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• Bone derived SCLEROSTIN associated with Alzheimer´s Disease

Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder and the primary cause of cognitive decline among older adults (1). In 2019, 55 million people were estimated to have dementia across the world, a figure predicted to increase to 139 million by 2050 according to the WHO (2).

Advancing age is a significant risk factor for both osteoporosis and Alzheimer’s disease (AD) as individuals with osteoporosis are more susceptible to developing AD later in life (3). Recent research has uncovered a connection between Alzheimer’s disease (AD) and osteoporosis (OP), emphasizing overlapping pathological characteristics that suggest they may share common regulatory and pathogenic mechanisms (4). It has been suggested that bone tissue can influence the function of other organs through the secretion of various proteins into the bloodstream (5).  Brain and bone tissues can regulate each other in different manners through bone-brain axis (3).

Bone derived SCLEROSTIN is associated with Alzheimer´s Disease

Alzheimer’s disease and Wnt Signaling

The Wnt signaling pathway plays a critical role in embryonic development and adult tissue homeostasis. This pathway also is vital in brain development and maintenance. Studies have shown that in AD, Wnt signaling is often dysregulated, and its deficiency can contribute to synaptic degeneration and cognitive decline (6, 7). 

Alzheimer’s disease and Sclerostin

Sclerostin (SOST) is a protein secreted by osteocytes, bone cells embedded in the bone tissue. Sclerostin is a key inhibitor of Wnt/β-catenin signaling. Increased sclerostin levels, often observed with aging, are linked to a higher accumulation of amyloid-beta (Aβ) and cognitive decline in both Alzheimer’s disease patients and older adults (8). In a mouse model researchers also demonstrated that osteocyte-derived sclerostin crosses the blood–brain barrier of old mice, where it dysregulates Wnt–β-catenin signalling (9).

Proposed Mechanism

Sclerostin’s inhibition of Wnt/β-catenin signaling can lead to increased BACE1 activity, which is involved in the production of Aβ, a key protein that forms plaques in the brains of AD patients (10). 

Therapeutic Implications

Understanding the role of sclerostin in AD has led to the exploration of strategies to target the Wnt pathway or sclerostin itself, potentially as a therapeutic approach for AD (9). 

Sclerostin ELISA, #BI-20492 developed and manufactured by BIOMEDICA

• TRUSTED – most referenced Sclerostin ELISA (+320 citations)
• LOW sample volume – 20µl sample /well
•  
• For SERUM & PLASMA samples
• RELIABLE – validated  following international quality guidelines

 

 

Also available:

 Bioactive Sclerostin ELISA, BI-20472

• CHARACTERIZED ANTIBODIES – targeting the receptor binding region
• EXTENSIVELY validated for clinical samples
• LOW sample volume – 20µl sample /well 

 

Literature

1. Worlds Alzheimer´s Report 2024 , Alzheimer’s Disease International. 2024. World Alzheimer Report 2024: Global changes in attitudes to dementia. London, England: Alzheimer’s Disease International.
2. Ageing and Health, World Health Organization.
3. Research progress in Alzheimer’s disease and bone-brain axis. Zhang F, Zhang W. Ageing Res Rev. 2024 Jul;98:102341. doi: 10.1016/j.arr.2024.102341. Epub 2024 May 15. PMID: 38759893.
4. The potential link between the development of Alzheimer’s disease and osteoporosis. Nasme F, Behera J, Tyagi P, Debnath N, Falcone JC, Tyagi N. Biogerontology. 2025 Jan 20;26(1):43. doi: 10.1007/s10522-024-10181-z. PMID: 39832071; PMCID: PMC12087362.
5. Biology of Bone Tissue: Structure, Function, and Factors That Influence Bone Cells. Florencio-Silva R, Sasso GR, Sasso-Cerri E, Simões MJ, Cerri PS. Biomed Res Int. 2015;2015:421746. doi: 10.1155/2015/421746. Epub 2015 Jul 13. PMID: 26247020; PMCID: PMC4515490.
6. The role of Wnt signaling in the development of Alzheimer’s disease: a potential therapeutic target? Biomed Res Int. 2014;2014:301575. Wan W, Xia S, Kalionis B, Liu L, Li Y. doi: 10.1155/2014/301575. Epub 2014 May 4. PMID: 24883305; PMCID: PMC4026919.
7. Wnt Signaling Deregulation in the Aging and Alzheimer’s Brain. Front Cell Neurosci. Palomer E, Buechler J, Salinas PC. 2019 May 22;13:227. doi: 10.3389/fncel.2019.00227. PMID: 31191253; PMCID: PMC6538920.
8. Elevated plasma sclerostin is associated with high brain amyloid-β load in cognitively normal older adults. Yuan J, Pedrini S, Thota R, Doecke J, Chatterjee P, Sohrabi HR, Teunissen CE, Verberk IMW, Stoops E, Vanderstichele H, Meloni BP, Mitchell C, Rainey-Smith S, Goozee K, Tai ACP, Ashton N, Zetterberg H, Blennow K, Gao J, Liu D, Mastaglia F, Inderjeeth C, Zheng M, Martins RN. NPJ Aging. 2023 Sep 4;9(1):17. doi: 10.1038/s41514-023-00114-4. PMID: 37666862; PMCID: PMC10477312.
9. Osteocyte-derived sclerostin impairs cognitive function during ageing and Alzheimer’s disease progression. Shi T, Shen S, Shi Y, Wang Q, Zhang G, Lin J, Chen J, Bai F, Zhang L, Wang Y, Gong W, Shao X, Chen G, Yan W, Chen X, Ma Y, Zheng L, Qin J, Lu K, Liu N, Xu Y, Shi YS, Jiang Q, Guo B. Nat Metab. 2024 Mar;6(3):531-549. doi: 10.1038/s42255-024-00989-x. Epub 2024 Feb 26. PMID: 38409606.
10. The Alzheimer’s disease beta-secretase enzyme, BACE1. Cole SL, Vassar R. Mol Neurodegener. 2007 Nov 15;2:22. doi: 10.1186/1750-1326-2-22. PMID: 18005427; PMCID: PMC2211305.
11. Inhibition of Wnt signaling induces amyloidogenic processing of amyloid precursor protein and the production and aggregation of Amyloid-beta (Abeta)42 peptides. Tapia-Rojas C, Burgos PV, Inestrosa NC. J. Neurochem. 2016;139

 

Elevated plasma sclerostin is associated with high brain amyloid-β load in cognitively normal older adults. Yuan J et al., Aging. 2023.  

Abstract

Osteoporosis and Alzheimer’s disease (AD) mainly affect older individuals, and the possibility of an underlying link contributing to their shared epidemiological features has rarely been investigated. In the current study, we investigated the association between levels of plasma sclerostin (SOST), a protein primarily produced by bone, and brain amyloid-beta (Aβ) load, a pathological hallmark of AD. The study enrolled participants meeting a set of screening inclusion and exclusion criteria and were stratified into Aβ- (n = 65) and Aβ+ (n = 35) according to their brain Aβ load assessed using Aβ-PET (positron emission tomography) imaging. Plasma SOST levels, apolipoprotein E gene (APOE) genotype and several putative AD blood-biomarkers including Aβ40, Aβ42, Aβ42/Aβ40, neurofilament light (NFL), glial fibrillary acidic protein (GFAP), total tau (t-tau) and phosphorylated tau (p-tau181 and p-tau231) were detected and compared. It was found that plasma SOST levels were significantly higher in the Aβ+ group (71.49 ± 25.00 pmol/L) compared with the Aβ- group (56.51 ± 22.14 pmol/L) (P < 0.01). Moreover, Spearman’s correlation analysis showed that plasma SOST concentrations were positively correlated with brain Aβ load (ρ = 0.321, P = 0.001). Importantly, plasma SOST combined with Aβ42/Aβ40 ratio significantly increased the area under the curve (AUC) when compared with using Aβ42/Aβ40 ratio alone (AUC = 0.768 vs 0.669, P = 0.027). In conclusion, plasma SOST levels are elevated in cognitively unimpaired older adults at high risk of AD and SOST could complement existing plasma biomarkers to assist in the detection of preclinical AD. 

 

Sclerostin is an osteocyte-derived secreted glycoprotein that suppresses bone formation.  Our Sclerostin ELISA assay was highlighted in a recent study investigating the effect of vitamin D3, omega-3 fatty acids (omega-3s), and exercise on serum sclerostin levels and bone turnover markers. The researchers evaluated the effects of vitamin D3, omega-3s, and a simple home-based strength exercise program (SHEP), alone or in combination, on serum sclerostin and bone turnover marker levels (1).

 

Sclerostin decreases through exercise and omega-3s

Key findings

Effect of vitamin D3, omega-3 fatty acids, and exercise on serum sclerostin levels and bone turnover markers. Tsourdi E et al., (1)

-In the 3-year prevention trial among largely vitamin D replete adults age 70 and older, structured home-based exercise program (SHEP) alone or in combination with omega-3s reduced serum sclerostin levels, while vitamin D3 and omega-3s alone had no effect on sclerostin levels.

-Omega-3s plus SHEP led to a greater decrease in sclerostin levels compared to no omega-3s/control exercise.

– The bone turnover markers P1NP and β-CTx showed no significant effects for any of the individual treatments and treatment combinations.

 

Biomedica´s SCLEROSTIN  ELISA (cat. no. BI-20492) kit features

• TRUSTED – most referenced Sclerostin ELISA (+320 citations)
• EFFICIENT – 20µl sample /well
• EASY HANDLING: 7 standards and 2 controls

 

About Sclerostin  

Sclerostin is a protein encoded by the SOST gene,  that is mainly produced by osteocytes which are bone cells embedded within the bone matrix. Sclerostin inhibits canonical Wnt signaling, a pathway promoting bone formation Sclerostin acts as a negative regulator of bone formation.

 

Literature

1. Effect of vitamin D3, omega-3 fatty acids, and exercise on serum sclerostin levels and bone turnover markers. Tsourdi E, Gängler S, Kistler-Fischbacher M, Rauner M, Dawson-Hughes B, Orav EJ, Tsai LT, Lang W, Kanis JA, Theiler R, Egli A, Bischoff-Ferrari HA, Hofbauer LC. J Clin Endocrinol Metab. 2024 Dec 9: dgae859. doi: 10.1210/clinem/dgae859. Epub ahead of print. PMID: 39657964.

 

Abstract

Context: Sclerostin inhibits canonical Wnt signaling, a pathway promoting bone formation. The effects of vitamin D3, omega-3 fatty acids (omega-3s), and exercise on serum sclerostin levels and bone metabolism are unclear.

Objective: To investigate the effects of 2000 IU/d vitamin D3, 1g/d omega-3s, and a simple home-based strength exercise program (SHEP), alone or in combination, on serum sclerostin and bone turnover marker levels.

Design, setting and participants: Sclerostin, procollagen type 1 N propeptide (P1NP) and C-terminal telopeptide (β-CTx) levels were pre-defined secondary outcomes of DO-HEALTH, a double blind, randomized controlled trial in healthy physically active older adults in five European countries.

Outcome measures: Changes in yearly serum sclerostin, P1NP and β-CTx levels over 3 years, adjusted for age, sex, prior falls, study site, baseline BMI, and baseline level of the respective outcome.

Results: 1,848 participants were included (mean age 74.8 ± 4.4 years, 58.9 % women, 41.4 % 25(OH)D < 20 ng/mL, 83.9 % at least moderately physically active at baseline). Vitamin D3 and omega-3s supplementation alone did not change sclerostin levels significantly, while SHEP compared with control exercise (joint mobility) led to greater decrease in sclerostin levels [-1.56 pmol/L (-2.54, -0.58), p=0.002]. Omega-3s plus SHEP led to a greater decrease in sclerostin levels compared to no omega-3s/control exercise [-1.93pmol/L (-3.31, -0.54), p=0.007]. For P1NP and β-CTx there were no significant effects for any of the individual treatments and treatment combinations.

Conclusions: In this 3-year prevention trial among largely vitamin D replete adults age 70 and older, SHEP alone or in combination with omega-3s reduced serum sclerostin levels, while vitamin D3 and omega-3s alone did not affect serum sclerostin levels.

 

 

The Biomedica SCLEROSTIN ELISA Assay Kit (cat. no. BI-20492) was utilized in a recent publication identifying high-risk frailty groups (full publication).  

Sclerostin (SOST) ELISA  (cat. no. BI-20492)

• Most referenced Sclerostin ELISA in over 300 citations
• Low sample volume – 20µl / well
• Validation following international guidelines

 

SCLEROSTIN – a biomarker for predicting the onset of frailty

SCLEROSTIN, a protein that is predominantly produced by osteocytes, has gained considerable attention for its role in inhibiting bone formation (1).  In addition to its effects on bone, sclerostin has been shown to have hormonal functions in non-skeletal tissues like adipocytes, blood vessels, muscles, and kidneys, where it plays a role in endothelial function, energy balance, glucose metabolism, physical performance, and kidney health (2-4). This broader systemic involvement highlights its potential effects on overall health.

Sclerostin circulates in the blood as a secreted protein and can easily be measured by ELISA assay technology, making it a promising biomarker for various age-related conditions, such as osteoporosis, sarcopenia, and cardiovascular diseases. The link between serum Sclerostin levels and frailty has not yet been studied. In a recent clinical study the relationship between circulating sclerostin levels and frailty, using both the phenotypic frailty model and the frailty index in a group of older adults has been investigated.

SCLEROSTIN – a biomarker for predicting the onset of frailty

Elevated Circulating Sclerostin Levels in Frail Older Adults: Implications beyond Bone Health. Baek JY et al., Endocrinol Metab (Seoul). 2025; 40(1):73-81. doi: 10.3803/EnM.2024.2100. PMCID: PMC11898323.

“Methods: We collected blood samples from 244 older adults who underwent comprehensive geriatric assessments. Sclerostin levels were quantified using an enzyme-linked immunosorbent assay. Frailty was assessed using two validated approaches: the phenotypic model by Fried and the deficit accumulation frailty index (FI) by Rockwood.

