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Sclerostin: Bad to the Bone?

  • 7/23/2012 1:05:00 PM
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Sclerostin: Bad to the Bone?

Brandon Macias, Ph.D

Most folks, especially those who do not suffer from bone debilitating diseases, might forget that their skeletons are “alive.”  Yes, the bone that protects your vital organs and works with your muscles to get you out of bed in the morning is constantly remodeling.  Bone cells called osteoblasts lay down new bone matrix, and bone cells called osteoclasts, “eat” or resorb bone tissue.  In a normal healthy human, this bone-forming activity by osteoblasts and bone-resorbing activity by osteoclasts is tightly regulated.  The “coupling” of bone formation-to-resorption is important to prevent bone loss.   It is a natural process that allows your body access to calcium and the ability to strengthen weak or damaged bone tissue sites.  In fact, the human skeleton is replaced, on average, every ten years.  However, if bone resorption exceeds bone formation, the skeleton will slowly lose bone mass.  An example of such a condition with higher resorption activity is osteoporosis, where bone formation and bone resorption become “uncoupled.”   Most bone mass is gained during adolescence; however, at adulthood (~ 30 years old), we slowly lose bone mass with aging. 


Exercise, especially during adolescence, is critical to maximize bone gain.  Why is exercise important?  Bone responds to the loading that occurs during exercise.  In other words, when we run, muscles attached to joints pull on bone to generate movement.  Then when the foot makes contact with the ground, an impact force is “felt” by the bone.  The muscle forces and impact forces act on bone cells to simulate bone formation and prevent resorption.


            Recent research has identified a natural factor in our bodies that inhibits bone cell forming activity, by examining individuals who had a condition of high bone mass, rather than the more common condition of low bone mass.  This disease is now named sclerosteosis, and patients show a life-long progressive increase in bone mass.  The cause is believed to be a genetic alteration that rendered the factor, now named sclerostin, non-functional.  Sclerosteosis is the opposite of osteoporosis.  The discovery of sclerostin has generated tremendous excitement in the scientific and medical communities.  Before this discovery, no strategy was known that had the single function of stimulating bone formation and thus making new bone.  Therefore, it is important to better understand how sclerostin levels in the body change with aging and exercise activity, across genders, or during therapeutic treatment.  Recent data show that human sclerostin levels circulating in the blood are higher in men than women.  In addition, human blood sclerostin levels gradually and continuously increase with aging in both men and women.  It has yet to be determined how sclerostin blood levels change with exercise or lack of exercise.  Current research in the Bone Biology Laboratory at Texas A&M University is working to determine how exercise or the lack of exercise affects blood sclerostin levels in animals.  Understanding how sclerostin levels change with exercise intensity or duration will help develop more effective exercise strategies to prevent bone loss.




  1.  Agostino Gaudio, Pietra Pennisi, Cornelia Bratengeier, Venerando Torrisi, Brigitte Lindner, Roberto A. Mangiafico, Ivana Pulvirenti, Gerhard Hawa, Giovanni Tringali and Carmelo E. Fiore. Increased sclerostin serum levels associated with bone formation and resorption markers in patients with immobilization-induced bone loss. J Clin Endocrinol Metab, 95:2248-2253.
  2. Ulrike IL Mödder, Jackie A Clowes, Kelley Hoey, James M Peterson, Louise McCready, Merry Jo Oursler, B Lawrence Riggs, Sundeep Khosla. Relation of Age, gender, and bone mass to circulating sclerostin levels in women and men. J Bone and Mineral Research. 26:27-34, 2011.



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