Biomedical Engineering Reference
In-Depth Information
Fig. 3. Biological stages of healing at the bone-dental implant interface Ambard & Swider
(2006); Dimitriou et al. (2005); Lang et al. (2003).
These fibers are accumulated to form the
fibrin clot
that completely detains blood flow and
also protects tissues left exposed after implantation Aukhil (2000).
Some fibrin fibers are broken down after coagulation to allow the flow of stem cells responsible
for restoring the tissues Collen & Lijnen (1991); Pasi (1999). Such degradation is accomplished
by
plasmin
, a protein present in blood plasma in its inactive form known as
plasminogen
Aukhil (2000); Collen & Lijnen (1991); Li et al. (2003), and macrophage and neutrophil cleaning
activity Davies (2003); Lang et al. (2003). Around the fourth day of healing, a process known
as
fibroplasia
begins the replacement of the fibrin clot into a new extracellular matrix known
as
granulation tissue
which mainly consist of collagen and new capillaries formed during
angiogenesis Aukhil (2000). This new matrix supports the
osteogenic cells
migration Lang et al.
(2003), stimulated by several molecules released during blood clotting and clot cleansing, such
as PDGF, TGF-
Davies (2003) and fibroblast growth factor (FGF) Dimitriou et al. (2005).
Between the 7-10th day of healing, some of the fibroblasts present in the interface are
transformed into
myoblasts
Häkkinen et al. (2000) characterized by smooth muscle
β
-actin
cytoplasmatic microfilaments, allowing them to generate contractile forces responsible for
wound contraction Aukhil (2000); Davies (2003); Häkkinen et al. (2000).
Osteogenesis
or new
bone formation along the vascular structures is started Lang et al. (2003); Meyer & Wiesmann
(2006) by day 14 after injury Dimitriou et al. (2005); Lang et al. (2003). Here, granulation tissue
is replaced by new collagen fibers that are slowly mineralized to create the new bone matrix
Meyer & Wiesmann (2006); Sikavitsas et al. (2001) by contact and direct osteogenesis Davies
(2003).
Biological activity regarding wound healing at the bone-dental implant interface concludes
with the modeling and subsequent bone remodeling Sikavitsas et al. (2001). Moreover, cell
adhesion, cell migration and proliferation on surrounding tissues, and internal and external
mechanical loads action modify the new tissue formation profile (Figure 4). Such phenomena
may act as follows. First, the adhesion phenomena produced by cells fixation to a substrate
Anselme (2000) activate chemical signaling Kasemo (2002) controlling cell proliferation and
differentiation, as in platelet aggregation and activation stages Collen & Lijnen (1991).
α
