Bone metabolism is a continual, cyclic interplay of bone growth and resorption that is carefully orchestrated by the dynamic relationship between osteoclasts, osteoblasts and an array of hormonal and regulatory influences. The relative levels of these signalling molecules dictate whether healthy, balanced bone metabolism ensues. Disturbances to this delicate equilibrium where resorption is greater than growth can weaken the skeletal architecture and put one at risk for the development of chronic and debilitating diseases such as Osteoporosis. As we continue to gain a better understanding of the intricacies of bone metabolism and the key regulators involved, we may gain further insights into mechanisms underlying other bone-related diseases as well. ALPCO’s portfolio of bone metabolism assays serves as a powerful tool for studying bone-related pathologies and may help guide the development of new, targeted therapeutics.
All products are for Research Use Only unless otherwise noted. Please refer to product pages via the Buy Now buttons for further information regarding kit specific regulatory status.
Sclerostin, a protein product of the SOST gene, inhibits osteoblast activity via antagonism of the Wnt signalling pathway and plays a key role in the regulation of bone formation. Reports show that sclerostin expression and/or circulating levels are elevated in osteoporosis, immobilisation-induced bone loss, rheumatoid arthritis, multiple myeloma and bone metastases, making it a therapeutic target of great interest for the fields of bone and cancer research 4,5 A growing body of evidence sheds light on sclerostin’s novel role in the cross-talk between diabetes, obesity and bone metabolism. As the population continues to age, so does the prevalence of chronic diseases such as obesity, type 2 diabetes and osteoporosis. A number of recent reports have shown that sclerostin levels are increased and bone turnover markers decreased in type 2 diabetes.6,7,8,9 Type 2 diabetes is associated with increased fracture risk, and it appears that the Wnt signalling pathway may be intimately involved, potentially at the level of insulin secretion from the pancreatic beta cells.
Featured Sclerostin Assays
Human Sclerostin ELISA
The measurement of serum sclerostin levels is a novel approach for studying the regulation of bone mass and may serve as a tool for better understanding the mechanisms behind certain bone disorders. The Human Sclerostin ELISA is a highly referenced kit for measurement of sclerostin in human samples, employing a six point standard curve and inclusion of a control reagent.
Catalogue No.: 04-BI-20492
Sample Type: Serum, plasma
Sample Size: 20 µl
Range: 15 – 240 pM
Sensitivity: 2.6 pM
Regulatory: Research Use Only
The Mouse Sclerostin ELISA is a highly sensitive assay utilising a polyclonal antibody based sandwich format for detecting low circulating levels of sclerostin in mouse samples. Specificity of the assay was confirmed using sera from sclerostin knock out mice and the ELISA’s small sample requirement facilitates measurement of multiple analytes from a single collection and/or multiple time points.
Catalogue No.: 41-SCLMS-E01
Sample Type: Serum, plasma
Sample Size: 15 µl
Range: 37.5 – 1200 pg/mL
Sensitivity: 17.4 pg/mL
Incubation: 5 hr 20 min
Regulatory:Research Use Only
The Human Sclerostin ELISA is manufactured by Biomedica and distributed exclusively by ALPCO in North America. A review of the Biomedica sclerostin assay can be found by clicking here: Clarke BL & Drake MT. Clinical Utility of Serum Sclerostin Measurements.
Bone metabolism is regulated by a complex array of hormonal influences and growth factors that foster communication between osteoclasts and osteoblasts and which have profound effects on the skeleton. The key players in the Hypothalamic-Pituitary-Gonadal Axis are the reproductive hormones (estrogen, progesterone and testosterone), while the Growth Hormone/Insulin Growth Factor Axis has direct impact on cartilage expansion, bone modelling and remodelling.
All products are for Research Use Only unless otherwise noted.