Tendon Adhesions: Causes, Symptoms, and Treatments

Tendon adhesions are bands of scar tissue that bind a tendon to the surrounding structures it normally glides past, restricting movement and often causing pain. They are one of the most common complications after tendon injuries and surgical repairs, with a meta-analysis of flexor tendon repairs reporting an adhesion rate of about 4% even with modern surgical techniques and rehabilitation protocols.¹ The reality behind that modest-sounding number is that adhesions range from barely noticeable stiffness to severe, function-stealing contractures, and the biology driving them is far messier than “scar tissue grows where it shouldn’t.”

How Adhesions Form

When a tendon is injured or surgically repaired, the body launches a healing response that relies heavily on inflammation and collagen production. A growth factor called TGF-β1 is one of the most powerful drivers of this process, stimulating cells to multiply, produce collagen, and bind to surrounding tissue.² In a perfect world, the new collagen would line up neatly along the tendon’s length, restoring its original gliding ability. In practice, the repair process tends to overshoot. TGF-β drives collagen production so aggressively that scar tissue forms not only within the tendon gap but also between the tendon surface and its surrounding sheath, nearby bone, or adjacent soft tissue.³

Research into the cellular level of this process has revealed something interesting about age and healing quality. In neonatal animals, healing involves a brief wave of outside cells followed by the tendon’s own resident cells taking over, rebuilding the tendon more or less normally. In adults, healing is dominated almost entirely by cells that migrate in from outside the tendon and never leave, forming permanent scar.⁴ That difference helps explain why children who undergo flexor tendon repair tend to heal with more pliable adhesions and better outcomes than adults, sometimes avoiding tenolysis surgery entirely.⁵

Major Risk Factors

Not every tendon repair ends in problematic adhesions. Several factors tip the odds. A large study examining risk factors for adhesion after hand tendon repair identified the following as the most significant, in descending order: degloving injuries (where skin is torn away from underlying tissue), skipping post-operative exercises, zone II flexor tendon injuries, delays of more than 12 hours between injury and surgery, combined vascular injury, and injuries involving multiple tendons.⁶

A few of those deserve unpacking. Zone II of the hand, the stretch between the base of the finger and the middle of the palm, is notoriously challenging for surgeons because two flexor tendons share a tight fibrous tunnel in that area. Any scarring at all in that confined space can lock the tendons to the sheath wall. Degloving injuries rank highest because they damage not just the tendon but the surrounding blood supply and soft tissue envelope, creating a much wider field of inflammation and repair.

The role of immobilization versus early movement deserves emphasis because it is probably the most actionable risk factor for patients. An animal model showed that immobilizing a repaired tendon led to a progressive rise in the resistance to finger bending: roughly 36% more resistance at one week and 63% more at three weeks compared to baseline. In contrast, tendons that were mobilized (with a short initial delay of about three days) returned to baseline resistance by three weeks.⁷ The message is clear: the longer a repaired tendon sits still, the more scar tethers it to its surroundings.

Metabolic conditions also play a role. Diabetes, high cholesterol, and obesity have all been linked to impaired tendon healing, and these conditions frequently overlap. The chronic low-grade inflammation associated with metabolic syndrome appears to disrupt normal collagen remodeling and prolong the inflammatory phase that encourages adhesion formation.

Symptoms and How Adhesions Are Identified

The hallmark symptom is a loss of active range of motion that does not improve, or barely improves, with further rehabilitation. You can often tell the difference between adhesion-related stiffness and joint stiffness by comparing active and passive motion. If someone else can bend your finger further than you can bend it yourself, the tendon is likely tethered, because the joint itself moves fine when pulled but the tendon cannot glide enough to produce the same range under its own power. If left untreated, these early limitations can lead to fixed deformities and lasting functional loss.⁸

Diagnosis is usually clinical, based on history and physical exam. When the situation is less straightforward, dynamic ultrasound can be valuable. In one case of persistent Achilles tendon dysfunction after surgical repair, a dynamic ultrasound scan revealed significant adhesion between the Achilles tendon and the fat pad behind it, something a static image would have missed.⁹ Watching the tendon in real time while the patient moves the joint lets clinicians see exactly where the tendon sticks and how badly.

