The Cellular Biology of Flexor Tendon Adhesion Formation

Abstract

Intrasynovial flexor tendon injuries of the hand can frequently be complicated by tendon adhesions to the surrounding sheath, limiting finger function. We have developed a new tendon injury model in the mouse to investigate the three-dimensional cellular biology of intrasynovial flexor tendon healing and adhesion formation. We investigated the cell biology using markers for inflammation, proliferation, collagen synthesis, apoptosis, and vascularization/myofibroblasts. Quantitative immunohistochemical image analysis and three-dimensional reconstruction with cell mapping was performed on labeled serial sections. Flexor tendon adhesions were also assessed 21 days after wounding using transmission electron microscopy to examine the cell phenotypes in the wound. When the tendon has been immobilized, the mouse can form tendon adhesions in the flexor tendon sheath. The cell biology of tendon healing follows the classic wound healing response of inflammation, proliferation, synthesis, and apoptosis, but the greater activity occurs in the surrounding tissue. Cells that have multiple "fibripositors" and cells with cytoplasmic protrusions that contain multiple large and small diameter fibrils can be found in the wound during collagen synthesis. In conclusion, adhesion formation occurs due to scarring between two damaged surfaces. The mouse model for flexor tendon injury represents a new platform to study adhesion formation that is genetically tractable. The clinical problem of flexor tendon injuries can be complicated when healing results in adhesions forming between the tendon and the surrounding synovial sheath. Although difficult to predict following surgical repair, adhesions have long been accepted as a cause of restricted tendon movement. Recent clinical studies on 315 primary flexor tendon repairs reported that approximately 28% of flexor tendon repairs had a fair to poor functional recovery, likely to be attributable to adhesion formation.

Tendon injury and repair – A perspective on the basic mechanisms of tendon disease and future clinical therapy

“…At the levels of the tissue and organ, the effect of this aberrant tissue remodeling is an increased tendon crosssection that can provide adequate overall strength, but with suboptimal stiffness and function [8,[200][201][202][203]. In synovial tendons such as the digital flexors of the hand, the scar tissue may become entwined with the tendon sheath [204][205][206]. Such adhesions can severely limit joint function, and are a common complication following surgical tendon repair [204][205][206].…”

Evaluating Adhesion Reduction Efficacy of Type I/III Collagen Membrane and Collagen-GAG Resorbable Matrix in Primary Flexor Tendon Repair in a Chicken Model

“…Injury to the tendon often involves damage to multiple tissue types including the skin, subcutaneous tissue, digital fascial structures, synovial sheath, and the tendon itself, each with unique healing properties [22]. When a tendon is lacerated in "no man's land," the normal intrinsic blood supply and nutrition to the tendon is disrupted in that portion of the tendon [14].…”

Controlled release of curcumin from curcumin-loaded nanomicelles to prevent peritendinous adhesion during Achilles tendon healing in rats

“…3 Tendon adhesion results primarily from an excessive fibrotic response between the tendons and the synovial sheath. 4 With increasing information available concerning the nature of the scar tissue responsible for the peritendinous adhesions, control of excessive scar formation is essential to restore the functional integrity of a healing tendon after surgery.…”