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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


Directional change


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.


Higher in men

Likely due to higher bone mass (osteocyte number); lower in premenopausal women because of estrogen effect.


Higher after menopause

Lack of inhibitory effect of estrogen or decreased bone formation leading to low osteocyte number.


Blunts sclerostin changes

In patients with anorexia nervosa, sclerostin does not decrease with estrogen therapy.



 Parathyroid hormone


Direct effect on osteoblast, osteocyte number, and on Wnt signaling.

 Vitamin D


Limited data; one study each in normal and dialysis patients; confounding by PTH is likely.



Direct effect of estrogen and possibly SERMs on osteoblast/osteocyte number and function.


Data unclear

Increased in prostate cancer patients and during androgen deprivation therapy.



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)


Lower levels compared with controls in untreated patients and normalize after parathyroidectomy.

  Paget’s disease of bone


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


Increased after treatment, suggesting suppressive effects on osteocyte and osteoblast function.

 Osteoporosis treatment effects


  Bisphosphonates and denosumab


Results may vary due to timing of data collection after denosumab or zolendronic acid administration.

  Teriparatide and strontium ranelate


Compensatory increase in Dkk1 levels may limit continued anabolic action.

  Estrogen and raloxifene


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


Age-related increase is absent, sclerostin response to PTH is impaired, and pioglitazone therapy increases sclerostin levels by 11 %.

  Chronic kidney disease


Sclerostin excretion increases with declining renal function with negative correlation with GFR.

  Kidney disease


Sclerostin levels increase despite increased PTH and increased excretion of sclerostin in renal failure.