Pain is variable. Some adhesions hurt, especially when you try to push through the restricted range. Others are painless but frustrating, producing a feeling of mechanical blockage without sharp discomfort. A “triggering” sensation, where the finger catches and then suddenly releases, can also occur when adhesion partially obstructs normal tendon gliding.

Rehabilitation and Early Motion Protocols

The single most important treatment for tendon adhesions is also the best way to prevent them: controlled early motion after repair. The details of exactly how and when to move matter more than most patients realize.

A randomized trial comparing controlled active motion (where you actively bend and extend under guidance) to early passive motion (where a therapist or splint moves the finger for you) found that controlled active motion produced superior results at every time point measured. By 12 weeks, 80% of patients in the active motion group achieved excellent outcomes on a standard grading scale, compared to 55% in the passive motion group.¹⁰ Grip strength and disability scores followed the same pattern.

A study of early active mobilization in zones II through V found excellent results in about 63% of digits and good results in another 19%, with complications like tendon rupture occurring in only about 3% of cases.¹¹ For extensor tendons, a trial comparing early active motion to immobilization found that the early motion group had better total active motion and returned to work sooner, with statistically significant advantages lasting up to 12 weeks.¹²

There is a real tension here between moving early enough to prevent adhesions and moving too aggressively and rupturing the repair. The animal data mentioned earlier suggests that delaying mobilization by about three days after surgery, then starting controlled movement, may be a sweet spot that allows the earliest inflammatory surge to settle without letting scar mature into strong tethers.⁷ Clinical protocols vary between surgeons and institutions, but the trend over the past two decades has been steadily toward earlier and more active motion.

Patient-reported outcomes track with the objective measurements. One study found a moderate correlation between total active motion and disability scores after flexor tendon repair, with mean disability scores improving substantially from about 46 points at four weeks to around 24 points by 12 weeks during a structured rehabilitation program.¹³ The practical implication is that the first three months of consistent therapy are where most of the functional gains happen.

When Surgery Is Needed

If active motion recovery stalls after three to six months of therapy, surgical release of the adhesions, called tenolysis, becomes a reasonable option. The procedure involves carefully cutting away the scar tissue binding the tendon to its surroundings, freeing it to glide again. A retrospective review of flexor tenolysis after zone II-III repairs found that total active motion improved from about 147° to 184° at the 12-week follow-up, and roughly half of the treated digits achieved excellent or good outcomes.¹⁴

A study of a traction tenolysis technique in 97 patients reported that roughly two-thirds achieved more than 75% of normal total active motion, and 80% reached at least half of normal motion. The gap between active and passive flexion, a direct measure of how much the adhesion was limiting the tendon, shrank from 28° before surgery to 9° after. The complication rate was 5%, including one tendon rupture during the procedure and three patients who required additional surgery.¹⁵

Those numbers are encouraging, but tenolysis has limits. Revision procedures (a second tenolysis when the first one did not work well enough), dual-tendon repairs, and cases with associated nerve injuries all predicted worse outcomes.¹⁴ Re-adhesion after tenolysis is a real phenomenon, because the surgery itself triggers a new round of inflammation and healing. That is why post-tenolysis rehabilitation is just as critical as post-repair rehabilitation, and why many of the preventive strategies described below are being developed specifically for use during tenolysis.

Barrier Materials and Anti-Adhesion Surfaces

Researchers have spent decades trying to find materials that can physically block scar tissue from forming between a healing tendon and the surrounding tissue. The concept is straightforward: wrap the repair in something slippery or semi-permeable that keeps nutrients flowing to the tendon while preventing invading cells from anchoring it to the sheath. A review of anti-adhesion biomaterials found that most studied materials, ranging from synthetic polymers to biologic scaffolds, act as barriers and show generally acceptable safety profiles in terms of compatibility and biodegradability.¹⁶

Hyaluronic acid, a naturally occurring substance in joint fluid, is among the most studied barrier agents. An animal study comparing cross-linked and non-cross-linked forms found that the non-cross-linked version was better at preventing adhesion, with significantly lower adhesion scores on histological analysis.¹⁷ Seprafilm, a commercially available anti-adhesion sheet originally developed for abdominal surgery, has also shown benefit in reducing tendon adhesions in animal tenolysis models.¹⁸

