Fibrous adhesion is disorganized, scar-like tissue that forms after injury, surgery, or repetitive strain and restricts normal movement between tissue layers. Our view is that it may be involved in more musculoskeletal problems than is usually recognized. It is rarely counted on its own because it sits under dozens of diagnostic names, depending on which specialist is looking and which tissue is involved. Unlike fibrosis in internal organs, musculoskeletal adhesion sits where examination and hands-on or device-based treatment can reach it.
The same process, a dozen different diagnoses
Fibrosis, the excess and disorganized buildup of collagen and scar-like tissue, is a major focus of modern medical research. Almost all of that research concerns organs: pulmonary fibrosis, liver fibrosis in metabolic disease, kidney fibrosis, scleroderma. A 2025 cross-organ review in Nature Reviews Drug Discovery laid out the shared biology across these conditions in detail.
The review's list of major fibrotic disease categories doesn't include musculoskeletal tissue at all. Yet the same cellular actors are active in a stiff shoulder capsule or a scarred-down tendon: activated fibroblasts turning into myofibroblasts, excess collagen deposition, and transforming growth factor-beta (TGF-β) driving the process.
Musculoskeletal fibrosis has likely been overlooked because it has never been filed under one name. It shows up as adhesive capsulitis (frozen shoulder), as arthrofibrosis after a joint injury or surgery, and as the disorganized collagen structure found in chronic tendinopathy. It appears as thickened, less mobile thoracolumbar fascia in chronic low back pain, and as the taut, restricted bands felt in myofascial trigger points. These belong to different specialists and different diagnostic codes. A growing body of research suggests a shared tissue process may connect them.
How common might it be?
The cells at the center of this are fibro-adipogenic progenitors, or FAPs. They are resident support cells in muscle and connective tissue. After injury, they can support clean, organized regeneration. Or they can default toward laying down disorganized fibrotic matrix. That tends to happen when inflammation doesn't resolve properly, when tissue isn't remodeled through normal movement, or when the injury repeats before it has healed.
A 2025 review in The Journal of Physiology frames this as a "fork in the road." The same cell population can go either way. Which path it takes depends heavily on the mechanical and inflammatory environment during healing, not on some conditions being inherently more "scar-prone" than others.
Consider how often that fork gets triggered. Global Burden of Disease data tracked roughly 494 million people living with other musculoskeletal disorders in 2020, more than double the 221 million recorded in 1990, with projections putting that figure past a billion by 2050. Many of those cases involve tissue that was injured, inflamed, or immobilized at some point, and so passed through that fork.
Surgery adds its own risk. Reported rates of arthrofibrosis after ACL reconstruction range from 2% to 35%, depending on how strictly it is defined (Sanders et al., Knee Surgery, Sports Traumatology, Arthroscopy, 2017). After a first total knee replacement, a 2026 review puts it at 3% to 10%, and up to 13% in some series (Hoveidaei et al., Journal of Knee Surgery, 2026). Add every joint surgery, muscle strain, bout of tendinopathy, and stretch of forced immobility. Healing with some degree of adhesion is plausibly common in musculoskeletal care. This is our reasoning from the evidence, not a measured prevalence.
Why it may be more treatable than organ fibrosis
The 2025 cross-organ review was candid about treatment for fibrotic lung, liver, and kidney disease. Turning mechanistic understanding of fibrosis into working drugs "continues to be limited and challenging." Only a handful of antifibrotic medications are approved, all for pulmonary fibrosis. Fibrotic tissue inside a lung or kidney is extraordinarily hard to reach and influence directly.
Musculoskeletal adhesion sits at or near the surface, in tissue we can physically access, load, and mechanically stimulate. The biology suggests that matters:
- Research on arthrofibrosis has found that the myofibroblasts depositing excess collagen aren't permanently locked into that identity. Under the right conditions, they can reverse differentiation toward a quieter, non-scarring state.
- A 2025 review on exercise and tissue fibrosis found that mechanical loading downregulates TGF-β signaling and helps rebalance the enzymes that build up and break down collagen matrix, in muscle and across fibrotic tissue generally.
- A 2026 review on fascial-targeted mechanical intervention described how more targeted, higher-intensity mechanical input, like that used in manual adhesion release and shockwave therapy, generates localized stress. That stress makes disruption of abnormal collagen cross-links more likely and triggers a fresh round of collagen turnover, giving tissue the chance to remodel toward a normal, mobile structure.
Put simply, the same cells that built the adhesion may, with the right mechanical input, help dismantle it. Fibrosis in most other organs doesn't offer that option yet.
Fixable doesn't mean automatic
None of this means every adhesion resolves the same way, or that more mechanical input is always better. The exercise-and-fibrosis research above included a real caveat: excessive or poorly dosed loading can worsen fibrosis. An overly aggressive return to activity can re-injure a tendon that was just starting to remodel.
Arthrofibrosis research also distinguishes "active" cases, where inflammation and collagen deposition are still ongoing, from "residual" cases, where the fibrotic process has burned out but the joint remains mechanically stiff. Those two states likely call for different approaches. Adhesion responds, when it responds, to the right mechanical input in the right amount at the right stage. Generic stretching or waiting it out is not the same thing.
What this means for an evaluation
If fibrous adhesion is involved in a large share of the conditions we diagnose separately, the evaluation question shifts. It becomes less "which named condition does this match?" and more "where has tissue lost its normal glide, and what combination of manual release, targeted shockwave, or movement-based loading will restore it?" That's the thinking behind treating each case as its own combination of tools.
If stiffness, restricted movement, or pain has outlasted the original injury by months or years, adhesion may be part of the picture, whatever name the problem has been given. Book a new patient exam and we'll examine what is involved.
Sources
- 2025 cross-organ review in Nature Reviews Drug Discovery. (link)
- 2025 review in The Journal of Physiology. (link)
- Global Burden of Disease data (2020) on musculoskeletal disorder prevalence. (link)
- 2025 review on exercise and tissue fibrosis (TGF-beta signaling). (link)
- 2026 review on fascial-targeted mechanical intervention. (link)
