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Bone Modeling and Remodeling

by Maria Luque, PhD on May 18, 2018

The skeleton is composed of two types of bone: cortical and trabecular. Cortical (compact) bone comprises 80% of the volume in the adult skeleton and forms the outer layer of bone (Lerner 2012). Trabecular (cancellous) bone makes up the inner layer; has a spongy, honeycomb structure; and is mostly found in the skull, pelvis, sacrum and vertebrae. Although peak bone mass is reached in late adolescence, bones never stop changing. An adult skeleton replaces its bone mass every 10 years (OSG 2004).

Bones adapt via processes called “modeling” and “remodeling”:

Modeling—formation of new bone in one site and removal of old bone in another—occurs during childhood and adolescence. This process allows bone to grow in size and shift in space so the skeleton can adapt on the way to adulthood. Modeling is crucial to bone because it’s in the modeling years that peak bone mass develops—a significant indicator of fracture risk in later life (Rizzoli 2014). A 10% higher peak bone mass may delay the development of osteoporosis by 13 years (Hernandez, Beaupre & Carter 2003).

Remodeling happens in the fully-formed adult skeleton. Remodeling does not change the size or shape of bones; it gradually replaces them.

Osteoblasts, Osteoclasts and Osteocytes

Three types of cells make modeling and remodeling possible: osteoblasts, osteoclasts and osteocytes. Osteoblasts form bone and cause it to mineralize. Osteoclasts do the opposite, degrading bone tissue. An optimum balance between osteoclasts and osteoblasts keeps bone mass constant. Too many osteoclasts cause too much bone to be dissolved, shrinking bone mass, but if osteoclasts are too few, bones will not be hollowed out enough for the marrow. Both of these imbalances can cause osteoporosis (Gilbert 2000).

Osteocytes, the third kind of cell, originate from osteoblasts and make up 90% of all bone cells (Lerner 2012). Osteocytes are deeply embedded in cortical and trabecular bone tissue and have extensive dendritic (branching) processes through which they communicate with osteoblasts and other osteocytes. These signaling pathways play a crucial role in the skeleton’s ability to continually adapt in response to mechanical loading, because osteocytes can sense total mechanical load and trigger biomechanical responses. These responses can either encourage formation of new bone to handle heavier loads or remove bone in the absence of load (Bonewald 2006).

The Bone-Muscle Unit

Mechanical loading is the most important determinant of bone strength, influencing muscle size and force, which in turn correlate with bone mineral density (BMD) (Tagliaferri et al. 2015). We call this concept the “bone-muscle unit” because the development of one directly influences the other. This unit has extra importance during childhood and adolescence because accruing lean tissue mass during the formative years affects adult bone strength (Tagliaferri et al. 2015). If you work with children and adolescents, the bone-muscle unit represents a prime opportunity to influence present and future bone health.

To read more about the workings of the skeleton and the risks of bone loss, please see "Bone Health: A Primer" in the online IDEA Library or in the June 2018 print issue of IDEA Fitness Journal. If you cannot access the full article and would like to, please contact the IDEA Inspired Service Team at (800) 999-4332, ext. 7.


Bonewald, L.F. 2006. Mechanosensation and transduction in osteocytes. Bonekey Osteovision, 3 (10), 7–15.

Chiba, R., et al. 2016. Human upright posture control models based on multisensory inputs; in fast and slow dynamics. Neuroscience Research, 104, 96–104.

Ferretti, J.L., et al. 2003. Bone mass, bone strength, muscle-bone interactions, osteopenias and osteoporoses. Mechanisms of Ageing and Development, 124 (3), 269–79.

Giangregorio, L.M., et al. 2014. Too fit to fracture: Exercise recommendations for individuals with osteoporosis or osteoporotic vertebral fracture. Osteoporosis International, 25 (3), 821–35.

Gilbert, S.F. 2000. Developmental Biology (6th ed.). Sunderland, MA: Sinauer Associates.

Hernandez C.J., Beaupre, G.S., & Carter, D.R. 2003. A theoretical analysis of the relative influences of peak BMD, age-related bone loss and menopause on the development of osteoporosis. Osteoporosis International, 14, 843–7.

IOF (International Osteoporosis Foundation). 2017. Facts and statistics. Accessed Mar. 3, 2018:

Karaguzel, G., & Holick, M.F. 2010. Diagnosis and treatment of osteopenia. Reviews in Endocrine and Metabolic Disorders, 11 (4), 237–51.

Lacour, M., Bernard-Demanze, L., & Dumitrescu, M. 2008. Posture control, aging, and attention resources: Models and posture-analysis methods. Neurophysiologie Clinique, 38 (6), 411–21.

Laskowski, E.R. 2012. The role of exercise in the treatment of obesity. PM & R: The Journal of Injury, Function, and Rehabilitation, 4 (11), 840–44.

Lerner, U.H. 2012. Osteoblasts, osteoclasts, and osteocytes: Unveiling their intimate-associated responses to applied orthodontic forces. Seminars in Orthodontics, 18 (4), 237–48.

McMillan, L.B., et al. 2017. Prescribing physical activity for the prevention and treatment of osteoporosis in older adults. Healthcare, 5 (4), e85.

NIH (National Institutes of Health). n.d. Trabecular bone. Accessed Mar. 19, 2018:

NOF (National Osteoporosis Foundation). 2016. Accessed Mar. 19, 2018:

ODPHP (Office of Disease Prevention and Health Promotion). 2018. Physical activity. Accessed Mar. 19, 2018:

OSG (Office of the Surgeon General). 2004. Bone health and osteoporosis: A report of the Surgeon General. Accessed Mar. 3, 2018:

Porter, J., et al. 2016. The effect of dietary interventions and nutritional supplementation on bone mineral density in otherwise healthy adults with osteopenia: A systematic review. Nutrition Bulletin, 41 (2), 108–21.

Rizzoli, R. 2014. Nutritional aspects of bone health. Clinical Endocrinology & Metabolism, 28 (6), 795–808.

Tagliaferri, C., et al. 2015. Muscle and bone, two interconnected tissues. Ageing Research Reviews, 21, 55–70.

Watson, S.L., et al. 2015. Heavy resistance training is safe and improves bone, function, and stature in postmenopausal women with low to very low bone mass: Novel early findings from the LIFTMOR trial. Osteoporosis International, 26 (12), 2889–94.

Wright, N.C., et al. 2014. The recent prevalence of osteoporosis and low bone mass in the United States based on bone mineral density at the femoral neck or lumbar spine. Journal of Bone Mineral Research, 29 (11), 2520–26.

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About the Author

Maria Luque, PhD

Maria Luque, PhD IDEA Author/Presenter

Dr. Maria Luque is a health educator and fitness expert with 15+ years experience. After serving in the US Air Force, this former military Fitness Program Manager, took her passion for health and education to the next level and now holds graduate and post-graduate degrees in health sciences. In addition to conducting workshops and group/personal training, she is a freelance writer. She currently teaches at the College of Health and Human Services at Trident University International.