When considering knee pain in runners, clinicians differentiate sources of symptoms and determine their cause. Knee problems arise when a runner increases the amount/frequency of the loading through the lower limb. The way the loading is distributed through the knee determines which tissues are abnormally loaded. Knee problems cannot be considered in isolation, requiring a thorough investigation of static and dynamic lower limb mechanics, and footwear and surfaces. This article examines potential sources of knee pain and explores the role of the infrapatellar fat pad and synovial plica in the mechanics of the knee and its involvement in knee symptoms.
Key points
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The infrapatellar fat pad (IFP) is highly innervated and when inflamed is responsible for inferior, medial, retropatellar, and in some cases posterior knee pain.
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The IFP stabilizes the patella in extremes of knee motion (<20° and >100°).
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The IFP can be injured with rapid extension or hyperextension of the knee, such as overextending the knee when running downhill.
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Inflammation of the IFP causes quadriceps atrophy.
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Inflammatory changes in the IFP seen on MRI are the consequence of trauma and degeneration, the commonest trauma being arthroscopy.
Introduction
Various intraarticular structures of the knee generate neurosensory signals that result in conscious pain perception. Pain is defined as an unpleasant sensory or emotional experience associated with actual or potential tissue damage (nociception). Pain involves an individual’s reaction to nociception, so it is very much a personal experience with a learned component. Pain can become memorized because pain mechanisms are not fixed (hard wired) but are plastic (soft wired). Through neuroplasticity, hyperalgesia can be learned and unlearned, from both tissue-based and environmental afferent inputs.
The tissue-based structures that can be the potential source of knee pain are the synovium, lateral retinaculum, subchondral bone, and the infrapatellar fat pad (IFP), with the articular cartilage because it is aneural, providing only an indirect source, perhaps either through synovial irritation or increasing subchondral bone stress.
There is, however, no correlation between the amount of articular cartilage degeneration and pain experienced by individuals with knee osteoarthritis (OA), for example. The severity of OA knee pain is associated with bone marrow lesions (edema) with subarticular bone attrition, synovitis/effusion, and degenerative meniscal tears, but it is not associated with presence of osteophytes or reduction in joint space. Hill and colleagues followed 270 subjects with tibiofemoral and patellofemoral (PF) OA for 30 months finding no correlation between baseline synovitis and baseline pain score but a decrease in synovitis at follow-up was correlated with a reduction in pain. These investigators found synovitis in 3 locations, namely, the superior, medial, and inferior patella, with infrapatellar synovitis being most strongly correlated with pain severity. The synovitis was not associated with cartilage loss in either the tibiofemoral or PF compartments.
Free nerve endings (IVa) are present in the synovium, so peripatellar synovitis is a possible source of knee pain. Despite the evidence supporting the synovium as a potential pain source, histologic changes in the synovium of patients with PF pain are only moderate. However, there is evidence of histologic changes in the lateral retinaculum with increased numbers of myelinated and unmyelinated nerve fibers, neuroma formation, and nerve fibrosis being found in some patients with PF pain. Additionally, increased intraosseous pressure of the patella has been found in patients with PF pain who complain of pain when sitting with a bent knee (“movie goers knee”), possibly secondary to a transient venous outflow obstruction. However, the structure that until recently has largely been ignored by the orthopedic community, even though it was first identified as a potent source of pain by Hoffa in 1904, is the (IFP). Hoffa described the symptoms originating from the IFP as being “pain felt quite suddenly on the medial side of the joint; with the patient having difficulty bending and straightening the knee and the presence of knee joint swelling on both sides of the patella.” Consequently, the IFP is often referred to as Hoffa’s fat pad, with most clinicians thinking of Hoffa’s syndrome as a result of a direct blow to the knee. Superolateral fat pad edema is a frequent finding with patellar maltracking and may precede clinically significant chondrosis. In a recent study by Matcuk and Cen, a patient with patellar maltracking was placed in the Hoffa group (superolateral fat pad edema), if 1 of 3 conditions was met: lateral patellar displacement greater than -3.6 mm and Insall–Salvati ratio (ratio of patellar tendon length and patellar length) greater than 0.99; lateral patellar displacement of -3.6 mm or less and Insall–Salvati ratio greater than 1.23; or lateral patellar displacement of -3.6 mm or less, Insall–Salvati ratio of 1.23 or less, and lateral trochlear inclination of 16.5° or less. These findings had 91.6% sensitivity and 88.9% specificity for identifying the Hoffa group.
