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Trabecular and bone plate are composed of osteocytes, osteoblasts, and osteoclasts that function in a coordinated manner during bone homeostasis.
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Our observation is also in line with previous data which demonstrate that soluble RANKL produced by hypertrophic chondrocytes is a biologically active molecule during bone growth [ 42, 43] that acts in a paracrine manner on the subchondral bone plate [ 44].
At any time during bone development or fracture healing, multiple growth/differentiation factors are functioning in a coordinated manner thus the combinations of bioactive factors might synergistically stimulate bone regeneration.
In particular, the attention will be focused on the type of osteogenesis of the newly formed bone during bone mass recovering that, as previously demonstrated [ 43, 44], can occur in two different manners (static and dynamic osteogenesis) and imply different bone quality by the mechanical viewpoint.
b Intraoperative findings during bone biopsy.
If 4HR inhibits the NF-kB pathway during bone regeneration, more bone formation can be anticipated.
Complications are common during bone fracture healing owing to incompatibility of the implants.
The storage moduli of the composites approached the lower range of storage modulus for cortical bone and may prevent stress shielding during bone regeneration.
Such ligands, incorporated in bone during bone formation, might activate osteoclasts when bone mineral is exposed by osteoblastic cells [50].
The detail mechanism of Cthrc1 during bone formation is unclear.
Thus, during bone development woven bone rich in versican alters into lamellar bone containing little versican.
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