Ifssh Flexor Tendon Committee Report

Abstract

At its most basic, biomechanics is the study of the effects of bending, twisting, pulling, pushing and rubbing (shear) forces on living tissue. These effects provide, as limits, a mechanical description of biological tissue; as they relate to loading experienced in vivo, they describe the mechanical milieu in which living tissues operate. To the extent that the latter affect the former, one can speak of a "Wolff's Law of Soft Tissue", to describe the effect of function on form. Within the realm of hand surgery, no topic exceeds tendon injury and repair in the wealth of biomechanical data available, the thought that has gone into the analysis of that data, and the knowledge that has been gained as a result. This review will summarize the influence of biomechanical thought and research on the management of flexor tendon injury. Conceptually, the loads applied to tendons physiologically become the lower limit for the material properties of the tissue, if it is to function normally. Thus it is relevant to know the tensile strength of normal tendon, of various tendon repairs, and the loads that might be applied to healing tendons either during daily activity or with rehabilitation. Tendon repairs commonly fail by breaking at some point during the healing period. In vitro studies have shown that thicker core sutures, repairs with more strands crossing the laceration, and repairs with locking loops are stronger, and such repairs have been adopted clinically. A running peripheral suture does not increase the ultimate breaking strength much, but does increase the load needed to cause the repair to gap, especially when the running suture is locked. This may be useful as well, for several mechanical reasons discussed below, and on the basis of these mechanical studies, peripheral finishing sutures have been incorporated into tendon repairs, although the details of such sutures remain subject to discussion. Tendon repairs have also been studied in vivo, in animal models. It has been known since the 1940s, when Mason and Allen wrote their classic study, that repairs tend to weaken for the first few weeks, especially in immobilized tendons. More recently, it has become clear that this effect can be moderated considerably if tendons are moved postoperatively, and so early motion regimens have become incorporated into all tendon rehabilitation protocols. Whether loading of the tendon is also important remains controversial. Loading clearly stimulates isolated tendon cells and, in some cases, tendon tissue in vitro, but the results of loading programs in vivo, either in animal models or in clinical studies, have been unimpressive when compared to similar protocols which assure motion, but with minimal loading. Some unanticipated findings have been noted in the studies of partial tendon injuries, which again have influenced clinical practice. For partial lacerations that affect less than 90% of the tendon cross-section, a repair results in a weaker tendon postoperatively than no repair. Even

Neuropeptide, Mast Cell, and Myofibroblast Expression After Rabbit Deep Flexor Tendon Repair

“…Other approaches, targeting the biomolecular aspects of the healing process, might be useful in achieving further progress in decreasing adhesion formation and optimizing the recovery and strength of flexor tendon repair. [1][2][3][4] Growth factors and inflammatory agents have been the major focus of research, but no single factor has yet proven to be the ultimate solution to either limit adhesion formation or augment tendon strength. The relative importance of different molecular and cellular participants during different phases, as well as potential negative effects of manipulation with down-regulation or up-regulation of a certain factor still remain, to a large extent, unknown.…”

Effectiveness of MicroRNA in Down-Regulation of TGF-β Gene Expression in Digital Flexor Tendons of Chickens: In Vitro and In Vivo Study

“…Early mobilization of the repaired tendon is effective in decreasing adhesions, although the motion does not eliminate adhesions and may rupture the repairs. [2][3][4][21][22][23] Numerous strategies were tested experimentally to combat adhesions; most either produced limited effects or had poor clinical applicability. A decade ago, Chang et al explored a novel approach of using antibody to neutralize TGF-␤1 to prevent adhesion formation.…”

“…[1][2][3][4][5][6][7] Transforming growth factor (TGF)-␤ is considered to be responsible for the formation of scars such as adhesions around the healing digital flexor tendons. Three isoforms of TGF-␤ have different biological functions.…”

Strength of Tendon Repair Decreases in the Presence of an Intact A2 Pulley: Biomechanical Study in a Chicken Model

“…20,21 The decrease was attributed to the fact that the tendon under curvilinear tension is subjected to both pulling and bending forces, which makes the repair more vulnerable to failure than linear tension alone. Rupture has been an important issue in clinical flexor tendon repair [22][23][24][25] ; previous studies have suggested a link between increased incidence of repair ruptures and the presence of the A2 pulley. [25][26][27] Pulley incision may reduce the detrimental effects of the bending forces on the repaired tendons, thereby decreasing the likelihood of repair failure.…”