Spondyloarthritis (SpA) is an umbrella term describing a family of chronic inflammatory diseases, that primarily affects the spine, sacroiliac and peripheral joints. The two most common members of this family are the psoriasis associated psoriatic arthritis (PsA) and ankylosing spondylitis (AS). SpA is characterized by articular manifestations (involving peripheral and axial skeleton, enthesitis, and dactylitis) and extra-articular (skin, gut and eye) manifestations.
In total, SpA affects around 0.5–2% of the population and is a major impact on quality of life. For AS, individuals with the gene HLA-B27 are more likely to develop AS, and men are also more likely to develop AS than women. There is no cure for SpA, but there are several treatment option that can ease symptoms, inhibit the inflammation and slow down disease progression.
The current diagnosis include physical examination, blood tests and medical history. Here, imaging techniques such as X-ray of the sacroiliac joints and a part of pelvis are used for initial analysis, and if available a magnetic resonance image (MRI) may also be used to diagnose SpA. Together with the imaging techniques, an HLA tissue typing is performed to detect whether HLA-B27 are present and c-reactive protein (CRP) to measure the total level of inflammation.

There is a great medical need for biomarkers in SpA. The diagnosis is often delayed 5-10 years due to the symptoms being lower back and buttock pain. Thus, earlier diagnosis may provide patients’ access to effective therapies and better possibility for remission. Biomarkers that could be used for diagnosis and monitoring of treatment response could improve patients’ life and reduce clinical trial size and length when developing new efficacious treatments.

Spondyloarthritis (SpA) is characterized by chronic inflammation and tissue destruction in the joints and involved several tissues. These tissues include bone, cartilage and soft tissue, which all consists of different types of extracellular matrix (ECM) proteins – especially collagens. The ECM proteins are remodeled as a part of the normal homeostasis of the joint, where they are broken down and rebuild as part of normal repair and maintenance of the tissue. In SpA this balance between degradation and formation of tissue is interrupted resulting in net degradation of the tissue. Protein fingerprint biomarkers can quantify this tissue turnover directly in a serum sample and serve as a liquid biopsy.

The SpA diseases involve several tissues and combining biomarkers measuring the tissue involved may provide information on disease pathology – we call this tissue profiling. Tissue profiling may aid the need of molecular subtyping - endotyping - patients and based on their profile choose the best treatment for the given patient. This may also be applied to clinical trials and development of novel drugs. The tissue profile can be quantified by the Protein Fingerprint biomarkers in serum.

Biomarkers for SpA:
Enthesitis: CRPM
Hypertrophicchrondrocytes: PRO-C2, C10-C
Osteoblasts:
OC, PINP, PRO-C1
Bone erosions:
CTX-I, ICTP, C1M
Synovitis: CRPM, VICM, C3M, C4M, C6M
Degradation of cartilage: C2M, CTX-II, huARGS


Specific Protein Fingerprint biomarkers measuring endochondral bone formation, quantified by type II collagen formation (PRO-C2) and type X collagen degraded by cathepsins (C10C), could distinguish healthy individuals from axSpA and PsA patients.


Biomarkers measuring specific fragments of type I collagen (C1M), type II collagen (C2M), type III collagen (C3M) and type IV collagen (C4M), can distinguish AS patients from nrAxSpA and healthy matched controls. This information can be used to separate patients with/without axial involvement.


Patients with AS may be treated with a TNF-a inhibitory therapy. The biomarker measuring a metabolite of type I collagen degradation (C1M), is together with high sensitive C-reactive protein (hsCRP) lowered in patients treated with TNF-a inhibitory therapy. This reflects a decrease of connective tissue degradation and a lowered inflammation with treatment.


SpA involves the remodeling of three different types of tissues:
- Connective tissue (fibrosis)
- Bone resorption and cartilage turnover (ankylosis)
- Flares, chronic and tissue inflammation (inflammation)

The involvement of the different tissues and pathways are associated with different level of disease activity and different stages of disease. Hence patients with SpA may be described by different molecular profiles (endotypes), which may be reflected by Protein Fingerprint biomarkers. This has previously been done in RA and OA, where you clearly see come cluster with a more prone bone and/or inflammation phenotype than others. This may be applied to SpA and used to endotype patients, based on their tissue profile.

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