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Purpose: To further the current understanding of the modifications of the morphology of the ACL tibial footprint in healthy knees during the ageing process. The hypothesis is that there are differences in the morphology of the ACL tibial footprint between the cadavers of the young and elderly due to a degenerative physiological process that occurs over time., Methods: The tibial footprint of the ACL was dissected in 64 knee specimens of known gender and age. They were divided into four groups by age and gender, setting 50 years of age as the cut-off point. Three observers analyzed the tibial footprint dissections and the shape was described and classified., Results: The knees from the cadavers of males older than 50 years of age presented a "C" morphology in 85% of the cases. In the group of males aged less than 50 years, an oval/elliptical morphology was found in 85.7% of the cases. In the group of women over 50 years-old, the "C" morphology was observed in 82.3% of the cases. In women under the age of 50, the oval/elliptical morphology was found in 84.6% of the cases. A significant difference was observed between the prevalence rates of the morphologies of the younger and older groups (p < 0.001 for both genders). However, no differences were observed between males and females of the same age group (n.s.)., Conclusions: The morphology of the tibial footprint of the ACL presents significant variations with ageing. It can go from an oval/elliptical shape to a "C" shaped morphology. The results of this work make for an advance in the individualization of ACL reconstruction based on the age and the specific morphology of the tibial footprint.

Animal models of cerebral ischemia have typically been established and performed using young animals, even though cerebral ischemia (CI) affects primarily elderly patients. This situation represents a discrepancy that complicates the translation of novel therapeutic strategies for CI. Models of transient global CI using aged animals have demonstrated an apparent neuroprotective effect on CA1 hippocampal neurons; however, this effect is not completely understood. Our study used a model in which young (3-6 months) and aged (18-21 months) male Wistar rats were subjected to 15 min of transient global CI using the four-vessel occlusion (4 VO) model. We determined that the 4 VO model can be performed on aged rats with a slight increase in mortality rate. In aged rats, the morphological damage was completely established by the 4th day after reperfusion, displaying no difference from their younger counterparts. These results demonstrated the lack of a neuroprotective effect of aging on CA1 hippocampal neurons in aged male Wistar rats. This study determined and characterized the morphological damage to the CA1 area after 15 min of 4 VO in aged male Wistar rats, validating the use of this model in CI and aging research.