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Ankle Arthrofibrosis

Do you wonder why your ankle is stiff, painful and lacks range of motion (ROM)? There is a good chance that you have ankle arthrofibrosis (fibrosis of the joint). However, since there are other causes of these symptoms, including mechanical problems, and these should be ruled out using scans such as magnetic resonance imaging (MRI). Osteoarthritis or Achilles tendinopathy can also cause similar symptoms, and these conditions are often associated with arthrofibrosis. Ankle arthrofibrosis is often referred to as Frozen Ankle or Adhesive Capsulitis [1, 2] and the term “hypertrophy” is sometimes used. Soft tissue impingement frequently indicates arthrofibrosis pathology.

The estimated rates vary from 40% to over 70% after surgical repair of ankle fractures and 22% following open removal of osteophytes and ankle joint replacement

Recent research indicates that ankle arthrofibrosis is relatively common, with fibrosis of the ankle found in 93.9% of patients who reported ankle pain following ankle fracture surgery [3]. However, despite this, ankle arthrofibrosis is rarely discussed [1] with some claiming that it’s rare. This may be because, like arthrofibrosis in other joints, ankle arthrofibrosis is difficult to diagnose. The estimated rates vary from 40% to over 70% after surgical repair of ankle fractures and 22% following open removal of osteophytes (abnormal bone growth) and ankle joint replacement [1]. Ligament ruptures and even relatively minor injuries such as repeated sprains can result in ankle arthrofibrosis or the cause may unknown, perhaps repeated micro-traumas, as for shoulder arthrofibrosis [2].


ROM can be restricted in either or both flexion and extension, which are referred to as dorsiflexion (pointing the toes upwards towards the knee) and plantarflexion (pointing the toes towards the ground) respectively. People with ankle arthrofibrosis often have an altered gait with shortened stride and early heal lift-off, and may have pain on palpitation of the joint margins [1] and pain during and after use. There may be muscle atrophy in the affected leg [2] which is a natural outcome of inflammation (see What you need to know about muscle wasting).


Fibrosis can affect tissues outside and inside the joint, including tendons and ligaments, fat pads and the joint capsule [1]. Ankle arthrofibrosis has the same pathology as arthrofibrosis of other joints [2], with specialised healing cells called myofibroblasts creating adhesions, contractions and excessive scar tissue that reduce range of motion and cause pain [4]. There is often obliteration of soft tissue structures or impingement (intrusions) [5]. Risk factors include prolonged immobilisation of the joint after surgery or trauma, together with a history of prior injuries or surgeries, inflammation and other medical conditions that increase inflammation or healing pathways such as autoimmune conditions, diabetes and thyroid problems [1, 2, 4].

Fibrosis impacting ankle ligaments, tendons and the joint synovial capsule is well known, but there are few references to fat pad fibrosis in ankles. The Hoffa’s fat pad (infrapatellar fat pad) is strongly implicated in the pathology of knee arthrofibrosis, so I was curious to see if fat pads are involved in ankle arthrofibrosis. Articular (joint) fat pads provide mechanical cushioning and are also immune organs crucial for joint health, releasing bioactive molecules that regulate healing, inflammation and tissue degradation [6]. Immune cells in articular fat pads regulate the joint’s immune response and there is a sensitive network of nerves and a rich supply of blood vessels in them that supply associated tendons [7]. The ankle joint has two large fat pads associated with it, and other fat pads are distributed around the foot.

It appears that ankle fat pads may be implicated in arthrofibrosis in a similar way to the Hoffa’s fat pad in knee arthrofibrosis, emphasising the importance of not damaging fat pads during surgery [8].

The Kager’s fat pad, also known as the pre-Achilles fat pad, is relatively large and located at the rear of the ankle, but there is scant research on its function. However, it’s apparent that the Kager’s fat pad is crucial in ankle health and pathology and is especially important to the Achilles’ tendon, supplying it with lubricants and protecting the blood vessels that supply it [6, 8]. The Kager’s fat pad can become fibrotic after injury or surgery and may form adhesions to the Achilles tendon or be obliterated by scar tissue [9], creating stiffness, reducing ROM and causing pain. In addition, scar tissue makes the fat pad less mobile and more likely to be impinged (pinched), causing pain [9]. Biopsies from the Kager’s fat pad in patients with Achilles’ tendinopathy demonstrated significantly higher expression of the major inflammatory cytokines (signalling molecules made by the body) and Substance P compared to healthy controls [6]. Substance P is a major pain signalling protein. It’s also thought that an inflamed and swollen Kager’s fat pad may diminish blood flow to the Achilles tendon, impacting its health.

The other fat pad in ankles is located at the front, about where the foot joins the leg, and is called the anterior tibiotalar fat pad. The soft tissues in this area can become fibrotic, with adhesions and scar tissue obliterating the normal structure [5]. Recent research suggests that the anterior tibiotalar fat pad becomes inflamed after ankle sprains and is associated with ankle pathology [10]. In support of this, ultrasound evidence indicates fibrosis of the synovium and anterior tibiotalar fat pad following ankle fracture surgery, causing stiffness and impingement during flexion [3].


