Elsevier

The Journal of Hand Surgery

Volume 42, Issue 9, September 2017, Pages 722-726
The Journal of Hand Surgery

Current concepts
Molecular Biology of Flexor Tendon Healing in Relation to Reduction of Tendon Adhesions

https://doi.org/10.1016/j.jhsa.2017.06.013Get rights and content

Tendon injuries are encountered after major and minor hand trauma. Despite meticulous repair technique, adhesion formation can occur, limiting recovery. Although a great deal of progress has been made toward understanding the mechanism of tendon healing and adhesions, clinically applicable solutions to prevent adhesions remain elusive. The goal of this paper is to review the most recent literature relating to the tendon healing and adhesion prevention.

Section snippets

Tendon Healing Process

Flexor tendons heal via intrinsic and extrinsic pathways in sequential and partially overlapping phases: inflammation, proliferation, synthesis, and remodeling, including apoptosis/necrosis and vascularization.5 Following injury, an acute inflammatory response is initiated, resulting in recruitment of circulating inflammatory cells including macrophages, monocytes, and neutrophils. This phase lasts approximately 3 to 7 days. Extrinsic cells, from the peritendinous soft tissue, as well as

Impact of Mechanical Load on Tendons

Tenocytes respond to mechanical stress cues by modifying the expression of ECM components and matrix degradation enzymes with the goal of guiding tendon maturation toward structural healing. Through mechanical stress input, tenocytes upregulate the expression of type III collagen mRNA expression and increase the concentration of growth factors, resulting in cell proliferation, differentiation, and matrix formation.7 Thus, tendon healing is increased along the intrinsic pathway and adhesions are

Cytokines and Biological Mediators

A great deal of research has been devoted to understanding the biomechanical pathway to tendon adhesion formation. Unfortunately, this has led to little progress in effective clinical application. However, these studies have identified critical growth factors, resulting in targeted studies to uncover treatment modalities that may be clinically applicable in the future.

Pharmacological Agents

The flexor digital tendon surface is specifically adapted for gliding. Human flexor tendons are intrasynovial. They have a gliding system with a coefficient of friction that is similar to that of articular cartilage and a surface that includes lubricants such as hyaluronic acid (HA), phospholipids, and lubricin. An ideal tendon gliding–enhancing drug should have no systemic side effects, require only a single application, and target the extrinsic healing mechanism as well as the inflammatory

Physical Barriers With Biochemical Agents

Barriers loaded with nonsteroidal anti-inflammatory drugs such as ibuprofen-loaded poly(l-lactic acid)–polyethylene glycol, poly(l-lactide) electrospun fibrous membranes, multilayer electrospun celecoxib-loaded membranes, or high-viscosity naproxen sodium and calcium acetate–made hydrogels have shown efficacy in reducing peritendinous adhesion formation.30, 31, 32 These results have been attributed to suppression of fibroblast proliferation and collagen expression. In vivo results using

Stem Cells Therapies

Zhao et al34 investigated the effect of lubricant and autologous bone marrow stromal cell augmentation on immobilized flexor tendon repairs. They compared repaired tendons treated with and without cd-HA-lubricin plus an interpositional graft of bone marrow stromal cells and growth differentiation factor-5. After analyzing histology and measuring the work of flexion, tendon gliding resistance, adhesion score, and failure strength, the authors concluded that the combination of lubricant and cell

Postoperative Therapy

Rehabilitation protocols must balance the impact of immobilization—which is necessary for tenocyte migration and tendon healing, but causes increased adhesions and joint stiffness—with the need for tendon gliding and tenocyte stimulation.7, 36 Mobilization places a higher load across the repair site for tendon gliding with the increased potential for gapping or even rupture. Repaired tendons require a greater force to achieve motion owing to edema within the confined tendon sheath, friction

Conclusions and Future Directions

The mechanism of injury, the degree of manipulation, and/or the presence of a tendon gap are the main intraoperative factors that influence adhesion formation. Other factors include the type of rehabilitation protocol and the length of immobilization. The outcome of the repair is also surgeon-dependent. Choice of suture technique and material as well as mastering atraumatic techniques and meticulous tendon dissection is essential for the surgeon.37 The benefits of preserving flexor tendon

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