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Hoffa’s Fat Pad

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 healing [1] and has a central role in knee pathology [1], including arthrofibrosis [2]. Indeed, treating IFP inflammation is now seen as a possible way to treat osteoarthritis [3,4]. The IFP can be inflamed from micro traumas, injury and surgery including ACL reconstructions [2].

Why the IFP causes pain

The IFP contains densely packed sensory nerves and is extremely sensitive [1]. 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 flexion [2]. When swelling is present pressures in the IFP increase further, stressing cells and creating inflammation in surrounding tissues [2], 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 unit [1].

In addition to pain, an inflamed and scarred IFP can limit ROM [1,2]. 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 tibia [2] 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 fibers in the IFP, and more pain [4] 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 sets [2] 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 irreversible [4]. The fibrosis is also associated with an increase in nerve density and pain and the IFP becomes highly sensitive to mechanical stress [4].

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.

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.

Fat cells, immune cells and fibroblasts

The IFP is made up of fat cells, immune cells (macrophages, mast cells and lymphocytes) and fibroblasts [1], 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 inflammation [2].

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 tendon [2]. 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 structures [1,2] in pathology. In a healthy joint the IFP helps to heal these structures via stem cells [1] 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) contraction [2]. 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 OA [1].

Aspects of Arthrofibrosis

Cells and Cytokines

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Myofibroblasts

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Hoffa’s Fat Pad

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Pathogenesis

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Predisposition

DNA Strand

Drivers

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References

  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).

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