[Post-traumatic repair of the tibia in rats]

Posttraumatic bone repair was studied histologically in 88 adult male Wistar rats. Thick, semithin and thin sections were stained with standard methods and investigated (microanatomy, histology, EM). The experimental animals were divided into five main groups: 1) control; 2) trained (swimming); 3) immobilized; 4) formalized (0.2 mg/kg i.m. every day); 5) alcoholised (3% alcohol instead of drinking water). The first group was divided into animals wit periost, contacted with endost and bone marrow and animals without periost contacts (with isolated periosteum). Bone perforation causes local hemorrhage and tissue destruction. Thr first reparative changes on the first-seventh days (proliferating fibroblasts and capillary sprouts grow into the blood clot and injured area, degranulation of neutrophils and tissue basophils, appearance of activated macrophages and osteoclasts) occur in soft tissue. Intensive collagen synthesis in fibroblasts began. On the fourteenth day collagen synthesis in osteoblasts was increased (packed collagen fibrils in vacuolated cytoplasm). Posttraumatic osteohistogenesis on d 4-21 was generally completed on d 28-42 bone formation (morphogenesis) and permanent remodeling were continued. Periosteal osteogenesis and bone repair require an existence of the periosteum contact with endosteum and bone marrow (growth and differentiation of endosteal bone callus was inhibited and those of periosteal callus was arrested in groups with isolated periosteum). Similar results were achieved in i.p. heterotopic autografts of repaired tissue in diffusion chamber (with isolated periosteal osteogenetic cells appearing only by 21st day after bone injury). In trained rats bone repair was stimulated, while in immobilised and in injured animals it was inhibited and resulted in chronic inflammation of bone marrow and abscesses.