The Medical Establishment centers osteoporosis diagnosis and treatment on just one measurable bone health parameter: bone density. The Osteoporosis Reversal Program emphasizes that not density, but rather bone quality and tensile strength are key to fracture resistance.
While it is desirable to increase bone density, not all bone density is created equal, as you’ll learn in today’s post.
So to elucidate this concept and to help you gain a better understanding of why bone quality is an essential element in bone health, we’re going to analyze and summarize a study authored by Dr. Charles H. Turner, a biomedical engineer, on the mechanical structure of bone.
An Engineer’s Perspective
Dr. Charles H. Turner earned a bachelor’s degree in Mechanical Engineering and a PhD in Biomedical Engineering in the mid and late 1980s. He is recognized internationally as a scientist and engineer, and his studies on the effect of genetic modification on bone and the mechanical adaptation of bone have resulted in some remarkable discoveries.
He authored more than 250 peer-reviewed papers, one of which we’re going to look at today, titled “Bone strength: current concepts”, published in the highly respected Annals of the New York Academy of Sciences.
The study begins with an overview of the skeleton’s various functions, as you’ll read next.
The Skeleton’s Functions
Most of us think of the skeleton as a sort of scaffold or armature that keeps our soft tissue from collapsing. While it does offer structural support, the skeleton plays some other fascinating roles as well.
Calcium: Bones provide a source of calcium, releasing this mineral into the bloodstream and raising serum calcium levels when necessary. This aids in proper muscle function, and it’s why calcium can relieve muscle cramps.
Hearing: It’s easy to forget that ears have bones. The tiny ossicles amplify sounds in the middle ear, and also manage the amount of sound transmitted in response to the input of sound waves.
Protection: Vital body systems and organs are protected from impact by bone. For example, the brain is protected by the skull, which deflects blunt force by transferring the energy of the impact to the spongy bone between the hard bony plates of the skull. The breastbone (sternum) protects the heart, the ribs provide a protective cage for the lungs.
Force distribution: The long bones in the arms and legs are wider at the ends to better distribute joint forces and therefore prevent bone damage. The long bones act as levers against muscle contraction, and this action alone could cause eventual damage if the bones were not shaped in this way.
In addition, bone is made up of layers including a spongy (trabecular) substance that absorbs pressure and impact. The ability to absorb impact without breaking is, of course, the key to fracture resistance.
How To Measure Fracture Resistance
As Savers know, DXA (previously DEXA) scans do not measure fracture resistance. They simply measure the quantity of bone, and a larger quantity of bone obviously means the bone is “denser.” But as we’ll see in a moment, Dr. Turner’s article shows that quality is far more important than quantity in evaluating fracture resistance.
He explains that when evaluating the ability of a bone to resist fracture, several key components have to be considered: stiffness, ultimate force, how much energy is required to break the bone, and displacement.
Stiffness relates to bone mineralization. Young children’s bones, for example, aren’t stiff and show less mineralization, but their bones are very flexible. This is why children are more prone to “greenstick” fractures, which are really deformities in the bone where it was bent but did not break.
They’re called “greenstick” because the bones act like a flexible green twig, which is how fracture-resistant bones are described in the Osteoporosis Reversal Program:
“…tensile strength must therefore be of primary concern. …picture a thin but supple and moist tree twig that has been saturated in protective oils and compare it to a thick slab of old dried-up wood. Even though this is not an exact comparison, it may clarify why a thick, hard outer bone layer can actually be more fragile than a thin but well-integrated whole…”
Ultimate force refers to this well-integrated whole, and is indicative of the bone’s overall structural integrity.
The amount of energy required to break a bone is measured by evaluating the stress-strain relationship and how much stress the bone can take before it breaks. Strength is an intrinsic property of bone itself, and is not dependent on the size and shape of the bone. But the point at which a bone breaks is influenced by bone shape and size. In other words, a thin bone such as a rib may break more easily than a thick bone like the femur, even if both bones are of optimal strength for their size and shape.
