Biomedical Engineering Reference
In-Depth Information
The fi brocartilage region is further divided into non-mineralized and miner-
alized fi brocartilage zones (Figure 17.1C). The ligament proper contains fi bro-
blasts embedded in a collagen I and III matrix. The non-mineralized fi brocartilage
matrix consists of ovoid fi brochondrocytes, and collagen types I and II are distrib-
uted within a proteoglycan-rich matrix. In the mineralized fi brocartilage zone,
hypertrophic fi brochondrocytes are surrounded by a calcifi ed matrix containing
collagen X (Niyibizi, Sagarrigo, Gibson, and Kavalkovich 1996; Petersen and
Tillmann 1999 ). The fi brochondrocyte phenotype at the ACL-bone interface has
been found to be similar to that of articular chondrocytes (Sun, Moffat, and Lu
2007). The last region is the subchondral bone, within which osteoblasts, osteo-
cytes and osteoclasts reside in a mineralized type I collagen matrix. The specifi c
organization and controlled matrix heterogeneity found at the ACL insertion are
believed to minimize the formation of stress concentrations and, in turn, facilitate
the transfer of complex loads between soft and hard tissues (Benjamin, Evans,
and Copp 1986; Woo and Buckwalter 1988).
The ACL is the most frequently injured knee ligament (Johnson 1982), with
over 100,000 ACL reconstruction procedures performed annually in the United
States alone (American Academy of Orthopedic Surgeons 1997; Gotlin and Huie
2000). Autologous soft tissue or hamstring tendon-based grafts are increasingly
utilized for ACL reconstruction due to donor site morbidity associated with
bone-patellar tendon-bone grafts (Barrett et al. 2002; Beynnon et al. 2002). While
these reconstruction grafts may restore the physiological range of motion and
joint function through mechanical fi xation, graft integration is not achieved as
disorganized scar tissue forms within the bone tunnels and the native insertion
site is lost during reconstruction. Without an anatomical interface, the graft-bone
junction has limited mechanical stability (Kurosaka, Yoshiya, and Andrish 1987;
Robertson, Daniel, and Biden 1986; Rodeo et al. 1999), and this lack of integra-
tion is the primary cause of graft failure (Friedman et al. 1985; Jackson et al. 1987;
Kurosaka, Yoshiya, and Andrish 1987; Robertson, Daniel, and Biden 1986; Yahia
1997). Therefore, to enable the biological fi xation of ACL reconstruction grafts,
the regeneration of the multi-tissue interface between soft tissue and bone is
critical.
Based on the complex multi-tissue organization inherent at the soft tissue-to-
bone junction, it is likely that interface formation will require
multiple types
of
cells, a
scaffold
system which supports interactions between these different cell
types, and the development of distinct yet continuous
multi - tissue regions
mimick-
ing the structure of the native insertion through physical and biochemical
stimuli. For functional soft tissue-to-bone integration, the mechanism governing
interface formation must be elucidated, in particular the role of heterotypic cel-
lular interactions in fi brocartilage formation and multi-tissue regeneration. These
interactions may be examined using multi-scale co-culture models that can deter-
mine the relevance of homotypic and heterotypic cellular communications for
interface regeneration and homeostasis. In addition, the success of any interface
tissue engineering effort will require an in-depth understanding of the structure-
function relationship at the native insertion in order to identify interface-relevant
Search WWH ::
Custom Search