Takeaway: Arthrofibrosis is common and can be debilitating. But because it doesn't have an agreed-upon diagnostic criteria, many professionals don't acknowledge or understand how important it is.

Imagine you've been through a common orthopedic surgery, and you’ve completed your follow-up care, but your knee (or elbow or ankle or shoulder) continues to hurt, and your range of motion is getting more and more limited. Your surgeon isn't interested, physical therapy is excruciating, and no one seems to be able or willing to explain what’s going on. This is the experience of many people with arthrofibrosis.

What is Arthrofibrosis?

Arthrofibrosis is a condition involving the manufacture of excessive extracellular matrix (ECM) inside and around joints because of dysregulation of the inflammatory and healing processes. This causes a buildup of connective tissue: mostly collagen, but heterotopic ossification—bone-like material in soft tissues—is possible too. And all this typically happens in and around a major synovial joint: a knee, an elbow, a shoulder (where it might be identified as adhesive capsulitis or frozen shoulder). It is often triggered by a surgery or injury, but it could be related to other factors too.

When it occurs as a complication of knee surgery, it has this definition: “. . . a limited ROM (range of motion) in extension and/or flexion, measured by active flexion and extension, which was not caused by infection or other specific causes.”¹

Another definition is a bit simpler: “Arthrofibrosis is defined as joint pain and stiffness that does not allow functional range of motion and is commonly due to adhesions, scarring, and contracture of the joint.”² This description suggests arthrofibrosis must be very common. But searches of well-respected sources of information about diseases and conditions (e.g., the National Institute of Arthritis and Musculoskeletal and Skin Diseases, and Emedicine.com) yield little or no discussion about this condition.

One obstacle to understanding arthrofibrosis is that it has no consistently-used diagnostic criteria. Some resources suggest it should only be diagnosed when the situation is severe enough to require surgical intervention; other resources include people with joint restrictions, but who don’t necessarily pursue surgery, as persons with arthrofibrosis. For this reason, estimates of how common it is range from accounting for 0.2 percent of post-surgical knee problems to 73 percent of post-ankle-fracture problems. 

Pathophysiology

To talk about the processes involved in arthrofibrosis, we need to look at what might be the body’s most interesting cell, the myofibroblast.

If you went to massage school in my era (the early ’80s), you might have learned that connective tissue is composed mainly of protein fibers suspended within a fluid or solid medium. Those fibers (varieties of collagen, elastin, and others) can be organized or disorganized, and they can be dense or loosely arranged. These variables give connective tissues their properties of strength, stretchiness, resistance, and different levels of stiffness and hardness. And embedded within this extracellular matrix we find the fibroblasts: literally, “fiber builders,” cells whose job is to produce new protein fibers and maintain the health of the connective tissue structure.

Since that time, our understanding of the construction, maintenance, and repair processes of connective tissue has evolved. Now we know that under certain circumstances (namely, mechanical distortion and/or exposure to pro-inflammatory chemicals), fibroblasts become more complex. Fibroblasts migrate to areas of injury, and they may change. From being smooth and spindle-shaped, they become broad and flat, and they develop numerous outreaching branches. Perhaps most importantly, they develop internal actin fibers that make them behave like smooth muscle cells: myofibroblasts are contractile. They play a vital role in wound healing, as they pull on damaged structures and produce ECM to help “glue” and pull injured surfaces together. In short, they make scar tissue (Image 1). 

Under normal conditions, fibroblasts migrate to an injured area, transform into myofibroblasts, proliferate as needed, and help knit the damaged tissue. Then their work is done, and they die. But in arthrofibrosis, they don’t; they just keep churning out ECM. Healthy myofibroblastic activity is important, but it can become pathologic when those cells don’t know when to stop and joint function is diminished instead of restored:

“On a cellular level arthrofibrosis is characterized by upregulated myofibroblast proliferation with reduced apoptosis, adhesions, aggressive synthesis of ECM that can fill and contract joint pouches and tissues and often also heterotrophic ossification. Although ECM is necessary for healing and wound repair, dysregulation of production and degradation leads to pathologic fibrosis.”³

Arthrofibrosis can damage internal joint structures, but external structures like bursae or fat pads may also become infiltrated with myofibroblasts and scar tissue. These may be continually irritated with movement, leading to more inflammation, and more ECM. In addition, excessive ECM may interfere with local blood flow, leading to hypoxia, which triggers the secretion of inflammatory cytokines. Ironically, that is the factor that keeps those myofibroblasts busy, and so a vicious circle is born: more ECM, less blood flow, more inflammation, and more ECM, ad infinitum. 

