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The advancement flap is the oldest and most straightforward type of adjacent tissue transfer, since it is basically a geometric and biomechanical extension of the fusiform or lenticular closure (Fig. 2.1). As compared to primary side-to-side closure, the advancement flap provides a small amount of additional tension release and no tension redistribution. The unique attribute of the advancement flap is the ability to redistribute and selectively position collections of tissue redundancy termed dog-ears when they are generated by wound closure.1 Advancement flaps have widespread utilization in the repair of facial operative wounds, and despite their relative simplicity, they are the most common type of nonlinear reconstruction utilized by most surgeons. Their design and execution is enhanced by a thorough understanding of the principals of tissue motion. Interestingly, less literature attention has been paid to the design of advancement flaps than to their more complex cousins, transposition, and rotation.
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An advancement flap moves tissue linearly from a site of origin to a recipient destination. The tension vector of closure is the same, or nearly the same, as would be the case if the wound were closed linearly. From an undermining standpoint, there is little mechanistic difference between the creation of an advancement flap and the execution of an elliptical closure. The edges of a primary closure may be undermined for a distance equivalent to that of a flap, generating equal degrees of deep tension release. Following appropriate undermining, the mobility of both advancement flaps and fusiform closures is primarily limited by a tension vector directed 180° away from the direction of the advancement. Nonetheless, there are subtle changes in mobility effected by the creation of an advancement flap.
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The amount of tension release achieved in any side-to-side closure is a function of intrinsic tissue properties, flap length, and undermining.2,3 Two undermining components exist: (1) undermining from the leading edge of the flap back to the pedicle and (2) undermining beneath the pedicle. These maneuvers release the advancing flap from the restraint of the underlying host bed (Fig. 2.2). Such deep restraint is transmitted via the intralobular septae of the fat from other limiting structures such as the fascia, muscle, or bone. The greater the undermining, the more motion may be achieved. Undermining does disrupt the vertical perforating vessels which nourish the flap. A balance must therefore be reached between tension release and vascular deprivation.
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