Other than by using shell allografts, it is not possible to replant whole cartilage or cells that even come close to a biological construct matching original cartilage. The old adage that cartilage, unlike bone, cannot repair itself holds true, as the natural damage repair of cartilage leads to the formation of “scar” cartilage (fibrocartilage).
However, there are connective tissue progenitor cells that can be found in multiple different tissues, and chondrogenic connective-tissue progenitors (CTP-Cs) are found within articular cartilage, even if it is osteoarthritic. Investigators recently designed a study to quantitatively define the CTP-Cs resident in cartilage and to compare overall cartilage-cell concentration, CTP-C prevalence, and biological potential of cells in tissues taken from patients with different grades of osteoarthritis.
Investigators procured samples of osteoarthritic articular cartilage from 23 patients undergoing elective total knee arthroplasty. All patients had grade 3-4 osteoarthritis on the medial side and grade 1-2 on the lateral side. Each patient sample was assessed for mean cell concentration and CTP prevalence by subjecting cells from a unit measure of cartilage to specific conditions to promote colony formation. The biological potential of the CTPs was measured using sophisticated imaging analysis.
Cell concentration was significantly greater (p < 0.001) in grade 3-4 cartilage than in grade 1-2 cartilage. This matches findings from previous histologic reports. Although the prevalence of CTP-Cs varied widely, it trended lower in grade 3-4 than grade 1-2 cartilage samples (p = 0.078). The biological performance of CTP-Cs from grade 1-2 and grade 3-4 cartilage was comparable. Increased cell concentration was a significant predictor of decreased CTP-C prevalence (p = 0.002). Sex was not a predictor of cell concentration, but age correlated negatively with prevalence of CTP-Cs. The number of cells per colony varied widely across the 23 patients, implying a highly individualized capacity.
This research contributes to our understanding of what might constitute appropriate cell selection for combination with biochemical interventions that could lead to robust cartilage repair that has greater longevity.