Results: After controlling for sex, age, and body mass index, we found that serum sclerostin levels were significantly elevated in frail individuals compared to their robust counterparts (P<0.001). There was a positive correlation between serum sclerostin concentrations and the FI (P<0.001). Each standard deviation increase in serum sclerostin was associated with an odds ratio of 1.87 for frailty (P=0.003). Moreover, participants in the highest quartile of sclerostin levels had a significantly higher FI and a 9.91-fold increased odds of frailty compared to those in the lowest quartile (P=0.003 and P=0.039, respectively).

Conclusion: These findings, which for the first time explore the association between circulating sclerostin levels and frailty, have significant clinical implications, positioning sclerostin as one of potential blood-based biomarkers for frailty that captures the comprehensive physical, mental, and social aspects of the elderly, extending beyond its traditional role in bone metabolism.”

 

Literature

1. Role of Wnt signaling and sclerostin in bone and as therapeutic targets in skeletal disorders. Marini F, Giusti F, Palmini G, Brandi ML.Osteoporos Int. 2023 Feb;34(2):213-238. doi: 10.1007/s00198-022-06523-7. Epub 2022 Aug 18. PMID: 35982318.
2. Sclerostin: From Molecule to Clinical Biomarker. Omran A, Atanasova D, Landgren F, Magnusson P. Int J Mol Sci. 2022 Apr 26;23(9):4751. doi: 10.3390/ijms23094751. PMID: 35563144; PMCID: PMC9104784.
3. Role of Sclerostin in Cardiovascular Disease. Golledge J, Thanigaimani S. Arterioscler Thromb Vasc Biol. 2022 Jul;42(7):e187-e202. doi: 10.1161/ATVBAHA.122.317635. Epub 2022 May 12. PMID: 35546488.
4. Exploring the Role of Sclerostin as a Biomarker of Cardiovascular Disease and Mortality: A Scoping Review. Sanabria-de la Torre R, González-Salvatierra S, García-Fontana C, Andújar-Vera F, García-Fontana B, Muñoz-Torres M, Riquelme-Gallego B. Int J Environ Res Public Health. 2022 Nov 30;19(23):15981. doi: 10.3390/ijerph192315981. PMID: 36498053; PMCID: PMC9739125.

Sclerostin and Periostin associated with vascular risk scales in type 2 diabetes

Exciting research news! The BIOMEDICA bioactive Sclerostin and Periostin ELISA kits were used in a groundbreaking study evaluating the association of these bone proteins related to cardiovascular disease (CVD), with the main vascular risk scales in patients with type 2 diabetes.

All Biomedica ELISA assays are fully validated following international quality guidelines.

Bioactive Sclerostin ELISA (cat. no. BI-20472)

• CHARACTERIZED ANTIBODIES – targeting the receptor binding region
• LOW sample volume – 20µl sample /well 

 

Sclerostin ELISA (cat. no. BI-20492)

• TRUSTED – most referenced Sclerostin ELISA (+280 citations)
• LOW sample volume – 20µl sample /well

 

Periostin ELISA (cat. no. BI-20433)

• LOW sample volume – 20µl sample /well
• SPECIFIC – Characterized, epitope mapped capture and detection antibodies:

Characterization of a sandwich ELISA for the quantification of all human periostin isoforms. Gadermaier, E et al.

 

Sclerostin and Periostin associated with vascular risk scales in type 2 diabetes

Type 2 diabetes is linked to an elevated risk of cardiovascular disease (CVD), affecting approximately 35% of patients with the condition (1). As a result, assessing cardiovascular risk is essential for effective disease management in individuals with type 2 diabetes. Various risk scores have been developed to estimate CVD in the general population, including the Framingham Risk Score (FRS), the REGICOR and more recently, the SCORE2-Diabetes was introduced, specifically tailored for individuals with type 2 diabetes (2).

While these computational tools are utilized in clinical practice, there remains a need to investigate new biomarkers that could enhance cardiovascular risk stratification for patients with type 2 diabetes.

Typical bone proteins, including Sclerostin and Periostin, have been linked to cardiovascular disease (CVD). Concurrently, various risk scores have been created to forecast CVD in the general population. The objective of the following study was to examine the relationship between these bone proteins connected to CVD and key vascular risk scales:

Bone proteins are associated with cardiovascular risk according to the SCORE2-Diabetes algorithm. González-Salvatierra S et al., Cardiovasc Diabetol. 2024.  

Key findings:

• Sclerostin and Periostin are associated with vascular risk in the SCORE2-Diabetes algorithm.
• This suggests that Sclerostin and Periostin may serve as useful diagnostic biomarkers for vascular risk in patients with type 2 diabetes.
• Future prospective studies are needed to validate the significance of these bone proteins in assessing vascular risk in the diabetic population.

 

Abstract

Background: Typical bone proteins, such as sclerostin and periostin, have been associated with cardiovascular disease (CVD). Simultaneously, several risk scores have been developed to predict CVD in the general population. Therefore, we aimed to evaluate the association of these bone proteins related to CVD, with the main vascular risk scales: Framingham Risk Score (FRS), REGICOR and SCORE2-Diabetes, in patients with type 2 diabetes. We focus in particular on the SCORE2-Diabetes algorithm, which predicts 10-year CVD risk and is specific to the study population.

Methods: This was a cross-sectional study including 104 patients with type 2 diabetes (62 ± 6 years, 60% males). Clinical data, biochemical measurements, and serum bioactive sclerostin and periostin levels were collected, and different risk scales were calculated. The association between bioactive sclerostin or periostin with the risk scales was analyzed.

Results: A positive correlation was observed between circulating levels of bioactive sclerostin (p < 0.001) and periostin (p < 0.001) with SCORE2-Diabetes values. However, no correlation was found with FRS or REGICOR scales. Both serum bioactive sclerostin and periostin levels were significantly elevated in patients at high-very high risk of CVD (score ≥ 10%) than in the low-moderate risk group (score < 10%) (p < 0.001 for both). Moreover, analyzing these proteins to identify patients with type 2 diabetes at high-very high vascular risk using ROC curves, we observed significant AUC values for bioactive sclerostin (AUC = 0.696; p = 0.001), periostin (AUC = 0.749; p < 0.001), and the model combining both (AUC = 0.795; p < 0.001). For diagnosing high-very high vascular risk, serum bioactive sclerostin levels > 131 pmol/L showed 51.6% sensitivity and 78.6% specificity. Similarly, serum periostin levels > 1144 pmol/L had 64.5% sensitivity and 76.2% specificity.

Conclusions: Sclerostin and periostin are associated with vascular risk in the SCORE2-Diabetes algorithm, opening a new line of investigation to identify novel biomarkers of cardiovascular risk in the type 2 diabetes population.

 

Literature

1. Cardiovascular disease in type 2 diabetes mellitus: progress toward personalized management. Ma CX, Ma XN, Guan CH, Li YD, Mauricio D, Fu SB. Cardiovasc Diabetol. 2022 May 14;21(1):74. doi: 10.1186/s12933-022-01516-6. PMID: 35568946.
2. Bone proteins are associated with cardiovascular risk according to the SCORE2-Diabetes algorithm. González-Salvatierra S, García-Martín A, García-Fontana B, Martínez-Heredia L, García-Fontana C, Muñoz-Torres M. Cardiovasc Diabetol. 2024 Aug 24;23(1):311. doi: 10.1186/s12933-024-02406-9. PMID: 39182106.

 

 

November is Diabetes Awareness Month bringing attention to diabetes and its impact on millions of individuals.

Diabetes mellitus has emerged as the third most significant non-communicable disease, following cardiovascular diseases and cancer. This condition encompasses a group of metabolic disorders marked by chronic hyperglycemia resulting from various causes, along with inadequate insulin secretion and impaired insulin action. According to the most recent statistics from the International Diabetes Federation, the global number of individuals with diabetes reached 530 million in 2021, with projections suggesting it could exceed 780 million by 2045. Due to the long-term nature of the disease, diabetes can lead to damage across multiple body systems or organs, resulting in various complications (1, 2). Beyond the more commonly known complications of diabetes such as heart disease, diabetes can also affect the skeletal system. This severe complication of diabetes leads to bone loss potentially resulting in osteoporosis and increased fracture risk.

Identifying biomarkers that may predict fracture risk in individuals with diabetes is crucial for improving patient care.

Sclerostin and Fracture Risk Prediction in Diabetes

Sclerostin (SOST) is a bone-related protein that is mainly produced by osteocytes, bone cells embedded in the bone matrix. Sclerostin is considered to be one of the major regulators of bone formation. It is a soluble antagonist of the Wnt signaling pathway and its inactivation leads to bone degradation, while the  of Wnt signaling promotes bone formation (3). Sclerostin has been a target of therapeutic antibodies for osteoporosis treatment due to its role in inhibiting bone formation.

Bone as an endocrine organ

Research indicates that bone, which is involved in lipid and glucose metabolism, is increasingly recognized as an endocrine organ. Recent findings suggest that sclerostin contributes to disorders related to lipid and glucose metabolism (4). Studies have shown that Sclerostin levels are increased in individuals with prediabetes and correlated with insulin resistance in the skeletal muscle, liver, and adipose tissue (5). In addition, Sclerostin levels have been shown to be negatively associated with insulin sensitivity in obese but not in lead woman (6).

Further studies have revealed that increased serum Sclerostin levels are associated with vertebral fractures in patients with type 2 diabetes mellitus (7, 8). Sclerostin, has also been suggested to have predictive value for fracture risk in patients with diabetes (9).

Sclerostin – a promising circulating marker of diabetic bone disease

Sclerostin has emerged as a promising circulating marker of diabetic bone disease. It may not only reflect the degree of osteocyte dysfunction and the suppression of bone formation that occurs in this disease, but it may also potentially reflect the vascular alterations that are associated with specific bone alterations such as cortical porosity (10).

Additional research is essential to enhance the understanding of biochemical markers in the assessment of diabetic bone disease. Specifically, the ability of bone markers to forecast fracture risk needs further examination.

Circulating Sclerostin levels can reliably be measured in human serum and plasma samples with a conventional SCLEROSTIN ELISA Assay Kit.

Sclerostin ELISA (cat. no. BI-20492)

• MOST referenced in more than 300 citations
• LOW sample volume – 20µl sample /well
• For SERUM & PLASMA samples
• RELIABLE – full validation package

 

Bioactive Sclerostin ELISA (cat. no. BI-20472)

• CHARACTERIZED ANTIBODIES – targeting the receptor binding region
• RIGOROUSLY validated for clinical samples
• LOW sample volume – 20µl sample /well
• RELIABLE – full validation package

 

Literature

1. International Diabetes Federation – Facts and Figures
2. Diabetes mellitus, the fastest growing global public health concern: Early detection should be focused. Hossain MJ, Al-Mamun M, Islam MR. Health Sci Rep. 2024; 7(3):e2004. doi: 10.1002/hsr2.2004. PMID: 38524769.
3. Role of Wnt signaling and sclerostin in bone and as therapeutic targets in skeletal disorders. Marini F, Giusti F, Palmini G, Brandi ML. Osteoporos Int. 2023; 34(2):213-238. doi: 10.1007/s00198-022-06523-7. PMID: 35982318.
4. The role of sclerostin in lipid and glucose metabolism disorders. Jiang H, Li D, Han Y, Li N, Tao X, et al., Biochem Pharmacol. 2023; 215:115694. doi: 10.1016/j.bcp.2023.115694. PMID: 37481136.
5. Sclerostin and Insulin Resistance in Prediabetes: Evidence of a Cross Talk Between Bone and Glucose Metabolism. Daniele G, Winnier D, Mari A, Bruder J, Fourcaudot M, Pengou Z, Tripathy D, Jenkinson C, Folli F. Diabetes Care. 2015; 38(8):1509-17. doi: 10.2337/dc14-2989. PMID: 26084344.
6. Serum sclerostin is negatively associated with insulin sensitivity in obese but not lean women. Aznou A, Meijer R, van Raalte D, den Heijer M, Heijboer A, de Jongh R. Endocr Connect. 2021; 10(2):131-138. doi: 10.1530/EC-20-0535. PMID: 33480863.
7. Increased serum sclerostin and decreased serum IGF-1 are associated with vertebral fractures among postmenopausal women with type-2 diabetes. M.S. Ardawi, D.H. Akhbar, A. Alshaikh, M.M. Ahmed, M.H. Qari, A.A. Rouzi, et al. Bone, 56 (2013), pp. 355-362
8. Elevated sclerostin levels are associated with vertebral fractures in patients with type 2 diabetes mellitus. Yamamoto M, Yamauchi M, Sugimoto T. J Clin Endocrinol Metab. 2013; 98(10):4030-7. doi: 10.1210/jc.2013-2143. PMID: 23894157.
9. Fracture risk assessment in diabetes mellitus. Front Endocrinol (Lausanne). Chen W, Mao M, Fang J, Xie Y, Rui Y. 2022; 13:961761. doi: 10.3389/fendo.2022.961761. PMID: 36120431.
10. Biochemical Markers of Bone Fragility in Patients with Diabetes. A Narrative Review by the IOF and the ECTS. Meier C, Eastell R, Pierroz DD, Lane NE, Al-Daghri N, Suzuki A, Napoli N, Mithal A, Chakhtoura M, El-Hajj Fuleihan G, Ferrari S. J Clin Endocrinol Metab. 2023; 108(10):e923–36. doi: 10.1210/clinem/dgad255. PMID: 37155585.

 

 

The Biomedica SCLEROSTIN ELISA Assay Kit (# BI-20492) was utilized in a recent publication assessing the associations between serum and bone sclerostin levels and biomarkers of bone turnover and bone histomorphometry. Read more: Sclerostin, Osteocytes, and Wnt Signaling in Pediatric Renal Osteodystrophy.

