| Biomarker | IL-1β | Full name | serum interleukin-1β | Molecular Type | cell factor |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Inflammatory mechanism research and targeted therapy evaluation | ||
| Disease(or Constitution) | Osteoarthritis (OA) | Disease Subtypes | Inflammatory osteoarthritis | ||
| Organ | Joint (Synovium) | Test Sample / Technology Platform | Serum (ELISA, flow cytometry) | ||
| Pathobiological Mechanisms | Promoting intra-articular inflammation and cartilage degradation is a key inflammatory factor in inflammatory osteoarthritis | ||||
| Clinical Availability Status | Research phase | ||||
| Notes and Dynamics | IL-1β inhibitors (such as anabyliside) have been used in clinical practice, and serum IL-1β levels can be assessed to evaluate treatment efficacy. | ||||
| Biomarker | CRP | Full name | Serum C-reactive protein | Molecular Type | acute phase protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Inflammation activity assessment and treatment response monitoring | ||
| Disease(or Constitution) | Osteoarthritis (OA) | Disease Subtypes | Inflammatory osteoarthritis | ||
| Organ | Joint (Synovium) | Test Sample / Technology Platform | Serum (colorimetric method, immunoturbidimetric method) | ||
| Pathobiological Mechanisms | Increased liver synthesis upon activation of inflammation reflects the degree of intra-articular inflammation | ||||
| Clinical Availability Status | Widely available | ||||
| Notes and Dynamics | Positively correlated with the patient's pain score, the post-treatment decline indicates effective control of inflammation. | ||||
| Biomarker | OPG | Full name | Serum osteoprotegerin | Molecular Type | cytokine recepto |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Bone erosion monitoring and prognosis assessment | ||
| Disease(or Constitution) | Osteoarthritis (OA) | Disease Subtypes | Erosive osteoarthritis | ||
| Organ | Joint (Bone) | Test Sample / Technology Platform | Serum (ELISA, immunohistochemistry) | ||
| Pathobiological Mechanisms | Regulation of osteoclast activity: A decrease in activity level indicates active bone resorption and increased risk of bone erosion. | ||||
| Clinical Availability Status | Scientific research verification | ||||
| Notes and Dynamics | Patients with OPG levels <3 pg/mL exhibit accelerated bone erosion progression and may serve as a reference indicator for bone-protective therapy. | ||||
| Biomarker | anti-CCP | Full name | Serum anti-cyclopeptidylcarbamide antibodies | Molecular Type | autoantibody |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Differential diagnosis, prognosis assessment | ||
| Disease(or Constitution) | Osteoarthritis (OA) | Disease Subtypes | Erosive osteoarthritis | ||
| Organ | Joint (Cartilage, Bone) | Test Sample / Technology Platform | Serum (ELISA, Western blot) | ||
| Pathobiological Mechanisms | Associated with articular cartilage and bone erosion, a positive result indicates erosive phenotype and elevated risk of bone erosion. | ||||
| Clinical Availability Status | Clinically available | ||||
| Notes and Dynamics | The positive rate is approximately 30%, significantly higher than that in non-erosive osteoarthritis, and can serve as a differential indicator for erosive phenotypes. | ||||
| Biomarker | TNF-α | Full name | Tumor necrosis factor-α | Molecular Type | cell factor |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Inflammation assessment and treatment response prediction | ||
| Disease(or Constitution) | Osteoarthritis (OA) | Disease Subtypes | Secondary osteoarthritis (post-traumatic) | ||
| Organ | Joint (Synovium) | Test Sample / Technology Platform | Synovial fluid (ELISA, immunoblotting) | ||
| Pathobiological Mechanisms | Mediates chronic intra-articular inflammation, promotes cartilage degradation and bone erosion, with a positive correlation between the degree of inflammation and the horizontal extent. | ||||
| Clinical Availability Status | In research | ||||
| Notes and Dynamics | Anti-TNF-α therapy can reduce the level of TNF-α in synovial fluid and improve patient symptoms, serving as an efficacy monitoring indicator. | ||||
| Biomarker | IL-6 | Full name | interleukin-6 in synovial fluid | Molecular Type | cell factor |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | inflammatory activity monitoring, progression prediction | ||
| Disease(or Constitution) | Osteoarthritis (OA) | Disease Subtypes | Secondary osteoarthritis (post-traumatic) | ||
