Many of you will remember Alan Smith suffering a horrific ankle injury playing for Manchester United against Liverpool in 2006. Those who witnessed this injury would no doubt be able to deduce that there was significant bone damage. Not all bone injuries are so blatantly obvious though and many go undiagnosed leading to problems further down the line.
A couple of years ago my wife came home from the gym with a badly swollen and bruised ankle after running on a treadmill. A few days later she visited her GP and despite not having suffered any trauma and despite reporting that the pain was worse at night than it was during the day she was diagnosed with an ankle sprain. After 3 weeks of my constant and relentless nagging, she finally succumbed and had an x-ray which revealed a stress fracture to the fibular!
That episode cemented my belief that if something doesn’t seem right, it probably isn’t.
Recently I assessed a footballer whose ankle had failed to respond to rehabilitation. An x-ray immediately after the injury failed to reveal any bone defect and the player was discharged from hospital, again with a diagnosis of an ankle sprain.
When he visited me a full 8 weeks later, he was still in considerable pain when walking and through the night as well. During the examination, I couldn’t reproduce the same pain the player felt when walking. I could provoke pain, but not the same pain. This disturbed me, as did the reports of night pain. Pain at night is a common finding with some bone related disorders, but it certainly isn’t normal with ligament damage associated with an ankle sprain.
I suspected an osteochondral defect (OCD) which is a defect affecting both the superficial cartilage of a joint and the underlying bone (‘Osteo’ – bone ‘chondral’ – cartilage).
In theory, OCD can occur in any joint in the body. The most commonly affected is the ankle joint and in particular the talar dome. The talar dome is the part of the talus bone in the ankle that the tibia (leg) sits on to form the ankle joint. Evidence suggests 1 in 20 ankle sprains and 1 in 4 ankle fractures result in a talar dome defect. What is even more alarming is that many defects cause neither pain nor dysfunction and the above statistics do not take into account these undiagnosed cases!
There are several factors that make the talar dome more prone to defects than other joints. Firstly, its articular cartilage is very thin, 1.3mm compared to the cartilage lining the hip (1.6mm) and the knee (2.2mm). The thickness of cartilage is directly related to the congruency of the joint. The ankle and elbow joints have the highest congruency which enables the compressive loads in these joints to be spread over a wider area.
Following a fracture or a sprain, malunion of the bones or laxity in the ligaments can allow the talus to move. Even a slight movement reduces the contact area and dramatically increases the load through the remaining cartilage.
In addition, the talus is a small and compact bone making it a poor shock absorber. The compactness of the bone, the thin articular cartilage and the likelihood of the talus shifting following trauma, makes it very susceptible to OCD.
The articular cartilage on a bone is the bright smooth shiny area at each end. Although the cartilage may look and feel hard, it actually contains a high percentage of fluid. This enables it to withstand large compressive loads. In a healthy joint, as one part of the cartilage is compressed, fluid within the cartilage is forced into an unloaded area (imagine sitting on a hot water bottle).
Following trauma, micro-fractures can appear in the articular cartilage and with every step; fluid is forced, at high pressure, from the cartilage into the underlying bone. This high pressure jet can result in a process called osteolysis where bone tissue is broken down and reabsorbed by the body.
Articular cartilage relies on the subchondral bone for support. Once the subchondral bone is damaged, it is less able to support the overlying cartilage. This lack of support results in further damage to the articular cartilage and a viscous cycle of degeneration starts.
X-rays do not show articular cartilage; therefore, they will only detect an OCD once it has progressed to involve the subchondral bone. Even then, evidence suggests x-rays will miss up to 40% of OCD, even if repeated several times over weeks or months.
So what now for the footballer? Well, I expressed my concerns to his club and the player was sent for a second x-ray which like the first reported no adverse findings. Unfortunately, as I have already said,
x-rays fail to identify a large percentage of OCD. MRI’s are the preferred imaging technique when an OCD is suspected. Had the player had an MRI and been given the all clear then I would have been happy. Regrettably we now have to play a waiting game. The player is back in rehab and only time will tell if my gut feeling was right or wrong. On this occasion I sincerely hope for the player’s sake that I’m wrong.