This is Part XII in 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 (at: www.osteonaturals.com 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
Osteoblasts and osteoclasts have a give-and-take relationship, and their activities are linked. As with any couple, their interactions must stay in balance for marital happiness to be maintained; the harmony of bone depends upon a similar balance. The tricky thing is that resorption, like any form of demolition, is faster than re-building. To offset this, bones produce larger numbers of osteoblasts, and these plentiful cells control the overall activity of osteoclasts.
If the coupling mechanism that balances the activities of osteoblasts and osteoclasts gets out of sync, osteoclasts may begin to resorb more bone than the osteoblasts can replace. Low bone density, and eventually osteoporosis, is the result. On rare occasions it is the osteoclasts that are underactive, resulting in too much bone, a condition called osteopetrosis. It is the balance, and the communication aspects, between the processes that is crucial, as with any relationship.
The communication system between bone cells is a series of linked stimuli and responses. Problems arise when signals are either blocked or amplified. If signals are muffled, the music that coordinates the cells' activities becomes too slow; if they are inappropriately amplified, the notes become distorted and the tempo too fast. In either case the dance between the bone remodeling partners, the osteoblasts and osteoclasts, gets out of step and bone density is lost. The molecules that conduct the music are cytokines, growth factors, and glycoproteins--all of which are woven throughout the bones' collagen foundation to orchestrate the periods of active remodeling.
At the cellular level, the current of our aliveness is carried by metabolic cascades linked through a series of biochemical interactions which adjust the body's state of being to demands being made of it. Cytokines are proteins that are involved in a host of different functions throughout the body, and which can stimulate or inhibit these cascades. They can even direct cells to live or die. It was the cytokines' involvement in mounting the body's immune defenses that caught my interest. Inflammation, as you will remember, is the immune system's response to injury. Whether the injury is the result of chemical, microbial, or physical assault, the body reacts with an increase in blood flow and the release of disease-fighting white blood cells to the area. Heat, redness, pain and swelling are the noticeable consequences of this swift and potent defense.
An athlete's life such as mine is characterized by intense engagements of body and will: inflammation is the mark left by the fires of this passionate encounter. Left to smolder, those hotbeds cause long-term damage to tendons, joints, and even bone. No matter where the inflammation originates—autoimmune problems, toxic gut, glucose imbalances, oxidative stress—the immune system's response will be to flood the body with a deluge of pro-inflammatory cytokines.
Because some of the same cytokines that are active in immune reactions are involved in bone resorption, I looked further into this important link between the inflamed tissues of my hip and the scorching erosion of the bone. One of these cytokines, interleukin-1 (IL-1) stimulates the production of PGE2, a powerful prostaglandin involved in the inflammatory process. Il-1 also happens to be one of the most powerful stimulators of bone resorption.
Another cytokine, interleukin-6 (Il-6), not only stimulates the production of the bone-eating osteoclasts, but it can also increase their destructive potential by extending their normal lifespan. Levels of this cytokine are also high in the inflamed tissues of an injured joint. The link between bone resorption and inflammation was becoming clearer.
And there was more: when Il-6 is elevated it can decrease the synthesis of cartilage proteoglycans, the water-loving molecules in joints whose synthesis depends on glutamine—the same glutamine which is depleted by both Gilbert's syndrome and intense exercise. Combining Gilbert's with elevated Il-6 could severely limit the production of proteoglycans, taking the bounce right out of joint cartilage, and stripping its ability to absorb the compressive forces of exercise. Take the resilience out of cartilage and even low-level activity can be destructive to joints and the surrounding bone.
One of the pro-inflammatory cytokines, tumor necrosis factor (TNF), is from a family of molecules that help regulate bone cell activity. Another important member of that family is receptor activator nuclear kappa-B ligand, or RANKL for short. (I talk A LOT about this molecule in my book, The Whole-Body Approach to Osteoporosis.) A ligand is a communication molecule. This particular communication molecule, RANKL, is released by the osteoblasts and attaches to a special membrane receptor that goes by the acronym RANK, on an osteoclast precursor cell. The
The key, at least for me, is that RANKL-induced aggressive bone resorptin can be stimulated by the over-production of pro-inflammatory cytokines and these same cytokines are capable of blocking osteoprotegerin (OPG). OPG is a "safety net" molecule released by osteoblasts that can prevent excess RANKL from over stimulating osteoclastic activity. With my N-TX (bone resorption marker) spiked so high, excessive osteoclastic activity in my bones was obvious. the linkage between stress, over-production of inflammatory cytokines, and the resulting over stimulation of the RANKL/RANK system suggested a trail to follow—a trail that might reveal the destructive pattern whose effects were showing up in symptoms and lab tests.
The athlete may not always be able to see it but high level competition is stressful. When I was training hard, I didn't think of it as stress, it was just what I did...who I was. But with pro-inflammatory cytokines making a clear link between bone loss and inflammatory states, I began to see my sports life in a different light. Could all of those miles that I ran, biked, and swam actually have contributed to the bone loss instead of stimulating its formation as we generally assume? The impact of healthy amounts of weight-bearing exercise is significantly different than flogging your body for hours upon hours, year upon year—especially if there is insufficient awareness of nutritional needs and an another underlying metabolic disorder (in my case Gilbert's).
Now the words of the acupuncturist began to make more sense. "A constitution dominated by the fire element, and the smell of being scorched." Had I done more than just bruise my wings? maybe I had been literally "scorched" by an unrelenting inflammatory cascade within me. An inability to limit the activity of the pro-inflammatory cytokines would continually fuel smoldering fires and steadily sap the bones' strength. Now I saw that I had never given the time or the extra nutrients necessary for my body to recover between the intensity of workouts. When the heat is kept up non-stop and the furnace is never allowed to cool between engagements, the walls can crack...and the bones will break.
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