| Organ | Joint (Synovium) | Test Sample / Technology Platform | Synovial fluid (ELISA, flow cytometry) | ||
| Pathobiological Mechanisms | Post-traumatic intra-articular inflammatory response activation, IL-6 promotes the inflammatory cytokine cascade, exacerbating cartilage damage | ||||
| Clinical Availability Status | In research | ||||
| Notes and Dynamics | The level of IL-6 in synovial fluid>10 pg/mL indicates active inflammation, and anti-inflammatory treatment should be intensified to delay the progression of osteoarthritis. | ||||
| Biomarker | COMP | Full name | serum chondrocyte oligomeric matrix protein | Molecular Type | chondroitin |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Early diagnosis and post-traumatic cartilage injury monitoring | ||
| Disease(or Constitution) | Osteoarthritis (OA) | Disease Subtypes | Secondary osteoarthritis (post-traumatic) | ||
| Organ | Joint (Cartilage) | Test Sample / Technology Platform | Serum (ELISA, immunoturbidimetry) | ||
| Pathobiological Mechanisms | Abnormal cartilage repair after trauma, with COMP released into the bloodstream and elevated levels indicating increased risk of cartilage injury | ||||
| Clinical Availability Status | Clinical trials | ||||
| Notes and Dynamics | atients with elevated serum COMP levels within 1 month post-trauma have a 2-fold increased risk of developing osteoarthritis within 2 years. | ||||
| Biomarker | MMP-13 | Full name | Serum matrix metalloproteinase-13 | Molecular Type | protease |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Study on the degradation m echanism of c artilage and m onitoring of t herapeutic effect | ||
| Disease(or Constitution) | Osteoarthritis (OA) | Disease Subtypes | Primary osteoarthritis | ||
| Organ | Joint (Cartilage) | Test Sample / Technology Platform | Serum (ELISA, immunohistochemistry) | ||
| Pathobiological Mechanisms | Specifically degrades type II collagen, promotes cartilage matrix degradation, and exhibits a positive correlation with the degree of cartilage injury. | ||||
| Clinical Availability Status | Scientific research verification | ||||
| Notes and Dynamics | A novel MMP-13 inhibitor has entered preclinical studies and can be used as an efficacy evaluation index for targeted therapy | ||||
| Biomarker | CTX | Full name | Type II collagen C-terminal peptide | Molecular Type | Collagen degradation products |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Chondrodegradation monitoring and prognosis assessment | ||
| Disease(or Constitution) | Osteoarthritis (OA) | Disease Subtypes | Primary osteoarthritis | ||
| Organ | Joint (Cartilage) | Test Sample / Technology Platform | Urine (ELISA, Western blot) | ||
| Pathobiological Mechanisms | Type II collagen is the primary collagen component of cartilage. After degradation, CTX-II is excreted in urine, and elevated levels indicate active cartilage destruction. | ||||
| Clinical Availability Status | Clinically available | ||||
| Notes and Dynamics | The degradation rate of cartilage can be dynamically monitored, and a decrease post-treatment indicates that cartilage destruction has been inhibited. | ||||
| Biomarker | HA | Full name | serum hyaluron11ic acid | Molecular Type | glycosaminoglycan |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | diagnosis and assessment of articular cartilage injury | ||
| Disease(or Constitution) | Osteoarthritis (OA) | Disease Subtypes | Primary osteoarthritis | ||
| Organ | Joint (Cartilage) | Test Sample / Technology Platform | serum (ELISA、Colorimetry) | ||
| Pathobiological Mechanisms | aggravated cartilage damage. | ||||
| Clinical Availability Status | Clinical gradual promotion | ||||
| Notes and Dynamics | Serum HA levels in patients with knee osteoarthritis are significantly higher than those in healthy individuals, showing a positive correlation with Kellgren-Lawrence classification. | ||||
| Biomarker | CTCs | Full name | circulating tumor cells | Molecular Type | Cell, nucleic acid |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | MRD monitor、clonal evolution tracing | ||
| Disease(or Constitution) | Multiple Myeloma (MM) | Disease Subtypes | / | ||
| Organ | Bone marrow, Peripheral blood | Test Sample / Technology Platform | peripheral blood | ||
| Pathobiological Mechanisms | CTCs reflect systemic tumor burden; ctDNA carries tumor mutations, indicating clonal evolution | ||||