Sclerostin (SOST) ELISA  (cat. no. BI-20492)

• Most referenced Sclerostin ELISA in over 290 citations
• Low sample volume – 20µl / well
• Validation following international guidelines

 

Sclerostin a biomarker in renal pediatric bone disease

Sclerostin, Osteocytes, and Wnt Signaling in Pediatric Renal Osteodystrophy. Laster M. et al., Nutrients. 2023 Sep 25;15(19):4127. doi: 10.3390/nu15194127. PMID: 37836411; PMCID: PMC10574198 . link to full text

Abstract

The pathophysiology of chronic kidney disease-mineral and bone disorder (CKD-MBD) is not well understood. Specific factors secreted by osteocytes are elevated in the serum of adults and pediatric patients with CKD-MBD, including FGF-23 and sclerostin, a known inhibitor of the Wnt signaling pathway. The molecular mechanisms that promote bone disease during the progression of CKD are incompletely understood. In this study, we performed a cross-sectional analysis of 87 pediatric patients with pre-dialysis CKD and post-dialysis (CKD 5D). We assessed the associations between serum and bone sclerostin levels and biomarkers of bone turnover and bone histomorphometry. We report that serum sclerostin levels were elevated in both early and late CKD. Higher circulating and bone sclerostin levels were associated with histomorphometric parameters of bone turnover and mineralization. Immunofluorescence analyses of bone biopsies evaluated osteocyte staining of antibodies towards the canonical Wnt target, β-catenin, in the phosphorylated (inhibited) or unphosphorylated (active) forms. Bone sclerostin was found to be colocalized with phosphorylated β-catenin, which suggests that Wnt signaling was inhibited. In patients with low serum sclerostin levels, increased unphosphorylated “active” β-catenin staining was observed in osteocytes. These data provide new mechanistic insight into the pathogenesis of CKD-MBD and suggest that sclerostin may offer a potential biomarker or therapeutic target in pediatric renal osteodystrophy.

 

Related Literature

FGF-23 and sclerostin in serum and bone of CKD patients. Lima F, Monier-Faugere MC, Mawad H, David V, Malluche HH. Clin Nephrol. 2023 May;99(5):209-218. doi: 10.5414/CN111111. PMID: 36970967; PMCID: PMC10286735. (Biomedica Sclerostin ELISA Assay Kit, cat. no. BI-20492 citation)

Sclerostin and Dickkopf-1 in renal osteodystrophy. Cejka D, Herberth J, Branscum AJ, Fardo DW, Monier-Faugere MC, Diarra D, Haas M, Malluche HH. Clin J Am Soc Nephrol. 2011 Apr;6(4):877-82. doi: 10.2215/CJN.06550810. Epub 2010 Dec 16. PMID: 21164019; PMCID: PMC3069382. (Biomedica Sclerostin ELISA Assay Kit, cat. no. BI-20492 citation)

Bone Disorders in Pediatric Chronic Kidney Disease: A Literature Review. Capossela L, Ferretti S, D’Alonzo S, Di Sarno L, Pansini V, Curatola A, Chiaretti A, Gatto A.Biology (Basel). 2023 Nov 2;12(11):1395. doi: 10.3390/biology12111395. PMID: 37997994; PMCID: PMC10669025.

 

Type 2 diabetes mellitus (T2DM) is characterized by a persistent state of elevated blood sugar levels and glucose intolerance, resulting from the body´s incomplete response to insulin, accompanied by an increase in insulin production and a subsequent insulin deficiency. Individuals suffering from T2DM have an increased risk of cardiovascular disease (CVD). High glucose levels, insulin resistance, and chronic inflammation, contribute to endothelial dysfunction (ED) and atherosclerosis (1). ED refers to an impairment of the endothelium, the inner lining of blood vessels, which play an important role in regulating vascular health.

Sclerostin is associated with endothelial dysfunction in patients with type 2 diabetes

Sclerostin is a protein known primarily for its role in bone metabolism. It has also been identified of being linked to endothelial dysfunction in individuals diagnosed with type 2 diabetes (2). Sclerostin is predominantly secreted by osteocytes, cells that are embedded in the bone. However, vascular endothelial cells have also been observed to produce sclerostin leading to the discovery of its significant anti-calcifying role (3).

Sclerostin is associated with endothelial dysfunction in patients with type 2 diabetes: In an investigation in individuals with T2DM, researchers measured endothelial dysfunction by digital thermal monitoring (2). This method is a valid and noninvasive technique to evaluate endothelial function using temperature change on finger as a surrogate measure of the magnitude of vascular reactivity index (VRI) (4) . Serum Sclerostin levels were measured in the T2DM cohort with the Biomedica ELISA.  The prospective cross-sectional study revealed that serum sclerostin levels are positively associated with endothelial dysfunction measured in patients with T2DM.

A previous cross-sectional study in patients with T2DM, with/without cardiovascular disease, determined Sclerostin levels and its expression by RT-qPCR and immunohistochemistry in calcified and non-calcified artery of the lower limb from T2D. Serum Sclerostin was measured with an ELISA from Biomedica. Moreover, in vitro experiments were performed in vascular smooth muscle cells under calcifying conditions investigating the cardioprotective function of Sclerostin (5). The study provided evidence that supports the protective function of Sclerostin in the development of vascular calcification. The findings suggest that Sclerostin could potentially reduce the susceptibility to atherosclerosis by decreasing atherosclerotic plaque formation and underscore the significance of the bone-vascular axis when developing therapeutic strategies for treating impaired bone metabolism or vascular diseases (5).

Features and Benefits when measuring Sclerostin with the Biomedica ELISA kits

Sclerostin ELISA, #BI-20492

• TRUSTED – most referenced Sclerostin ELISA (+280 citations)
• LOW sample volume – 20µl sample /well
• For SERUM & PLASMA samples
• RELIABLE – fully validated  following international quality guidelines

 

 Bioactive Sclerostin ELISA, BI-20472

• CHARACTERIZED ANTIBODIES – targeting the receptor binding region
• EXTENSIVELY validated for clinical samples
• LOW sample volume – 20µl sample /well 

 

Literature

1. Endothelial Cell Dysfunction and the Pathobiology of Atherosclerosis. Garcia-de Los Ríos C, Medina-Casado M, Díaz-Chamorro A, Sierras-Jiménez M, Lardelli-Claret P, Sclerostin as a biomarker of cardiovascular risk in women with systemic lupus erythematosus. Cáliz-Cáliz R, Sabio JM. Sci Rep. 2022 Dec 14;12(1):21621. doi: 10.1038/s41598-022-25651-y. PMID: 36517533; PMCID: PMC9749620. Gimbrone MA Jr, García-Cardeña G. Circ Res. 2016 Feb 19;118(4):620-36. doi: 10.1161/CIRCRESAHA.115.306301. PMID: 26892962; PMCID: PMC4762052.
2. Serum sclerostin level is positively associated with endothelial dysfunction measured by digital thermal monitoring in patients with type 2 diabetes: A prospective cross-sectional study. Hsu BG, Wu DA, Yang HY, Chen MC.Medicine (Baltimore). 2023 Sep 8;102(36):e34649. doi: 10.1097/MD.0000000000034649. PMID: 37682176; PMCID: PMC10489308.
3. Sclerostin Protects Against Vascular Calcification Development in Mice. De Maré A, Opdebeeck B, Neven E, D’Haese PC, Verhulst A J Bone Miner Res. 2022 Apr;37(4):687-699. doi: 10.1002/jbmr.4503. Epub 2022 Feb 15. PMID: 35038187; PMCID: PMC9303214.
4. Digital thermal monitoring techniques to assess vascular reactivity following finger and brachial occlusions. Heath M, Gourley D, Naghavi M, Klies S, Tanaka H. J Clin Hypertens (Greenwich). 2020 Dec 7;23(1):122–7. doi: 10.1111/jch.14115. PMCID: PMC8030097.
5. Cardioprotective function of sclerostin by reducing calcium deposition, proliferation, and apoptosis in human vascular smooth muscle cells. González-Salvatierra S, García-Fontana C, Lacal J, Andújar-Vera F, Martínez-Heredia L, Sanabria-de la Torre R, Ferrer-Millán M, Moratalla-Aranda E, Muñoz-Torres M, García-Fontana B. Cardiovasc Diabetol. 2023 Nov 2;22(1):301. doi: 10.1186/s12933-023-02043-8. PMID: 37919715; PMCID: PMC10623848.

November is “Diabetes Awareness Month” raising attention to this fast growing and life-threating epidemic. Patients suffering from diabetes have a risk of additional health complications, including heart disease, strokes, and diabetic kidney disease (DKD). People who develop DKD mostly have few symptoms in the early stage of the disease, although the risk of developing severe kidney damage is very high. High blood sugar levels may damage the small blood vessels in the kidney leading to kidney damage, kidney failure, and high blood pressure (1). 

FGF23 and Sclerostin – novel biomarkers in diabetic kidney disease

Traditionally, the bone is regarded as a structural organ that gives the human body support and facilitates physical movement. However, bone is also a source of various hormones including fibroblast growth factor 23 and sclerostin that play an important role in regulating glucose metabolism and DKD (2).

FGF23 and Sclerostin  – novel biomarkers in diabetic kidney disease

 

FGF23 and Sclerostin – bone derived hormones regulate glucose metabolism

 

Fibroblast growth factor 23 (FGF23) is a bone-derived protein that regulates phosphate metabolism, by inhibiting renal phosphate reabsorption. There is increasing evidence that FGF23 plays a role in type 2 diabetes (T2DM), as FGF23 levels are elevated in these patients, even in individuals with preserved kidney function when compared to the general population (3). Phosphate independent effects on FGF23 following glucose loading were shown in a recent study demonstrating that FGF23 is associated with glucose, insulin and proinsulin levels, as well as obesity (4 ). Furthermore, FGF23 has also been shown to be associated with the development of gestational diabetes mellitus (5).

Sclerostin is a protein that is produced by bone cells that inhibits bone formation. Recent research suggests that Sclerostin also plays a role in lipid and glucose metabolism as serum sclerostin is negatively associated with insulin sensitivity as measured in obese, but not lean women (5). Sclerostin levels have also been shown to be increased in individuals with prediabetes (6).

FGF23 and Sclerostin can reliable by measured with conventional ELISA assays from BIOMEDICA.

FGF23 (C-terminal), #BI-20700 and FGF23 intact ELISA, #BI-20700

• RELIABLE – validated following international quality guidelines
• CITED in over 60 publications
• EASY – 8 standards and 2 controls included
• For SERUM & PLASMA samples
• HIGH QUALITY guaranteed!

 

Sclerostin ELISA, #BI-20492

• MOST referenced in more than 280 citations
• LOW sample volume – 20µl sample /well
• For SERUM & PLASMA samples
• RELIABLE – full validation package

 

Bioactive Sclerostin ELISA, BI-20472

• CHARACTERIZED ANTIBODIES – targeting the receptor binding region
• RIGOROUSLY validated for clinical samples
• LOW sample volume – 20µl sample /well

 

Literature

1. Renal microvascular disease predicts renal function in diabetes. Futrakul N, Futrakul P. Ren Fail. 2012;34(1):126-9. doi: 10.3109/0886022X.2011.623490. Epub 2011 Oct 20. PMID: 22010784.
2. The Emerging Role of Bone-Derived Hormones in Diabetes Mellitus and Diabetic Kidney Disease. Li Y, Gu Z, Wang J, Wang Y, Chen X, Dong B. Front Endocrinol (Lausanne). 2022 Jul 11;13:938830. doi: 10.3389/fendo.2022.938830. PMID: 35966090; PMCID: PMC9367194.
3. Earlier onset and greater severity of disordered mineral metabolism in diabetic patients with chronic kidney disease Wahl P., Xie H., Scialla J., Anderson C.A.M., Bellovich K., Brecklin C.et al.. (2012)  Diabetes Care 35, 994–1001 10.2337/dc11-2235 
4. Fibroblast Growth Factor 23, Glucose Homeostasis, and Incident Diabetes: Findings of 2 Cohort Studies, Amarens van der Vaart, Coby Eelderink, André P van Beek, Stephan J L Bakker, Peter R van Dijk, Martin H de Borst, The Journal of Clinical Endocrinology & Metabolism, Volume 108, Issue 10, October 2023, Pages e971–e978, https://doi.org/10.1210/clinem/dgad246.
5. Fibroblast growth factor 23 is associated with the development of gestational diabetes mellitus. Hocher CF, Chen X, Zuo J, Horvathova K, Hocher B, Krämer BK, Chu C. Diabetes Metab Res Rev. 2023 Aug 8:e3704. doi: 10.1002/dmrr.3704. Epub ahead of print. PMID: 37553983.
6. Serum sclerostin is negatively associated with insulin sensitivity in obese but not lean women. Aznou A, Meijer R, van Raalte D, den Heijer M, Heijboer A, de Jongh R. Endocr Connect. 2021 Feb;10(2):131-138. doi: 10.1530/EC-20-0535. PMID: 33480863; PMCID: PMC7983521.
7. Sclerostin and Insulin Resistance in Prediabetes: Evidence of a Cross Talk Between Bone and Glucose Metabolism. Daniele G, Winnier D, Mari A, Bruder J, Fourcaudot M, Pengou Z, Tripathy D, Jenkinson C, Folli F. Diabetes Care. 2015 Aug;38(8):1509-17. doi: 10.2337/dc14-2989. Epub 2015 Jun 17. PMID: 26084344.

Bone markers are currently used to monitor skeletal diseases and treatments. The proteins Sclerostin and Dickkopf-1 (DKK-1) reflect distinct biological processes and have gained attention as potential biomarkers for bone-related conditions. They may provide valuable information for diagnosis, prognosis, and monitoring of bone diseases and treatments.

Sclerostin and DKK-1 emerging biomarkers for bone disease

Sclerostin and Dickkkopf-1 are two important osteocyte proteins that are involved in the regulation of bone metabolism, particularly through their interactions with the Wnt signaling pathway.

SCLEROSTIN (SOST) is a glycoprotein that is primarily secreted by osteocytes, the most abundant cells in bone tissue. It inhibits Wnt signaling, which is a critical pathway regulating bone formation and remodeling. Sclerostin acts as a negative regulator of bone formation by binding to the LRP5/6 co-receptors (low-density lipoprotein receptor protein), which activate Wnt signaling. By binding to LRP5/6, sclerostin inhibits the interaction between Wnt ligands and the Frizzled receptor, thereby inhibiting Wnt signaling and suppressing bone formation. Inhibition of Sclerostin has led to the development of a novel anabolic therapy for osteoporosis.

