteoporosis
With progression of osteoporosis, bone density decreases. As a result, the shape of affected bone changes to maximise its strength. Rigidity of tubes is a product of the diameter of the tube, thickness of the wall, and construction material. As the material itself cannot be modulated, the end result is a change in geometry with increasing diameter as the cortical thickness decreases. The progressive increase in cortical diameter provides a progressive increase in resistance to bending forces and a slight increase in resistance to compressive forces, for a static bone density score. Given that osteoporosis features decreases in bone density and reduction in cancellous bone density, overall strength will still decrease, but maintains sufficient strength for physiological / daily activity purposes until it drops below the threshold to develop a pathological fracture.

Changes in bone exposed to bisphosphonates
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Bone graft and substitutes

Autograft

Allograft

Synthetic

References

  • Orthobullets
  • Wu, D., Isaksson, P., Ferguson, S. J., & Persson, C. Young’s modulus of trabecular bone at the tissue level: A review. Acta Biomaterialia. 78,1-12
  • Rho, J. Y., Ashman, R. B., & Turner, C. H. Young’s modulus of trabecular and cortical bone material: Ultrasonic and microtensile measurements. Journal of Biomechanics, 26(2), 111–119, (1993)
  • Leucht, P., Kim, J. B., Currey, J. A., Brunski, J., & Helms, J. A. (2007). FAK-mediated mechanotransduction in skeletal regeneration. PLoS One, 2(4).
  • Huang, C., Ogawa, R. Mechanotransduction in bone repair and regeneration. FASEB J. 24, 3625–3632 (2010)
  • Mano M, et al. Prostaglandin E2 directly inhibits bone-resorbing activity of isolated mature osteoclasts mainly through the EP4 receptor. Calcif Tissue Int. 2000 Jul;67(1):85-92.
  • Li M, Thompson DD, Paralkar VM. Prostaglandin E(2) receptors in bone formation. Int Orthop. 2007;31(6):767‐772. doi:10.1007/s00264-007-0406-x
  • Bouxsein, M.L., Karasik, D. Bone geometry and skeletal fragility. Curr Osteoporos Rep 4, 49–56 (2006).
  • Bono CM, Einhorn TA. Overview of osteoporosis: pathophysiology and determinants of bone strength. Eur Spine J. 2003;12 Suppl 2(Suppl 2):S90‐S96.

Author Contributions

Sean Griffiths, WH Resident, 2020

Reviewed by Professor Phong Tran, Head of Orthopaedic Surgery, Western Health. Last updated 10 October 2026.