It appears that some people have a genetic predisposition for this dysfunctional overactivity of myofibroblasts and scar tissue formation. Some studies have begun to find connections and overlap in people who have frozen shoulder, Dupuytren’s contracture, idiopathic pulmonary fibrosis, and other fibrotic problems. It may be that this population is also prone to developing this common complication of joint injuries or surgeries.  

In addition, research points to connections between inflammation-based diseases like osteoarthritis, type 2 diabetes, and others to a risk for fibrotic conditions. We see this in the finding that people with diabetes are five times more likely to develop frozen shoulder compared to the rest of the population.⁴

Most of the literature about arthrofibrosis discusses it in the context of the knee, especially as a surgical complication of ACL repair or total knee replacement. But it has been documented at the elbow, wrist, hip, and ankle. It is often associated with a joint injury or surgery, but it can occur with neurological deficits, and it is an especially common complication of hemophiliac arthropathy: a person with hemophilia may bleed into a joint space, and this is a powerful impetus for the cellular activities that cause arthrofibrosis.

Some experts discuss frozen shoulder or adhesive capsulitis as a form of arthrofibrosis. Certainly the cellular processes are the same or similar, but frozen shoulder has some different patterns: it tends to occur in middle-aged women (where arthrofibrosis is more common in younger people); it often has a spontaneous onset (where arthrofibrosis is usually linked to injury or surgery); and while the prognosis for arthrofibrosis is often poor in many cases, most cases of frozen shoulder are expected to have a nearly full recovery, regardless of what kind of intervention is used—at least, that’s been the traditional expectation. This belief has recently come under scrutiny, however, and it may be unrealistically optimistic: Many people with frozen shoulder live with long-term pain, stiffness, and loss of range of motion.  

Signs and Symptoms 

The symptom patterns we see with arthrofibrosis suggest that this condition appears in two main forms or stages: active and residual.

A typical presentation involves a trigger, followed by pain, inflammation, new scar tissue production, and a decreased range of motion that worsens over a period of time. This active, inflammatory period may persist for an undetermined amount of time, and it may lead to peripheral and central sensitization: changes in neural processing of nociceptive signals. In fact, this presentation of arthrofibrosis may often be misdiagnosed as complex regional pain syndrome, a pain-processing disorder that usually begins with an injury to an extremity.

Some people with arthrofibrosis get stuck in this state of active inflammation, pain, and loss of function, and that is their lifelong experience. But others may move on to the second residual arthrofibrosis stage: inflammation subsides, scar tissue constricts, and the person is left with persistent stiffness and loss of function. Pain may no longer be a constant problem. However, if this person then pushes the affected joint past a comfortable range of motion and initiates a new inflammatory process—especially within the first year of recovery when the fibroblasts may still be easy to reactivate—they may reenter that acute stage of pain and scar tissue formation.

Treatment Controversies

Because arthrofibrosis is not well understood, we have few strategies to prevent or even lower the risk of its development. Over the past decades, orthopedic surgical and post-surgical protocols have evolved to try to improve long-term outcomes, but we have not seen significant changes in the frequency with which arthrofibrosis develops as a complication. Orthopedists and others may assume that some patients develop arthrofibrosis because they are not compliant with their physical therapy or other postsurgical treatment, but this is probably not the case. Instead, arthrofibrosis is a situation that involves dysregulated inflammatory and healing responses.

The “old school” approach to arthrofibrosis involves aggressive physical therapy, sometimes followed by forceful joint manipulation or manipulation under anesthesia to try to break up internal joint adhesions. Alternatively, surgery to destroy or remove scar tissue may be recommended. In the short term these interventions have been seen to improve range of motion, but they are also associated with a risk of exacerbating symptoms and leaving the patient in a worse situation than before. 

Alternatively, a nonaggressive approach might include exercise of other areas, stretching, and manual therapies that all stay well within boundaries for pain and injury. The disadvantage to this approach is that it is slow, and improvement may take place only over a period of months or longer. 

Many variables can influence the outcomes of arthrofibrosis treatment. These include how long it was since the triggering event, how much of the joint is affected, and the individual’s unique immune and inflammatory responses. Some patients appear to tolerate aggressive interventions well, and others react badly, sometimes with permanent damage. This suggests some differences in those internal chemical environments, and those differences are impossible to predict.

The future of arthrofibrosis treatment may look extremely different than it does today. As we learn more about myofibroblastic activity and inflammatory cytokines, we may also learn how to influence those signals and cellular activities in ways that can reduce the hyper-production of scar tissue that impairs function.

