Abstract

THE usual cause of failure after primary repair of flexor tendons in no man’s land is adhesion between tendon and bed. The view that adhesions are inevitably necessary for tendon healing has been challenged by some (Furlow, rg75), and disproved both experimentally (Matthews and Richards, 1976) and in practice (Kessler and Nissim, 1969; Lister et al., 1977). Anatomical studies describing the intrinsic blood supply of sheathed flexor tendons (Caplan et al., 1975; Lundborg and Myrhage, 1977) and the effects of suturing methods on intrinsic blood supply (Bergljung, 1970) have led to speculation about the relevance of blood supply to healing and adhesion formation. Matthews and Richards have suggested that sheath synovial fluid may nourish the outer avascular layers of the tendon by diffusion. Experimental evidence to support this has also come from Lundborg (1976). The following study was designed to elucidate the role of sheath function and intrinsic tendon blood supply on adhesion formation and repair in experimentally severed chicken flexor tendons. The long flexor system of the 2 distal joints of the middle digit of the chicken’s foot closely resembles that of the human finger in the anatomy of both the sheath system (Greenlee, 1975) and the extrinsic (Fig. I) and intrinsic (Fig. 2) blood supply to the tendon.

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