Early preventive management is critical for minimising the risk of ankle arthrofibrosis after surgery, and care should be taken to avoid aggressive therapy [1]. This is consistent with the treatment of other joints. As for knee arthrofibrosis, non-weight bearing for an extended period following surgery is likely to reduce risk by reducing fat pad inflammation. Dynamic splinting with a low load is recommended by some to stretch the connective tissue and regular gentle range of motion therapy is believed to be essential [1]. I personally feel that regular continuous passive motion (CPM) immediately after surgery has significant advantages over long stretch holds, preventing the formation of adhesions as well as reducing contractions. In addition, animal research indicates that CPM reduces inflammation [11]. Although there is scant research on CPM as a preventive/treatment for ankle arthrofibrosis, research in rabbits suggests that continuous CPM of ankles after surgery prevents stiffness [12]. This is supported by research comparing 22 patients treated with immediate full-time CPM for three weeks following surgery to repair an ankle fracture with 22 patients whose ankle was immobilised for 3 weeks after similar surgery, with a 10-year follow-up [13]. All ankles in the CPM group had good ROM, whereas 7 out of 22 ankles in the immobilised group had restricted ROM. In addition, only minor or moderate osteoarthritis was observed in 2 of the 22 CPM ankles, while 7 of the 22 immobilised ankles developed minor to severe osteoarthritis [13]. Patients in both groups could immediately use crutches without weight bearing. Unfortunately, CPM of knees post-surgery is frequently poorly applied, resulting in contradictory outcomes [14].

Corticosteroid injections may be prescribed but are reported to have a low rate of success [1] and are only effective in the short term. Corticosteroids have also been implicated in fat atrophy [8] and could therefore be detrimental to fat pad health. Other serious side-effects associated with corticosteroids include Achilles tendon rupture, cartilage damage, death of bone tissue, calcification and infection [15].

There are not a lot of quality studies on the success of surgical treatment of ankle arthrofibrosis, but some surgeons recommend the release of adhesions and contractions of tissues [1]. Based on arthrofibrosis pathology, the IAA believes that arthrofibrosis surgery is more likely to be successful if a tourniquet is not applied, a cauterising tool is used rather than a mechanical shaver, and there is careful attention to the control of bleeding and pain.

For further information on treatment approaches for arthrofibrosis please see information on this website.

  1. Velasco, B. T. et al. Arthrofibrosis of the Ankle. Foot & Ankle Orthopaedics 5, 247301142097046 (2020).

  2. Aguilar-Nunez, D. et al. Adhesive Capsulitis of the Ankle (Frozen Ankle): An Infrequent Syndrome. Biomedicines 11 (2023).

  3. Osanami, H. et al. Validation of anterior ankle soft tissue dynamics and shear modulus for anterior ankle impingement syndrome after ankle fracture surgery. Sci Rep 14, 5863 (2024).

  4. Usher, K. M. et al. Pathological mechanisms and therapeutic outlooks for arthrofibrosis. Bone Research 7 (2019).

  5. Cerezal, L. et al. MR Imaging of Ankle Impingement Syndromes. American Journal of Roentgenology 181, 551-559 (2003).

  6. Pingel, J. et al. Inflammatory and Metabolic Alterations of Kager's Fat Pad in Chronic Achilles Tendinopathy. PLoS One 10, e0127811 (2015).

  7. Labusca, L. & Zugun-Eloae, F. The Unexplored Role of Intra-articular Adipose Tissue in the Homeostasis and Pathology of Articular Joints. Front Vet Sci 5, 35 (2018).

  8. Theobald, P. et al. The functional anatomy of Kager's fat pad in relation to retrocalcaneal problems and other hindfoot disorders. J Anat 208, 91-97 (2006).

  9. Gupta, A., Mulvihill, E. & Turner, D. Is Real-Time Ultrasound Reliably Able to Determine Kager's Fat Pad Motion during Walking? Ultrasound Med Biol 48, 217-222 (2022).

  10. Arnaert, S. et al. Anterior Tibiotalar Fat Pad Involvement in Ankle Osteoarthritis: MRI Features in Patients 1 Year After a Lateral Ankle Sprain. Cartilage 14, 285-291 (2023).

  11. Ferretti, M. et al. Anti-inflammatory effects of continuous passive motion on meniscal fibrocartilage. J Orthop Res 23, 1165-1171 (2005).

  12. Namba, R. S., Kabo, J. M., Dorey, F. J. & Meals, R. A. Basic Science AND Pathology: Continuous Passive Motion Versus Immobilization: The Effect on Posttraumatic Joint Stiffness. Clinical Orthopaedics and Related Research® 267 (1991).

  13. Farsetti, P. et al. Immediate continuous passive motion after internal fixation of an ankle fracture. J Orthop Traumatol 10, 63-69 (2009).

  14. O'Driscoll, S. W. & Giori, N. J. Continuous passive motion (CPM): theory and principles of clinical application. Journal of rehabilitation research and development 37, 179-188 (2000).

  15. Stone, S., Malanga, G. A. & Capella, T. Corticosteroids: review of the history, the effectiveness, and adverse effects in the treatment of joint pain. Pain Physician 24, S233 (2021).

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