Massage for Arthrofibrosis?

Arthrofibrosis is a problem that usually starts inside large synovial joints—beyond the reach of our hands. However, external ligaments, fat pads, bursae, tendons, and muscles may also become constricted, adhered to each other, and pathologically fibrotic. Further, the muscular patterns that develop around a joint with a limited ROM may reinforce that constraint: Proprioceptors adapt to limitations, so the neuromuscular signals may perpetuate and even advance the problem as the tight muscles further compress and irritate the joint structures.

Massage therapy cannot undo the results of an overactive inflammatory response with the accumulation of excessive scar tissue, but our work could probably help with many of the auxiliary consequences.

What are some possible risks related to working with a client who has arthrofibrosis? If the injury or surgery is still in the healing phase, it’s not appropriate to disrupt those tissues, of course. 

Manual therapies for frozen shoulder sometimes recommend aggressive stretching to try to “break through” the scar tissue and reestablish a normal range of motion. Given what we know about inflammation and scar tissue accumulation, I propose that this is not in the client’s best interest. Any work that stimulates inflammation and the production of collagen can exacerbate the processes that cause this problem.

By contrast, in a situation where the surgery or trauma was recent, then pain-free massage in combination with pain-free exercise and stretching could help prevent the processes that start arthrofibrosis to begin with, and it could undo some of the contributing factors that restrict range of motion as the condition develops. When inflammation settles, neuromuscular strategies like proprioceptive neuromuscular facilitation or muscle energy technique may help reset the resting tone of affected muscles, which could then improve range of motion at the joint—but only if this work does not initiate any adverse reactions in terms of pain, heat, or swelling at the joint.

How much difference massage therapy might make for a long-term fibrotic joint is an open question, however. But even for clients with longstanding limitations, the experience of educated touch that respects their pain tolerance, range of motion, and other physical compensations that they have had to make to accommodate for a “frozen” joint could be strength- and health-promoting. 

Kayley Usher, PhD, a leading expert on arthrofibrosis and founder of the International Arthrofibrosis Association, suggests a conservative approach to avoid causing inadvertent injury and renewed ECM production is preferable. But to date, the only published study about massage and arthrofibrosis is a case report that suggests that a modified version of cross-fiber friction using tools (the Graston technique) and exercise to “release adhesions, scar tissue, and fascial restrictions” was effective. This type of work can cause bruising, and the supposition that this strategy does indeed “break down” scar tissue is questionable. But the results of this single-person case report were clear: The client had improvement in range of motion and muscle strength, where other interventions had not succeeded. That said, the data describes only one person, and covered only short-term effects. We don’t know the long-term outcomes for this patient.⁵ 

I agree with Dr. Usher that a strategy that does not promote more scar tissue is better than one that causes inflammation and bruising for a person whose injury-response processes have a history of being hyperreactive. The video that accompanies this column shows more of my conversation with Dr. Usher about her experience with arthrofibrosis, the inflammatory process, and the work of the International Arthrofibrosis Association. 

Notes

1. K. M. Usher et al., “Pathological Mechanisms and Therapeutic Outlooks for Arthrofibrosis,” Bone Research 7, 9 (2019): https://doi.org/10.1038/s41413-019-0047-x. 

2. B. T. Velasco et al., “Arthrofibrosis of the Ankle,” Foot & Ankle Orthopaedics 5, no. 4 (2020): https://doi.org/10.1177/2473011420970463. 

3. Usher et al., “Pathological Mechanisms and Therapeutic Outlooks for Arthrofibrosis.” 

4. B. P. Dyer et al., “Diabetes as a Prognostic Factor in Frozen Shoulder: A Systematic Review,” Archives of Rehabilitation Research and Clinical Translation 3, no. 3 (2021): 100141, https://doi.org/10.1016/j.arrct.2021.100141. 

5. D. W. Black, “Treatment of Knee Arthrofibrosis and Quadriceps Insufficiency after Patellar Tendon Repair: A Case Report Including Use of the Graston Technique,” International Journal of Therapeutic Massage & Bodywork 3, no. 2 (2010): 14–21.

Author’s note: I want to offer my special gratitude to Kayley Usher, PhD, a leading expert on arthrofibrosis and founder of the International Arthrofibrosis Association. Dr. Usher was the lead author on a 2019 review article published in Bone Research titled “Pathological Mechanisms and Therapeutic Outlooks for Arthrofibrosis,” and she generously let me interview her twice: once for a podcast about arthrofibrosis (see page 73), and again for this column.