DICKKOPF-1 (DKK-1) is a protein that also inhibits the Wnt signaling pathway. DKK-1 binds to the LRP5/6 co-receptors thereby preventing Wnt ligand interaction thus inhibiting bone formation and promoting bone resorption.

The Wnt-signaling pathway is one of the most important pathways controlling bone metabolism. Sclerostin and Dickkopf-1 act as Wnt inhibitors and play a crucial role in controlling bone formation and resorption.

Sclerostin and DKK-1 can easily be measured in blood samples with an ELISA assay

BIOMEDICA offers two kits to measure Sclerostin

Bioactive Sclerostin ELISA cat. no. BI-20472

• serum, plasma, cell-culture
• characterized antibodies
• day test
• 20µl sample volume
• sample values provided
• full validation package

 

The epitope of the monoclonal capture antibody is in loop 2 of the Sclerostin molecule, which is the binding site for the LRP5/6 complex.

All Sclerostin molecules including potential fragments containing this receptor binding region can be detected.

Bioactive Sclerostin ELISA – antibody binding sites

 

Sclerostin ELISA cat. no. BI-20492

• most referenced more than 280 citations
• 20µl sample volume
• for serum, plasma
• full validation package

 

DKK-1 ELISA cat. no. BI-20413

• widely cited
• day test
• no sample dilution
• full validation package

 

All assays are developed and manufactured by BIOMEDICA

Related Publications

New Emerging Biomarkers for Bone Disease: Sclerostin and Dickkopf-1 (DKK1). Dincel AS, Jørgensen NR; IOF-IFCC Joint Committee on Bone Metabolism (C-BM). Calcif Tissue Int. 2023 Feb;112(2):243-257. doi: 10.1007/s00223-022-01020-9. Epub 2022 Sep 27. PMID: 36165920.

Abstract

A healthy skeleton depends on a continuous renewal and maintenance of the bone tissue. The process of bone remodeling is highly controlled and consists of a fine-tuned balance between bone formation and bone resorption. Biochemical markers of bone turnover are already in use for monitoring diseases and treatment involving the skeletal system, but novel biomarkers reflecting specific biological processes in bone and interacting tissues may prove useful for diagnostic, prognostic, and monitoring purposes. The Wnt-signaling pathway is one of the most important pathways controlling bone metabolism and consequently the action of inhibitors of the pathway such as sclerostin and Dickkopf-related protein 1 (DKK1) have crucial roles in controlling bone formation and resorption. Thus, they might be potential markers for clinical use as they reflect a number of physiological and pathophysiological events in bone and in the cross-talk with other tissues in the human body. This review focuses on the clinical utility of measurements of circulating sclerostin and DKK1 levels based on preanalytical and analytical considerations and on evidence obtained from published clinical studies. While accumulating evidence points to clear associations with a number of disease states for the two markers, and thus, the potential for especially sclerostin as a biochemical marker that may be used clinically, the lack of standardization or harmonization of the assays still hampers the clinical utility of the markers.

 

Therapeutic approaches to activate the canonical Wnt pathway for bone regeneration. Nelson AL, Fontana G, Miclau E, Rongstad M, Murphy W, Huard J, Ehrhart N, Bahney C. J Tissue Eng Regen Med. 2022 Nov;16(11):961-976. doi: 10.1002/term.3349. Epub 2022 Sep 16. PMID: 36112528; PMCID: PMC9826348.

Decrease of bone biomarker Sclerostin in women with anorexia nervosa during nutrition therapy – indication of reduced bone loss

Anorexia nervosa (AN) is an eating disorder and has one of the highest mortality rates of any mental illness.  It affects roughly 2.9 million people and many experience bone loss and increased fracture risk. In a 3-year prospective study, Swedish researchers looked into the long-term effects of nutrition therapy. They  investigated bone and mineral metabolism and biomarkers young women with AN. Their results showed that body mass index (BMI) and fat mass was increased. The regulatory bone biomarker Sclerostin decreased during nutrition therapy and further over 3 years, indicating reduced bone loss.

Read more: Bone mass and biomarkers in young women with anorexia nervosa: a prospective 3-year follow-up study.

Biomedica Sclerostin ELISA kit 

• The internationally most referenced Sclerostin ELISA with more than 270 citations!
• Rigorously validated according to international quality guidelines
• Low sample volume

 

Bone mass and biomarkers in young women with anorexia nervosa: a prospective 3-year follow-up study.

Svedlund A, Pettersson C, Tubic B, Ellegård L, Elfvin A, Magnusson P, Swolin-Eide D. J Bone Miner Metab. 2022 Aug 12. doi: 10.1007/s00774-022-01359-x. Epub ahead of print. PMID: 35960382.

Abstract

Introduction: Anorexia nervosa (AN) increases the risk of impaired bone health, low areal bone mineral density (aBMD), and subsequent fractures. This prospective study investigated the long-term effects of bone and mineral metabolism on bone and biomarkers in 22 women with AN.

Materials and methods: Body composition and aBMD were measured by dual-energy X-ray absorptiometry (DXA) and peripheral quantitative computed tomography. Total and free 25-hydroxyvitamin D (25OHD), C-terminal collagen cross-links (CTX), osteocalcin, bone-specific alkaline phosphatase (BALP), leptin, sclerostin, and oxidized/non-oxidized parathyroid hormone (PTH) were analyzed before and after 12 weeks of intensive nutrition therapy and again 3 years later. An age-matched comparison group of 17 healthy women was recruited for the 3-year follow-up.

Results: Body mass index (BMI) and fat mass increased from baseline to 3 years in women with AN. Sclerostin decreased during nutrition therapy and further over 3 years, indicating reduced bone loss. CTX was elevated at baseline and after 12 weeks but decreased over 3 years. BALP increased during nutrition therapy and stabilized over 3 years. Free 25OHD was stable during treatment but decreased over 3 years. Non-oxidized PTH was stable during treatment but increased over 3 years. Trabecular volumetric BMD in AN patients decreased during the first 12 weeks and over 3 years despite stable BMI and bone biomarkers implying increased BMD.

Conclusion: Our findings highlight the importance of early detection and organized long-term follow-up of bone health in young women with a history of AN.

Keywords: DXA; Eating disorder; Osteoporosis; Sclerostin; Vitamin D

Related publications

Anorexia nervosa: 30-year outcome.

Dobrescu SR, Dinkler L, Gillberg C, Råstam M, Gillberg C, Wentz E. Br J Psychiatry. 2020 Feb;216(2):97-104. doi: 10.1192/bjp.2019.113. PMID: 31113504; PMCID: PMC7557598.

Abstract

Background: Little is known about the long-term outcome of anorexia nervosa.

Aims: To study the 30-year outcome of adolescent-onset anorexia nervosa. 

Method: All 4291 individuals born in 1970 and attending eighth grade in 1985 in Gothenburg, Sweden were screened for anorexia nervosa. A total of 24 individuals (age cohort for anorexia nervosa) were pooled with 27 individuals with anorexia nervosa (identified through community screening) who were born in 1969 and 1971-1974. The 51 individuals with anorexia nervosa and 51 school- and gender-matched controls were followed prospectively and examined at mean ages of 16, 21, 24, 32 and 44. Psychiatric disorders, health-related quality of life and general outcome were assessed. 

Results: At the 30-year follow-up 96% of participants agreed to participate. There was no mortality. Of the participants, 19% had an eating disorder diagnosis (6% anorexia nervosa, 2% binge-eating disorder, 11% other specified feeding or eating disorder); 38% had other psychiatric diagnoses; and 64% had full eating disorder symptom recovery, i.e. free of all eating disorder criteria for 6 consecutive months. During the elapsed 30 years, participants had an eating disorder for 10 years, on average, and 23% did not receive psychiatric treatment. Good outcome was predicted by later age at onset among individuals with adolescent-onset anorexia nervosa and premorbid perfectionism.

Conclusions: This long-term follow-up study reflects the course of adolescent-onset anorexia nervosa and has shown a favourable outcome regarding mortality and full symptom recovery. However, one in five had a chronic eating disorder.

Anorexia Nervosa.

Mitchell JE, Peterson CB. N Engl J Med. 2020 Apr 2;382(14):1343-1351. doi: 10.1056/NEJMcp1803175. PMID: 32242359.

 

Effect of Sclerostin Inhibition on Cardiovascular Safety for the Treatment of Severe Osteoporosis

Osteoporosis is a skeletal disorder characterized by diminished bone strength that is responsible for an increased fracture risk. The glycoprotein sclerostin acts as an inhibitor of bone formation. Therapies directed against this molecule have been developed. A humanized antibody against sclerostin has been approved for the treatment of severe osteoporosis in postmenopausal women in many parts of the world. A recent review by Langdahl BL and colleagues sumarizes the current knowledge of the effect of sclerostin inhibition on cardiovascular safety.

Cardiovascular Safety and Sclerostin Inhibition – a mini-review.
Langdahl BL, Hofbauer LC, Forfar JC. J Clin Endocrinol Metab. 2021 Mar 23:dgab193. doi: 10.1210/clinem/dgab193. Epub ahead of print. PMID: 33755157. 

Biomedica´s Sclerostin ELISA kit:
• The internationally most referenced Sclerostin ELISA!
• Rigorously validated according to FDA/ICH/EMEA guidelines
• Low sample volume

 

RELATED Publications – Sclerostin Inhibition and Cardiovascular Safety

 

Evaluating the cardiovascular safety of sclerostin inhibition using evidence from meta-analysis of clinical trials and human genetics.

Bovijn J, Krebs K, Chen CY, Boxall R, Censin JC, Ferreira T, Pulit SL, Glastonbury CA, Laber S, Millwood IY, Lin K, Li L, Chen Z, Milani L, Smith GD, Walters RG, Mägi R, Neale BM, Lindgren CM, Holmes MV. Sci Transl Med. 2020 Jun 24;12(549):eaay6570. doi: 10.1126/scitranslmed.aay6570. PMID: 32581134; PMCID: PMC7116615.

Abstract

The glycoprotein Sclerostin is mainly secreted by osteocytes and acts as a negative regulator of bone mass and strength by inhibiting bone formation. Studies have shown that high intensity exercise induces an increase in serum Sclerostin levels suggesting that it may be a key protein involved in muscle and bone interaction.
A recent study by Śliwicka E and colleagues https://buff.ly/3qx6V4U evaluated the effects of a marathon race on selected myokines and Sclerostin in male recreational runners. Results show that in response to the marathon run, a complex network of endocrine interactions is initiated. Further research is needed to fully elucidate the long-term impact of prolonged high intensity exercise on the human body.
Exercise-induced increase in sclerostin- related finding: https://buff.ly/3atiBA4

Check out the Biomedica Sclerostin ELISA kit https://buff.ly/2N4iVsK

• The internationally most referenced Sclerostin ELISA!

• Rigorously validated according to FDA/ICH/EMEA guidelines

• Low sample volume

Biomedica’s Sclerostin ELISA:  

√ HIGH QUALITY – fully validated assay according to ICH/FDA/EMEA guidelines

√ LOW SAMPLE VOLUME – only 20 µl sample / well

√ EASY – convenient ready to use protocol 

√ MOST REFERENCED

 

Also available: Bioactive Sclerostin ELISA

√ specific antibodies targeting the receptor binging region 

 

Complete ready to use ELISA kits for superior performance and reproducibility.

Related ELISAs: free soluble RANKL, OPG, DKK-1, FGF23 – Analytical Service Measurements

Planning your study? Contact us by e-mail or phone to receive your special study quote.

Serum levels of sclerostin reflect altered bone microarchitecture in patients with hepatic cirrhosis. Sclerostin, a glycoprotein secreted mainly by osteocytes, regulates bone mass by decreasing bone formation.

In patients with hepatic cirrhosis, areal bone mineral density (aBMD) is decreased especially at the lumbar spine. aBMD alone can be insufficient to explain increased fracture risk and bone microarchitecture can provide additional information. However, since assessment of bone microarchitecture is complex, biomarkers could help assess fracture risk. In a study of several biomarkers, Wakolbinger et al. found a correlation between sclerostin and altered bone microarchitecture in hepatic cirrhosis https://link.springer.com/article/10.1007/s00508-019-01595-8.

Biomedica´s bioactive sclerostin ELISA  measures bioactive sclerostin by using a monoclonal antibody directed at the LRP5/6 binding region, capturing all circulating sclerostin forms containing the free-receptor binding site. It is validated in depth according to FDA quality standards, to ensure the ELISA reliability.

Researchers have identified the soluble WNT pathway inhibitor SCLEROSTIN as an independent risk factor for all-cause #mortality in patients after kidney transplantation.
600 stable renal transplant recipients were followed for all-cause mortality for 3 years.

Sclerostin is an independent risk factor for all-cause mortality in kidney transplant recipients.
Zeng S et al., Clin Exp Nephrology (2020). Click link for full text.

Biomedica Sclerostin ELISA: https://www.bmgrp.com/product/cardiovascular/sclerostin-elisa-human-sost-biomedica/

√ HIGH QUALITY – fully validated assay according to ICH/FDA/EMEA guidelines
√ LOW SAMPLE VOLUME – only 20 µl sample / well
√ EASY – convenient ready to use protocol
√ MOST REFERENCED Sclerostin ELISA

Also available: Bioactive Sclerostin ELISA https://www.bmgrp.com/product/cardiovascular/biomedica-bioactive-sclerostin-elisa-human-sost/
√ specific antibodies targeting the receptor binging region

The only Sclerostin ELISA that utilizes specific EPITOPE MAPPED ANTIBODIES enabling the analysis of bioactive Sclerostin in clinical samples. 

