Table 1 Changes in serum sclerostin levels in various physiologic and pathological conditions
From: Role of sclerostin in the pathogenesis of chronic kidney disease-mineral bone disorder
Condition | Directional change | Comments |
|---|---|---|
Physiologic states | ||
Age: adults and elderly | Increase with age | Serum sclerostin levels increase with age, but bone marrow sclerostin mRNA is not increased in older patients. |
Gender | Higher in men | Likely due to higher bone mass (osteocyte number); lower in premenopausal women because of estrogen effect. |
Menopause | Higher after menopause | Lack of inhibitory effect of estrogen or decreased bone formation leading to low osteocyte number. |
Malnutrition | Blunts sclerostin changes | In patients with anorexia nervosa, sclerostin does not decrease with estrogen therapy. |
Hormones | ||
Parathyroid hormone | Decrease | Direct effect on osteoblast, osteocyte number, and on Wnt signaling. |
Vitamin D | Increase | Limited data; one study each in normal and dialysis patients; confounding by PTH is likely. |
Estrogen | Decrease | Direct effect of estrogen and possibly SERMs on osteoblast/osteocyte number and function. |
Androgen | Data unclear | Increased in prostate cancer patients and during androgen deprivation therapy. |
Leptin | Increased | Sclerostin levels were higher in obese patient and correlated with leptin and PTH levels. |
Growth hormone/IGF | Data unclear | IGF is obligatory to the anabolic action of PTH; may be for osteocyte function and sclerostin as well. |
Pathologic conditions | ||
Bone and mineral disorders | ||
Hyperparathyroidism (Primary) | Decrease | Lower levels compared with controls in untreated patients and normalize after parathyroidectomy. |
Paget’s disease of bone | Increased | Sclerostin did not correlate with P1NP or CTX. |
Glucocorticoid-induced osteoporosis | Early increase/later decline | Varies with timing of the study with reference to steroid use. |
Cushing’s disease | Decreased | Increased after treatment, suggesting suppressive effects on osteocyte and osteoblast function. |
Osteoporosis treatment effects | ||
Bisphosphonates and denosumab | Increase | Results may vary due to timing of data collection after denosumab or zolendronic acid administration. |
Teriparatide and strontium ranelate | Decreased | Compensatory increase in Dkk1 levels may limit continued anabolic action. |
Estrogen and raloxifene | Decreased | Suggesting estrogen and estrogen effect of raloxifene may modulate osteocyte and osteoblast function. |
Systemic disorders | ||
Diabetes mellitus type 1 | Slight increase | Age-related increase maintained, but sclerostin response to PTH is blunted. |
Diabetes mellitus type 2 | Increased | Age-related increase is absent, sclerostin response to PTH is impaired, and pioglitazone therapy increases sclerostin levels by 11 %. |
Chronic kidney disease | Increased | Sclerostin excretion increases with declining renal function with negative correlation with GFR. |
Kidney disease | Increased | Sclerostin levels increase despite increased PTH and increased excretion of sclerostin in renal failure. |