Displacement refers to the position of the bone after a fracture. Brittle bone will snap apart with greater displacement than a flexible bone, which may simply bend as in the greenstick fracture. So the kind of fracture sustained can say a lot about bone quality.
Anatomy Of A Fracture – Why Do Bones Break?
It may seem obvious at first – bones break because force is applied to them. But it’s much more complex than that.
For example, the same force can be applied to two similar bones – say, two ribs – and one will break while the other will not. Why is this?
The Medical Establishment will tell you it’s due to the bone’s BMD, or bone mineral density, which they place great emphasis on as a measure of bone health. But in actuality, a bone with a high BMD may break under pressure more easily than a less dense but more flexible bone. In fact, there is an inverse relationship between a bone’s hardness and how much strain it can take.
When force is applied to a bone, the energy must go somewhere. If the impact is very forceful and fast, then the energy escapes quickly via cracking, and the bone is more prone to shatter in pieces under this kind of force. Lower amounts of force cause simple fractures as the energy releases more slowly through one crack.
The angle and type of force plays a role, too. Bone is strongest in compression and weakest under tension. Torsion, or twisting, naturally tends to cause spiral-shaped fractures. Thus, bone breakage has much to do with how the bone absorbs the energy of impact. And that is influenced by the bone’s structure and quantity of mineralization.
The Geometry And Matrix Of Bone
Bone is composed of collagen and minerals, with collagen being the tough yet elastic protein that forms the matrix, or scaffold-like structure of bone. The mineral component is hard, and adds strength and stiffness to bone tissue. Both are important for bone health, and the ratio of collagen to mineral is crucial to overall bone health and fracture resistance.
Your bones are a mix of both, and if they are stiff, they’re more likely to break than if e more spongy, trabecular bone is present. Yet bones that are made up of a high proportion of cancellous matter will show as denser in a DXA scan. Once again, this points to the limited nature of bone scans; they simply indicate quantity, but not fracture resistance.
Dr. Turner notes that:
“A bone that is highly mineralized is also stiff and brittle and will require much less energy to fracture (the area under the curve) than a bone that is more compliant.”1
Back to the structure of bone – long bones are not unlike a tube in structure, with the outer walls thick and firm but the inside more open. This structure allows bones to be very strong without being overly heavy. Combining light weight with strength is a concept that engineers like Dr. Turner know very well. This plays into the concept of building and increasing bone, which we’re going to look at next. Bones need to remain light, flexible, and “aerated” even when building density.
Mechanotransduction: How Bones Strengthen Under Load
Bones rebuild themselves through the activities of various kinds of cells that undergo mechanotransduction, which refers to any of various processes by which cells respond to mechanical stimulation and convert it into electromechanical action. Applied to bone, mechanotransduction refers to the way bone increases density and strength in response to mechanical forces – for example, in response to exercise.
Mechanical stimulation activates many biochemical pathways, and this happens almost instantaneously. Bone cells respond to stimulation immediately, releasing prostaglandins and nitric oxide within minutes of osteogenic loading, which is the application of force along the longitudinal body axis (the top of your head through your hips).
It’s worth pointing out that non-steroidal, anti-inflammatory drugs (NSAIDs) work by blocking prostaglandins that play a role in carrying pain signals to the brain. NSAIDs, therefore, suppress this biomechanical pathway and greatly hinder bone formation. Not surprisingly, research clearly shows that NSAIDs slow fracture healing.
The complex interplay between stimulation and repression of osteoclasts (bone-removing cells) and osteoblasts (bone-building cells) continues as the bones respond to loading. This is why exercise is such an important component to building bone, as stated in Chapter 13 of the Osteoporosis Reversal Program:
“Scientists have confirmed that bone growth is stimulated by an applied force, and therefore, increasing muscular stress can increase bone tissue. Muscles help bone growth in two ways: when they apply stress on bones, the latter develop their size to support the stress. Secondly, muscles also apply their weight on bones causing an increase in bone mass.”
The Hormone Connection
The process of bone remodeling involves interactions between various hormones, namely parathyroid hormone (PTH) and estrogen. In the absence of a parathyroid gland, the anabolic effect – that is, the building of bone from smaller molecules – is no longer observed in response to osteogenic loading. PTH’s role in building bone is likely the mobilization of calcium ions within the cells.
