Biomedical Engineering Reference
In-Depth Information
28 CHAPTER 2. CARTILAGE AGINGAND PATHOLOGY
results in loads several times body weight to be applied [
279
,
280
]. Indeed, knee and hip cartilages
show greater incidences of lesions than other anatomical regions. A survey of all cartilage lesions
across all ages shows that the patellar articular surface and the medial femoral condyle were the
most frequently damaged, accounting for 36% and 34%, respectively, of the cases surveyed [
165
].
These joints are also the ones that enable mobility and have a great impact on the quality of life.
Arthroscopic evaluation in young Finnish males showed that 73.5% of the lesions were patellar, 12.0%
in the medial condyle of the femur, and 8.0% in the femoral groove. Roughly, 75% of the patients
had superficial (grade I-II) and 25% deep lesions (grade III-IV) [
229
]. This is particularly alarming
as data from 1995, 1996, and 1997 indicate that roughly 20% of the knee injuries in adolescents
required surgery [
281
-
283
]. Unfortunately, current therapies, as reviewed in the last section of this
topic, are not sufficient in effecting long term relief and activity resumption. Follow up studies of 5,
10, and greater years have consistently shown a need for improvement in the outcomes of arthroplasty,
osteochondral, and autologous cell transplantation. Effective solutions are clearly needed, and these
can be improvements on current therapies, chondrocyte transplantation, which can be considered
as a form of
in vivo
tissue engineering, or controlled manipulation of cells and materials
in vitro
to
form implantable neocartilage.
2.6 CHAPTER CONCEPTS
The cartilages of the limbs mostly form by mesenchymal condensation, proliferation, and
differentiation.
A variety of chemical signals, such as TGF-
β
, BMP, VEGF, shh, etc., regulate the process of
cartilage formation, and these signals have been manipulated to study and to recapitulate this
process.
Immature cartilage can contain vasculature. As cartilage ages, the vascular regions calcify, and
cartilage thins.
Aging results in increased collagen crosslinking, lowered collagen alignment, and slower col-
lagen turnover. Proteoglycans also decrease in amount and size with age.
Hormones and steroids can negatively affect cartilage material properties.
Cartilage can be injured by impact, repeated loading, torsional loading, joint malalignment,
and foreign bodies in the joint space.
Sometimes, injuries to the cartilage show no gross morphological changes, and chondrocytes do
not respond adversely to the insult immediately. However, chondrocyte death and catabolism
have been shown to occur even for these “clinically silent” injuries.
Chondral lesions do not heal, and osteochondral lesions are filled with mechanically inferior
fibrocartilage that breaks down with use.