Introduction
Various intraarticular structures of the knee generate neurosensory signals that result in conscious pain perception. Pain is defined as an unpleasant sensory or emotional experience associated with actual or potential tissue damage (nociception). Pain involves an individual’s reaction to nociception, so it is very much a personal experience with a learned component. Pain can become memorized because pain mechanisms are not fixed (hard wired) but are plastic (soft wired). Through neuroplasticity, hyperalgesia can be learned and unlearned, from both tissue-based and environmental afferent inputs.
The tissue-based structures that can be the potential source of knee pain are the synovium, lateral retinaculum, subchondral bone, and the infrapatellar fat pad (IFP), with the articular cartilage because it is aneural, providing only an indirect source, perhaps either through synovial irritation or increasing subchondral bone stress.
There is, however, no correlation between the amount of articular cartilage degeneration and pain experienced by individuals with knee osteoarthritis (OA), for example. The severity of OA knee pain is associated with bone marrow lesions (edema) with subarticular bone attrition, synovitis/effusion, and degenerative meniscal tears, but it is not associated with presence of osteophytes or reduction in joint space. Hill and colleagues followed 270 subjects with tibiofemoral and patellofemoral (PF) OA for 30 months finding no correlation between baseline synovitis and baseline pain score but a decrease in synovitis at follow-up was correlated with a reduction in pain. These investigators found synovitis in 3 locations, namely, the superior, medial, and inferior patella, with infrapatellar synovitis being most strongly correlated with pain severity. The synovitis was not associated with cartilage loss in either the tibiofemoral or PF compartments.
Free nerve endings (IVa) are present in the synovium, so peripatellar synovitis is a possible source of knee pain. Despite the evidence supporting the synovium as a potential pain source, histologic changes in the synovium of patients with PF pain are only moderate. However, there is evidence of histologic changes in the lateral retinaculum with increased numbers of myelinated and unmyelinated nerve fibers, neuroma formation, and nerve fibrosis being found in some patients with PF pain. Additionally, increased intraosseous pressure of the patella has been found in patients with PF pain who complain of pain when sitting with a bent knee (“movie goers knee”), possibly secondary to a transient venous outflow obstruction. However, the structure that until recently has largely been ignored by the orthopedic community, even though it was first identified as a potent source of pain by Hoffa in 1904, is the (IFP). Hoffa described the symptoms originating from the IFP as being “pain felt quite suddenly on the medial side of the joint; with the patient having difficulty bending and straightening the knee and the presence of knee joint swelling on both sides of the patella.” Consequently, the IFP is often referred to as Hoffa’s fat pad, with most clinicians thinking of Hoffa’s syndrome as a result of a direct blow to the knee. Superolateral fat pad edema is a frequent finding with patellar maltracking and may precede clinically significant chondrosis. In a recent study by Matcuk and Cen, a patient with patellar maltracking was placed in the Hoffa group (superolateral fat pad edema), if 1 of 3 conditions was met: lateral patellar displacement greater than -3.6 mm and Insall–Salvati ratio (ratio of patellar tendon length and patellar length) greater than 0.99; lateral patellar displacement of -3.6 mm or less and Insall–Salvati ratio greater than 1.23; or lateral patellar displacement of -3.6 mm or less, Insall–Salvati ratio of 1.23 or less, and lateral trochlear inclination of 16.5° or less. These findings had 91.6% sensitivity and 88.9% specificity for identifying the Hoffa group.
Anatomy
The IFP is a highly vascular, richly innervated, intracapsular, extrasynovial structure, lined by synovium, filling the anterior knee compartment with between 21 to 39 mL of adipose tissue, although there is considerable individual volumetric variation. The IFP covers the extraarticular part of the posterior patellar surface and merges superiorly with the peripatellar fold. Posteriorly, the IFP extends into ligamentum mucosum, which in many individuals is continuous with the anterior cruciate ligament (ACL), finally connecting to the intercondylar notch of the femur. Inflammation of the pericruciate portion of the IFP causes posterior knee pain in athletes.
The IFP also attaches to the proximal patellar tendon, inferior pole of the patella, transverse meniscal ligament, medial and lateral meniscal horns, and the retinaculum, as well as the periosteum of the tibia. The medial and lateral patellomeniscal ligaments appear as thickening of the edges of the IFP as it merges with the capsular synovium.