Interestingly enough, the precise role of estrogen in building bone in response to mechanical loading is still unclear. We do know that loading increases certain estrogen receptors in osteoblasts, and that the bone cells of low-estrogen mice exhibit less response to mechanical stimulation. It appears that estrogen affects bone components differently in response to loading, with estrogen suppressing bone resorption of trabecular bone and also suppressing bone formation of the periosteum (external membrane surrounding bone).
Estrogen, then, plays seemingly opposing roles in bone remodeling; but healthy bone turnover is the result of a balanced interplay between bone loss and bone gain.
Dr. Turner’s Conclusion Regarding Bone Strength
Dr. Turner credits “matrix composition and geometry”1 as the primary determinants of bone strength, noting that:
“Increased mineralization of bone has the combined effects of stiffening the tissue while making it more brittle. This has implications for osteoporosis therapies that change bone turnover.”1
The statement above is in perfect alignment with the Osteoporosis Reversal Program, which points out in Chapter 3 the problem with “osteoporosis therapies that change bone turnover” – in other words, osteoporosis drugs:
“[Bisphosphonates] attach themselves to the collagen matrix of the bone (hydroxyapatite) and block resorption, while bone formation continues for approximately 6 to 12 months thereafter. During that time, there is an increase in bone volume (and bone mass), and scientists have observed that typically, bone volume stabilizes and the increases are minimal after that period of time.
The explanation for the bone density increases seen after the first year is that it most likely represents increased mineralization, so that bone mineral is more densely packed and therefore, bone density increases. However, bone volume does not increase, since there is no new bone formation after the initial period mentioned earlier.”
This explains the vast difference between drug-induced bone density, which is ultimately very harmful to bones and actually increases fracture risk, and healthful bone density built through nutrition and exercise. The latter takes bone quality into account; the former considers only bone quantity.
Even The Researcher Who Discovered Bisphosphonates Admitted That Osteoporosis Drugs Can Actually Cause Fractures!
Shockingly, Dr. Herbert Fleisch himself, the late Swiss researcher who specialized in metabolic bone disease and discovered the role of bisphosphonates as antiresportive therapy, openly acknowledged the harm bisphosphonates can cause. In an article titled “Bisphosphonates: Mechanisms of action”, published in the Endocrine Reviews Journal back in 1998, he writes the following:
“The effect of the bisphosphonates upon the mechanical properties of the skeleton has been addressed only recently. This issue is important since long lasting, strong inhibition of bone resorption can lead to increased bone fragility and, therefore, to fractures caused by the inability to replace old bone by young bone … ”2 [my emphasis]
It Couldn’t Be More Clear: Bisphosphonates Increase Fracture Risk
The evidence is undeniable, and the Osteoporosis Reversal Program was right on track from the get-go about the true nature of bisphosphonates. Dr. Turner’s work explains in great detail why bisphosphonates undermine true bone health and increase the risk of fractures. This is extremely ironic considering the scare tactics some doctors use to get their patients to take osteoporosis drugs, warning them about fractures they’ll sustain if they don’t take the drugs!
Stop Worrying About Your Bone Loss
Join thousands of Savers from around the world who have reversed or prevented their bone loss naturally and scientifically with the Osteoporosis Reversal Program.
But Savers like you know better. The Program has been informing Savers of the dangers of osteoporosis drug therapy since 2007. Rest assured that our goal at the Save Institute always has been and always will be to expose myths and promote the truth!
Till next time,
1 Turner, C.H. “Bone strength: current concepts.” Ann N Y Acad Sci. 1068. (2006): 429-46. PDF. http://www.fields.utoronto.ca/programs/scientific/08-09/biomedical/proposed_problems/Turner_bone_strength.pdf
2 Fleisch, H. “Bisphosphonates: Mechanisms of action.” Endocrine Rev. 18. (1998): 80-100. http://press.endocrine.org/doi/full/10.1210/edrv.19.1.0325