In our experience many people with arthrofibrosis who have increased pain with standing, and after exercise, have an inflamed and scarred Infrapatellar Fat Pad (IFP). This is also known as the Hoffa’s Fat Pad. This important organ is located at the front of the knee underneath the patella and the patellar tendon (see diagram). It’s packed with nerves, fat cells, fibroblasts, stem cells and immune cells that are interspersed with collagen bundles. Although the IFP used to be considered as space filler and was ignored, recent research indicates that it’s an essential organ for knee health and healing1 (see more under Go Deeper) and has a central role in knee pathology1, including arthrofibrosis2. Indeed, treating IFP inflammation is now seen as a possible way to treat osteoarthritis3,4. The IFP can be inflamed from micro traumas, injury and surgery including ACL reconstructions2.
Why the IFP causes pain. The IFP contains densely packed sensory nerves and is extremely sensitive1. When inflamed, the IFP swells and is not able to properly move out of the way of the bones of the knee as the angle of the joint changes. During standing the IFP is placed under pressure as the patella is pulled downwards and inwards, trapping an inflamed IFP between the patella and the femur, creating micro trauma, pain and more inflammation. Dragoo et al.2 state that pain when the knee is straight is diagnostic of IFP inflammation, although patella tendon inflammation can also cause this.
Even in a healthy knee, pressure in the IFP increases substantially at less than 200 (nearly straight) and more than 1000 of flexion2. When swelling is present pressures in the IFP increase further, stressing cells and creating inflammation in surrounding tissues2, including the synovial membrane and patellar tendon, to which it is attached. In fact, the IFP and synovial lining share a boundary and can be considered as single functional unit1.
In addition to entrapment (impingement) of the IFP when standing, an inflamed IFP can also become trapped between the femur and tibia when the knee flexes under load, such as getting into a chair, going down steps and performing deep squats. The load (body weight) on the knee can make the scissoring action of the bones on the IFP severe, and when this occurs it can be excruciatingly painful and very damaging. The degree of pain and damage is likely dependent on how inflamed and fibrotic the IFP is in that area, and therefore how much is protruding into the space between the bones.
In addition to pain, an inflamed and scarred IFP can limit ROM1,2. Inflammation transforms fibroblasts into myofibroblasts which produce scar tissue and more inflammation. In “anterior interval scarring” scar tissue from the IFP is adhered to the front of the tibia2 and patellar tendon.
Exercise. Unfortunately, it is very easy to cause further inflammation in an already inflamed IFP. Inflammation causes the formation of more nerve fibres in the IFP, and more pain4 and swelling in a feedback effect that can become a viscous cycle. Exercises that involve body weight on a bent knee may do this as well as the straight leg lifts, quadriceps sets2 and standing, as mentioned. This is likely why many people with arthrofibrosis find that standing is one of the most painful activities they can do.
Prolonged inflammation leads to fibrosis, and after a time fibrosis of the IFP becomes irreversible4. The fibrosis is also associated with an increase in nerve density and pain and the IFP becomes highly sensitive to mechanical stress4.
Many forms of exercise using the affected leg are unwise in the setting of an inflamed IFP, and the pain may make it difficult to undertake daily living activities. The aim of any treatment is to prevent the pain and limitations from becoming a permanent condition. Continuous passive motion (CPM) may be beneficial because if stretches tissues to counteract contraction without activating leg muscles and therefore without creating IFP pressure and entrapment. The increased movement also helps to reduce inflammation, and pumps fluids through the joint flushing out cell debris and inflammatory cytokines, and bringing essential nutrients to nourish cells and reduce stress.
Because of the central importance of the IFP in knee health, accessing the degree of inflammation and scarring of this organ when somebody is in pain and has arthrofibrosis should be a priority. If scans and an exam determine that the IFP is inflamed then exercise will need to be managed very carefully until this has resolved.
Treatment. It would likely be beneficial to offload the knee for a period of 4 to 6 weeks with crutches, in a similar way to the care for a meniscus tear or fracture, while using passive stretching such as CPM (see above) in order to allow the IFP to heal. However, we are not aware of any research using this approach. Increased pain is an indication that exercise/standing has been too long in duration or intensity, and should be wound back. In our opinion, it’s important not to continuously damage the IFP with daily activities and exercises. Building muscle can occur after the IFP has healed.
Some physiotherapists suggest taping of the knee to offload the IFP, orthotics if there is over pronation of the feet and ultrasound-guided injections containing an anaesthetic and corticosteroid. The later can be helpful in diagnosing the source of knee pain, but the effects are short-lived. Surgery can be performed to remove scar tissues, but the risk of creating more inflammation and scar tissue is always present.
This web page has more diagrams and descriptions (please note that we are not advocating their services)
Imaging. Sagittal MRI is the most commonly used scan to image fibrosis and inflammation of the IFP2, but in our experience, where a prosthesis is present ultrasound can be used providing the operator is experienced.
The IFP is made up of fat cells, immune cells (macrophages, mast cells and lymphocytes) and fibroblasts1, a rich vascular supply and a lot of nerves throughout it. Many of these nerves are capable of releasing Substance P (think P for pain) and consequently the IFP is a “potent source of pain” 2,4. In fact, Substance P increases both pain and inflammation2.
The IPF is attached to a number of knee structures in normal knees, including the synovial lining, meniscus, meniscal ligament, patellar tendon, and in some patients the ACL, and this association implicates it in many knee pathologies including arthrofibrosis and contracture of the patellar tendon2. Inflammatory signalling molecules from an inflamed IFP can travel via the shared vascular supply which has connections to the ACL, synovial lining and other structures, and this likely to be the way in which the IFP adversely affects these structures1,2 in pathology. In a healthy joint the IFP helps to heal these structures via stem cells1 and the production of cytokines and other important compounds such as adiponectin.
Experimental short-term induction of IFP inflammation caused shallow and deep pain in the IFP, and altered the coordination and strength of the quadriceps and vastus medialus obliquus (VMO) contraction2. However, total excision of the IFP has worse outcomes for TKR patients, and can lead to patella baja (tendon shortening), due to the importance of this organ to knee health.
Other fat pads occur in the knee (and other joints), including the suprapatellar fat pad (consisting of the quadriceps and prefemoral fat pads) and the posterior fat pad. However the IFP appears to have a unique role in the development of pathologies such as OA1.
1 Belluzzi, E. et al. Contribution of Infrapatellar Fat Pad and Synovial Membrane to Knee Osteoarthritis Pain. Biomed Res Int 2019, 6390182, doi:10.1155/2019/6390182 (2019).
2 Dragoo, J. L., Johnson, C. & McConnell, J. Evaluation and Treatment of Disorders of the Infrapatellar Fat Pad. Sports Med 42, 51-67, doi:10.2165/11595680-000000000-00000 (2012).
3 Belluzzi, E. et al. Infrapatellar Fat Pad Gene Expression and Protein Production in Patients with and without Osteoarthritis. Int J Mol Sci 21, doi:10.3390/ijms21176016 (2020).
4 Onuma, H. et al. Fibrotic changes in the infrapatellar fat pad induce new vessel formation and sensory nerve fiber endings that associate prolonged pain. J Orthop Res 38, 1296-1306, doi:10.1002/jor.24580 (2020).