Bioactive Sclerostin ELISA (cat.no. BI-20472) Assay Highlights:

• HIGHLY SPECIFIC and DEFINED: capture antibody directed against Sclerostin’s bioactive site. Learn more
• RELIABLE: human serum based calibrators and controls, rigorously validated
• LOW SAMPLE VOLUME: 20 µl / well
• QUICK: total incubation time 3.5 h

First bioactive Sclerostin ELISA for clinical samples

 

Areas of interest: osteoporosis, cancer induced bone diseases, rheumatoid arthritis, chronic inflammation, kidney diseases, therapy monitoring of anabolic treatment.

 

For detailed information please click corresponding links:

BI-20472 bioactive Sclerostin product website
BI-20472 bioactive Sclerostin ELISA IFU
BI-20472 bioactive Sclerostin ELISA Validation Data
BI-20472 bioactive Sclerostin ELISA MSDS

 

RELATED PUBLICATIONS

Circulating bioactive sclerostin levels in an Austrian population-based cohort. Kerschan-Schindl K, Föger-Samwald U, Gleiss A, Kudlacek S, Wallwitz J, Pietschmann P. Wien Klin Wochenschr. 2022 Jan;134(1-2):39-44. doi: 10.1007/s00508-021-01815-0. Epub 2021 Feb 5. PMID: 33544208; PMCID: PMC8813720.

Abstract

Sclerostin ELISA | BI-20492 Highlights:

• 
  The internationally most referenced human Sclerostin ELISA!
• 
  Rigorously validated according to FDA/ICH/EMEA guidelines
• 
  Low sample volume 
• New finding: Sclerostin in Alzheimer´s Disease

Bioactive Sclerostin ELISA Kit (Human SOST):

• 
  Specific antibodies targeting the receptor binding region
• 
  Rigorously validated for clinical samples according to FDA/ICH/EMEA guidelines
• 
  Low sample volume – 20 µl of serum/plasma per well 

Maintaining strong and healthy bones is crucial for overall well-being. Bones not only provide structural support for the body but also protect vital organs and serve as reservoirs for essential minerals like calcium and phosphorus. Key aspects of bone health include bone density and bone strength.

Osteoporosis is a condition characterized by weakened and fragile bones. It is the most prevalent metabolic bone disorder worldwide and can affect people of all ages, though it is more commonly associated with aging (1). Both men (2) and women can develop osteoporosis, but postmenopausal women are at a higher risk due to declining estrogen levels, which normally help protect bone health (3). Prevention strategies include maintaining a balanced diet and engaging in regular exercise.

Bone remodeling is a continuous, tightly regulated process involving the resorption of old or damaged bone and the formation of new bone tissue. Various hormones and factors influence bone metabolism. The bone cycle encompasses different phases, and markers of bone metabolism can be classified into markers of bone formation, markers of bone resorption, and markers involved in the regulation of bone metabolism.

Biomarkers of bone regulation

Protein biomarkers are frequently utilized in clinical research and practice to evaluate bone health and monitor the effectiveness of osteoporosis treatments. Some of these biomarkers offer insights into the regulatory processes governing bone metabolism and turnover. Measuring these markers can help assess overall bone health. Key regulatory biomarkers include:

Sclerostin (SOST): Produced by osteocytes, the bone cells embedded within bone tissue, sclerostin is a bone-specific inhibitor of the Wnt signaling pathway. It negatively influences bone formation by promoting osteoclastogenesis and increasing bone resorption. Elevated levels of sclerostin may indicate reduced bone formation.

Dickkopf-1 (DKK-1): Similar to sclerostin, DKK-1 inhibits Wnt signaling, which is essential for bone formation. Increased serum DKK-1 levels can promote bone resorption, potentially signaling suppressed bone formation.

The Wnt signaling pathway is one of the most vital mechanisms regulating bone metabolism. Sclerostin and Dickkopf-1 function as inhibitors of Wnt signaling and are essential in the regulation of bone formation and resorption.

 

Receptor Activator of Nuclear Factor-Kappa B Ligand (RANKL): A critical regulator of osteoclast development and activation, RANKL promotes bone resorption by stimulating osteoclast activity. It is secreted by osteocytes and plays a central role in osteoclast formation.

Osteoprotegerin (OPG): Serving as a decoy receptor for RANKL, OPG modulates bone resorption. The ratio of OPG to RANKL influences bone remodeling processes, with alterations potentially impacting bone strength.

Fibroblast Growth Factor 23 (FGF23): This hormone regulates phosphate balance and vitamin D metabolism. Abnormal FGF23 levels are linked to bone disorders such as hypophosphatemic rickets, which can impair bone health.

 

These biomarkers can easily be measured in human blood samples with an ELISA assay

 

Sclerostin (SOST) ELISA  (BI-20492)

• • Most internationally referenced Sclerostin ELISA with more than 320 citations
  • Low sample volume – 20µl / well
  • Full validation package

 

Bioactive Sclerostin ELISA (BI-20472)

• • Targets the receptor binding region
  • Full validation package
  • Low sample volume – 20 µl of serum/plasma per well 

 

Dickkopf-1 (DKK-1) ELISA  (BI-20413)

• • Widely cited +180 publications
  • Direct measurement
  • Validated following international quality guidelines

 

Osteoprotegerin (OPG) ELISA (BI-20403)

• • most referenced human OPG ELISA in +280 citations
  • day test, ready to use color coded reagents
  • controls included

 

Free soluble RANKL ELISA (BI-20462)

• • Highly sensitive  – measurable concentrations in healthy subjects
  • Only assay measuring free, uncomplexed soluble RANKL
  • Cited in over +320 citations 

 

FGF23 c-terminal multi-matrix ELISA (BI-20702)

• • for serum and plasma samples
  • full validation package 
  • cited in +60 publications

 

FGF23 intact ELISA (BI-20700)

• • for serum and plasma samples
  • full validation package
  • one-step ELISA

 

Literature 

1. Bone Health and Osteoporosis Prevention and Treatment. Muñoz M, Robinson K, Shibli-Rahhal A.Clin Obstet Gynecol. 2020 Dec;63(4):770-787. doi: 10.1097/GRF.0000000000000572. PMID: 33017332.
2. Osteoporosis in men. Lancet Diabetes Endocrinol. Vilaca T, Eastell R, Schini M. 2022 Apr;10(4):273-283. doi: 10.1016/S2213-8587(22)00012-2. Epub 2022 Mar 2. PMID: 35247315.
3. Postmenopausal Osteoporosis: A Review of Latest Guidelines. Subarajan P, Arceo-Mendoza RM, Camacho PM. Endocrinol Metab Clin North Am. 2024 Dec;53(4):497-512. doi: 10.1016/j.ecl.2024.08.008. Epub 2024 Oct 5. PMID: 39448132.

Chronic kidney disease (CKD) is a major global health concern, affecting roughly 10 percent of the population, totaling more than 850 million people (1, 2).

CKD involves progressive nephron loss, compensatory hyperfiltration in remaining nephrons, and subsequent glomerulosclerosis (3, 4). This process is often driven by etiologies such as diabetic nephropathy (5), glomerulonephritis, and other systemic or intrinsic renal diseases.

Biochemical hallmarks include decreased clearance of nitrogenous waste products such as urea and creatinine, leading to azotemia (6). The disruption of electrolyte homeostasis may result in hyperkalemia, metabolic acidosis, and disturbances in calcium-phosphate balance, contributing to secondary hyperparathyroidism and vascular calcification (7).

CKD progression is associated with increased cardiovascular morbidity and mortality (8).The disease course can be monitored via estimated glomerular filtration rate (eGFR), albuminuria levels, and imaging findings of renal morphology (9).

Role of the Kidneys

Kidneys are vital organs that regulate fluid balance, blood pressure and produce hormones that stimulate the production of red blood cells . Kidney disease is a condition in which kidneys lose their ability to effectively filter waste products and excess fluids from the blood. Kidney disease commonly leads to a decline in kidney function that may lead to kidney failure, characterized by the complete loss of kidney function. At this stage dialysis or kidney transplantation become the only treatment option.

Kidney problems can emerge suddenly (acute) or gradually over time (chronic). Various conditions, diseases and medications can contribute to acute and chronic kidney problems.  Chronic kidney disease (CKD) is characterized by a prolonged period of kidney abnormalities that last for more than three months (10), whereas acute kidney disease – acute kidney injury (AKI) is characterized by a sudden loss of excretory kidney function (11).

Other forms of kidney disease include polycystic kidney disease (PKD) a genetic disorder that leads to kidney enlargement and impaired kidney function over time and glomerulonephritis (GN) (12). GN is a group of diseases characterized by inflammation of the glomeruli, the filtration units of the kidney (13).

Novel Biomarkers in Nephrology

FGF23  •  SCLEROSTIN  •  ENDOSTATIN  •  VANIN-1  •  PERIOSTIN

Advancements in nephrology have led to the identification of several emerging biomarkers that enhance early detection, prognosis, and understanding of kidney injury and disease progression. These novel biomarkers could provide more sensitive and specific insights compared to traditional measures like serum creatinine and albuminuria.

FGF23  – in Acute Kidney Injury

Fibroblast growth factor 23 (FGF23) is a hormone produced by bone that plays a key role in regulating phosphate excretion by the kidneys. In the context of kidney disease, declining renal function leads to an increase in serum phosphate levels, which in turn stimulates the secretion of FGF23. Elevated phosphate levels are also frequently observed in patients with acute kidney injury (AKI) (14).

FGF23 as a Marker of Adverse Outcomes in AKI

Levels of FGF23 rise rapidly during AKI and have been associated with the need for renal replacement therapy (14-17). Furthermore, FGF23 levels possess prognostic value, as demonstrated in a large study  in over 1500 patients with AKI (16).

FGF23 and Sclerostin – Novel Biomarkers in Diabetic Kidney Disease

Growing evidence indicates that FGF23 may be involved in type 2 diabetes (T2DM), as levels of FGF23 are elevated in these patients—even among those with normal kidney function—when compared to the general population (18). A recent study demonstrated phosphate-independent effects of FGF23 following glucose loading, showing associations between FGF23 and levels of glucose, insulin, and proinsulin, as well as obesity (19). Additionally, FGF23 has been linked to the development of gestational diabetes mellitus (20).

Sclerostin is a protein produced by bone cells that inhibits bone formation. Recent research suggests that sclerostin also influences lipid and glucose metabolism, as serum sclerostin levels are negatively associated with insulin sensitivity in obese women, but not in lean women (21). Elevated sclerostin levels have also been observed in individuals with prediabetes (22).

 FGF23 and Sclerostin can reliable by measured with conventional ELISA assays from BIOMEDICA.

• FGF23 (C-terminal) |BI-20700 and FGF23 intact ELISA |BI-20700               
• Sclerostin ELISA |BI-20492 and Bioactive Sclerostin ELISA |BI-20472    

 

Endostatin – A Potential Biomarker for Renal Fibrosis, CKD, and Prognosis in AKI

Endostatin is a protein found in the extracellular matrix that is expressed during the progression of renal fibrosis. Elevated serum levels of endostatin may result from increased degradation of the extracellular matrix in patients with chronic kidney disease (CKD) (23, 24). Additionally, endostatin has been explored as a prognostic marker in individuals with acute kidney injury (AKI) (25) and has been independently linked to the occurrence of cardiovascular events in CKD patients (26).

Endostatin can reliably be quantified in serum, plasma and urine samples:

• Endostatin ELISA | BI-20742

 

VANIN-1 – A Potential Biomarker for Acute Kidney Injury and Drug-Induced Renal Injury

Vascular non-inflammatory molecule-1 (Vanin-1) is highly expressed in the kidney (27) and has been proposed as a biomarker for acute kidney injury (AKI) and drug-induced renal damage (28). It has also been identified as an indicator of kidney injury in a rat model of type 1 diabetic nephropathy (29).

Urinary Vanin-1 has been studied in children with renal fibrosis (30) and as a potential predictor of acute pyelonephritis in young children with urinary tract infections (31). More recently, research has explored the role of urinary Vanin-1 in kidney transplant recipients (32).

Vanin-1 can easily be measured with a conventional ELISA assay:

• Vanin-1 (urine) ELISA | BI-VAN1U  (33)

 

PERIOSTIN – A Potential Early Biomarker of Renal Tubular Injury

Periostin is a matricellular protein involved in tissue remodeling and wound healing processes. Research has shown that Periostin expression in the kidney correlates with the extent of interstitial fibrosis and a decline in renal function (34). Elevated levels of urinary Periostin have been observed in patients with type 2 diabetes, even before the appearance of microalbuminuria. These findings suggest that urinary Periostin may serve as an early marker of renal tubular injury (35).

Periostin can be accurately measured in serum, plasma, and urine through a fully validated ELISA assay (36).

