by Maria Luque, PhD
A strong skeleton is just as important as a healthy heart.
Bones form the frame that keeps our bodies from collapsing and serve as a bank for minerals essential to multiple bodily functions. In fact, 99% of the body’s calcium is found in the bones and teeth (NIH n.d.). The skeleton anchors everything fitness professionals deal with every day: muscles, joints, tendons, the whole kinetic chain.
But how much do you really know about bones? Although bones are vital to life itself, knowledge and interventions geared at preventing unnecessary bone loss and subsequent osteopenia and osteoporosis are still lacking. According to the Surgeon General, “The biggest problem is a lack of awareness of bone disease among both the public and health care professionals” (OSG 2004).
Bone loss and sarcopenia (muscle loss) are a normal part of aging, and being aware of the pathophysiology of these processes can help fitness professionals to develop effective preventive strategies and to better inform clients. Consider that half of women over 50 and a quarter of their male counterparts suffer broken bones because of osteoporosis (NOF 2016). Health authorities project about 17.2 million new cases of osteoporosis or osteopenia between 2010 and 2030, a 32% growth rate compared with 2005–2010 (Wright et al. 2014). No doubt, you’re aware of the ample opportunity—and great earnings potential—in this population.
To excel at informing these clients and helping them develop effective preventive strategies, you need insight on the basic pathophysiology of aging bone. We’ll start by reviewing how bones grow, why they shrink with age, and what the difference is between osteoporosis and osteopenia.
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.
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).
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.
Bone loss and aging are inseparable: “The skeleton is a systemically regulated mass of mineralized material that is born, grows, reaches a more or less high peak, and then declines faster or slower as to develop a correspondingly high or low fracture risk”(Ferretti et al. 2003). Musculoskeletal aging—declining bone and muscle mass, increasing joint pain and stiffness, and decreasing physical mobility—is a normal part of aging. However, how rapidly or slowly bone mass declines depends on different factors. While genetic abnormalities account for 70% of the variance in skeletal strength (Rizzoli 2014), other factors—like hormones, nutrition, physical activity and toxins—play crucial roles in developing bone and losing it.
Understanding bone loss starts with distinguishing between the two basic diagnoses: osteopenia (low bone mass) and osteoporosis (advanced loss of bone tissue). Then, the smart thing to do is learn about risk factors and preventive measures.
For activities to promote good bone health, as well as a full reference list, please see “Bone Health: A Primer” in the online IDEA Library or in the June 2018 print edition 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.
IDEA Fit Tips, Volume 16, Issue 7
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