A comparative study of fresh autogenous and preserved homogenous tendon grafts in rabbits.

The problems of repair and grafting of tendons have received considerable attention. However, conclusions have been hampered by lack of a standard terminology and by attempts to assign the origin oftendon, paratenon, and cicatrix to distinct types ofcell. The potentialities of cells under stress have been insufficiently recognised. Beltzow (1883), Viering (1891), Busse (1892), Rehn (1919) and Schwarz (1922) concluded that though tendon stumps took some part in the new formation of tendon, the intervening tissue, despite histological resemblances, was essentially scar and not regenerated tendon. They agreed that the clot at the tendon ends was gradually replaced by granulation tissue from the paratenon. Adams (1860) attributed the regeneration of new tendon to activity by the sheaths rather than by the stumps of the tendons. There has been disagreement about the role of the tendon cells. Busse (1892) described tendon cell proliferation, as did Viering (1891), Enderlen (1893), Seggel (1903), Borst (1903), Imayoshi (1925) and Migliavacca (1925). Mason and Allen (1941) and Peer (1955) thought that the parenchymal cells of autogenous tendon grafts could survive and participate in the process of repair. However, Bizzozero (1868), Schradieck (1900), Marchand (1901), Schwarz (1922), Bloch and Bonnet (1929) and Lange (1929) concluded that tendon cell proliferation played little or no part in healing tendon defects. Skoog and Persson (1954) maintained that degenerative changes were inevitable in autogenous tendon transplants, and that replacement by invading cells from the host tissues must occur before healing was complete. Viering (I 891) was the first to note that, with use, nuclei and fibres of tendon lined up in rows parallel to the line of pull. Kirschner (1909) studied autogenous grafts of tendon and fascia and found that tendon, whether functioning or not, remained at least partly alive but that its fibres tended to lose their normal parallel arrangement. Gallie and LeMesurier (1922) stated that after tendon injury healing ultimately occurred by the production of ordinary scar, tendon cells and fibres apparently taking no active part in repair. There was no proliferation of the tendon cells themselves. Mayer (1921) stated that in the free transfer of a tendon the blood supply was destroyed and the vitality of the tendon was entirelydependent on the accuracyofcoaptation. Neuhof(l923) thought that all the transplanted tendon tissue died and was replaced by cellular proliferation from surrounding tissues. Mason and Shearon (1932) found, with autogenous tendon grafts, that during the first two weeks grafts and stumps were united by proliferation of paratenon or peritendinous tissues ; this phase overlapped that of tenoblastic proliferation which began at the fourth or fifth day after grafting. Twelve to fourteen days after grafting, tenoblasts proliferating in the graft extended into the stumps if apposition had been good. This nuclear increase in the graft was present in longitudinal strips or oval zones. After the second week healing was produced by organisation of the scar between the ends of graft and stumps, in the formation of which the tenoblasts themselves played the most important part. During the fourth and fifth weeks after operation the sheath separated progressively more easily from the organising tendon and a well organised tendon with a paratenon arrangement about it was eventually produced. They could not demonstrate any new synovial sheath formation. Teneff and Fonda (1953) found no differences in the rate, completeness, or character of growth in autogenous, homogenous, or heterogenous grafts of frozen tendon. They thought that the fibrillar portion