New bone formation in ankylosing spondylitis (AS) is sometimes known as "fusing". Fusion of the spine and other joints, such as the knees, is known to occur in some of those with AS. The full process as to exactly how this occurs is still not fully understood.
It is currently thought that the inflammation caused by AS can cause injury by releasing powerful chemicals, which include cytokines and proteolytic enzymes that actually damage the surrounding tissues. As the inflammation subsides, the lesions, which are injured areas, begin to heal by forming scar tissue. This scar tissue then replaces the destroyed cartilage or joint capsule. Sometimes the scar tissue
calcifies and turns into new bone formation in areas of the body where none usually exists.
The objective of a study published in the Annals of Rheumatic Diseases was to "demonstrate that while acute lesions resolve completely, more advanced lesions, characterized by evidence of reparation, are associated with new bone formation." Thus, the thinking was that the advanced lesions are the type mostly responsible for bone formation. These are more often found in more advanced disease.
The researchers also state that, "anti-tumour necrosis factor a therapies have not been shown to prevent new bone formation." Meaning, TNF-a Inhibitor / biologic class medications have not been proven to prevent new bone formation in AS. However, if a window exists between when lesions are discovered early on and they are not in an advanced stage, TNF-a inhibitors may be much more effective in treatment. Click here for information on AS medications.
The authors of the study conclude that "Our data supports the hypothesis that new bone formation is more likely in advanced inflammatory lesions and proceeds through a process of fat metaplasia, supporting a window of opportunity for disease modification."
To read the study abstract, click here.