More creative approaches are also being tested. Decellularized tendon matrix membranes, made by stripping donor tendon tissue of its cells while preserving the structural proteins, reduced adhesion and improved repair quality in a rabbit Achilles model.¹⁹ Similarly, decellularized amniotic membrane has been used experimentally to reconstruct the tendon sheath itself, effectively giving the tendon a new sleeve that promotes internal healing while blocking external scar formation.²⁰ In one of the more unusual material experiments, decellularized tilapia fish skin was used as a scaffold combined with tendon stem cells and showed reduced fibrous scarring compared to repairs without the scaffold.²¹ A synovial fluid-based gel coating for tendon grafts also significantly reduced adhesion scores and improved finger joint motion in a long-term study.²²

It is worth noting that almost all of these barrier materials are still in animal or early clinical testing. None has become a universal standard of care, though hyaluronic acid-based products are the closest to routine clinical use.

Biologic and Drug-Based Approaches

Beyond physical barriers, researchers are targeting the molecular machinery of adhesion formation directly. Since TGF-β1 is one of the most potent drivers of fibrosis during tendon healing, silencing the gene that produces it is an appealing strategy. A 3D-printed tendon scaffold loaded with a gene-silencing agent targeting TGF-β1 was shown in preclinical work to both prevent adhesion and promote functional tendon repair.²³ The challenge is doing this precisely enough to reduce scarring without undermining the tendon’s ability to heal at all. TGF-β promotes both helpful collagen production within the tendon and harmful adhesion formation outside it, so simply shutting it off is not an option.

Platelet-rich plasma, or PRP, takes a different approach by concentrating the patient’s own growth factors and applying them at the repair site. PRP contains a cocktail of signaling molecules that modulate inflammation, stimulate the tendon’s own cells to proliferate, and support blood vessel formation.²⁴ Tendon stem cells, which can self-renew and differentiate into the cells responsible for tendon maintenance, are being explored alongside PRP as a combined therapy.²⁵ Mesenchymal stromal cells derived from fat or synovial tissue have shown promising preclinical effects by dialing down inflammation, reducing scar-related gene activity, and improving tendon gliding, though the results have not always reached statistical significance.²⁶

An older but still-studied drug strategy uses 5-fluorouracil, a chemotherapy agent, at very low doses applied locally. The drug works by inhibiting the proliferation of the fibroblasts that invade from outside the tendon and lay down adhesion-forming scar.²⁷ In a hen model using slow-release gelatin blocks, a low dose (10 mg) reduced adhesion formation compared to untreated controls, while higher doses (20 and 30 mg) caused severe inflammation and were counterproductive.²⁸ This illustrates a recurring theme in anti-adhesion research: the therapeutic window is narrow, and finding the right dose or delivery method is the hard part.

Where Adhesions Happen Beyond the Hand

Most of the clinical literature focuses on flexor tendons in the hand because that is where adhesions cause the most dramatic functional loss and where the anatomy is tightest. But adhesions can form after repair or injury of any tendon. Achilles tendon adhesions, as noted in the ultrasound case above, can bind the tendon to the fat pad behind the ankle, creating pain and restricted push-off during walking. Rotator cuff repairs in the shoulder, patellar tendon procedures around the knee, and even peroneal tendon surgeries at the ankle can all produce clinically relevant adhesions.

The common thread is that any tendon expected to glide within a sheath, channel, or against adjacent soft tissue is vulnerable. The tighter the anatomical corridor, the less room for error. Zone II of the hand remains the most studied and most problematic site, but the principles of early controlled motion, careful surgical technique, and minimizing tissue trauma apply everywhere tendons need to slide.

Adhesions That Do Not Follow Surgery

While surgical repair is the most well-known cause, adhesions can also develop after non-operative tendon injuries, prolonged immobilization for fractures near tendon paths, infections of tendon sheaths, and inflammatory conditions like rheumatoid arthritis. Crush injuries are particularly prone to adhesion because of widespread soft tissue damage. Metabolic conditions such as diabetes may impair the normal resolution of inflammation, leading the healing process to linger in its fibrotic phase longer than it otherwise would.

These non-surgical adhesions tend to be diagnosed later because there is no repair date on the calendar prompting a structured rehab program. A person who had a wrist fracture treated in a cast for six weeks may notice a stiff finger months later without connecting the two. By the time they seek help, the adhesion may have matured enough that therapy alone is insufficient, and tenolysis becomes the discussion. Early recognition, even in cases where no tendon surgery was performed, makes a real difference in how treatable the problem is.