| Biomarker | GSTP1 | Full name | Glutathione S-transferase P1 | Molecular Type | protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Oxidative stress and bone metabolism | ||
| Disease(or Constitution) | Osteoporosis (OP) | Disease Subtypes | Idiopathic Osteoporosis (Adolescent/Young Adult Type) | ||
| Organ | Bone | Test Sample / Technology Platform | Bone tissue (immunohistochemistry, Western blot) | ||
| Pathobiological Mechanisms | Participates in antioxidant stress, with reduced GSTP1 expression in the bone tissue of idiopathic patients, leading to increased ferroptosis of osteocytes and decreased bone strength. | ||||
| Clinical Availability Status | Research phase | ||||
| Notes and Dynamics | Positively correlated with iron accumulation in bone tissue, which may explain the mechanism of iron overload in idiopathic osteoporosis; its inhibitor can alleviate bone loss in mouse models. | ||||
| Biomarker | peripheral blood exosomes circRNA_0007059 | Full name | Molecular Type | Circular RNA | |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Regulation of osteocyte differentiation | ||
| Disease(or Constitution) | Osteoporosis (OP) | Disease Subtypes | Idiopathic Osteoporosis (Adolescent/Young Adult Type) | ||
| Organ | Bone | Test Sample / Technology Platform | peripheral blood exosomes(qRT-PCR、RNA-seq) | ||
| Pathobiological Mechanisms | As a ceRNA, it binds to miR-378, upregulates BMP-2 expression, and promotes osteogenic differentiation; its level is significantly reduced in exosomes of idiopathic patients. | ||||
| Clinical Availability Status | Research phase | ||||
| Notes and Dynamics | circRNA_0007059 shows promise as a non-invasive biomarker for juvenile osteoporosis | ||||
| Biomarker | LCN2 | Full name | Serum Lipid Carrier Protein 2 | Molecular Type | protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Inflammation and bone metabolism | ||
| Disease(or Constitution) | Osteoporosis (OP) | Disease Subtypes | Secondary osteoporosis (diabetes-related type) | ||
| Organ | Bone, Immune system | Test Sample / Technology Platform | Serum (ELISA, Western blot) | ||
| Pathobiological Mechanisms | Diabetes-associated chronic inflammation induces LCN2 upregulation, which promotes osteoclast differentiation by activating the NF-κB pathway | ||||
| Clinical Availability Status | Research phase | ||||
| Notes and Dynamics | Can serve as an inflammatory biomarker for diabetic osteoporosis | ||||
| Biomarker | IGF-1 | Full name | Serum insulin-like growth factor-1 | Molecular Type | protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | bone formation regulation | ||
| Disease(or Constitution) | Osteoporosis (OP) | Disease Subtypes | Secondary osteoporosis (diabetes-related type) | ||
| Organ | Bone | Test Sample / Technology Platform | Serum (Chemiluminescence, ELISA) | ||
| Pathobiological Mechanisms | Insulin resistance in diabetic patients leads to reduced IGF-1 synthesis, which inhibits osteoblast proliferation and collagen synthesis, thereby exacerbating bone loss. | ||||
| Clinical Availability Status | Clinically available (for auxiliary evaluation) | ||||
| Notes and Dynamics | It is positively correlated with lumbar BMD in diabetic patients; IGF-1 <100 ng/mL indicates impaired bone formation function and increased fracture risk. | ||||
| Biomarker | sPD-L1 | Full name | Serum soluble PD-L1 | Molecular Type | protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Immune Regulation and Bone Metabolism | ||
| Disease(or Constitution) | Osteoporosis (OP) | Disease Subtypes | Secondary osteoporosis (glucocorticoid-induced) | ||
| Organ | Bone, Immune system | Test Sample / Technology Platform | Serum (ELISA, flow cytometry) | ||
| Pathobiological Mechanisms | Glucocorticoids induce immunosuppression, and elevated sPD-L1 suppresses T cell activity, indirectly promoting osteoclast activation | ||||
| Clinical Availability Status | Research phase | ||||
| Notes and Dynamics | It is positively correlated with the dosage of glucocorticoids; patients with sPD-L1>2 ng/mL exhibit a 25% reduced response rate to bisphosphonate therapy. | ||||
| Biomarker | FGF23 | Full name | Fibroblast Growth Factor 23 | Molecular Type | protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | phosphorus metabolism regulation | ||
| Disease(or Constitution) | Osteoporosis (OP) | Disease Subtypes | Secondary osteoporosis (glucocorticoid-induced) | ||
| Organ | Bone, Kidney | Test Sample / Technology Platform | Serum (ELISA, Immunoassay by Radioimmunoassay IRMA) | ||
| Pathobiological Mechanisms | Glucocorticoids inhibit renal 1α-hydroxylase activity, leading to elevated FGF-23 levels, which promotes phosphorus excretion and results in impaired bone mineralization. | ||||
