Therefore, current orthopae dic practice aims to preserve meniscal integrity and restore function. The success of clinical repairs www.selleckchem.com/products/Vandetanib.html depends on a number of factors including age, time to surgery, and the type and location of the meniscal tear. In general, repairs involving the outer one third of the meniscus, the vas cularized red red zone, have the highest likelihood of success. Repairs are less favorable in the inner two thirds of the meniscus, the avascular white white zone. However, in vitro studies of integrative repair suggest that the intrinsic repair capabilities of the outer and inner zones are similar, supporting the hypothesis that the in vivo presence of vasculature aids in the repair of the outer zone. Nonetheless, differences in extracellular matrix and cell composition between the inner and outer zones may also influence repair.

The outer zone contains fibroblast like cells that pro duce predominantly Inhibitors,Modulators,Libraries type I collagen. The inner zone consists of fibrochondrocyte like cells, both type I and II collagen, and increased aggrecan content relative to the outer zone. Meniscal plugs from the outer zone inserted into inner zone tissue demonstrate enhanced healing, suggesting that repair capability is related to the intrinsic healing potential of the outer region, rather than the vasculature alone. The integrative repair of meniscal lesions is associated with increased cell accumulation in the repair site. However, the respective roles of cell prolifera tion and migration in integrative repair, and the influ ence of soluble mediators Inhibitors,Modulators,Libraries on these Inhibitors,Modulators,Libraries processes are not fully understood.

An in vivo canine model consisting of a fibrin clot surgically inserted into an avascular menis cal defect showed that the clot functioned as a scaffold for cell migration and a chemotactic stimulus for cell proliferation. Furthermore, cells can migrate Inhibitors,Modulators,Libraries Inhibitors,Modulators,Libraries into an acellular meniscal plug in vivo and remodel the tissue. An important factor that may strongly influence meniscal repair is the inflammatory this environment within the joint. The inflammatory cytokines interleukin 1 and tumor necrosis factor alpha are up regulated in injured and OA knee joints. In addition, IL 1 and TNF a decrease integrative meniscal repair in vitro by increasing matrix metalloproteinase activity, sulfated glycosaminoglycan release, and nitric oxide production, while simulta neously decreasing cell accumulation and tissue forma tion at the meniscal repair interface, and ultimately compromising the shear strength of repair. Initial acute exposure to IL 1 for 1 to 3 days potently suppresses meniscal repair for at least 28 days, sug gesting that the initial inflammatory environment in a joint post injury may have long term degenerative effects.