Knee Pain: Where Does It Come From?

Australian College of Physiotherapy, Sydney, Australia.
Patellofemoral pain (PFP) is a multifactorial problem with weighting which factors (local, proximal, or distal) have the greatest significance with respect to causing the symptoms.6 However, what seems to be missing in the debate is the source of the pain. Foot pronation, femoral anteversion, poor gluteal control, or the delay in the onset timing of vastus medialis obliquus (VMO) are not in themselves the source of PFP, even though their presence is associated with pain. The presence of pain will certainly decrease muscle activity, timing, and endurance, as well as alter movement patterns.12 As we know, however, pain is very much a cortical experience, so extrinsic factors, such as fear of pain, stress, and anxiety,15,20 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 PFP. This lecture will examine some of these issues in the context of PFP.
Hodges et al12 have reported that inducing pain in the knee of asymptomatic individuals decreases both VMO and vastus lateralis (VL) activity. But when a painful electric shock is randomly and intermittently applied to the knee of the same individuals (ie, mimicking the fear-of-pain state experienced by patients with PFP), only VMO activity is decreased. Exposure to fear and stress initiates the secretion of several hormones, including corticosterone/cortisol, catecholamines, prolactin, oxytocin, and rennin. This is part of the survival mechanism. Such conditions are often referred to as “stressors” and can be divided into 3 categories: external conditions resulting in pain or discomfort, internal homeostatic disturbances, and learned or associative responses to the perception of impending endangerment, pain, or discomfort.20 Release of cortisol can be detrimental to a patient’s recovery. In fact, it has been found that stress-related hormones can alter inner ear fluid homeostasis and auditory function.13 This could have implications for the balance of individuals exhibiting fear/avoidance behavior, so instead of just blaming poor gluteal function for balance problems in patients with PFP, other factors may need to be considered.
The structures that may be the possible source of PFP are the synovium, lateral retinaculum, subchondral bone, and the infrapatellar fat pad. Articular cartilage is aneural and thus provides only an indirect source of pain, perhaps either through synovial irritation or increasing subchondral bone stress. Interestingly, there is no correlation between amount of articular cartilage degeneration and pain experienced by patients with osteoarthritis (OA) of the knee, with many patients with knee OA having episodic bouts of pain for years before requiring surgical intervention. The severity of OA knee pain is associated with bone marrow lesions (edema) with subarticular bone attrition,16,18 synovitis/effusion, and degenerative meniscal tears, but is not associated with the presence of osteophytes or reduction in joint space.16 Hill and colleagues11 followed 270 subjects with tibiofemoral and patellofemoral OA for 30 months and found no correlation between baseline synovitis and baseline pain; however, a decrease in synovitis at follow-up correlated with a reduction in pain. These investigators found synovitis in 3 locations: superior, medial, and inferior patella, with infrapatellar synovitis being the most strongly correlated with pain severity. Synovitis was not associated with cartilage loss in either the tibiofemoral or patellofemoral compartments.11
Free nerve endings (IVa) are present in the synovium.9 As such, peripatellar synovitis is a possible source of PFP. Despite the evidence supporting the synovium as a potential pain source, histological changes in the synovium of patients with PFP are only moderate.1 However, there is evidence of histological changes in the lateral retinaculum in some patients with PFP, as shown by increased numbers of myelinated and unmyelinated nerve fibers, neuroma formation, and nerve fibrosis.10,15,19 Additionally, increased intraosseous pressure of the patella has been found in patients with PFP who complain of pain when sitting with a bent knee (“moviegoer’s knee”), possibly secondary to a transient venous outflow obstruction.9,10 However, the structure that has largely been ignored by the orthopaedic community, even though it was first identified as a potent source of pain by Hoffa in 1904, is the infrapatellar fat pad.