| Clinical Availability Status | Clinical trials in progress | ||||
| Notes and Dynamics | A level> 80 pg/mL indicates abnormal mineralization induced by glucocorticoids; combined with serum phosphorus testing, the diagnostic accuracy can be improved to 79%. | ||||
| Biomarker | PBMC | Full name | peripheral blood monouclear cells | Molecular Type | microRNA |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Regulation of osteocyte differentiation | ||
| Disease(or Constitution) | Osteoporosis (OP) | Disease Subtypes | Primary osteoporosis (senile) | ||
| Organ | Bone | Test Sample / Technology Platform | Peripheral blood PBMC (qRT-PCR、RNA-seq) | ||
| Pathobiological Mechanisms | Targeted inhibition of osteoblast transcription factor ATF4 and high expression of miR-133a in peripheral blood mononuclear cells (PBMCs) of elderly patients suppress osteogenic differentiation, exacerbating bone loss | ||||
| Clinical Availability Status | Research phase | ||||
| Notes and Dynamics | negatively correlated with lumbar BMD; it can serve as a potential molecular biomarker for the early diagnosis of senile osteoporosis | ||||
| Biomarker | S1P | Full name | Plasma sphingosine-1-phosphate | Molecular Type | lipid |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Regulation of osteocyte migration | ||
| Disease(or Constitution) | Osteoporosis (OP) | Disease Subtypes | Primary osteoporosis (senile) | ||
| Organ | Bone, Bone marrow | Test Sample / Technology Platform | Plasma (LC-MS/MS, High Performance Liquid Chromatography HPLC) | ||
| Pathobiological Mechanisms | Regulation of osteoclast precursor migration via the S1PR1/S1PR2 pathway, elevated plasma S1P levels in elderly patients promote bone resorption, and imbalance of bone marrow-S1P gradient | ||||
| Clinical Availability Status | Research phase | ||||
| Notes and Dynamics | Elderly patients with S1P>3.5 μmol/L exhibit a 5.5-fold increased risk of hip fracture; the plasma/bone marrow ratio provides a more accurate assessment of bone resorption activity. | ||||
| Biomarker | DKK-1 | Full name | serum Dickkopf-1 | Molecular Type | protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | inhibition of bone formation | ||
| Disease(or Constitution) | Osteoporosis (OP) | Disease Subtypes | Primary osteoporosis (senile) | ||
| Organ | Bone | Test Sample / Technology Platform | Serum (ELISA, Western blot) | ||
| Pathobiological Mechanisms | Inhibition of Wnt pathway activity: In elderly patients, the decline in osteocyte function leads to increased secretion of DKK-1, which further suppresses osteogenesis. | ||||
| Clinical Availability Status | Research phase | ||||
| Notes and Dynamics | It is negatively correlated with lumbar BMD in elderly males (r=-0.42); teriparatide treatment can reduce its levels and reverse the state of bone formation inhibition. | ||||
| Biomarker | Cathepsin K | Full name | Serum cysteine protease K | Molecular Type | protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | bone resorption monitoring | ||
| Disease(or Constitution) | Osteoporosis (OP) | Disease Subtypes | Primary osteoporosis (senile) | ||
| Organ | Bone | Test Sample / Technology Platform | Serum (ELISA、LC-MS/MS) | ||
| Pathobiological Mechanisms | Osteoclast-specific proteases degrade type I collagen and non-collagenous proteins in the bone matrix, with elevated levels in elderly patients due to excessive osteoclast activation. | ||||
| Clinical Availability Status | Clinical trials in progress | ||||
| Notes and Dynamics | Positively correlated with bone resorption rate, it can predict the risk of vertebral fractures in elderly patients; a ≥50% reduction in cathepsin K inhibitor (e.g., odanacatib) levels post-treatment indicates significant therapeutic efficacy. | ||||
| Biomarker | POSTN | Full name | Serum periostin | Molecular Type | protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | bone cortical metabolism | ||
| Disease(or Constitution) | Osteoporosis (OP) | Disease Subtypes | Primary Osteoporosis (Postmenopausal) | ||
| Organ | Bone (Cortical bone) | Test Sample / Technology Platform | Serum (ELISA, immunohistochemistry) | ||
| Pathobiological Mechanisms | Primarily secreted by periosteal osteoblasts, it regulates collagen cross-linking and cortical bone strength. A decline in postmenopausal levels leads to increased cortical bone fragility. | ||||
| Clinical Availability Status | Scientific research verification | ||||
| Notes and Dynamics | It is independently associated with the risk of non-vertebral fractures (HR=1.89), particularly suitable for evaluating areas predominantly composed of cortical bone (e.g., hip); it holds promise as a periperal metabolic marker. | ||||
