  Injuries to articular cartilage result in the development of lesions that
form on the surface of the cartilage. Such lesions are associated with
articular cartilage degeneration and osteoarthritis. The typical injury
response often causes collateral damage, primarily an effect of inflammation,
which results in the spread of lesions beyond the region where the initial
injury occurs. We present a minimal mathematical model based on known
mechanisms to investigate the spread and abatement of such lesions. In
particular we represent the "balancing act" between pro-inflammatory and
anti-inflammatory cytokines that is hypothesized to be a principal mechanism in
the expansion properties of cartilage damage during the typical injury
response. We present preliminary results of in vitro studies that confirm the
anti-inflammatory activities of the cytokine erythropoietin (EPO). We assume
that the diffusion of cytokines determine the spatial behaviour of injury
response and lesion expansion so that a reaction-diffusion system involving
chemical species and chondrocyte cell state population densities is a natural
way to represent cartilage injury response. We present computational results
using the mathematical model showing that our representation is successful in
capturing much of the interesting spatial behaviour of injury associated lesion
development and abatement in articular cartilage. Further, we discuss the use
of this model to study the possibility of using EPO as a therapy for reducing
the amount of inflammation induced collateral damage to cartilage during the
typical injury response. The mathematical model presented herein suggests that
not only are anti-inflammatory cytokines, such as EPO necessary to prevent
chondrocytes signaled by pro-inflammatory cytokines from entering apoptosis,
they may also influence how chondrocytes respond to signaling by
pro-inflammatory cytokines.
