Successful outcome after flexor tendon repair requires a delicate balance between tendon healing and limiting scar tissue formation. Recent studies have highlighted the importance of the number of core sutures crossing the repair and the benefits of specific suture configurations in determining the strength of tendon repair. Researchers have attempted to augment the biological environment to improve the speed and strength of tendon repair.
Key points
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Tendon healing is a complex process that must coordinate healing within the tendon while limiting the amount of fibrosis in the surrounding tissues.
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The ultimate goal of surgical intervention has remained constant: to achieve enough strength to allow early motion, to prevent adhesions within the tendon sheath, and to restore the finger to normal range of motion and function.
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Although certain suture materials may have superior tensile properties, the number of strands crossing a repair site is the most important factor in the overall strength of the repair.
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Recent research has been focused on using pharmacologic agents to modify the healing environment to increase the healing response within the tendon while decreasing the adhesion formation between the tendon and its sheath.
Introduction
Before the 1960s, tendon repairs in the digits were rarely performed because of the universally poor outcomes, particularly in zone II, lending to the term “no man’s land.” Sterling Bunnell is often credited as being one of the first to stress the necessity of gentle and precise surgical technique in the treatment of flexor tendon injuries. Additional research has focused on different suture configurations or number of core sutures to maximize the strength of tendon repair and postoperative rehabilitation protocols to maximize function. The ultimate goal of surgical intervention has remained constant: to achieve enough strength to allow early motion, to prevent adhesions within the tendon sheath, and to restore the finger to normal range of motion and function. In recent years, basic science research has focused on biological factors that will increase the tendon stability after surgical repair, increase intratendinous healing, and decrease extratendinous fibrosis in order to maximize clinical outcomes. It is in this area that there is the potential for great advancement of our understanding of tendon healing.
The purpose of this article is to review the relevant tendon anatomy, biology of tendon healing, biomechanics of tendon healing, biological strategies to augment tendon healing, and suture configurations to maximize strength and motion.
Introduction
Before the 1960s, tendon repairs in the digits were rarely performed because of the universally poor outcomes, particularly in zone II, lending to the term “no man’s land.” Sterling Bunnell is often credited as being one of the first to stress the necessity of gentle and precise surgical technique in the treatment of flexor tendon injuries. Additional research has focused on different suture configurations or number of core sutures to maximize the strength of tendon repair and postoperative rehabilitation protocols to maximize function. The ultimate goal of surgical intervention has remained constant: to achieve enough strength to allow early motion, to prevent adhesions within the tendon sheath, and to restore the finger to normal range of motion and function. In recent years, basic science research has focused on biological factors that will increase the tendon stability after surgical repair, increase intratendinous healing, and decrease extratendinous fibrosis in order to maximize clinical outcomes. It is in this area that there is the potential for great advancement of our understanding of tendon healing.
The purpose of this article is to review the relevant tendon anatomy, biology of tendon healing, biomechanics of tendon healing, biological strategies to augment tendon healing, and suture configurations to maximize strength and motion.
Tendon anatomy
Tendons are collagen-based tissues that connect muscle to bone. Tendons are primarily composed of type I collagen, whereas the surrounding endotenon and epitenon are primarily composed of type III collagen. Collagen is synthesized and secreted by tenocytes present within the tendon. Once secreted, the collagen fibers arrange into triple helices and undergo cross-linking to increase their strength and stability. The surrounding extracellular matrix (ECM) is thought to help with gliding between collagen fibrils and to provide functional stability to the fibers.
The collagen fiber units are bound together by endotenon fascicles. These fascicles bind together within the epitenon to form the tendon ( Fig. 1 ). Lymphatic, vascular, and neural elements are present within the endotenon to supply the fibroblasts. The epitenon contains the blood vessels and tracts for the lymphatics and nerves. The tendon sheath is covered with synovial cells that provide lubrication to aid in gliding of the tendon within the sheath. Outside of the hand, tendons are not typically enclosed within a sheath and are covered by a continuous paratenon that contains the vascular elements to supply the endotenon and epitenon.
