Brace yourself: anterior knee pain
John Hardy looks into the aetiology, diagnosis and effective treatments of chondromalacia patellae.
Anterior knee pain is one of the most frequent musculoskeletal problems seen in general practice. It is an umbrella term for a range of diseases, each with a spectrum of presentation of different severities. As each condition becomes more severe with time it becomes more difficult to treat.
Treatment without accurate diagnosis is a futile waste of healthcare resources. Treatments range from conservative to surgical, and there is a good evidence base for some of the treatments available.
There are many causes of anterior knee pain that we should bear in mind when taking a patient history. The first thing to consider is that anterior knee pain may not be coming from the knee at all – it may be referred pain from the spine (usually irritation of L3 or L4 spinal nerve roots) or from the hip. One clue which indicates that pain could be referred is that the pain is diffuse in nature rather than localised. For other causes of anterior knee pain it is useful to consider the underlying structures as a clockface pattern around the knee. Moving in a clockwise direction, the following should be considered:
- suprapatella plical pain;
- intra-articular adhesions;
- quadriceps tendinopathy;
- medial plical impingement syndrome and secondary chondromalacia patellae grades 0–4
- Outerbridge;
- Hoffa’s Superior fat pad impingement syndrome and secondary chondromalacia patellae grades 0–4
- Outerbridge;
- torn ligamentum mucosum;
- patella tendinosis;
- sleeve fracture of the patella;
- Sinding–Larsen and Johansson syndrome;
- lateral plical impingement syndrome;
- patella maltracking;
- infective or chemical prepatella bursitis;
- post-traumatic synovitis; and
- intrabursal adhesions.
I am going to limit the scope of this article to addressing chondromalacia patellae (CP) alone. I will address its aetiology, diagnosis of its stages and effective treatments.
In the UK we have got to such a stage in the development of surgical trainee teaching in orthopaedics and trauma that all trainees will learn the necessary pathology, biomechanics and tribology to understand and manage anterior knee pain well.
As long ago as 1961, Outerbridge, a fellow Canadian, took an interest in the frequency of chondromalacia seen at the time of surgery for meniscal tear. The understanding of fatigue in material science was still in its infancy and Outerbridge admitted that the aetiology of chondromalacia was not well understood.
In the past, Outerbridge considered CP to be “the result common to a wide variety of unusual traumata. Treatment must be directed primarily not toward the damaged patellar cartilage but toward a correction of the mechanical abnormality causing it” [1]. Today we understand the aetiology of chondromalacia in terms of the mechanical abnormality better than in the 1960s.
In the1970s patella maltracking was considered a common cause of chondromalacia in young women [2]. This was before the advent of MRI and the understanding that mechanical principles like Young’s modulus, Hooke’s law and fatigue could be considered as biomechanical principles pertaining to the cause of localised failure of hyaline cartilage.
Outerbridge realised that the degenerate change was well localised to just one or other part of the patella. He realised that the medial facet of the patella was most prone to degenerate change. This countered the lateral patella maltracking hypothesis of wear so another mechanical problem needed to be recognised and addressed for successful management. Outerbridgee dismissed the theory that degeneration was due to constitutional change, writing: “it seems unlikely that a constitutional disturbance should make the medial patellar facet more susceptible to injury”. This was a clear and accurate observation; however, he and others were not yet aware of the genetic predisposition of some patients to weak hyaline cartilage. These patients have subsequently been identified – by evidence of family history and Heberden’s nodes – to be more prone than the general population to progression of knee osteoarthritis [3].
We know that most materials are prone to ‘single load to failure’, and cyclic loading above the endurance limit also causes fatigue failure. Even complex viscoelastic materials such as hyaline cartilage conform to Young’s modulus.
As late as 1972, Mike Freeman suggested that the primary event in the pathogenesis of osteoarthritis could be a fatigue failure of articular cartilage [4]. We also know that hyaline cartilage demonstrates different fatigue properties, depending not on the area, but depth of cartilage [5]. Cyclic loading of cartilage demonstrates that the different layers have differing biomechanical properties. There is a ring of different tissues around the patella that move with the patella in flexion and extension. This ring of tissue is in layers of skin, fibrous retinacular, fat and fibroelastic plical tissue in different thicknesses and layers. We know that the fat is the most highly innervated layer, especially with pain receptors [6]. We also recognise that the fat – like Hoffa’s fat pad – can be injured acutely and then chronically scarred [7]. Scarring occurs with impingement between the condyles and this then causes secondary degenerate changes in the adjacent hyaline cartilage of either the patella or the trochlea (chondromalacia) [8,9].
I often explain what is happening in anterior knee pain using an analogy of a stone in a shoe. It explains both the progressive nature of the condition and the treatment:
Surgeon: What would you do if you had a stone in your shoe?
Patient: I would take it out.
Surgeon: Yes, because if you didn’t it would start to hurt. Then if you kept walking you would develop a blister and subsequently an ulcer.