The fat pad covers the extra-articular posterior patellar surface, merges superiorly with the peripatellar fold, extends into the ligamentum mucosum posteriorly, and is lined by synovium.7 The fat pad attaches to the proximal patellar tendon, inferior pole of the patella, transverse meniscal ligament, medial and lateral meniscal horns, the retinaculum, and the periosteum of the tibia.7 The fat pad is highly vascular and richly innervated, so it is one of the most pain-sensitive structures in the knee.7,8 The innervation of the fat pad is linked to the entire knee joint structure, so the fat pad may be affected by pathology in various knee joint components.7 To simulate early knee OA change, Clements and colleagues5 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. These authors concluded that the infrapatellar fat pad may contribute to pain in the early stages of knee OA. Experimentally induced chemical irritation of the fat pad in asymptomatic individuals confirms that the pain is not just confined to the infrapatellar region but can refer to the proximal thigh as far as the groin.2 In fact, the fat pad and medial retinaculum of patients with PFP contain a higher number of substance-P nerve fibers than the same structures in individuals without PFP.21
The fat pad facilitates distribution of synovial fluid, stabilizes the patella in the extremes of knee motion (ie, less than 20° and greater than 100° of knee flexion), and increases tibial external rotation.4 A total resection of the fat pad decreases patellofemoral contact area.4 Inflammatory changes in the fat pad seen on MRI are most commonly the consequence of trauma and degeneration, with the commonest traumatic lesions following arthroscopy, which in 50% of cases fibrous scarring can still be present 12 months later.17 Impingement of the fat pad with diffuse edema occurs following patellar dislocation, often mimicking a loose body.14
An ongoing clinical trial being conducted by our group currently consists of 65 patients (mean age, 41 years; range, 14–79 years) presenting to an outpatient setting for treatment of knee pain. The patients completed a KOOS questionnaire, as well as provided detailed information about the area of their knee pain. Visual analog pain scales at rest and during activities such as walking, stair climbing, squatting, quadriceps setting, and passive knee extension were obtained. The widest diameter of the fat pad of both knees was measured with a tape measure. MRI scans were performed on a random subset of the subjects, prepatella and postpatella tape, and pretreatment and posttreatment. Treatment consisted of taping to unload the fat pad so that the patients were pain free, stretching the anterior hip structures, and weight-bearing gluteal training, and was provided weekly for the first 2 weeks, once every 2 weeks for the next 2 treatments, then once a month for the next 2 treatments. Follow-up assessments were made at 3, 6, and 12 months.
At initial presentation, 46% of the 65 patients reported pain in the inferior patellar region, 43% medial knee pain, 23% retropatellar pain, and 20% lateral pain. Fifty-three percent of patients reporting retropatellar pain also reported inferior or medial knee pain. Sixty-one percent of patients complained of pain doing a quadriceps contraction, ranging from 1 to 8 on the visual analog scale, and 45% of patients experienced pain on extension overpressure ranging from 1 to 9 on the visual analog scale. The size of the fat pad on the affected side averaged 10 cm and 8.5 cm on the unaffected side. These findings support the hypothesis that the fat pad was the source of the symptoms. At the time of entry into the trial, scans were available for 20 subjects. In 12 of these scans, the radiologists had commented on fat pad inflammation. The diagnoses of these 20 patients included ACL injury (n = 1), meniscal tear (n = 2), tricompartmental OA (n = 2), patellar tendinopathy (n = 1), patellar dislocation (n = 3), medial femoral softening (n = 3), chondromalacia patella (n = 1), and patellofemoral arthrosis (n = 7).
Ten subjects received an MRI scan prepatella and immediately postpatella taping, in which the taping had to decrease the symptoms on stairs or squatting by at least 80%. The patella was tilted out of the fat pad and the fat pad was unloaded anteriorly and posteriorly. The MRI results showed various areas of fat pad inflammation, depending on the underlying pathology. The posttaping MRI scans demonstrated an inferior patellar shift in all cases, an increase in fat pad depth, and either an anterior or posterior tibial shift, compared with the pretape condition. MRI results of another subset of subjects 6 to 12 months following cessation of treatment revealed a decrease in fat pad volume, an increase in patellar height, a medial patellar drift, and an increase in patella varus alignment, suggesting an improvement in VMO strength.
In summary, the infrapatellar fat pad is highly innervated and a probable source of knee pain. Knee pain inhibits quadriceps activity, and fear of pain specifically inhibits the VMO. Taping to unload the infrapatellar fat pad significantly reduces pain and causes an inferior patellar shift and a slight increase in fat pad depth. Physical therapy treatment results in an increase in patellar varus alignment, an increase in patellar height, a medial drift of the patella, and decreased fat pad volume, suggestive of an improved resting VMO tone.
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