This is Part XI of a multi-part essay chronicling my personal experience with osteoporosis. In this series I have been taking readers through the diagnostic and treatment phases of my care that began over 18 years ago when I was diagnosed with severe osteoporosis. Over the years, the combination of experiencing multiple fragility fractures along with an intense immersion into the study of bone pathophysiology has given me a unique understanding of this disease. If you are just joining the series, I encourage you to skim through the previous DX Severe Osteoporosis essays on my blog as they provide background to each new installment. It is my hope that this series will provide you with a better understanding of osteoporosis in general, plus a few “pearls” that you may be able to incorporate into your own quest for better bone health. If you have been reading the essays all along…welcome back. Dr.M
“And now here is my secret, a very simple
secret: It is only with the heart that one can
see rightly; what is essential is invisible
to the eye.”
The Little Prince
Antoine de Saint-Exupery
Not only was I beginning to discover ways to improve my skeletal and overall health but I was also starting to see osteoporosis through a much different lens—and this lens was projecting multiple images from seemingly divergent rays of medical and biochemical data. For example, exercise signals the body to form bone. Well, I had certainly engaged in enough exercise in my life to build several skeletons if this was the case. So why was my skeleton, or at least its density, so paltry?
Concussive forces and the shear strain (an engineering term for the application of force at a specific angle) from muscular activity send waves of vibration rippling through the body and into bone. Here, cells called osteocytes detect and respond to these mechanical signals, translating them into biochemical signals that stimulate bone-building. Osteocytes start off as osteoblasts, the very cells that build bone. When osteoblasts have finished forming the collagen matrix foundation of bone, each osteoblast then builds a small chamber around itself. This chamber is like a cocoon offering a protected site for the osteoblast’s transformation into an osteocyte while the matrix around it is being flooded with solidifying minerals such as calcium, phosphorous, and magnesium. Once the bone is calcified, the now chambered (in an elongated cartilage sac called a lacuna) osteocyte is in place and able to receive those vibrating wave forces—the signals necessary to activate future bone remodeling activity.
|Osteocytes in lacunae|
Osteocytes have a star-like configuration with appendages reaching out through bony tunnels that radiate from them. These tunnels are fluid-filled corridors extending to neighboring osteocytes, and along them the vibrating mechanical signal is communicated from one osteocyte to the next. Thus, from every movement of the body, there comes the potential to alter the shape of each osteocyte’s cell membrane. It is at this point that the signal changes from a mechanical one to a biochemical one. Receivers in the cell’s membrane transmit the signal (if the membrane is healthy enough) into the cell where substances that promote bone formation are then released.
Because of this link between physical activity and osteogenic (bone forming) signaling, it makes sense that athletes generally have better bone density than non-athletes. But for athletes who have pushed themselves to excess for years…decades…this positive response to exercise may indeed turn into a negative response. Over stressing the body regularly with excessive, adrenal cortisol-releasing stress, coupled with neglecting to sufficiently refuel the body with important nutrients, puts the active aging athlete at considerable addition risk for osteoporosis. In addition, exercise alone does not necessarily make for better bones. Young adults who take up an exercise program will only gain a small amount of bone density. A post-menopausal woman who starts working out in a gym won’t typically gain any density. Her low estrogen causes a continued loss of bone, although her rate of loss will not be as rapid as a post-menopausal woman who does not exercise. So exercise helps to stimulate osteogenic signaling, and it is vitally important for both bone and overall health, but it will not result in increased bone density beyond a certain age—and it is not the primary determinant of bone density at any age.
I was not only seeing that bone was very much alive and amazingly complex but I was beginning to sense that it had a hidden dynamic life. Bone is amazing in that it can undergo change both by remodeling its architecture in response to external mechanical demands, and to internal physiological needs. A hefty percentage of bone is fairly quiescent at any given time. It is just there, doing its job of supporting the body and providing a reservoir for minerals. But in areas in need of repair or when the body is desperate for mineral reserves, metabolic and remodeling activity increases dramatically. Continuous cycles of remodeling are necessary to maintain skeletal health for normal, everyday activity—but when the stresses of life (both physical and emotional) increase, or when the concussive forces of weight-bearing activity are particularly high, micro-fracturing of bone and the need for
repair increases. Weakened bone must be replaced with new, resilient bone. This renewal process is accomplished by coordinated cell groups called basic multicellular units (BMUs).
At any given time there can be millions of BMUs, areas where osteoclasts are actively tearing down old micro-fractured bone and new bone is being formed in its place. Osteoclasts move like predators on the prowl for injured prey. They feast on old microfractured bone, leaving gouged out tunnels and troughs, and then move on. The osteoblasts come in behind, filling the stripped out areas with strong, new collagen matrix. This bone-like substance, called “osteoid,” is then mineralized over the next several weeks by osteoblasts. These cells deposit crystalline mineral salts (hydroxyapatite, such as in OsteoMineralBoost) between the collagen fibers to make them rigid and increase their overall strength. Once this biomineralization has occurred and the hydroxyapatite crystals are in place, the bone formation process is complete.
My job was to try and find out if this process was going on in my body and if not…why? Intermittently, as I learned more about bone biology and it hidden physiology, I would scan the slide from the biopsy of my pelvis looking for clues. I could see the BMUs very clearly in their lit-up red tetracycline “ink.” Instead of the uniform mineralized bone formation typically seen in “normal”
|Zebra-striping: red is new mineralized bone|
bone, my BMUs were filled with alternating layers of mineralized bone and un-mineralized matrix, giving it a zebra-striped look.
To me, this suggested there may be a mineralization defect of some kind that was involved in my osteoporosis. It really looked like my severe bone loss—bone weakness—wasn’t just from over-activity of the osteoclasts breaking down excessive amounts of bone, but that there was something else going on in addition. It looked as though the crystalline mineral salts weren’t “sticking” to the osteoid matrix after it was formed. Or that maybe there was something intermittently inhibiting mineralization. Maybe there was a mineral missing?…or a toxin infiltrating and preventing the hydroxyapatite crystal from forming? Maybe the levels of my testosterone and estrogen hormones were fluctuating every few days? Could the vitamin D and parathyroid hormones which are responsible for pulling in calcium from the gut and kidneys, and maintaining its optimal levels in bone and blood somehow be ineffective? Their levels, after all, had been tested several times over the past year and shown to be normal which meant that the calcium should be there in high enough quantities. Maybe my low level of essential fatty acids (that I discovered through lab testing) was involved? Fatty acids are needed for absorption and deposition of calcium into bone. But if the fatty acids were keeping me from bringing in enough calcium, then shouldn’t my parathyroid hormone have been elevated in response to low levels of calcium? My questions seemed endless, and my dearth of information was evident and discouraging. I was seeing that this last question, that of parathyroid function, was of prime importance when evaluating the causes of bone loss, and that is where I placed my next investigatory lens.
“I need to put up with two or three
caterpillars if I want to get to
know the butterflies.”
The Little Prince
Antoine de Saint-Exupery