PubMed · 5640251
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C M Lanphier. 1968. Clique and complementarity.. https://doi.org/10.1080/00224545.1968.9919801
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The spontaneous healing of osteochondral defects in the knee joints of immature rabbits within the first 12 weeks after surgery showed a faster filling and earlier tissue specialization than in adult animals. The purpose of the present study was to investigate whether the better short-term quality of spontaneous repairs in immature animals lasted over a period of 48 weeks. A full-thickness osteochondral defect was created on the medial femoral condyle in both knees of 10 young, 10 adolescent, and 10 adult rabbits. Equal numbers of animals were evaluated after 24 and 48 weeks. At both time intervals, bonding to adjacent cartilage and proteoglycan content of the matrix were better in the repairs of young than in adult animals. Repairs in the former had cellularity similar to the adjacent cartilage and were composed of 90% hyaline-like cartilage, which did not decrease with time. In contrast, repairs in older animals formed less hyaline-like cartilage and had a lower cellularity than the adjacent cartilage. However, the surface of the repaired tissue was similarly disrupted in all age groups, and the mechanical properties remained inferior to adjacent or normal cartilage. Repairs in older animals showed signs of degeneration with time. The initial better repair quality in a young, growing animal remained up to 48 weeks when the animal had already reached maturity, indicating that successful initial promotion of cartilage repair may even lead to better results in the long term. However, it has to be pointed out that the morphologically good repairs with hyaline-like cartilage appearance, normal cellularity, and durability of up to 48 weeks were unable to reestablish and maintain a cartilage-like mechanical function.
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Astrocyte populations were analyzed over a period of 1 month in the hippocampus following lateral fluid percussion (FP) brain injury. Rats (n = 23) were subjected either to a brain injury of moderate severity, or to anesthesia and surgery without injury (n = 7). At 3 days, 1, 2, or 4 weeks postinjury, subgroups of animals were sacrificed and the brains removed and sectioned for histochemical analysis. The density of astrocytes, identified with gold sublimate staining, decreased significantly in the ipsilateral hippocampus of injured rats 3 days following injury, eventually falling to 64% of the total astrocyte population present in uninjured animals by 1 week postinjury. One month postinjury, the density of hippocampal astrocytes had returned to 85% of the total number of astrocytes observed in the hippocampus of uninjured animals. In order to characterize the post-traumatic formation of new astrocytes, immunohistochemistry was performed using antibodies to proliferating cell nuclear antigen (PCNA) and to glial fibriallary acidic protein (GFAP). Positive immunolabeling for both PCNA and GFAP was most abundant at 3 days following FP brain injury in regions where the blood brain barrier was compromised, and was not detectable by 1 month postinjury. These results indicate that astrocyte proliferation after injury may be evoked by mitogens released from vascular sources, and may be an attempt to compensate for some of the astrocytic cell loss observed after injury.