| Biomarker | Sclerostin | Full name | seric scleroprotein | Molecular Type | protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | inhibition of bone formation | ||
| Disease(or Constitution) | Osteoporosis (OP) | Disease Subtypes | Primary Osteoporosis (Postmenopausal) | ||
| Organ | Bone | Test Sample / Technology Platform | Serum (ELISA, electrochemiluminescence assay) | ||
| Pathobiological Mechanisms | Secreted by osteocytes, it inhibits osteoblast differentiation by blocking the Wnt/β-catenin pathway, and elevated levels after menopause exacerbate bone formation inhibition. | ||||
| Clinical Availability Status | Clinical trials in progress | ||||
| Notes and Dynamics | negatively correlated with lumbar BMD (r=-0.38); the degree of reduction in levels after treatment with sclerosing protein antibody (Romosozumab) was positively correlated with BMD increase | ||||
| Biomarker | OPG | Full name | serum osteoprotegerin | Molecular Type | protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | bone metabolism regulation | ||
| Disease(or Constitution) | Osteoporosis (OP) | Disease Subtypes | Primary Osteoporosis (Postmenopausal) | ||
| Organ | Bone | Test Sample / Technology Platform | Serum (ELISA, Western blot) | ||
| Pathobiological Mechanisms | As a decoy receptor for RANKL, it inhibits osteoclast differentiation and activity. The decline in estrogen levels after menopause leads to reduced OPG expression, resulting in an imbalance in bone resorption. | ||||
| Clinical Availability Status | Clinical trials in progress | ||||
| Notes and Dynamics | The diagnostic value of individual detection is limited, whereas combined detection with RANKL (OPG/RANKL ratio) improves the accuracy of postmenopausal osteoporosis risk stratification, with a ratio <0.8 indicating high risk. | ||||
| Biomarker | β-CTX | Full name | Serum β-collagen cross-linked C-terminal peptide | Molecular Type | protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Bone Resorption Assessment | ||
| Disease(or Constitution) | Osteoporosis (OP) | Disease Subtypes | Primary Osteoporosis (Postmenopausal) | ||
| Organ | Bone | Test Sample / Technology Platform | Serum (Chemiluminescence, ELISA) | ||
| Pathobiological Mechanisms | Type I collagen degradation products during bone resorption specifically reflect osteoclast-mediated bone matrix destruction, with significantly elevated levels in postmenopausal estrogen deficiency. | ||||
| Clinical Availability Status | Widely available | ||||
| Notes and Dynamics | Significantly influenced by diet, blood sampling requires fasting; positively correlated with hip fracture risk, with a 2.3-fold increase in fracture risk when levels exceed 0.5 ng/mL. | ||||
| Biomarker | PINP | Full name | Serum type I procollagen N-terminal prepeptide | Molecular Type | protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Bone formation monitoring | ||
| Disease(or Constitution) | Osteoporosis (OP) | Disease Subtypes | Primary Osteoporosis (Postmenopausal) | ||
| Organ | Bone | Test Sample / Technology Platform | Serum (fully automated chemiluminescence immunoassay analyzer, ELISA) | ||
| Pathobiological Mechanisms | The precursor fragments released by osteoblasts during type I collagen synthesis directly reflect the collagen synthesis rate and serve as a sensitive indicator of bone formation. | ||||
| Clinical Availability Status | Widely available | ||||
| Notes and Dynamics | Bone formation reference markers recommended by IOF/IFCC; an increase of ≥20% within 3 months post-treatment indicates the onset of anabolic drug (e.g., teriparatide) and is significantly associated with increased spinal BMD. | ||||
| Biomarker | BALP | Full name | Serum bone-specific alkaline phosphatase | Molecular Type | protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Bone formation assessment | ||
| Disease(or Constitution) | Osteoporosis (OP) | Disease Subtypes | Primary Osteoporosis (Postmenopausal) | ||
| Organ | Bone | Test Sample / Technology Platform | Serum (Enzyme-Linked Immunosorbent Assay (ELISA), Chemiluminescence Assay) | ||
| Pathobiological Mechanisms | Secreted by osteoblasts, it catalyzes bone matrix mineralization. Elevated levels reflect enhanced osteoblast activity and may early indicate abnormal bone formation. | ||||
| Clinical Availability Status | Widely available | ||||
| Notes and Dynamics | It was negatively correlated with lumbar BMD, and combined with PINP, the diagnostic sensitivity of postmenopausal osteoporosis was improved to 82%; A decline of ≥40% indicates efficacy of anti-osteoporosis therapy | ||||