Ankylosing Spondylitis (AS) localises to sites of high mechanical stressing at entheses and the bone adjacent to fibrocartilage at sites including the sacroiliac joint. Research in man into enthesitis and animal model data increasingly supports the role of mechanical factors in AS. This means that important questions about injury and occupation and AS onset can be revisited. These questions include:
Was my AS caused by an accident?
Did my work bring on AS?
Is my work worsening my AS and causing disease flares?
Should I advise my children to avoid joint stress to prevent AS development?
In Psoriatic Arthritis, which is closely related to AS, there is evidence pointing towards a role for site specific injury and the development of arthritis, skin disease and nail disease. However, there is a comparative lack of direct evidence in AS.
A study in AS showed that most people who developed symptoms following an injury already had X-ray changes reflecting pre-existing AS prior to the injury. This suggests that the disease comes to clinical attention after an injury but was already there . However, the authors commented that "unquestionably" a small group of patients with AS report disease onset after initial trauma .
Certainly patients sometimes report disease onset after an accident.
It is worth pointing out that mechanical stressing of the spine and sacroiliac joint can lead to an identical pattern of abnormalities on MRI as those seen in full blown AS. This indicates that mechanical stressing affects the normal entheses and not just in AS cases. However, genetic and other environmental factors determine if someone susceptible to AS actually go on and develops disease.
Compared to Psoriatic Arthritis, it can be surmised that the jury is still out as to the role of injury in the development of AS.
It is true to say that AS typically starts around the age young people start to work. People from all walks of life and all occupations get AS. There is no direct evidence that a particular joint can bring on AS. This area needs research. Now that patients can be recognised at an earlier stage of disease using MRI this question could be addressed.
Historically flares in most rheumatic disease has been linked to injury, physical activity or work and eases with rest. For example, in the case of Rheumatoid Arthritis, the commonest joint autoimmune disease, joint damage is usually worse in the dominant hand.
Patients with established AS in more physically active jobs were found to be more likely to be on permanent work disability payments .
In the United States researchers have shown a link with spinal fusion and heavy work related occupations. This is not obviously linked to disease onset but disease severity.
In particular, bending, twisting, and stretching were linked to more X-ray fusion in cases with longstanding AS. In the same study, exposure to whole body vibration was also associated with more radiographic damage .
The normal skeleton is subject to microdamage and repair and this is prominent at the entheses and bone in the spine. It seems likely that normal levels of joint loading may be sufficient to trigger disease.
If somebody carries the HLA-B27 gene and have a parent with AS then it is likely that even normal levels of stressing (in conjunction with other genes and environmental factors) may trigger disease. This is what happens in animal models.
The enthesitis mechanical stressing model of AS is supported by the effect of occupational factors on the severity of disease symptoms, work incapacity and X-ray fusion of the spine. More research is needed in this area.
In this new era of therapies there is evidence that such therapies may prevent occupational related disability . That AS is now potentially treatable may lessen the importance of mechanical factors in disease onset.
Spondyloarthritis Association of America Can AS be triggered by trauma?
Hindawi Publishing Corporation Integrative Structural Biomechanical Concepts of Ankylosing Spondylitis Dr Alfonso Masi and colleagues discuss the enthesitis mechanical stress theory of AS.