Imaging, Diagnosing and Causes of Arthrofibrosis After Total Knee Replacement: An Interview with Dr. Marco Valoroso

Knee arthrofibrosis — a condition marked by pain, stiffness and, often, limited motion — remains one of the most challenging complications following total knee replacement (TKR) and other knee surgeries. Despite advances in surgical techniques and rehabilitation, many patients continue to struggle with this underrecognized condition, which can deeply affect mobility and quality of life.

To shed light on this complex topic, I had the pleasure of speaking with Dr. Marco Valoroso, Head of Knee Surgery at the EOC hospitals in Lugano, Switzerland, and a leading specialist in the management of arthrofibrosis. In the first of this two-part blog, Dr. Valoroso shares his insights into imaging knees post-TKR, the causes and mechanisms behind knee arthrofibrosis, his multidisciplinary treatment approach, and what both patients and surgeons should know to optimize outcomes after TKR.

Let’s start at the beginning - diagnosing arthrofibrosis. Dr. Valoroso, when a patient comes in with a reduced range of motion after a TKR, how do you go about identifying the problem?

Dr. Valoroso: Thank you for the question. I begin with a thorough clinical assessment. Key indicators include persistent stiffness beyond 3 months, pain that is disproportionate to radiographic findings, and restricted range of motion—typically less than 90° of flexion or more than 10 degrees of extension lag. I also evaluate for mechanical block, infection, or implant malalignment.

And once you suspect arthrofibrosis, what imaging studies do you typically use?

Dr. Valoroso: So, first of all, I use X-ray to assess the implant position if there is some problem with the implant. But now there are other technologies that can be used, like MRI.

Metal implants can make imaging tricky. Are MRI centers with metal artifact suppression widely available? 

Dr. Valoroso: MRI with metal artifact suppression is increasingly available in specialized centers, although the assets are still limited globally. At EOC, we are very lucky to have multiple 3 Tesla MRI systems that are equipped with advanced metal artifact suppression protocols, which significantly enhance soft tissue visualization around prosthetic components. This MRI allows us to assess capsular fibrosis, synovial thickening, and periprosthetic inflammation with greater precision.

So, we could say that you actually consider this type of MRI useful to diagnose arthrofibrosis in TKR knees.

Dr. Valoroso: It's very useful, especially for visualizing soft tissue fibrosis, thickening, and capsular contractures. However, I think that it's not essential for the diagnosis because the clinical evaluation remains the cornerstone of identifying arthrofibrosis.

And, let's say if an MRI is done, is there a magnetic field strength preferred for knees with a prosthesis, like 1.5 Tesla, for example?

Dr. Valoroso: 1.5 Tesla MRI is preferred due to reduced susceptibility to artifacts compared to 3 Tesla systems. However, with the advent of advanced metal artifact suppression software, 3 Tesla MRI machines can now achieve excellent image quality even in the presence of prosthetic components.

And are there some types of prosthetics that can't go into an MRI scanner due to the type of metal?

Dr. Valoroso: So, you know, most modern prostheses are MRI compatible, but cobalt-chromium alloy may still present challenges. So always verify implant specifications before doing an MRI.

You also already mentioned that the clinical assessment is the cornerstone of diagnosing arthrofibrosis. Is a biopsy necessary for its diagnosis?

Dr. Valoroso: Not routinely. Biopsy is reserved for cases with suspected infection or unusual processes. But, for sure, histopathology can confirm proliferation, but it is not essential for the diagnosis.

Excellent. Have you noticed differences in the presentation of knee arthrofibrosis in patients with or without TKR?

Dr. Valoroso: Yes, of course. In non-TKR knees, arthrofibrosis typically develops as a response to acute trauma or surgical intervention, such as anterior ligament reconstruction. In this case, the fibrotic process is often triggered by direct injury to the joint capsule and cartilage, or prolonged immobilization, leading to excessive scar tissue formation and capsular contracture. In contrast, arthrofibrosis in TKR patients tends to have a more insidious onset. It may not be immediately apparent and often evolves gradually over weeks or months. The underlying mechanisms are multifactorial: surgical trauma during joint replacement can initiate an inflammatory cascade; implant malpositioning or oversizing can cause chronic mechanical irritation; infection, often subclinical, can sustain a pro-fibrotic environment within the joint. Factors contribute to a persistent inflammatory scenario, thickening, and progressive loss of motion.

Let's talk about what might actually cause arthrofibrosis in a TKR. In your experience, is misplacement or improper sizing of the prosthesis a common factor?