• Periostin ELISA | BI-20422

 

BIOMEDICA – HIGH QUALITY ASSAYS – Fully validated according to international quality guidelines

• TRUSTED – Widely cited in over 1800 publications

 

 

See our brochure on Biomarkers in Clinical Nephrology  

 

Literature

1. ISN- International Society of Nephrology
2. Global Facts: About Kidney Disease
3. Remnant nephron physiology and the progression of chronic kidney disease. Schnaper HW. Pediatr Nephrol. 2014; 29(2):193-202.  PMID: 23715783.
4. Mechanisms of progression of chronic kidney disease. Fogo AB. Pediatr Nephrol. 2007;  22(12):2011-22. PMID: 17647026.
5. Classification and Differential Diagnosis of Diabetic Nephropathy. Qi C et al.,  J Diabetes Res. 2017; 2017:8637138. PMID: 28316995.
6. Azotemia. Tyagi A, Aeddula NR. 2023;  In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan–. PMID: 30844172.
7. Understanding Vascular Calcification in Chronic Kidney Disease: Pathogenesis and Therapeutic Implications. Siracusa C et al., Int J Mol Sci. 2024; 25(23):13096. PMID: 39684805.
8. The Dual Burden: Exploring Cardiovascular Complications in Chronic Kidney Disease. Biomolecules. Caturano A et al., 2024: 14(11):1393. PMID: 39595570.
9. The KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease (CKD), 2024. Chronic Kidney Disease Diagnosis and Management: A Review. Chen TK, Knicely DH, Grams ME. JAMA. 2019 Oct 1;322(13):1294-1304. doi: 10.1001/jama.2019.14745. PMID: 31573641; PMCID: PMC7015670.
10. Chronic Kidney Disease Diagnosis and Management: A Review. Chen TK et al.,  JAMA. 2019; 322(13):1294-1304.  PMID: 31573641.
11. Acute kidney injury. Kellum JA et al.,. Nat Rev Dis Primers. 2021; 15;7(1):52. PMID: 34267223.  
12.  Treatment of Autosomal-Dominant Polycystic Kidney Disease. Jdiaa SS et al.,. Am J Kidney Dis. 2025; 85(4):491-500.  PMID: 39424253.
13. Advances in primary glomerulonephritis. Ellison B et al.,  J Hosp Med (Lond). 2024; 30;85(7):1-11. PMID: 39078905.
14. Fibroblast Growth Factor 23 and Klotho in AKI. Christov M, Neyra JA, Gupta S, Leaf DE. Semin Nephrol. 2019 Jan;39(1):57-75. doi: 10.1016/j.semnephrol.2018.10.005. PMID: 30606408. 
15. Fibroblast Growth Factor 23 Regulation and Acute Kidney Injury. Zhou W et al.,  Nephron. 2022;146(3):239-242. PMID: 34284404. 
16. Fibroblast growth factor 23 associates with death in critically ill patients. Leaf DE et al., Am Clin J Am Soc Nephrol. 2018. 13(4):531–41. 
17. FGF-23 levels in patients with AKI and risk of adverse outcomes. Leaf DE et al., Clin J Am Soc Nephrol. 2012. 7(8):1217-23. 
18. Earlier onset and greater severity of disordered mineral metabolism in diabetic patients with chronic kidney disease Wahl P et al. 2012.  Diabetes Care 35, 994–1001.  
19. Fibroblast Growth Factor 23, Glucose Homeostasis, and Incident Diabetes: Findings of 2 Cohort Studies, Amarens van der Vaart et al., 2023. The Journal of Clinical Endocrinology & Metabolism,  108, 10,  e971–e978.
20. Fibroblast growth factor 23 is associated with the development of gestational diabetes mellitus. Hocher CF et al., Diabetes Metab Res Rev. 2023. 8:e3704. PMID: 37553983.
21. Serum sclerostin is negatively associated with insulin sensitivity in obese but not lean women. Aznou A et al., Endocr Connect. 2021. 10(2):131-138. PMID: 33480863.
22. Sclerostin and Insulin Resistance in Prediabetes: Evidence of a Cross Talk Between Bone and Glucose Metabolism. Daniele G et al., Diabetes Care. 2015. 38(8):1509-17.  PMID: 26084344.
23. A defective angiogenesis in chronic kidney disease. Futrakul N et al., Ren Fail. 2008. 30(2):215-7.  PMID: 18300124.
24. Endostatin in Renal and Cardiovascular Diseases. Li M et al., Kidney Dis (Basel). 2021.9;7(6):468-481. PMID: 34901193.
25. Prognostic value of dynamic plasma endostatin for the prediction of mortality in acute kidney injury: A prospective cohort study. Jia HM et al.,  J Int Med Res. 2020.  48(7):300060520940856. PMID: 32691651.
26. Endostatin in chronic kidney disease: Associations with inflammation, vascular abnormalities, cardiovascular events and survival. Kanbay M et al., Eur J Intern Med. 2016. 33:81-7.  PMID: 27394925.
27. Chemical biology tools to study pantetheinases of the vanin family. Schalkwijk, J, Jansen, P. Biochem Soc Trans. 2014. 42, 1052–1055.
28. Urinary Vanin-1 As a Novel Biomarker for Early Detection of Drug-Induced Acute Kidney Injury. Hosohata K et al.J  Pharm  Exp Ther. 2012. 341, 656–662.
29. Proteomic identification of vanin-1 as a marker of kidney damage in a rat model of type 1 diabetic nephropathy. Fugmann T et al., Kidney Int. 2011. 80, 272–281.
30. The Usefulness of Vanin-1 and Periostin as Markers of an Active Autoimmune Process or Renal Fibrosis in Children with IgA Nephropathy and IgA Vasculitis with Nephritis-A Pilot Study. Mizerska-Wasiak M et al.,  J Clin Med. 2022. 11(5):1265. PMID: 35268356. 
31. Urinary vanin-1 for predicting acute pyelonephritis in young children with urinary tract infection: a pilot study. Krzemień G et al., Biomarkers. 2021. 26(4):318-324.
32. Urinary vanin-1, tubular injury, and graft failure in kidney transplant recipients. Alkaff FF et al., Sci Rep. 2024. 4(1):2283.  PMID: 38280883.
33. Development of an immunoassay that reveals altered uninary Vanin-1 in human with kidney disease. Wallwitz, J.,  et al.,. 2018. Nephrology Dialysis Transplantation, Volume 33, Issue suppl_1, Page i126. 
34. Periostin in the Kidney. Wallace DP et al., Adv Exp Med Biol. 2019, 1132:99-112.
35. Periostin as a tissue and urinary biomarker of renal injury in type 2 diabetes mellitus. Satirapoj B et al., PLoS One. 2015, 17;10(4):e0124055.
36. Characterization of a sandwich ELISA for the quantification of all human periostin isoforms. Gadermaier E et al., J Clin Lab Anal. 2018, 32(2):e22252.

Osteogenesis imperfecta (OI), also known as brittle bone disease, is a rare hereditary bone disorder with an estimated incidence of about 1 in 10,000 to 1 in 20,000 (1). It is characterized by low bone mass, increased bone fragility and recurrent fractures. The condition results from mutations that disrupt the synthesis and post-translational modification of type I collagen. Recent research indicates that the severity of OI phenotypes is influenced not only by abnormalities in type I collagen metabolism but also by alterations in osteoblast function (2), although the underlying mechanisms remain unclear. So far, none of the current available treatments have shown an overall efficacy in treating OI, thus demonstrating the unmet clinical need for managing OI (3). A recent study in mice has shown that  DKK1-antisense treatment can improve bone mechanical strength, restore the expression of osteogenic genes, stimulate osteogenesis, and suppress osteoclastogenesis in OI mice (3).

 

The Wnt/β-catenin pathways plays a key role in the regulation of osteogenesis. Dickkopf-1 (DKK-1) is a direct inhibitor of Wnt/β-catenin signaling by binding with high affinity to LRP5/LRP6 and Kremen proteins, inhibiting osteoblast function and bone formation. It is a soluble protein secreted in the bone microenvironment and can be detected in the circulation. In a recent study researchers measured DKK-1 concentrations in children with OI and examined its association with bone mineral density (BMD), fracture frequency, bone turnover markers, and the underlying genetic mutations of OI (4).

DKK-1 a potential biomarker and therapeutic target in Osteogenesis Imperfecta                                      

Key findings:

– concentrations were significantly higher in children with OI compared to healthy children

– DKK-1 is closely correlated to the skeletal phenotype of children with OI

– DKK-1 may become a novel biomarker and a potential therapeutic target of OI

 

Biomedica´s high quality human DKK-1 ELISA cat. no. BI-20413

• widely cited in over 180 publications
• day test
• no sample dilution
• full validation package

 

Related Products: SCLEROSTIN ELISA (BI-20492), BIOACTIVE SCLEROSTIN ELISA (BI-20472)

 

Correlation of serum DKK1 level with skeletal phenotype in children with osteogenesis imperfecta.  Wang Y et al., J Endocrinol Invest. 2024

Abstract

Purpose: We aim to detect serum DKK1 level of pediatric patients with OI and to analyze its relationship with the genotype and phenotype of OI patients.

Methods: A cohort of pediatric OI patients and age-matched healthy children were enrolled. Serum levels of DKK1 and bone turnover biomarkers were measured by enzyme-linked immunosorbent assay. Bone mineral density (BMD) was measured by Dual-energy X-ray absorptiometry. Pathogenic mutations of OI were detected by next-generation sequencing and confirmed by Sanger sequencing.

Results: A total of 62 OI children with mean age of 9.50 (4.86, 12.00) years and 29 healthy children were included in this study. The serum DKK1 concentration in OI children was significantly higher than that in healthy children [5.20 (4.54, 6.32) and 4.08 (3.59, 4.92) ng/mL, P < 0.001]. The serum DKK1 concentration in OI children was negatively correlated with height (r = – 0.282), height Z score (r = – 0.292), ALP concentration (r = – 0.304), lumbar BMD (r = – 0.276), BMD Z score of the lumbar spine and femoral neck (r = – 0.32; r = – 0.27) (all P < 0.05). No significant difference in serum DKK1 concentration was found between OI patients with and without vertebral compression fractures. In patients with spinal deformity (22/62), serum DKK1 concentration was positively correlated with SDI (r = 0.480, P < 0.05). No significant correlation was observed between serum DKK1 concentration and the annual incidence of peripheral fractures, genotype and types of collagen changes in OI children.

Conclusion: The serum DKK1 level was not only significantly elevated in OI children, but also closely correlated to their skeletal phenotype, suggesting that DKK1 may become a new biomarker and a potential therapeutic target of OI.

Literature

1. Osteogenesis imperfecta: an update on clinical features and therapies. Marom R, Rabenhorst BM, Morello R. Eur J Endocrinol. 2020; 83(4):R95-R106. PMID: 32621590.
2. Osteogenesis Imperfecta: Mechanisms and Signaling Pathways Connecting Classical and Rare OI Types. Jovanovic M, Guterman-Ram G, Marini JC. Endocr Rev. 2022; 43(1):61-90. PMID: 34007986.
3. Dickkopf-1 (DKK1) blockade mitigates osteogenesis imperfecta (OI) related bone disease. Ko JY, Wang FS, Lian WS, Yang FS, Chen JW, Huang PH, Liao CY, Kuo SJ. Mol Med. 2024; 30(1):66. PMID: 38773377; PMCID.
4. Correlation of serum DKK1 level with skeletal phenotype in children with osteogenesis imperfecta. Wang Y, Hu J, Sun L, Zhou B, Lin X, Zhang Q, Wang O, Jiang Y, Xia W, Xing X, Li M. J Endocrinol Invest. 2024; 47(11):2785-2795. PMID: 38744806.

.

We are excited to be soon attending the ECTS Congress in Innsbruck, Austria from May 23-26, 2025. Meet us at our banner exhibition “Biomedica´s Bone Marker ELISAs” and explore our kits including SCLEROSTIN, OPG, RANKL, FGF23, PERIOSTIN, and many others.

We look forward to connecting with you!

Join us at ECTS 

Click here for more information about the congress.

The ECTS 2025 Congress is recognized as the premier annual gathering in Europe dedicated to this field. The congress offers a comprehensive and engaging scientific program that covers the most recent advances, challenges, and debates related to bone and calcified tissues. The program aims to unite researchers,  clinicians, and health professionals, showcasing their latest research.

Biomarkers in Bone Biology
Bone cells produce biomarkers throughout the process of bone remodeling. These biomarkers are valuable for evaluating bone diseases and serve as potential therapeutic targets. They can be readily identified in serum and plasma samples using immunoassay techniques.

A recent review by Fernández-Villabrille S et al.,  Novel Biomarkers of Bone Metabolism explores some emerging biomarkers in mineral and bone metabolism like:

Receptor Activator of NFkappa B lingand (RANKL), Osteoprotegerin (OPG), Sclerostin (SOST), Dickkopf-1 (DKK-1), Periostin (POSTN) and others.

 

BIOMEDICA offers quality Bone Marker ELISA assay kits: 

-Sclerostin ELISA (SOST; cat.no. BI-20492)  

-OPG ELISA (Osteoprotegerin; cat.no. BI-20403)  

-RANKL ELISA (soluble RANKL; cat.no. BI-20462)  

-DKK-1 ELISA (Dickkopf-1; cat.no. BI-20413)  

-FGF23 intact ELISA (Fibroblast growth factor-23 intact; cat.no. BI-20700) 

-FGF23 C-terminal ELISA  (Fibroblast growth factor-23 C-terminal; cat.no. cat.no. BI-20702) 

-PERIOSTIN ELISA (POSTN, BI-20433) 

-NT-proCNP ELISA (NT-C-type natriuretic peptide, BI-20812)

 

 TRUSTED – cited in over 1300 publications

• Kit validations follows international quality guidelines
• Developed & manufactured by Biomedica in Austria

 

About SCLEROSTIN

Sclerostin (SOST), primarily produced by osteocytes, is regarded as a key regulator of bone formation. It functions as a soluble antagonist of the Wnt signaling pathway. Inhibition of this pathway results in bone resorption, whereas activation of Wnt signaling stimulates bone formation.

About PERIOSTIN

Periostin (POSTN) is an extracellular matrix protein predominantly expressed in the periosteum, the membrane covering the outer surface of bones that plays a role in bone growth. It is involved in various processes, including bone biology, tissue repair, cancer, cardiovascular and respiratory conditions, as well as in numerous inflammatory conditions such as asthma.

Osteoporosis is a bone disease characterized by progressive loss of bone density, leading to an increased risk of fractures, particularly in the hip, spine, and wrist. It occurs when the balance between bone resorption and bone formation is disrupted, often due to factors such as aging, hormonal changes (especially post-menopause in women), nutritional deficiencies (such as calcium and vitamin D), sedentarism, and certain medications or medical conditions (1).

The prevalence of osteoporosis among older adults is significant: it is estimated that over 200 million people suffer from osteoporosis worldwide, with about one in three women and one in five men over the age of 50 experiencing an osteoporotic fracture in their lifetime (1). Osteoporosis represents a major public health concern due to its impact on mobility, quality of life, and healthcare costs associated with fracture management and treatment. Surprisingly, in women over 45 years of age, osteoporosis accounts for more days in hospital than may other diseases, including diabetes, myocardial infarction and breast cancer (3).

Bone Health and Osteoporosis

How can Osteoporosis be prevented ?

Regular exercise and a healthy diet, including the intake of key nutrients like Vitamin D and Calcium, are some key factors that can help in preventing the disease (2).

