The Bone–Cartilage Interface - Structural Interfaces and Attachments in Biology - page 104

Finite element analysis of juxtarticular stresses showed that increased stiffness of
the SCB plate (that presumably included the SCB and ZCC) correlated with elevated
shear stresses at the bone-cartilage interface [ 144 ]. However, similar analyses
demonstrated that subchondral stiffening leads only to modest increases in stress
within the overlying hyaline cartilage [ 145 , 146 ]. These results, in combination with
the elevated incidence of radial fractures in aged subjects with presumably higher
ZCC mineralization, indicates that damage at the osteochondral interface may
precede, and ultimately cause, hyaline articular degradation and damage.
How the mineralized cartilage participates in functional grading within the
osteochondral region requires further study. An improved understanding of the
function of the ZCC and SCB will help to elucidate how alterations in mineraliza-
tion, porosity, and remodeling of the ZCC and SCB contribute to degeneration with
aging and disease in both synovial and cartilaginous joints.
5.4.3 Failure of the Bone-Cartilage Interface
Because the soft, hyaline cartilage forms an abrupt boundary with the underlying
ZCC, failure in this region tends to parallel, rather than to penetrate, the interface in
synovial joints [ 147 ]. However, twisting or dislocation can expose convex joint
surfaces to lateral forces and shear-induced lesions or failure within the
osteochondral region [ 148 - 150 ]. Osteochondral failure depends mainly on the
load intensity and the integrity of the cartilage material—a factor that varies
substantially with aging and disease.
Polar forces between water and the negatively charged proteoglycans within the
matrix create a significant Donnan pressure effect and thus resist flow—especially
at high strain rates such as those most commonly experienced in vivo [ 37 , 45 ].
The total swelling pressure contributes to the high-energy state of the hyaline
cartilage and results from a physiochemically derived osmotic pressure and the
repulsive charges between closely spaced proteoglycan molecules [ 37 ]. Articular
cartilage is constrained in its superficial zone by radially oriented (i.e., parallel to
the articular surface) collagen fibrils and by the underlying mineral, as evidenced by
its immediate expansion upon being cut away from the ZCC and SCB [ 1 , 151 , 159 ].
This complex high-energy state, and the water stored within the cartilage,
conveys rigidity and toughness [ 1 ]. Yet failure of the tissue enables release of
stored potential energy to cause significant tissue damage. For example, adolescent
individuals, who lack a substantially calcified cartilage layer, can experience
traumatic fractures that transmit deep into the osteochondral junction and penetrate
the SCB [ 152 , 153 ]. In elderly adults, where the ZCC possesses a significant
mineral volume fraction, regions of tissue failure tend to locate along, but do not
penetrate through, the leading tidemark [ 154 ]. In excised human tissues,
microcracks often occur in the ZCC from 58- to 75-year-old subjects [ 155 , 156 ].
Separately, a controlled, ex vivo study of shear impact loading of articular cartilage
demonstrated age-dependent patterns of osteochondral failure [ 148 ]. In immature