CARTILAGE-FLOW PHENOMENON AND EVIDENCE FOR IT IN PERICHONDRIAL GRAFTING

The cartilage-flow phenomenon has been frequently described but not in connection with transplantation procedures for treatment of cartilage lesions. Consequently, we examined this particular phenomenon in an e xperimental sheep model originally set up to study the use of perichon drial grafts for repair of full-thickness cartilage lesions. Osteochon dral lesions were made in non-weight-bearing and weight-bearing areas of knee joints in 36 sheep. The defects were filled with autologous ri b perichondrial grafts and secured by either collagen sponges or fibri n glue (n = 24 animals). Defects without perichondrial grafts served a s controls (n = 12 animals). Following 1 week of immobilisation of the operated leg, the plaster was removed, and the animals were allowed t o move freely. Animals were killed after 4, 8, 12 and 16 weeks. Grafts including rims of original surrounding cartilage and bone were remove d and investigated by means of macroscopy, histology and micromorpholo gy, including scanning electron microscopy and analysis under polarize d light. Cartilage flow was observed in all specimens by 4 weeks after drilling the defects, independent of the weight-bearing condition. Th ese flow formations exhibited a bending of the collagen fibres central ly into the defects, reduction of metachromasia, cell cluster formatio n and areas of reduced cell density. Time-dependent flow formations we re observed related to the weight-bearing condition and whether or not the defects had been grafted. In grafted, non-weight-bearing defects further cartilage flow was stopped 8 weeks after transplantation by th e growing perichondrial transplants, which had filled the defects comp letely. In contrast, control defects exhibited further flaw formations in both areas. The same was observed in grafted defects in the weight -bearing area. In defects without complete filling as not enough spont aneously growing fibrous tissue had arisen from the bottom of the defe cts, two different observations were made: either the defects exhibite d a fungiform mass of fibrous tissue that had overgrown the lateral fl ow formations, or the central mass of fibrous tissue was overgrown by the lateral flow formations. In conclusion, cartilage flow seems to be a mechanically induced phenomenon at the rims of cartilage lesions th at contributes little to the reduction of size of large osteochondral defects. There was no evidence for new cartilage proliferation or prod uction of cartilaginous matrix at the rims of the lesions.