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.
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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.
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