That is what happens with impingement in the knee. Osteoarthritis from impingement of the fat pad or a plical fold is no different from an ulcer due to a stone in the shoe.
Walking produces the cyclic loading. Impingement of a tissue like Hoffa’s fat pad that is not normally subject to these pressure causes fibrosis of the tissue, and then high-profile pressure causes failure of the adjacent hyaline cartilage.
The progressive nature of the condition is apparent to most orthopaedic surgeons with experience. The progression from initial impingement to chondral damage and the chronic periarticular pathological changes drives us to try to identify knees at risk and prevent degenerate change using conservative or surgical techniques.
We have many clinical symptoms and signs that can help us determine the stage of progression and there are few surgeons that will not use MRI scanning to demonstrate the stages of degenerate change as this is so closely correlated to prognosis.
Present
In the knee we know that impingement from a plical fold, the superior portion of Hoffa’s fat pad or a torn ligamentum mucosum can cause fatigue failure of the hyaline cartilage of the patella or trochlea.
At first there is pain from pinching the plica or fat pad without chondromalacia. Patients usually notice a sharp pain while rising from a chair or stair climbing. If a patient is taught to mobilise the patella medially and laterally while the quadriceps is relaxed (the ‘Shuffle test’), they can frequently flip the fold from beneath the patella – standing from sitting will confirm whether this has happened as the symptom of sharp pain is relieved.
If the pinch persists, it tends to result in local oedema within the tongue of fat. The patient still has pain crouching under load but no crepitus; swelling precedes fibrosis of the fat and a swollen fat pad impinges even further into the joint. The localised oedema is worse after exercise, as is the pain, but better after rest. We can use this observation to assist in the accuracy of confirmation of diagnosis using exercise before MRI. If the patient is sent to do the exercise that causes pain before the MRI scan is performed, it is my experience that the localised pain correlates with the site of oedema on the fat pad. In this circumstance, where the MRI shows no evidence of chondromalacia, I recommend conservative management: a non-steroidal anti-inflammatory and physiotherapy. A physiotherapist good at trialling different types of patella taping sometimes resolves the impingement. It is also useful to try one of a number of knee supports and braces, especially if taping helps but the tape causes an allergic reaction. For example, following successful infrapatella taping I would recommend the Aircast Infrapatella band (Figure 1), which uses an aircell to focus compression on the patellar tendon. Available in black only, it is a universal fit.
One of the most successful new braces for plica syndrome and Hoffa’s superior fat pad impingement is the new DonJoy Reaction WEB knee brace (Figure 2). This works by loading the soft tissues around the patella to equalise the support for the patella from the surrounding soft tissues. It works well in cases where a trial of medial and lateral taping has improved symptoms.
If there is a component of lateral patella maltracking and medial shift taping techniques have helped, then the Drytex Lateral ‘J’ brace is an old favourite (Figure 3).
By the time chondromalacia has appeared, patients have pain and crepitus on crouching. An MRI confirms chondromalacia and in my experience the patient does not do well with conservative management but has an excellent prognosis with arthroscopic resection of the impinging tissue and chondroplasty. The gold standard is both and persistent pain usually means the surgeon has undertaken chondroplasty only (www.youtube.com/watch?v=7tcr61HItUs). The analogy here would be to debride the ulcer on the heel but not remove the stone from the shoe.
Author
John Hardy is a consultant knee surgeon practising in London and Bristol. To find out more Google knee surgeon or visit www.OrthopaedicsAndTrauma.com.
References
R.E. Outerbridge (1961) The etiology of chondromalacia patellae. J. Bone Joint Surg. Br. 43B, 752–757
Outerbridge, R.E. & Dunlop, J.A. (1975) The problem of chondromalacia patellae. Clin. Orthop. Relat. Res. 110, 177–196
Cooper, C., Snow, S., McAlindon, T.E., et al. (2000) Risk factors for the incidence and progression of radiographic knee osteoarthritis. Arthritis & Rheumatism. 43(5), 995–1000
M.A.R. Freeman (ed.) (1972) Modern Trends in Orthopaedics, Butterworths, London
Belluchi, G. & Seedholm, B.B. (2001) Mechanical behaviour of articular cartilage under tensile cyclic load. Rheumatology 40, 1337–1345
Bohnsack, M., Meier, F., Walter, G.F., et al. (2005) Distribution of substance-P nerves inside the infrapatellar fat pad and the adjacent synovial tissue: a neurohistological approach to anterior knee pain syndrome. Arch. Orthop. Trauma. Surg. 125(9), 92–97
Magi, M., Branca, A., Bucca, C. & Langerame, V. (1991) Hoffa disease. Ital. J. Orthop. Traumatol. 17(2), 211–216
Hoffa, A. (1904) Influence of adipose tissue with regard to the pathology of the knee joint. JAMA 43, 795–796
Ogilvie-Harris, D.J. & Giddens J. (1994) Hoffa’s disease: arthroscopic resection of the infrapatellar fat pad. Arthroscopy 10(2), 184–187
