← Questions/TREATMENT
Will my spine fuse, and can treatment stop it?
The short answer
Not everyone fuses, and treatment appears to slow it: people on bimekizumab showed almost no X-ray progression over two years, and early diagnosis is linked to less damage decades later. The surprise in recent research is that new bone forms partly on its own track, driven by worn-out stem cells, rare gene variants and a protein signature that classic inflammation markers miss. That is why some people fuse despite well-controlled disease, and why the next generation of drugs may target bone formation directly.
6 papers behind this answer, best first
Clicking through to a study? How to read a paper is the ten-minute version.
Early diagnosis of axial spondyloarthritis is associated with less long-term spinal structural damage: a longitudinal analysis of the Swiss Clinical Quality Management in rheumatic diseases registry.
Arthritis & rheumatology (Hoboken, N.J.)
In a Swiss registry of 376 people followed for an average of 11 years, those diagnosed within two years of their first back symptoms developed less spinal fusion on X-ray than those diagnosed later, even though short-term treatment responses were the same. Getting a diagnosis early appears to protect the spine over decades, which is the strongest argument yet against the long diagnostic delays most people with AS experience.
Impact of Dual Interleukin-17A and Interleukin-17F Inhibition with Bimekizumab on Inflammatory and Structural Lesions in Axial Spondyloarthritis: MRI and Radiographic Outcomes from the Phase 3 BE MOBILE 1 and 2 Studies and their Open-Label Extension.
Arthritis & rheumatology (Hoboken, N.J.)
Across both bimekizumab (Bimzelx) phase 3 trials, MRI inflammation in the sacroiliac joints and spine dropped substantially within a year, erosion scores fell gradually, and X-rays at two years showed almost no progression in either the joints or the spine. For a drug this new, that is early evidence it may slow structural damage, not just symptoms, though two years is short for a disease measured in decades.
Impact of bimekizumab on CANDEN spinal MRI inflammation & structural lesions in radiographic axial spondyloarthritis: 2-year phase 3 results.
Rheumatology (Oxford, England)
In 102 people with radiographic axial spondyloarthritis scanned repeatedly over two years on bimekizumab (Bimzelx), spinal inflammation on MRI fell sharply by 16 weeks and stayed down, fat lesions rose a little early then stopped changing, and erosion and new bone barely moved. The inflammation the drug is aimed at clears quickly and the structural damage that worries people most showed minimal change over two years.
Plasma Proteomics Identifies Molecular Signatures and Biomarkers Associated with High Structural Damage in Ankylosing Spondylitis
Arthritis & Rheumatology
Measuring hundreds of blood proteins in people with ankylosing spondylitis, researchers found a five-protein signature, driven by platelet and tissue-remodelling proteins rather than classic inflammation markers, that identified those with heavy structural damage with high accuracy in a separate validation group. Bone damage in AS seems to run partly on a different track from inflammation, and a blood test for it looks feasible.
Single-cell profiling reveals senescent bone marrow mesenchymal stem cell subpopulations driving pathological ossification in ankylosing spondylitis.
Rheumatology (Oxford, England)
Single-cell analysis of bone marrow stem cells from people with ankylosing spondylitis found a worn-out, senescent group of cells that dominated in those with advanced spinal fusion and churned out bone-forming signals. New bone in AS may come from exhausted stem cells rather than healthy ones, which points to a different kind of drug target than inflammation.
EXTL3 dysfunction identified as a driver of aberrant bone development in severe familial ankylosing spondylitis.
Annals of the rheumatic diseases
In a family with unusually severe ankylosing spondylitis, a rare change in a gene called EXTL3 was found, and mice carrying it developed early joint bridging and abnormal bone through a pathway involving heparan sulfate and Wnt signalling. It identifies a bone-formation mechanism separate from inflammation, which may explain why some people fuse despite well-controlled disease.
Plain-language guides on this from patient organisations
Reviewed sources written for patients. They cover the “what do I do” part that research papers can’t.
- NHS: Complications of AS ↗
NHS (UK)
- NASS: Living well with axial SpA (PDF guide) ↗
National Axial Spondyloarthritis Society (UK)