Dr. R. Keith McCormick, DC of Belchertown, MA, gave an insightful talk at the recent Boulderfest 2007 in which he described the realities of osteoporosis and the problems with the family of drugs being purveyed by the pharmaceutical industry known as bisphosphonates. In part one of a three part series, Dr. McCormick has been gracious enough to explain to my blog readers why bisphosphonates are NOT the right thing to do to prevent or treat osteoporosis.  Here is part 1.

Osteoporosis is a disease process characterized by skeletal weakening from low bone mass and a deterioration in micro-architectural quality. The physical and financial burden of this disease is substantial with over 50 percent of women and 13 percent of men in America destined to sustain an osteoporotic-related fracture within their lifetime. With these high-stakes costs it is important that our method of treatment is not only efficacious but also conducive to the patient’s over-all good health.

Bone health is naturally maintained in a person’s body by a balanced remodeling system that ensures continued replacement of old worn-out bone with strong new bone. During normal bone remodeling, the bone-forming cells (osteoblasts) produce enough new bone to replace that which was resorbed by the osteoclasts. It is when this coupled remodeling process is in balance that bone health is maintained. When the osteoclasts resorb excessive amounts of bone, remodeling becomes uncoupled and there is a net decrease in bone tissue. Drug therapy has therefore concentrated on reducing osteoclastic activity in an attempt to correct this imbalance that leads to bone loss. The antiresorptive agents, bisphosphonates, have become the most commonly used pharmaceuticals for this task. With less osteoclastic activity, remodeling slows and there is less bone loss. Most physicians and millions of patients who have taken bisphosphonates view them as harmless drugs that increase bone mineral density and reduce the risk of fractures. But after decades of use, concerns are now rising over the safety of bisphosphonates.

HOW DO BISPHOSPHONATES WORK?  Bisphosphonates are synthetic analogs of inorganic pyrophosphates (commonly used antiscaling or water-softening chemicals) that bind to the divalent calcium ion (Ca2+) in the hydroxyapaitite crystal of bone. It is here that nitrogen-containing bisphosphonates are able to decrease excessive osteoclast activity. They do so by repressing farnesyl diphosphate synthase, an enzyme important for the synthesis of osteoclast cell regulatory proteins. Without these proteins, osteoclasts can no longer function and bone resorption is substantially reduced. With decreased osteoclastic activity, resorption sites are reduced, which lessens the risk that a minor external mechanical load could impart a breakpoint strain leading to trabecular buckling and catastrophic structural failure. It is from this reduction in resorption sites that bisphosphonates are able to reduce fractures. From a glance, and from statistics showing that bisphosphonates reduce both vertebral and nonvertebral fractures, this seems a very positive therapeutic outcome. But is this mode of therapy improving the actual “health” of bone? And, are there drawbacks to these powerful drugs that must be considered before prescribing their use?

Tune in tomorrow for part II and Wednesday for the completion of this important series.