Rabbit flexor tendons with a 90 per cent mid-section transverse
laceration demonstrated the intrinsic capacity to participate in the repair
process in the absence of extrinsic cell sources and without the benefit of
nutrition from a circulating blood supply or the influence of synovial
fluid. Two cellular processes were involved in the in vitro repair process:
(1) phagocytosis occurred by differentiation of fibroblasts from the
epitenon--the cells migrated into the repair site and removed cellular
debris and collagen fragments, and (2) collagen synthesis occurred
primarily within the endotenon cells. Clinical Significance: The results of
this experimental study support the concept that flexor tendons have the
intrinsic capacity to phagocytize old collagen and synthesize new collagen
fibrils. Consequently, clinical attempts to prevent or control the
peripheral adhesions appear valid, since these adhesions do not appear to
be an essential component of the repair process.