Vascularization
The IFP is vascularized by a rich anastomotic network. Branches of the inferior genicular arteries run vertically through the IFP just posterior to the borders of the patellar tendon. Branches of the superomedial and superolateral genicular arteries wrap posteriorly around the distal half of the patella to enter the proximal aspect of the IFP and anastomose with the inferior genicular arteries. Two to 3 horizontal arteries connect the vertical arteries at the level of the femoral condyles, tibial plateau, or tibial tubercle. A network of smaller arteries extending from the inferior genicular arteries infiltrate the remainder of the fat pad, although the central portion remains the least vascularized. In some individuals, a branch of the middle genicular artery, which runs through the ligamentum mucosum during embryonic development, persists as a robust connection between the arterial supplies of the ACL and the IFP. Without this middle genicular vascularization, the vascular network of the IFP sends smaller branches into the surrounding synovial lining as well as that of the cruciate ligaments. The rich vascular supply found in the IFP supports the hypothesis that the IFP can aid in healing the ACL and other nearby structures, but also supports the hypothesis of IFP fibrosis after an injury.
Innervation
The IFP is a potent source of knee pain owing to its rich innervation and relationship with the highly innervated synovium. The innervation of the fat pad is linked with the entire knee joint structure, so the IFP may be affected by pathology in various knee joint components. The IFP is supplied by several nerves, including the terminal branch of the obturator nerve; branches of the femoral nerve, supplying the vastus medialis and vastus lateralis muscles; the lateral articular and recurrent peroneal branches of the common peroneal nerve; and the infrapatellar branch of the saphenous nerve and the posterior articular nerve, a branch of the posterior tibial nerve.
Histologically nerves within the IFP stain positively for S-100, tyrosine hydroxylase, and nociceptive fibers, which contain substance P as well as type IVa free nerve endings, which are most dense in the central and lateral portions of the IFP and the surrounding synovium. In fact, the IFP and medial retinaculum of PF pain patients contain a higher numbers of substance P nerve fibers than the same structures of individuals without PF pain.
Knee pain has been induced experimentally by injecting hypertonic saline into the fat pad of asymptomatic individuals. All individuals complained of severe infrapatellar pain, with most also experiencing retropatellar pain and some reporting medial thigh, and even groin pain. Experimentally inducing pain in the fat pad causes a decrease in vastus medialis obliquus and vastus lateralis activity. Simulated acute knee joint pain leads to hyperalgesia and facilitated temporal summation in the IFP, as well as in the muscles located distant to the injection site, in subjects with no history of knee pain. Injection or infusion of local anesthetic into the IFP after an operation or injury decreased patient use of opioids, decreased overall pain, and facilitated rehabilitation of the knee.
To simulate early knee OA change, Clements and colleagues injected monoiodoacetate into the right knee of 150 rats and after 21 days of weight-bearing asymmetry found marked inflammatory changes in the fat pad, concluding that the IFP contributed to the pain in the early stages of knee OA.
Biomechanics
Although there has been debate about the role of the IFP, recent evidence of outcomes of patients 12 months after total knee arthroplasty has shown that the individuals where the IFP was preserved had significantly better Oxford Knee Score associated with rising from a chair, pain, limping, giving way, and pain interfering with work than those who had the IFP resected. The role of the IFP is to stabilize the patella in the extremes of knee motion (that is less than 20° and >100° of knee flexion), increase tibial external rotation and facilitate distribution of synovial fluid. A total resection of the IFP decreases PF contact area, but has no effect in reducing PF pain. Excision of the IFP also results in a shortened patellar tendon after total knee arthroplasty. Edema in the IFP increases the volume of the anterior interval and leads to irritation of nearby tissue. Inflammatory changes in the IFP seen on MRI are most commonly the consequence of trauma and degeneration, with the commonest traumatic lesions after arthroscopy, where in 50% of cases fibrous scarring can still be present 12 months later. Impingement of the fat pad with diffuse edema occurs after patellar dislocation, often mimicking a loose body.
Clinical Features
Fat pad irritation is a poorly described and underdiagnosed condition. It is frequently confused with patellar tendinopathy and if acute in onset is associated with a rapid extension of knee such as overextending the knee when running downhill. Patellar tendinopathy is often owing to an increased amount or volume of eccentric loading, such as increased hill or stair descent in running. Because the pain in both conditions is in the inferior patellar region, differential diagnosis can be difficult. Brukner and colleagues found that found that 78% of college athletes diagnosed with patellar tendinopathy showed an increased uptake in the fat pad on T2-weighted MRI, suggestive of inflammation of the fat pad. It seems that the fat pad, rather than the patellar tendon, may be the source of the primary pathology of many athletes with a patellar tendinopathy diagnosis, particularly because the IFP also attaches to the proximal patellar tendon, or a combination of the 2 conditions may exist.
