Tissue-engineered repair of osteochondral defects: effects of the age of donor cells and host tissue.

Transplantation of a tissue-engineered construct containing cells of a chondrocytic phenotype into an osteochondral defect provides a biological solution to this type of injury. Among the factors that affect cell proliferation and phenotypic expression, age is one that has not been well characterized. In this study adult and aged male donor cells, derived from perichondrium, were cultured and adsorbed into a polylactic acid (PLA) scaffold and transplanted into osteochondral defects created in adult (8- to 10-month-old) and aged (4- to 5-year-old) female rabbits. Three groups were investigated: (1) adult cells transplanted into aged defects, (2) aged cells transplanted into aged defects, and (3) aged cells transplanted into adult defects. In vitro characterization of adult and aged cells and in vivo assessment of osteochondral repair tissue at 12 weeks posttransplantation were carried out. The in vitro studies demonstrated that the proliferation rate of aged cells was less than that of mature cells during the earliest stage of culture. Also, the chondrocytic phenotype was reduced in aged cells compared with mature cells. The in vivo results showed that donor (SRY-positive) cell survival differed among the three groups: survival of adult cells into aged defect > survival of aged cells into aged defect > survival of aged cells into adult defect. The biological acceptability of the repair, defined as smooth firm cartilaginous tissue filling the defect, was < 25% of the operated specimens in each of the three groups. This repair tissue contained only 20-25% of the amounts of type II collagen and glycosaminoglycans found in normal articular cartilage. These data suggest that the outcome of tissue-engineered repair of osteochondral defects is affected by both the age of donor cells and the age of the host.