Both the flexor digitorum profundus (FDP) and flexor digitorum superficialis (FDS) tendons in the digits receive dual nutritional supply from vascular perfusion and synovial diffusion. The vascular supply is through vincula with each tendon having 2: a longus and a brevis. Proceeding from proximal to distal, the first vinculum encountered is the vinculum longus superficialis (VLS), arising just proximal to the decussation of the FDS and coming off the floor of the digital sheath of the proximal phalanx ( Fig. 2 ). The vinculum brevis superficialis consists of small triangular mesenteries near the insertion of the FDS. The vinculum longus profundus arises from the superficialis at the level of the proximal interphalangeal (PIP) joint. Finally, the vinculum brevis profundus arises near the insertion of the FDP. Each vinculum inserts on the dorsal aspect of the tendon, creating a richer blood supply on the dorsal side of the tendon. The vincula are important in the repair of injured tendons as they may hold the tendons out to length after injury, and one must be careful not to injure any maintained vincula while repairing an injured tendon, thereby decreasing the already tenuous blood supply.
The flexor tendons pass through the carpal canal and then enter a series of pulleys, creating the flexor tendon sheath in the digits. The flexor tendon sheath starts with the first annular pulley, or A1, overlying the metacarpal heads. There are a total of 5 annular pulleys (A1–A5) and 3 cruciate pulleys (C1–C3). The more stout annular pulleys help hold the tendon close to the phalanges, whereas the cruciate pulleys allow for some mobility of the sheath with finger flexion. The tendon sheath needs to be preserved, if at all possible, to maintain the normal function of the repaired tendon. The A1, A3, and A5 pulleys all arise from the volar plates of the metacarpophalangeal, PIP, and distal interphalangeal joints, respectively. These pulleys may be incised and used as windows through which to perform tendon repairs. The A2 and A4 pulleys should be maintained to prevent bowstringing of the tendon after repair.
Biology of tendon healing
Tendon healing is a complex process that must coordinate healing within the tendon while limiting the amount of fibrosis in the surrounding tissues. The initial healing of flexor tendons consists of 3 separate stages: inflammatory, fibroblastic or reparative, and remodeling.
Starting within the first week after injury, blood vessels within the tendon and tendon sheath form a clot at the injury site that is involved in the recruitment of vasodilators and proinflammatory cells. These cells migrate to the injury site from both local tissues as well as from distant sites. They also help with removal of necrotic tissue, fibrin clot, and cellular debris through phagocytosis. Canine models have shown that angiogenic factors, such as vascular endothelial growth factor (VEGF), help initiate the vascular invasion to the site of injury.
In the third week after injury, the tendon enters the fibroblastic stage. In this stage, the fibroblasts rapidly proliferate, synthesize immature collagen in an unorganized manner, and assist with the production of ECM. The initial collagen laid down is type III collagen, a weaker form of collagen than the type I collagen present in native tendons. The combination of type III collagen and previously initiated vascular network leads to scar formation within the tendon, initially decreasing its strength before entering into the final stage of healing.
The remodeling stage begins 6 to 8 weeks after injury. In this stage, type I collagen fibers are reoriented in a longitudinal manner along the long axis of the tendon and collagen fibrils begin cross-linking to one another, increasing the strength of the tendon complex. Unfortunately, the end result of the tissue repair never completely mimics the normal native tendon. It is during this stage that adhesions between the tendon and its sheath become more apparent.
Two separate models have been proposed to explain the overall mechanism of tendon healing. Extrinsic healing occurs when the fibroblasts and inflammatory cells move in from outside the tendon and invade the healing site. This process is thought to include the initial formation of adhesions. In contrast, intrinsic healing occurs through the migration of cells from the endotenon and epitenon. In most cases of tendon healing both types are present. Typically the extrinsic mechanism is activated earlier than the intrinsic mechanism and is thought to be responsible for the adhesion formation, whereas the intrinsic system is thought to help with collagen realignment and cross-linking.
Biomechanics of tendon healing
Although primary tendon repair with current techniques maximizes tendon healing and decreases tendon adhesions, it is not currently possible to recreate the biomechanical properties of the normal tendon. Native tendons have a stress-strain curve that is not directly linear in nature. The collagen fibrils are aligned with one another but are not on full tension while at rest. On tensioning of the tendon, there is an initial toe region in which the tendon fibrils fully align with one another ( Fig. 3 ). The curve then follows a linear progression as the tendon is increasingly tensioned. It maintains this linear slope until reaching the failure area of the curve. When tendons initially undergo surgical fixation, they have a decrease in their tension strength. It is not until the sixth to eighth week after repair when the strength of the tendon starts to increase as the collagen fibrils are realigning and the type I collagen begins to replace the initial type III collagen.
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