DESIGNING NANOFIBROUS SCAFFOLDS FOR TISSUE ENGINEERING - Advanced Biomaterials: Fundamentals, Processing, and Applications - page 463

In vivo bone regeneration using nanofi ber-based scaffolds was demonstrated
by Shin et al. who reported the osteogenic differentiation ability of MSCs seeded
on PCL electrospun scaffolds in a rat model [235]. The initial differentiation of
MSCs (isolated from rat bone marrow) on PCL matrices was performed in rota-
tional oxygen permeable bioreactors for four weeks, followed by in vivo implan-
tation in the omentum of a rat model. They demonstrated successful differentiation
of MSCs into osteoblasts with laid down osteoids following four weeks of implan-
tation. Further, characteristic mineralization and the presence of collagen type I
throughout the harvested cellular constructs strengthened the potential for bone
graft development from highly porous electrospun PCL nanofi bers.
13.5.2.2 Cartilage. Cartilage is a tough, elastic, and fl exible connective
tissue that comprises cells in combination with a fi brous network. It is an avascu-
lar, alymphatic, and aneural tissue with limited innate ability for repair and regen-
eration [236]. Cartilage in the human body exists as three types: fi brocartilage,
elastic cartilage, and hyaline cartilage [237,238]. Hyaline cartilage is the predomi-
nant type of cartilage that coats the surface of articulating joints [35,136,239] and
hence is referred to as articular cartilage. Healthy articular cartilage is a water
rich tissue (60-85%) with the remainder being ECM (mainly collagen type II:
15-22% and proteoglycans 4-7%) and chondrocytes (2-5%). High water content
enables cartilage to withstand the forces associated with joint loading. Chondro-
cytes are the only cellular component of normal cartilage. Although low in
number, chondrocytes continuously remodel and organize the surrounding ECM
in a unique and complex anisotropic structure [136].
Collagen type II is the predominant component of cartilage ECM and pro-
vides tensile strength, whereas macromolecules-like glycosaminoglycans (GAGs)
produced by chondrocytes contribute to the viscoelastic property of cartilage.
GAGs attached to protein molecules form proteoglycans that impart compres-
sive strength to cartilage tissue [136,239]. Cartilage defects, irrespective of their
origin, are not life-threatening, but result in debilitating affl iction and gradual loss
in mobility [240]. Statistical data indicates that the disorders linked with damaged
cartilage have rapidly increased in the last century and are expected to affect a
large section of the population worldwide in the future [3,203]. Currently avail-
able treatment options heavily rely on tissue grafts (autograft and allograft) or on
artifi cial prosthetic joints. Although a fair degree of success has been achieved
with these treatment methods, challenges such as limited availability and donor
site morbidity (autograft), disease transmission, and immunogenic response
(allograft) still remain [3]. Total joint replacement is a successful treatment in
most severe cases of arthritis; however, the implant has a limited life span, with an
average of 10-15 years [241,242].
When cartilage is damaged or injured, a cascade of events occurs to restore
and repair the damaged tissue. Only full thickness defects that penetrate the
subchondral bone elicit a healing response [243]. Furthermore, despite the elicita-
tion of repair processes in full thickness defect, mechanically inferior fi brocarti-
lage is formed [240]. Consequently, a sequential permanent loss of structure and