Biomedical Engineering Reference
In-Depth Information
and migratory cell types, both during development and in the adult
animal [15].
1.6.7 Fibroblast Growth Factor
Fibroblast growth factors, or FGFs, are a family of growth factors involved
in angiogenesis, wound healing, and embryonic development. The FGFs are
heparin-binding proteins, and their interactions with cell-surface associated
heparan sulfate proteoglycans have been shown to be essential for FGF signal
transduction. FGFs are key players in the processes of proliferation and dif-
ferentiation of a wide variety of cells and tissues. The function of FGFs is
not restricted to cell growth. Although some of the FGFs do, indeed, induce
fibroblast proliferation, the original FGF molecule (FGF-2 or FGF basic) is
now known also to induce proliferation of endothelial cells, chondrocytes,
smooth muscle cells, and melanocytes, as well as other cells [16]. It can also
promote adipocyte differentiation, induce macrophage and fibroblast IL-6
production, stimulate astrocyte migration, and prolong neuronal survival.
Thus, the FGF designation is clearly limited by its description as one target
cell and one implied biological activity.
1.7 Introduction to Bone Remodeling
Bone remodeling is a complex process performed by the coordinated activi-
ties of osteoblasts and osteoclasts. Together, these cells form temporary
anatomical structures, called BMUs, which execute bone remodeling. The
interactions between osteoblasts and osteoclasts, which guarantee a proper
balance between bone gain and loss, is known as coupling [6].
Specific regions of bones are targeted for remodeling due to structural
microdamage, thus maintaining the mechanical strength of the skeleton
(targeted remodeling) [17,18]. Furthermore, bone remodeling plays a major
role in mineral homeostasis by providing access to stores of calcium and
phosphate [19]. In this case, bone remodeling occurs at random locations
(random remodeling), so every part of the skeleton is remodeled periodi-
c a l l y [1 7, 1 8 ] .
The net amount of old bone removed and new bone restored in the remod-
eling cycle is a quantity called the bone balance. While coupling is rarely
affected, bone balance can vary quite widely in many disease states; for
example, in osteoporotic patients, resorption and formation are coupled but
there is a negative bone balance (i.e., more bone is resorbed than is replaced
by the typical BMUs).
BMUs are constantly remodeling bone tissue in the growing, adult, and
senescent skeleton. Most metabolic bone diseases appear when a biochemical