–Calcium: a healthy adult body contains around 1 kg of calcium, 99% of which is deposited in bone and teeth (4). Good sources of calcium include dairy products, leafy green vegetables, fortified foods, and fish with bones (1).

–Vitamin D: vitamin D plays an important role in regulating calcium and maintaining bone health. Although vitamin D influences various aspects of bone and calcium metabolism, one of its most important functions is the regulation of the efficiency of intestinal calcium (Ca) absorption (5).

The primary source of vitamin D is sunlight; it is synthesized in the skin. The form of vitamin D produced in the skin is known as vitamin D3 (cholecalciferol), while the dietary forms can be either vitamin D3 or a closely related plant-derived compound called vitamin D2 (ergocalciferol). Only a limited number of foods are naturally high in vitamin D. Dietary sources include fatty fish like salmon, sardines, and mackerel, as well as eggs, liver, and in some regions, fortified products such as margarine, dairy items, and cereals. For more information on sources on vitamin D and Vitamin D recommendations : https://www.osteoporosis.foundation/vitamin-d-recommendations.

-Other potentially risk factors for osteoporosis are smoking, alcohol consumption, low or excessive phosphorus intake, protein deficiency or a high-protein diet, excessive consumption of coffee, a sedentary lifestyle or lack of mobility, and insufficient exposure to the sun (6). 

Role of the human skeleton

The human skeleton provides support and structure for the body, protecting vital organs like the brain and heart. It is an important component of the musculoskeletal system, enabling movement. The skeleton also produces blood cells in its bone marrow and stores essential minerals like calcium. The skeleton is  constantly remodeled throughout life, with old bone being broken down and replaced by new tissue to maintain bone mass. This ongoing process of bone resorption and growth is called bone metabolism.

Bone remodeling

Bone remodeling is a continuous and regulated process where various specialized cells primarily osteoclasts breaking down old bone tissue, and osteoblasts building new bone, are involved. These cells constantly interact via factors like osteoprotegerin (OPG) and RANKL (receptor activator of nuclear factor kappa-B ligand) to maintain a healthy balance between bone resorption and bone formation. Imbalances in this process can lead to bone diseases like osteoporosis.  

Bone cells act as endocrine cells, influencing other organs. Osteocytes, the most common bone cell type embedded within the bone, are key regulators of bone formation. They play an important role in bone remodelling and release specific biomarkers such as sclerostin (SOST), fibroblast growth factor 23 (FGF23), and Dickkopf-1 (DKK-1).

 

Biomedica offers a range of ELISA kits to measure bone biomarkers in serum, plasma, and cell cultures

SCLEROSTIN (SOST; cat.no. BI-20492)

OPG  (Osteoprotegerin; cat.no. BI-20403)

RANKL  (soluble RANKL; cat.no. BI-20462)

DKK-1  (Dickkopf-1; cat.no. BI-20413)

FGF23 intact (Fibroblast growth factor-23, intact; cat.no. BI-20700)

FGF23 C-terminal  (Fibroblast growth factor-23, C-terminal; cat.no. cat.no. BI-20702)

PERIOSTIN  (POSTN, BI-20433)

 

• TRUSTED – cited in over 1200 publications
• Kit validations follows international quality guidelines
• Developed & manufactured by Biomedica in Austria

 

Literature

1. Assessment of osteoporosis at the primary health-care level. WHO Scientific Group Technical Report. Kanis J. 2007  [Accessed 22.02.2019];
2. The clinician’s guide to prevention and treatment of osteoporosis. LeBoff M et al. Osteoporos Int 33, 2049–2102 (2022).
3. The prevalence of vertebral deformity in european men and women: the European Vertebral Osteoporosis Study. O’Neill TW et al., J Bone Miner Res, 1996. 11(7): p. 1010-8.
4. Physiology of Calcium Homeostasis: An Overview. Matikainen N et al., Endocrinol Metab Clin North Am. 2021; 50(4):575-590. PMID: 34774235.
5. Vitamin D-Mediated Regulation of Intestinal Calcium Absorption . Fleet JC. Nutrients. 2022 Aug 16;14(16):3351. PMID: 36014856.
6. Osteoporosis – risk factors, pharmaceutical and non-pharmaceutical treatment. Tański W et al., Eur Rev Med Pharmacol Sci. 2021; 25(9):3557-3566. PMID: 34002830.

 

Biomedica’s FGF23 ELISA kits now available for the US Biotech community at 25% trial discount.

FGF23 (fibroblast growth factor 23) is a 32 kDa protein with 251 amino acids that is proteolytically processed between arginine179 and serine180 to generate N-terminal and C-terminal fragments. FGF23 is mainly secreted by osteocytes and controls phosphate and 1,25(OH)2 vitamin D homeostasis. Epidemiological data suggest that higher FGF23 concentrations are associated with all-cause mortality, cardiovascular mortality, a higher risk of myocardial infarction, stroke and heart failure.
➡️ Learn more: FGF23 – An Overview

FGF23 ELISA kits available for the US & CA

Biomedica’s FGF23 (intact) and FGF23 (C-terminal) ELISA kits

Biomedica’s FGF23 ELISA kits, widely recognized in Europe and Asia, are now also available in the US.

💡 What makes them a game-changer?

✓ MULTI-MATRIX: for plasma, serum, cell-culture
✓ CONVENIENT: 50 µl sample/well, all buffers included
✓ RELIABLE: validated following quality guidelines
✓ COMPARABLE: good correlation with existing kits
✓ EASY HANDLING: 7 prediluted standards, 2 controls
✓ TRUSTED: cited in more than 80 publications

Biomedica offers world-leading quality products at competitive pricing.

FGF23 ELISA kits available for the US & CA

🚨 Don’t miss out and order your trial kit at 25% discount. Promotion extended until June 30, 2025.

➡️ Contact our US partners or CA partner for your study quote.

Related kits: Sclerostin . OPG . Periostin . Vanin-1 . NT-proBNP . NT-proANP 

 

Literature

Non-Classical Effects of FGF23: Molecular and Clinical Features. Martínez-Heredia L, Canelo-Moreno JM, García-Fontana B, Muñoz-Torres M.Int J Mol Sci. 2024 Apr 30;25(9):4875. doi: 10.3390/ijms25094875. PMID: 38732094; PMCID: PMC11084844.

The role of fibroblast growth factor 23 in regulation of phosphate balance. Wilson R, Mukherjee-Roy N, Gattineni J. Pediatr Nephrol. 2024 Dec;39(12):3439-3451. doi: 10.1007/s00467-024-06395-5. Epub 2024 Jun 14. PMID: 38874635.

FGF23 signalling and physiology. Ho BB, Bergwitz C. J Mol Endocrinol. 2021 Feb;66(2):R23-R32. doi: 10.1530/JME-20-0178. PMID: 33338030; PMCID: PMC8782161.

Kidney dysfunction causes disruptions in bone and mineral metabolism and changes in the regulators of the renal-bone axis through various mechanisms. Studies have demonstrated that fibroblast growth factor 23 (FGF23) and inflammatory markers rise, while iron status may decline (1, 2). In healthy individuals, FGF23 is regulated by phosphate, Vitamin D (1,25(OH)₂D), and parathyroid hormone (PTH). However in the early stages of chronic kidney disease (CKD), FGF23 levels begin to increase even before plasma phosphate levels increase (3).

Thus, CKD causes disruptions in bone and mineral metabolism that also includes the regulatory hormones, resulting chronic kidney disease-mineral bone disorder (CKD-MBD).

Bone biomarkers in early renal impairment

A recent study investigated the effects of Vitamin D supplementation in a cohort of healthy community-dwelling older people. Baseline blood concentrations of bone regulatory markers including Sclerostin (SOST), Dickkopf-related Protein 1 (DKK1); Osteoprotegerin (OPG) and soluble RANKL (sRANKL), Fibroblast growth factor 23 (intact and c-terminal FGF23) and TNF-alpha, Interleukin-6 (IL-6) were analysed. The results showed that SOST, cFGF23, iFGF23, PTH and TNF-alpha were elevated in the group of individuals with early kidney impairment compared to those with normal kidney function. Following Vitamin D supplementation, only cFGF23, 25(OH)D, and IL-6 showed differences between the groups.

The study identified alterations in the renal bone-axis that occur prior to clinical monitoring of patients. Early diagnosis in the initial stages of renal impairment may offer opportunities for preventing the progression of renal disease and chronic kidney disease-mineral bone disorder (CKD-MBD).

Learn more: Alterations in regulators of the renal-bone axis, inflammation and iron status in older people with early renal impairment and the effect of vitamin D supplementation. Christodoulou M et al., Age Ageing. 2024; 53(5):afae096. doi: 10.1093/ageing/afae096. PMID: 38770543.

Bone biomarkers in early renal impairment

Biomedica offers quality ELISA Assay Kits for bone regulatory biomarkers

Sclerostin (SOST; cat.no. BI-20492)

Bioactive Sclerostin (bioSOST; cat. no. BI-20472)

OPG  (Osteoprotegerin; cat.no. BI-20403)

RANKL (soluble RANKL; cat.no. BI-20462)

DKK-1  (Dickkopf-1; cat.no. BI-20413)

FGF23 intact  (Fibroblast growth factor-23 intact; cat.no. BI-20700)

FGF23 C-terminal  (Fibroblast growth factor-23 C-terminal; cat.no. cat.no. BI-20702)

 

Key Features

• TRUSTED – cited in over 1000 publications
• Kit validations follows international quality guidelines
• Ready to use standards and controls included
• Developed & manufactured by Biomedica in Austria

 

Literature

1. Iron Deficiency Anemia in Chronic Kidney Disease. Gafter-Gvili A, Schechter A, Rozen-Zvi B. Acta Haematol. 2019;142(1):44-50. doi: 10.1159/000496492. Epub 2019 Apr 10. PMID: 30970355.
2. Iron-Deficiency Anemia in CKD: A Narrative Review for the Kidney Care Team. Hain D, Bednarski D, Cahill M, Dix A, Foote B, Haras MS, Pace R, Gutiérrez OM. Kidney Med. 2023 May 25;5(8):100677. doi: 10.1016/j.xkme.2023.100677. PMID: 37415621; PMCID: PMC10319843.
3. The bone-renal axis in early chronic kidney disease: an emerging paradigm. Danziger J. Nephrol Dial Transplant. 2008 Sep;23(9):2733-7. doi: 10.1093/ndt/gfn260. Epub 2008 May 9. PMID: 18469306.

 

Join us at the ASBMR (American Society of Bone and Mineral Research) Conference at booth number 145. The annual meeting is taking place in Toronto, ON, Canada from September 27-30, 2024.

The American Society of Bone and Mineral Research (ASBMR) meeting is considered to be the largest event worldwide covering fields in bone, mineral and musculoskeletal research. The meeting attracts over 2,500 participants across the globe, including both clinicians and researchers working in different disciplines and at all career levels. The meeting provides attendees with exciting opportunities to exchange knowledge and to learn about the latest scientific and medical advances in the field.

Discover some of our biomarker assays for clinical research in bone and mineral disorders

–FGF23 intact and c-terminal

–Sclerostin and bioactive Sclerostin

–Osteoprotegerin(OPG)  and soluble RANKL

–Dickkopf-1 and Periostin

 

 

Exploring Biomarkers in Bone Biology

During the process of bone remodeling, bone cells release biomarkers that can aid in the evaluation of bone diseases and serve as valuable therapeutic targets. These bone biomarkers can be readily detected in serum and plasma samples using immunoassays.

A recent review by Nicolas H Hart et al., provides researchers and clinicians involved in bone and mineral metabolism with a comprehensive contemporary update on the Biological basis of bone strength: anatomy, physiology and measurement. J Musculoskelet Neuronal Interact. 2020; ;20(3):347-371.

Abstract

Understanding how bones are innately designed, robustly developed and delicately maintained through intricate anatomical features and physiological processes across the lifespan is vital to inform our assessment of normal bone health, and essential to aid our interpretation of adverse clinical outcomes affecting bone through primary or secondary causes. Accordingly this review serves to introduce new researchers and clinicians engaging with bone and mineral metabolism, and provide a contemporary update for established researchers or clinicians. Specifically, we describe the mechanical and non-mechanical functions of the skeleton; its multidimensional and hierarchical anatomy (macroscopic, microscopic, organic, inorganic, woven and lamellar features); its cellular and hormonal physiology (deterministic and homeostatic processes that govern and regulate bone); and processes of mechanotransduction, modelling, remodelling and degradation that underpin bone adaptation or maladaptation. In addition, we also explore commonly used methods for measuring bone metabolic activity or material features (imaging or biochemical markers) together with their limitations.

 

 

 

September is Blood Cancer Awareness Month raising awareness about the various types of blood cancers, including leukemia, lymphoma, myeloma, and other hematologic malignancies. The goal of this month-long initiative is to educate the public about the signs, symptoms, and the risks that are associated with these cancers, as well as the importance of early detection and treatment.

Some cancer treatments may lead to bone loss and increases the risk of osteoporosis and fractures. Learn more about the impact of intensive chemotherapy and glucocorticoid treatment on bone remodeling markers in children with acute lymphoblastic leukemia in the study described below (1).

The campaign also focuses on highlighting the latest advancements in blood cancer research and treatment, emphasizing that ongoing research is essential for improved outcomes and quality of life for patients.

September is Blood Cancer Awareness Month

Acute lymphoblastic leukemia (ALL) is a type of cancer that affects the blood and bone marrow. ALL is the most common cancer in children. Intensive chemotherapy has improved the 5-year survival rate for ALL patients up to 90%. However, this improved survival has resulted in long-term complications associated with chemotherapy, including negative effects on bone health including osteopenia/osteoporosis, osteonecrosis, and increased fragility fractures.

Skeletal health relies on a balance between bone resorption and bone formation

The health of the skeleton relies on a balance between bone resorption and bone formation, a process known as “bone remodeling,” which is regulated by the RANKL/RANK/osteoprotegerin (OPG) and Wnt/β-catenin signaling pathways.

