The role of movement and the forces generated by walking, running and other activities and the ability of strenuous exercise to cause tissue damage that might trigger AS is a new area of research. The role of mechanical factors in entheseal related disease was first suggested in the late 1950s and again mentioned, but mostly ignored, in the 1980s. This page summarises the role of movement and mechanics in AS. The current lack of knowledge around injury as a cause of AS or as an exacerbating factor is discussed
Even gentle movement is associated with mechanical stressing. Resisting the forces of gravity actually takes a lot of effort and has major effects on the skeleton. As an example of this, astronauts residing in space stations, where there is zero gravity develop brittle bones or osteoporosis. This indicates the major impact that normal forces acting on the skeleton that are associated with movement can have a major effect.
Given that very high forces are exerted at the normal enthesis, it is possible that these forces might be sufficient to trigger or drive AS in susceptible individuals. The normal tissue at the enthesis bone interface and in the sacroiliac joint is lined by fibrocartilage, a tissue whose development is determined by mechanical stressing in joints.
Just after the millennium a new theory of AS and the Spondyloarthropathies was put forward that proposed how mechanical stress, tissue microdamage and access of bacteria or other germ products to the enthesis could drive disease in susceptible individuals [1].
Dr Peggy Jacques, Prof Dirk Elewaut and colleagues in Ghent in Belgium have shown that mechanical stress to the joints in the course of normal movement, without any injury is sufficient to cause arthritis in a mouse model. This model has similarities with human Spondyloarthropathy including lower limb inflammation, sacroiliitis and Crohns Disease like features. It provides experimental proof that normal levels of mechanical stress at the enthesis is key to the Spondyloarthropathy pattern of disease. [2]
These publications have raised new questions about the role of exercise and activity in AS.
There is no evidence to stop exercise in patients with AS. This is of the utmost importance because exercise is key for patient wellbeing and cardiovascular fitness.
Lack of movement is likely a big cause in the bones of the spine knitting together or fusing so patients certainly need to keep active.
Movement and stretching exercise and maintaining a supple skeleton might actually protect a relatively immobile skeleton, such as that in AS patients, from microdamage.
Exercise has valuable psychological effects and pain alleviating effects by the release of endorphins and other chemical with pain relieving properties.
However, this new research has raised some legitimate questions for AS patients and their relatives. This is especially relevant since the newer biological therapies may retard spinal fusion progression in AS.
A study showed that patients with AS with more manual heavy jobs had more spinal fusion [3]. A second study from the same US based group of Ward and colleagues linked the level of work related activity and spinal fusion in AS [4]. More work is needed in this area since there are many potential factors that differentiate workers in manual jobs from those with other jobs.
Patients with AS do report that vigorous exercise has aggravated their symptoms
Likewise very vigorous physiotherapy has been reported as an aggravating factor in some patients. These findings come for a patient survey that we carried out on the UK NASS patient group.
Not infrequently we get contacted by AS patients who report that an injury such as car accident, has seemingly triggered AS. In the related Spondyloarthropathy group of diseases including psoriatic arthritis there is a reasonably strong case for skin, nail, or joint injury being associated with arthritis development in patients with psoriasis.
From a medicolegal perspective, a link with Psoriatic Arthritis and prior joint injury is often accepted in different jurisdictions around the world but less so in AS. More scientific research in AS will address these questions.
Of relevance to biomechanics and AS, it is evident that children with the disease typically get it in the lower part of the body including knees and ankles and large entheses. It is only with skeletal maturity that the disease migrates to the sacroiliac joint-whose mechanics is changing due to the gain in weight and growth.
Teenagers developing AS who are part of elite sports academies or other high level competitive activities may be mis-diagnosed as a mechanical tendonitis. This has lots of implications in the modern era where therapies may be transformative for patients.
This site devoted to enthesitis and enthesopathy and related conditions discusses all aspects of disease including stress and skeletal microdamage at the enthesis.
Reflecting that this is a new area there are no specific resources that we can recommend on the role of mechanics in AS.