Biomedical Engineering Reference
In-Depth Information
20 CHAPTER 2. CARTILAGE AGINGAND PATHOLOGY
that the defect's diameter is less than 1.5 cm. When fissuring does extend to the level of the sub-
chondral bone, in an area with a diameter more than 1.5 cm, the lesion is classified as Grade III.
Lastly, articular cartilage injuries that result in exposure of the subchondral bone is classified as
Grade IV [
164
]. Noyes and Stabler [
166
] developed a scale specifically for arthroscopic grading of
cartilage. A similar scale modified from the Outerbridge scale [
167
] has been shown to correlate
well with the Histological/Histochemical Grading System (HHGS) when the severity of the lesions
was Grade III or below [
168
]. Several grading scales have also been developed for osteoarthritis,
such as the Osteoarthritis Research Society International (OARSI) and Cartilage Histopathology
Assessment System (OOCHAS) [
169
].
Cartilage microfractures do not result in immediate changes in the matrix that are visible
to the naked eye. However, the damage to the collagen network begins to effect superficial GAG
loss [
170
]. As the network loosens, increased hydration is also observed [
171
]. Microfractures can
also lead to altered load distribution of the matrix, resulting in stress concentrations that can cause
further damage or a greater proportion of forces borne by the bone. These loading alterations, as
well as fractures to the calcified layer that can occur, lead to eventual thickening of the subchondral
bone [
172
]. The calcified layer also thickens as the cartilage thins. Since cartilage is aneural, repeated
loading of microfractured cartilage can continue without pain, leading to further degeneration [
173
].
Though the GAG loss stimulates chondrocyte activity, the metabolic response is typically inadequate,
leading to a net loss of GAG, increased wear, and the eventual development of fissures.
Chondral fissures are defects that do not extend to the subchondral bone. These defects are
visible to the naked eye, often via India ink staining. Chondral defects can proceed from cartilage
microfractures or from trauma, improper loading, or foreign bodies. Without blood, the intrinsic
metabolic activity after such an injury is insufficient to result in adequate repair, leading to the
eventual development of osteochondral fissures [
173
]. Osteochondral fissures are lesions that cross
the tidemark and penetrate the underlying bone. Though growth factors and progenitor cells are
recruited from the bone's vasculature, there is impaired functionality of the repair tissue, a mix
of fibro- and articular cartilages [
174
], resulting in eventual degeneration into osteoarthritis. It is
important to recall that, with age, both chondrocytes and progenitor cells decrease in number and
metabolic activity, thus contributing to the cartilage healing problem.
2.3.2 CAUSES OF CARTILAGE INJURIES
Cartilage injuries can result from impact and repeated loading, and these can occur under a wide
range of loads, time scales, and frequencies. Determining thresholds that can correlate to certain
elicited cellular responses is important in understanding cartilage injuries and degeneration. Because
of the viscoelastic nature of articular cartilage, load rate affects tissue stiffness and thus failure. The
rates of applied stress, strain, and load must be considered. For example, using a confined compression
loading protocol, the dynamic modulus has been shown to increase from 225 to 850 MPa as the
load rate was increased from 25 to 1000 MPa/s [
175
].