| Clinical Availability Status | Research validation | ||||
| Notes and Dynamics | ctDNA enables non-invasive monitoring of clonal evolution and detects drug-resistant mutations earlier than bone marrow biopsy; CTC detection demonstrates superior sensitivity in extramedullary multiple myeloma (MM) compared to bone marrow minimal residual disease (MRD) assessment. | ||||
| Biomarker | Telomerase and telomerase complex | Full name | Telomerase and telomerase complex | Molecular Type | protein/nucleic acid |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | prognosis, therapeutic targets | ||
| Disease(or Constitution) | Multiple Myeloma (MM) | Disease Subtypes | / | ||
| Organ | Bone marrow, Serum | Test Sample / Technology Platform | Marrow, serum | ||
| Pathobiological Mechanisms | Telomerase activation maintains unlimited proliferation; TRF2 abnormalities lead to chromosomal instability and promote clonal evolution | ||||
| Clinical Availability Status | research and verification phase | ||||
| Notes and Dynamics | Patients with high TERT expression exhibited a 30% reduction in median OS; telomerase inhibitor MST-312 induced apoptosis in MM cells, showing synergistic efficacy when combined with lenalidomide. | ||||
| Biomarker | CTLA-4 | Full name | Cytotoxic T-Lymphocyte-Associated Protein 4 | Molecular Type | protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | assessment of immune status and prognosis | ||
| Disease(or Constitution) | Multiple Myeloma (MM) | Disease Subtypes | / | ||
| Organ | Bone marrow, Serum | Test Sample / Technology Platform | serum、marrow | ||
| Pathobiological Mechanisms | CTLA-4 overexpression leads to Treg accumulation and weakens anti-tumor immunity | ||||
| Clinical Availability Status | research verification | ||||
| Notes and Dynamics | CTLA-4 gene polymorphisms (rs231775, rs3087243) are associated with myeloma susceptibility and immune therapy efficacy, showing promise as potential biomarkers for personalized medicine. | ||||
| Biomarker | sPD-L1 | Full name | Soluble Programmed Death-Ligand 1 | Molecular Type | protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | assessment of immune status and prognosis | ||
| Disease(or Constitution) | Multiple Myeloma (MM) | Disease Subtypes | / | ||
| Organ | Bone marrow, Serum | Test Sample / Technology Platform | serum、marrow | ||
| Pathobiological Mechanisms | sPD-L1 inhibits T cell activity; | ||||
| Clinical Availability Status | research verification | ||||
| Notes and Dynamics | sPD-L1 levels are associated with MRD positivity and predict the efficacy of pembrolizumab; a decrease in sPD-L1 after ASCT indicates immune recovery and prolongs PFS. | ||||
| Biomarker | CD163, CD206, versican | Full name | Cluster of Differentiation 163、Cluster of Differentiation 206 | Molecular Type | protein/nucleic acid |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | prognosis, microenvironment assessment | ||
| Disease(or Constitution) | Multiple Myeloma (MM) | Disease Subtypes | / | ||
| Organ | Bone marrow, Serum | Test Sample / Technology Platform | serum、marrow | ||
| Pathobiological Mechanisms | Tumor-derived extracellular vesicles carry immunosuppressive molecules and regulate the microenvironment; versican promotes adhesion and angiogenesis. | ||||
| Clinical Availability Status | Frontier research phase | ||||
| Notes and Dynamics | miR-203 and miR-30d in EVs can be used for early diagnosis; Versican promotes tumor growth through FAK/STAT3 pathway, and its inhibitor combined with lenalidomide shows synergistic effect. | ||||
| Biomarker | Gly、Pro、Gln、Glu | Full name | glycine, proline, glutamine/glutamate | Molecular Type | Metabolite |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | diagnosis, prognosis, therapeutic targets | ||
| Disease(or Constitution) | Multiple Myeloma (MM) | Disease Subtypes | / | ||
| Organ | Bone marrow, Serum | Test Sample / Technology Platform | serum、marrow | ||
| Pathobiological Mechanisms | Glycine disrupts glutathione balance and promotes proliferation; Proline originates from collagen degradation and is associated with osteolytic lesions; Glutamine metabolism provides energy. | ||||
| Clinical Availability Status | Research validation/early clinical | ||||
| Notes and Dynamics | Glycine inhibitors enhance bortezomib sensitivity; Proline dehydrogenase (PRODH) downregulation is associated with drug resistance; Glutamine transporter LAT1 inhibitors show preclinical efficacy | ||||