I have a client who has been diagnosed with arthrofibrosis.

There is very little information on how to work with this condition. This client is 29 years old and had some stubborn, tight fibularis muscles that ended up affecting his knee to the point that his orthopedist told him he needed an anterior cruciate ligament repair. I’m not sure if there was ever any injury. 

After the ACL repair, his body laid down bone and fibers that have left this young father of a 16-month-old in about 60 degrees of flexion, in a fixed position. He gets around with crutches.

His case kind of broke my heart.

– Excerpt from “I Have a Client Who . . .”  Pathology Conversations with Ruth Werner, episode 311

Resources 

Baum, J. and H. S. Duffy. “Fibroblasts and Myofibroblasts: What Are We Talking About?” Journal of Cardiovascular Pharmacology 57, no. 4 (2011): 376–79. https://doi.org/10.1097/FJC.0b013e3182116e39. 

Black, D. W. “Treatment of Knee Arthrofibrosis and Quadriceps Insufficiency after Patellar Tendon Repair: A Case Report Including Use of the Graston Technique.” International Journal of Therapeutic Massage & Bodywork 3, no. 2 (2010): 14–21. 

D’Urso, M. and N. A. Kurniawan. “Mechanical and Physical Regulation of Fibroblast–Myofibroblast Transition: From Cellular Mechanoresponse to Tissue Pathology.” Frontiers in Bioengineering and Biotechnology 8 (2020). www.frontiersin.org/articles/10.3389/fbioe.2020.609653.  

Dyer, B. P. et al. “Diabetes as a Prognostic Factor in Frozen Shoulder: A Systematic Review.” Archives of Rehabilitation Research and Clinical Translation 3, no. 3 (2021): 100141. https://doi.org/10.1016/j.arrct.2021.100141. 

Healthline. “Arthrofibrosis After Knee Replacement.” Updated September 29, 2017. healthline.com/health/total-knee-replacement-surgery/arthrofibrosis. 

Injured Athlete’s Toolbox. “Arthrofibrosis.” 2015. www.injuredathletestoolbox.com/aboutarthrofibrosis.  

International Arthrofibrosis Association. “What is Arthrofibrosis.” Accessed March 2023. www.arthrofibrosis.info/what-is-arthrofibrosis.   

Lubowitz, J. “Arthrofibrosis.” James H. Lubowitz, M. D. (March 31, 2013). www.jameslubowitzmd.com/arthrofibrosis.

Martinez-Lozano, E. et al. “Management of Arthrofibrosis in Neuromuscular Disorders: A Review.” BMC Musculoskeletal Disorders 23, no. 1 (2022): 725. https://doi.org/10.1186/s12891-022-05677-z. 

Medscape. “Anterior Cruciate Ligament Injury.” Updated February 26, 2021. https://emedicine.medscape.com/article/89442-overview.  

Sapudom, J. et al. “The Interplay of Fibronectin Functionalization and TGF-ß1 Presence on Fibroblast Proliferation, Differentiation and Migration in 3D Matrices.” Biomaterials Science 3, no. 9 (2015): 1,291–301. https://doi.org/10.1039/C5BM00140D. 

ScienceDirect. “Arthrofibrosis.” Accessed March 2023. www.sciencedirect.com/topics/medicine-and-dentistry/arthrofibrosis.

Smith, S. P., V. S. Devaraj, and T. D. Bunker. “The Association Between Frozen Shoulder and Dupuytren’s Disease.” Journal of Shoulder and Elbow Surgery 10, no. 2 (2001): 149–51. https://doi.org/10.1067/mse.2001.112883. 

Tai, Y. et al. “Myofibroblasts: Function, Formation, and Scope of Molecular Therapies for Skin Fibrosis.” Biomolecules 11, no. 8 (2021): 1,095. https://doi.org/10.3390/biom11081095. 

Usher, K. M. et al. “Pathological Mechanisms and Therapeutic Outlooks for Arthrofibrosis.” Bone Research 7 (2019): 9. https://doi.org/10.1038/s41413-019-0047-x. 

Velasco, B. T. et al. “Arthrofibrosis of the Ankle.” Foot & Ankle Orthopaedics 5, no. 4 (2020). https://doi.org/10.1177/2473011420970463. 

WebMD. “Knee Scar Tissue: What to Know.” Reviewed May 24, 2021. www.webmd.com/pain-management/knee-pain/what-to-should-know-about-knee-scar-tissue.