Damage and recovery of the bone growth mechanism in young rats following 5‐fluorouracil acute chemotherapy

摘要: Chemotherapy-induced bone growth arrest and osteoporosis are significant problems in paediatric cancer patients, yet how chemotherapy affects remains unclear. This study characterised development resolution of damage caused by acute with antimetabolite 5-fluorouracil (5-FU) young rats the plate cartilage metaphyseal bone, two important tissues responsible for lengthening. In metaphysis, 5-FU induced apoptosis among osteoblasts preosteoblasts on days 1-2. plate, chondrocyte appeared 5-10. Interestingly, Bax was prior to Bcl-2 upregulated during recovery. also suppressed cell proliferation While returned normal day 3 it recovered partially 3, overshot 5-7 normalised 10 plate. Histologically, heights decreased 4-5 10. primary spongiosa height reduced, mirroring changes thickness. secondary spongiosa, a reduced volume observed 7-10 as there were fewer but more separated trabeculae. Starting from 4, expression some cartilage/bone matrix proteins factors (TGF-beta1 IGF-I) increased. By 14, cellular activity, histological structure gene had both tissues. Therefore, directly inducing inhibiting at bone; after damage, mechanism can recover, which is associated factors.