Dr. Valoroso: Absolutely. Malrotation, overstuffing the joint, or improper soft tissue balancing are what I’d call mechanical contributors to arthrofibrosis following TKR. Malrotation, particularly of the femoral or tibial component, can lead to abnormal patellofemoral tracking, increasing joint stress and persistent pain, all of which promote a pro-inflammatory intraarticular environment. Overstuffing the joint, due to an oversized femoral component or excessive polyethylene thickness, can increase tension in the surrounding soft tissues, limiting motion and triggering a fibrotic response. Similarly, inadequate balancing of the flexion and extension gaps may result in asymmetric loading and micro-instability, which can exacerbate synovial irritation and a fibrotic response. So, these biomechanical factors, if unaddressed, can perpetuate a cycle of inflammation, pain, and progressive stiffness.

Okay. And, low-grade infections—are these a frequent underlying cause as well?

Dr. Valoroso: These are very recognised as drivers. Cutibacterium acnes and other bacteria like coagulase-negative Staphylococci may evade detection yet trigger persistent inflammation, and despite the absence of overt clinical signs of infection such as fever, elevated CRP, or purulence (pus), these organisms can sustain a chronic low-grade inflammatory response within the joint. This persistent inflammation promotes synovial hyperplasia (overgrowth), capsule thickening, and excessive extracellular matrix deposition, all of which contribute to fibrotic cascade.

And TKR implant loosening can also lead to knee arthrofibrosis. Does this happen often in your experience?

Dr. Valoroso: Yeah, although less common than other causes, implant loosening remains a clinically significant contributor to arthrofibrosis following total knee replacement. Micromotion of the bone-implant interface, often due to suboptimal fixation or progressive osteolysis, can lead to mechanical irritation of the surrounding synovial tissue, and this repetitive microtrauma stimulates a chronic inflammatory response, which in turn promotes synovial hyperplasia and capsule thickening. Additionally, wear particles from polyethylene components or metal debris can activate macrophages and other immune cells, triggering the release of pro-inflammatory cytokines (signaling molecules) such as interleukin-6 or TNF-alpha, and these mediators drive fibroblast proliferation and excessive extracellular matrix (scar tissue) deposition, leading to arthrofibrosis and joint stiffness. Clinically, these patients may present with pain, swelling, and progressive loss of motion, often without signs of infection. So the diagnostic workup includes imaging to assess implant stability and laboratory tests to rule out infection, and management may involve revision surgery to address mechanical instability and remove the inflammatory stimulus.

So when you suspect a low-grade infection or implant loosening as the underlying trigger, how do you go about ruling them out, and how do you treat them if confirmed?

Dr. Valoroso: When evaluating patients with suspected arthrofibrosis after TKR, it is essential to rule out underlying causes such as low-grade infection or implant loosening, as this can significantly alter both prognosis and treatment strategy. What is my diagnostic workup? First of all, inflammatory markers. I begin with several tests, including CRP, the C-reactive protein, and while not definitive, elevated levels may suggest an inflammatory or infectious process. I also perform joint aspiration. Fluid analysis is critical. I perform aspiration under sterile conditions and send samples for cell count and differential Gram stain, and culture. It is important to extend incubation up to 14 days to detect low-virulence organisms. I also test alpha-defensin, which can improve sensitivity. Imaging evaluation starts with standard X-rays and CT scans to assess implant positioning, signs of loosening, and periprosthetic osteolysis, and nuclear imaging is also very important. In fact, if clinical suspicion remains high despite inconclusive lab results, I utilize localized nuclear medicine techniques, such as SPECT, which can localize infection around the prosthesis, or PET CT, which may help differentiate between infection and aseptic loosening.

What is the treatment approach if confirmed?

Dr. Valoroso: For infection, surgical options include irrigation and debridement or one- or two-stage arthroplasty depending on chronicity and pathogen virulence, along with targeted antibiotic therapy based on culture results. For implant loosening, revision surgery is typically required to restore mechanical stability. It is important to remove the component and re-implant with appropriate fixation, and postoperative rehabilitation is always tailored to minimize recurrence of arthrofibrosis. Early and accurate differentiation between infection and mechanical causes is vital, as misdiagnosis can lead to ineffective treatment and worsening symptoms.

Stay tuned for part 2, where Dr. Valoroso explains why he never performs a MUA without lysis of adhesions first, and gives us invaluable insights on his surgical practice.

Disclaimer

Arthrofibrosis is a controversial subject and the views expressed by the clinicians do not necessarily represent the views of the International Arthrofibrosis Association (IAA). The materials presented on this website are provided voluntarily as a public service. It is of a general nature, based on the scientific literature. The information and advice provided is made available in good faith but is provided solely on the basis that readers will be responsible for managing their own assessment of the matters discussed herein and that they should verify all relevant representations, statements and information. Please consult your doctor.