Jenny McConnell and John W Read

The source of osteoarthritic (OA) knee pain is perplexing. Bone marrow Lesions (BMLs) and the Infrapatellar Fat Pad (IPFP) are hypothesized to cause symptoms in this patient population. With escalating costs for OA treatment, physiotherapy could be an inexpensive option for managing OA knee pain. The aim of this study was to examine the Magnetic Resonance Imaging (MRI) of OA knee pain patients, pre and post, a specific physiotherapy program to determine if there were any changes in patellar position, IPFP volume and appearance as well as BMLs. The study included 12 patients with radiological evidence of tibio-femoral, patello-femoral or tri-compartmental OA. 1.5 T MRIs were obtained pre and 4 months post 6 physiotherapy sessions. MRI comparisons were made for changes in (a) IPFP oedema signal b) patellar alignment c) IPFP depth, area and perimeter and d) cyst presence or size in the subspinous tibial bone marrow and subchondral bone marrow. After treatment, both pain scores and IPFP signal reduced in all subjects. The patella was 1.7 mm higher (p=0.004), 1.2 mm more medial (patellar drift, p=0.0001) and 2° more varus (patellar roll, p=0.001). No consistent pattern was found in distribution, size or intensity in BMLs. IPFP oedema seems to be associated with increased pain in knee OA.

Keywords: Knee osteoarthritis; MRI; Physical therapy; Infra-patellar fat pad; Bone marrow lesions


Worldwide, arthritis is a major cause of long-term disability, costing governments billions of dollars annually in both direct (health care) and indirect (loss of income and early retirement) costs [1-6]. Knee osteoarthritis (OA) is the most commonly diagnosed cause of knee pain in individuals over 50 years of age [7]. Pain is the major reason for an individual with OA to seek a knee joint replacement. The severity of pain can range from barely perceptible to immobilizing, but the cause of pain in OA is poorly understood, particularly as the reported pain intensity does not always correlate with the severity of change on X-ray [8-11].

As articular cartilage is completely aneural, it is unlikely to be the actual pain generator. Alternative explanations for OA-related knee pain have been suggested and include both primary effects on subchondral bone or synovium and secondary effects on structures such as menisci or ligaments [12-18]. However, a recent study by Guermazi et al. [19] involving 710 participants of more than 50 years age found that, although 89% had structural abnormalities on MRI consistent with OA, only 29% complained of pain. The most common abnormalities were osteophytes (74%) followed by bone marrow lesions (52%). These authors concluded that most middle aged and elderly people with “normal” knee X-rays have degenerative tibiofemoral joint lesions on MRI regardless of the presence or absence of pain. Nevertheless, Javaid et al. [13] found that the presence of bone marrow lesions (BMLs), particularly in the non-weight bearing, subspinous tibial region of asymptomatic, radiographically normal knees, predicted the development of pain 15 months later.

Interestingly, Felson et al. [12] found that BMLs could fluctuate in volume over 6-12 weeks, suggesting that BMLs were strongly related to focal overloading of the joint, usually from mal-alignment. They postulated that the rapid change in volume of these lesions could either reflect a fluctuating mechanical environment or some as yet undescribed temporary pathological change causing oedema and inflammation.

The deep infrapatellar fat pad (IPFP), a large intra-capsular but extra-synovial collection of adipose tissue, has also been proposed as a potential significant source of OA-related knee pain [20-22]. The posterior surface of the IPFP is covered with synovium and extends posteriorly through the intercondylar notch of femur contiguous with the anterior cruciate ligament [23]. The IPFP is a highly vascular and pain sensitive structure which influences knee biomechanics [24]. Nerves within the IPFP contain substance P fibres as well as type IVa free nerve endings, making this one of the most pain sensitive structures in the knee [25-27]. Knee pain has been experimentally induced, by injecting hypertonic saline into the fat pad of asymptomatic individuals [28]. Pro-inflammatory cytokines have been found in the infrapatellar fat pads of patients with knee OA [22]. Using an established OA model in rodents, Clements et al. [21] injected monoiodoacetate into the knee joint and found marked IPFP inflammatory changes on day 1, suggesting the fat pad as an early source of OA pain. After 21 days of marked weight-bearing asymmetry, the rodents exhibited IPFP fibrosis. IPFP fibrosis has been shown to cause chronic knee pain and stiffness in humans [20].

Non-operative management of knee OA is relatively successful in improving OA symptoms [29,30]. There is good evidence that improved quadriceps strength and perhaps even gluteal strength may decrease knee symptoms sufficiently, reducing the need for TKR [31-34]. There have been no studies however, evaluating MRI scans, pre and post successful physiotherapy intervention for patients with knee OA, to give some insight into the potential causes of the episodic acute, disabling pain experienced by patients with knee OA. Thus, the aim of this pilot study was to determine whether any changes in patellar alignment, indirectly implying improved quadriceps muscle tone, IPFP volume, IPFP appearance or BMLs could be observed on MRI in patients with OA-related knee pain pre and post a specific physiotherapy intervention.

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