Currently, there is a lack of data regarding the impact of intensive chemotherapy on bone remodeling markers in children with ALL. In a recent study, researchers in Italy investigated the role of bone remodeling markers in children with acute lymphoblastic leukemia after intensive chemotherapy and glucocorticoid (GC) treatment (1). The bone remodeling markers such as RANKL, OPG and the WNT signaling molecules Sclerostin and DKK-1 were also measured with ELISA kits from BIOMEDICA.

The researchers found “higher levels of RANKL and OPG in ALL children compared to the controls, with a balance of RANKL/OPG ratio, whereas the levels of sclerostin and DKK-1, the main inhibitors of osteoblastogenesis, were similar in the two groups of subjects. These results suggest that in our cohort of ALL subjects, the intensive chemotherapy and GCs increased osteoclastic activity and, thereby, bone resorption” (1).

About the RANK/RANKL/OPG system

The receptor-ligand duo, RANK and RANKL are crucial regulators of bone metabolism and osteoclast development. Osteoprotegerin (OPG) acts as a decoy receptor for RANKL. It competitively binds to RANKL and interferes with the interaction of RANKL–RANK, thus blocking bone resorption. Beyond its role as a regulator of bone remodeling, the RANK/RANKL/OPG system has direct effects on the development of tumor cells, as it is implicated in the progression of breast and prostate cancer as well as leukemia.

About the WNT signaling molecules Sclerostin and DKK-1

Sclerostin (SOST) is mainly produced by osteocytes and is considered as the major regulator of bone formation. It is a soluble antagonist of the Wnt signaling pathway. Inactivating this pathway leads to bone degradation, while induction of Wnt signaling promotes bone formation.

Dickkopf-1 (DKK-1) is an extracellular protein. DKK-1 plays a role in the regulation of bone metabolism, and is a secreted inhibitor of the Wnt signaling pathway. DKK-1 inhibits the differentiation of osteoblasts and thereby bone formation. The dysregulation of DKK1 can lead to cancer progression.  

Biomedica offers quality kits for the measurement of these bone biomarkers

-Osteoprotegerin (OPG) ELISA (cat. no. BI-20403)

-Soluble free RANKL ELISA (cat. no. BI-20462)

-Sclerostin (SOST) ELISA (cat.no. BI-20492)

-Bioactive Sclerostin (SOST) ELISA (cat. no. BI-20472)

-DKK-1 (Dickkopf-1) ELISA (cat.no. BI-20413)

 

• Widely cited in + 1000 publications
• Validated kits following international quality guidelines

 

Literature

1. Bone Remodeling Markers in Children with Acute Lymphoblastic Leukemia after Intensive Chemotherapy: The Screenshot of a Biochemical Signature. Muggeo P, Grassi M, D’Ascanio V, Brescia V, Fontana A, Piacente L, Di Serio F, Giordano P, Faienza MF, Santoro N. Cancers (Basel). 2023 Apr 29;15(9):2554. doi: 10.3390/cancers15092554. PMID: 37174020; PMCID: PMC10177249.
2. The RANK-RANKL-OPG System: A Multifaceted Regulator of Homeostasis, Immunity, and Cancer. Medicina (Kaunas). De Leon-Oliva D, Barrena-Blázquez S, Jiménez-Álvarez L, Fraile-Martinez O, García-Montero C, López-González L, Torres-Carranza D, García-Puente LM, Carranza ST, Álvarez-Mon MÁ, Álvarez-Mon M, Diaz R, Ortega MA. 2023 Sep 30;59(10):1752. doi: 10.3390/medicina59101752. PMID: 37893470; PMCID: PMC10608105.
3. Understanding the Wnt Signaling Pathway in Acute Myeloid Leukemia Stem Cells: A Feasible Key against Relapses. Biology (Basel). Láinez-González D, Alonso-Aguado AB, Alonso-Dominguez JM. 2023 May 5;12(5):683. doi: 10.3390/biology12050683. PMID: 37237497; PMCID: PMC10215262.

We are present in over 60 countries, ensuring global availability and customer support through partnerships with selected local distributors on almost every continent. Regardless of your location, we are here to help you reach your goals.

With over 30 years of experience, we specialize in developing and manufacturing high-quality ELISA assay kits for biomarkers in clinical research.

Check out our ELISA Assay product brochure

Our ELISA Kits Travel Worldwide – contact us or your local representative 

About us

BIOMEDICA develops and manufactures high quality and widely cited immunoassays for clinical and pre-clinical applications in bone and cardiorenal diseases. For specific biomarkers, Biomedica has become a world-wide leader, e.g. Sclerostin, free sRANKL, OPG, DKK-1, and NT-proCNP.   

All Biomedica ELISA assays are fully validated following international quality guidelines. The assays include ready-to-use serum-based calibrators and controls enabling researchers to collect biologically reliable data.

This year’s ELISA assay highlights  

Cardiac Safety Biomarkers : Rat NT-proBNP, NT-proANP ELISA kits

FGF23  : FGF23 intact , FGF23 (C-terminal) ELISA kits

Cytokines  : VEGF, Angiopoietin-2, IL-6   

Discover our PROMOTION : Take 15% OFF of the human IL-6 ELISA Assay now through end of 2024! Making IL-6 ELISA Kits more affordable!

 

Features & Benefits of BIOMEDICA ELISA Assay Kits

• Highly Specific – many of our kits employ  characterized epitope-mapped antibodies
• Excellent Quality – our kits are validated according to international quality guidelines (ICH, FDA..)
• Convenient Use  –offering ready to use and color coded reagents – controls are included in all kits! 

 

Other Products

EZ4U – Cell Proliferation & Cytotoxicity Assay (cat. no. BI-5000) for reliable testing of cell viability in 96-well microtiter plates.

 Features & Benefits EZ4U Assay

-easy and convenient singe-step incubation for use on living cells

-non-radioactive

-cultivation can be continued after cell numbers are determined

-widely cited in more than 240 publications e.g.

• BRD4-targeting PROTACs Synergize With Chemotherapeutics Against Osteosarcoma Cell Lines
  Lang et al., Anticancer Res; 2024; 44 (3), 971-980.  PMID: 38423674
• Expression of cytokines in pleural effusions and corresponding cell lines of small cell lung cancer
  Rath et al., Transl Lung Cancer Res; 2024; 13 (1), 5-15. PMID: 38405004

July is acknowledged as Bone Cancer and Sarcoma Awareness Month, focusing on increasing awareness about rare and challenging cancers affecting children and adolescents. Sarcoma is a type of cancer that originates in the bones and soft tissues. Soft tissues include muscle, fat, blood vessels, fibrous tissues such as tendons and ligament. More than 70 different subtypes of sarcomas have been reported. However, all sarcomas can be divided into two main groups: soft tissue sarcomas and bone cancers.

Soft Tissue Sarcomas is a rare type of cancer that originates from the growth of cells within the body´s soft tissue. More than 50 different soft tissue sarcomas have been reported (3 ) Soft tissue sarcoma can occur anywhere in the body, but it most frequently develops in arms, legs, and abdomen (4).

Osteosarcoma is the most prevalent type of bone cancer in children and adolescents with and incidence of around 4.4. cases per million children reported each year (1). Genomic alterations, particularly the inactivation of TP53 and RB, are present in most cases of osteosarcoma.

Ewing sarcoma is the second most common bone tumor occurring most frequently in teenagers, with a median age of 15 years. Ewing sarcomas is an aggressive tumor that develops usually in bone, but sometimes in soft tissue, most commonly affecting the lower extremity and pelvis. At diagnosis, up to 25% of patients , commonly found in the lung, bones, and bone marrow (2). This condition is biologically driven by a chromosomal translocation, typically involving the EWS and FLI1 genes.

July is Sarcoma and Bone Cancer Awareness Month

• 5 Things to Know About Bone Cancer and Sarcoma Awareness Month- link

 

Wnt Signalling molecules Sclerostin (SOST) and Dickkopf-1 (DKK-1) in Sarcoma

 

SCLEROSTIN has been shown to be expressed in bone and cartilage forming skeletal tumors. Sclerostin is widely localized to areas in osteoblastic differentiation and ossification (5). In a study using an osteosarcoma mouse model, the administration of sclerostin resulted in inhibited tumor growth and extended survival periods (6).

DKK-1 is a wnt inhibitor that has been shown to partially improve osteosarcoma survival by upregulating aldehyde-dehydrogenase-1A1, neutralizing reactive oxygen species originating from nutritional stress and chemotherapeutic challenge (7). In a mouse model researches demonstrated the use of a DKK-1 targeting vivo morpholino that reduces tumour progression (7).

FGF23 in uterine sarcoma

Human FGF23 has been shown to be highly expressed in uterine sarcoma highlighting its potential as a biomarker for the diagnosis and prognosis of the disease (8).

Sclerostin, DKK-1 and FGF23 can easily be measured in blood, urine and cell culture supernatants with an ELISA assay.

– Sclerostin ELISA (cat. no. BI-20492)

– DKK-1 ELISA (cat. no. BI-20413)

– FGF23 ELISAs (cat. no. BI-20700, BI-20702)

Literature

1. Osteosarcoma. Pediatr Blood Cancer. Eaton BR, Schwarz R, Vatner R, Yeh B, Claude L, Indelicato DJ, Laack N. 2021 May;68 Suppl 2:e28352. doi: 10.1002/pbc.28352. Epub 2020 Aug 11. PMID: 32779875.
2. Ewing sarcoma. Pediatr Blood Cancer. Eaton BR, Claude L, Indelicato DJ, Vatner R, Yeh B, Schwarz R, Laack N. 2021 May;68 Suppl 2:e28355. doi: 10.1002/pbc.28355. PMID: 33818887.
3. More Than 50 Subtypes of Soft Tissue Sarcoma: Paving the Path for Histology-Driven Treatments. Katz D, Palmerini E, Pollack SM. Am Soc Clin Oncol Educ Book. 2018 May 23;38:925-938. doi: 10.1200/EDBK_205423. PMID: 30231352.
4. Malignant Soft-Tissue Sarcomas. Hematol Oncol Clin North Am. Brownstein JM, DeLaney TF. 2020 Feb;34(1):161-175. doi: 10.1016/j.hoc.2019.08.022. Epub 2019 Oct 28. PMID: 31739942.
5. Sclerostin expression in skeletal sarcomas. Shen J, Meyers CA, Shrestha S, Singh A, LaChaud G, Nguyen V, Asatrian G, Federman N, Bernthal N, Eilber FC, Dry SM, Ting K, Soo C, James AW. Hum Pathol. 2016 Dec;58:24-34. doi: 10.1016/j.humpath.2016.07.016. Epub 2016 Aug 3. PMID: 27498059; PMCID: PMC6560186.
6. Antitumor Effect of Sclerostin against Osteosarcoma. Ideta H, Yoshida K, Okamoto M, Sasaki J, Kito M, Aoki K, Yoshimura Y, Suzuki S, Tanaka A, Takazawa A, Haniu H, Uemura T, Takizawa T, Sobajima A, Kamanaka T, Takahashi J, Kato H, Saito N. Cancers (Basel). 2021 Nov 29;13(23):6015. doi: 10.3390/cancers13236015. PMID: 34885123; PMCID: PMC8656567.
7. Morpholino-driven blockade of Dkk-1 in osteosarcoma inhibits bone damage and tumour expansion by multiple mechanisms. Pan S, Cesarek M, Godoy C, Co CM, Schindler C, Padilla K, Haskell A, Barreda H, Story C, Poole R, Dabney A, Gregory CA. Br J Cancer. 2022 Jul;127(1):43-55. doi: 10.1038/s41416-022-01764-z. Epub 2022 Mar 11. PMID: 35277659; PMCID: PMC9276700.
8. Fibroblast Growth Factor 23 is a Potential Prognostic Biomarker in Uterine Sarcoma. Yang L, Cai Y, Wang Y, Huang Y, Zhang C, Ma H, Zhou JG. Technol Cancer Res Treat. 2024 Jan-Dec;23:15330338241245924. doi: 10.1177/15330338241245924. PMID: 38613349; PMCID: PMC11015760.

We are excited to be soon exhibiting at the International Conference on Children’s Bone Health (ICCBH) in Salzburg, Austria from June 22-25, 2024.

Join us at booth number 4 and explore our widely trusted Biomarker ELISA Assay Kits including Fibroblast Growth Factor (FGF23), Sclerostin, Periostin, NT-proCNP, and many others.

We look forward to connecting with you!

Join us at the International Conference on Children’s Bone Health

Click here for more information about the conference for anyone who is interested in 

bone metabolism and bone mass in children, adolescents and young adults.

The ICCBH conference aims to unite researchers, clinicians, health professionals, and others from different fields to gain an understanding of the developing skeleton with regards to childhood health and disease. Latest advancements, innovative therapies, and genetic discoveries will be discussed.

More about Biomarkers in Bone Biology  

Bone cells release biomarkers during bone remodeling. They can be used in assessing bone diseases and represent useful therapeutic targets. Bone biomarkers can easily be detected in serum and plasma samples by immunoassay.  

A recent review by Ponds-Belda OD et al., Mineral Metabolism in Children: Interrelation between Vitamin D and FGF23 focuses on various aspects of FGF23 metabolism in children, reference values,  and other key variables involved in mineral homeostasis. 

BIOMEDICA offers quality kits to measure various bone biomarkers 

Sclerostin ELISA (SOST; cat.no. BI-20492)  

OPG ELISA (Osteoprotegerin; cat.no. BI-20403)  

RANKL ELISA (soluble RANKL; cat.no. BI-20462)  

DKK-1 ELISA (Dickkopf-1; cat.no. BI-20413)  

FGF23 intact ELISA (Fibroblast growth factor-23 intact; cat.no. BI-20700) 

FGF23 C-terminal ELISA (Fibroblast growth factor-23 C-terminal; cat.no. cat.no. BI-20702) 

PERIOSTIN ELISA (POSTN, BI-20433) 

NT-proCNP ELISA (NT-C-type natriuretic peptide, BI-20812)

 TRUSTED – cited in over 1300 publications

• Kit validations follows international quality guidelines
• Developed & manufactured by Biomedica in Austria