The patient’s history may help to differentiate patellar tendinopathy from typical fat pad irritation. The patient with patellar tendinopathy must have a history of eccentric loading of the quadriceps muscle such as running downhill, whereas a patient with a fat pad irritation presents after a forceful extension maneuver. Both patient groups have inferior patellar pain; with patellar tendinopathy the pain is exacerbated by squatting, whereas pain with acute fat pad irritation is exacerbated by both flexion and extension maneuvers. Thus, rehabilitation consisting of short arc quadriceps, straight leg raises, and non–weight-bearing knee extension exercises will increase fat pad symptoms The athlete can complain of pain during prolonged standing and can experience pain going up, as well as, down stairs. The athlete stands with hyperextended or “locked back” knees, but if the fat pad is acutely inflamed and extremely painful the patient will not be able to extend the knee. The fat pad seems to be fatter than the other asymptomatic side. On palpation, the inferior pole of the patella is embedded in underlying tissues. The patient may have focal tenderness of the inferior pole. The symptoms are often exacerbated by knee extension and quadriceps contractions.
The presence of pain decreases muscle activity, timing, and endurance as well as alters movement patterns. However, because we know pain is very much a cortical experience, so extrinsic factors such as fear of pain, stress, and anxiety can amplify the pain experience for the patient and the contribution of these factors must be understood if we are to satisfactorily improve the rehabilitation of individuals with PF pain. Fear of pain decreases vastus medialis obliquus activity, but does not decrease vastus lateralis activity, causing an increase in the dynamic valgus vector force, which results in further PF problems.
Athletes with hyperextended knees often have increased internal femoral rotation. Femoral internal rotation means that the gluteal muscles, maximus and medius posterior fibers, are elongated in standing, so these muscles may be inadequate in maintaining a stable pelvis during running, further increasing the dynamic valgus vector force and continuing the PF pain cycle.
As with all overuse knee problems, the clinician must be aware of the impact of the foot and the shoe, as well as the surface the athlete is running on, has on the symptoms, so a thorough examination of the landing pattern of the runner, the foot, and shoe type is essential when managing runners with inflamed fat pads.
Although not a common problem in runners, the infrapatellar plica, which is an inflammation of the ligamentum mucosum (an embryonic remnant), needs to be considered in the differential diagnoses of fat pad injuries. The ligamentum mucosum is one of several remnants of synovial membranes separating the embryonic knee into compartments. These gradually disappear, although the ligamentum mucosum remains in adulthood in 65% to 90% of knees and is mostly asymptomatic. Normal ligamentum mucosum appear isointense to the IFP on T2-weighted MR.
When symptomatic, the ligamentum mucosum becomes thickened and inflamed, and is referred to as an infrapatellar plica. The plica is rarely inflamed in runners but more commonly in elite cyclists, owing to high resistance repetitive knee flexion and extension movements. The patients report symptoms of popping and snapping with knee movement and have a positive Faber’s test (palpation of the medial border of the patella in supine with the knee in a figure of 4 position will elicit pain). Unlike IFP pain, which is often exacerbated by an inferior tilt of the patella, pain from an inflamed plica is exacerbated by medial glide of the patella. Pathologic infrapatellar plicae have been shown to be hypointense on T2-weighted MR appearing along the ACL.
Treatment
IFP problems are usually successfully managed with physical therapy. Physical therapy aims to unload abnormally inflamed tissue, both passively using tape and actively by improving the lower limb mechanics, which involves optimizing hip muscle control as well as foot function, which in turn, significantly decreases the patient’s symptoms.
Unloading the inflamed soft tissue requires shortening of the inflamed tissue. With IFP problems, the inferior pole patella needs to be tilted out of the fat pad to decrease the repeated inflammation. One or 2 pieces of tape from the superior part of the patella may be sufficient to achieve this. If this procedure does not reduce the patient’s symptoms, a further 2 pieces of tape need to be applied from the tibial tubercle to the medial and lateral joint lines, forming a V to unload the IFP further. The aim is to create a “muffin top” so that the fat pad is unloaded as much as possible. If the athlete is still experiencing some pain, the fat pad can be further unloaded by taping just distal to the popliteal fossa from posterior to anterior to pull the tibia forward ( Fig. 1 ). Hug and colleagues found that unloading tape significantly reduced muscle stress during contraction, as well as contraction of the muscle. Taping the knee is required until the runner is no longer experiencing symptoms. Patients should be taught how to tape themselves, so they can easily apply the tape before going for a run so they do not exacerbate their symptoms.
