**5.1 Compact bone**

The behavior of fresh compact bone, loaded in the longitudinal direction, is elastic up to a strain of 0.7% in tension or in compression [1, 3], failure occurs at 3% strain (**Figure 5**). In the transverse direction, in tension, the bone is less rigid and the rupture occurs at a strain of 0.6%. These values correspond to fresh bones. If they are dry, the Young's modulus increases and the tensile strength decreases. Dry bone is also more fragile. The Young's modulus of fresh compact bone is about 17 GPa longitudinally and 11.5 GPa transversely. The maximum compressive stress is 193 MPa in the longitudinal direction and 133 MPa in the transverse direction. In traction, the maximum stresses are 148 MPa in the longitudinal direction and 49 MPa in the transverse direction.

The elastic mechanical properties of bone ultrastructure scale levels depends on several geometrical and mechanical parameters such as Young's modulus bone elementary com- pounds (mineral, collagen) [6, 7], the nature of collagen (dry, wet) [6], size of the mineral crystal and the number of cross- links [8]. In order to clarify, the averaged elastic constants have been presented in **Table 1** to compare

**Figure 5.** *Tensile-compression test of compact bone [5].*


**Table 1.**

*The average elestic mechanical properties of the bone ultrastructure scales [8].*

our results with experi- mental and numerical results of further works performed on the same components. There are few works focused on the mechanical properties characterization of MCFR (mineralized collagen fibers (MCFRs)), for this reason, the comparison of the results is limited on MCM (Mineralized Collagen Microfibrils) and MCF (Mineralized Collagen Fibrils) scale levels.

MCFRs are formed by the assembly of MCFs surrounded by a matrix of mineral and are offset from each other with an apparent pe- riodicity noted D. Then, MCFs are made the same way by MCMs related to each other by cross-links. Finally, MCMs, a particu- lar assembly of five helical TC molecules, longitudinally offset them with the same apparent periodicity D.

#### **5.2 Bone remodeling or renewal**

Bone is constantly being renewed. It is a continuous cycle of bone formation and destruction, which is living tissue. This phenomenon is called "bone remodeling". Two types of cell are involved: osteoclasts which will first destroy the bone that has been formed in the past, and osteoblasts which will rebuild new bone.

At first, the osteoclasts arrive and dig real "holes" called gaps: this is the resorption phase.

Then, the osteoblasts arrive in the gaps dug previously. These cells will then fill in with bone tissue without calcium (called osteoid tissue), this is the formation phase. Finally, on this young osteoid bone tissue, the calcium will be fixed: this is the phase of the mineralization.

Bone tissue is a dynamic tissue which is constantly renewed by synthesis and resorption. This mechanism is induced by the action of hormones and local factors (parathyroid hormone, vitamin D3, prostaglandin E2) or mechanical constraints (stresses, alterations in bone tissue). Permanent remodeling makes it possible to renew bone tissue to compensate for the aging of osteocytes, to modify the architecture of bone tissue according to mechanical constraints and finally to control phosphocalcic homeostasis by recirculating calcium and phosphorus during the resorption phase.

There are 5 main phases in the bone remodeling process: the activation phase, the resorption phase, the inversion phase, the formation phase and the quiescence phase. Bone remodeling is a cellular cooperation between osteoblasts and osteoclasts. The phenomenon of bone remodeling takes place within a multicellular temporary remodeling unit called the BMU "Bone Multicellular Unit".

#### *5.2.1 The activation phase*

The activation phase is initiated by the osteocytes. These cells are anchored in the bone matrix and have numerous cytoplasmic extensions. They are able to communicate with other cell types, but also to detect mechanical signals (stresses, alterations in bone tissue such as microfractures) or hormonal signals. Faced with these signals, the osteocytes die by apoptosis and induce, through this programmed cell death, the retraction of the bordering cells to expose the bone surface which

must be remodeled. Stromal cells, mesenchymal stem cells, which are found in the environment on the surface of bone tissue, differentiate into pre-osteoblasts. These express on their surfaces RANKL, a cytokine-type ligand whose role is the recruitment of pre-osteoclastic cells, coming from the medullary environment, and the differentiation of these into mature cells by the RANK bond (expressed at the surface of pre-osteoclasts) and RANKL. Mature osteoclasts thus formed adhere to the bone surface.
