The aging of the population has been pronounced over the past 3-4 decades with the 45 and up age group growing approximately 3 times greater than those under 45 years.  A natural result has been increasing numbers of persons with diseases that are highly related to aging including osteoporosis and osteopenia.

Osteoporosis is a major public health problem, particularly in elderly women, affecting approximately 10 million Americans. Over 300,000 hip fractures per year can be attributed to osteoporosis resulting in direct patient care costs of over 18 billion dollars in 2005. As the population ages, this cost is anticipated to rise to approximately 25.3 billion dollars by 2025.

The concern with osteoporosis is fragility fracture which is a fracture from either no stress other than weight bearing or from less force than would be needed to fracture healthy bone.  Osteoporosis increases fracture risk approximately 70% compared to that in healthy bone.  Osteopenia is not benign and increases the risk 31% compared to healthy bone.

Many patients are concerned about the potential adverse effects of medications available to treat the disease and would prefer a non-drug approach.  The first line medications called bisphosphonates such as Fosamax (alendronate) have been shown to increase bone mineral density (BMD) by 5-7% and 1.6-5% in the spine and femoral neck (hip) respectively after 3 years of treatment.  While these medications do reduce fracture risk, they do not completely prevent them and their use is associated with adverse effects. Common adverse effects include:

More serious, less common adverse effects are atypical femoral fractures and osteonecrosis of the jaw.

Atypical femoral fracture is thought to result from the treatment weakening the collagen matrix which holds the bone minerals and an uneven improvement in bone density distribution which may occur with these medications.  Osteonecrosis of the jaw is thought to result from medication induced slowing of normal bone remodeling and changes in bone vascularity.

As an alternative to medication treatment of osteoporosis, many persons will try supplemental use of the raw materials needed to build bone; minerals such as calcium, magnesium and boron, and vitamins D and K2.  While it is true that these factors are needed to maintain and build bone, the success of this supplemental use once significant bone loss has occurred has proven largely inadequate in making important increases in BMD. 

The reason supplying these nutrients once bone loss occurs has not proven to be adequate corrective therapy is that the cells responsible for using these in bone are functioning abnormally.  While it is very important to have these nutrients available, bone cell activity must be re-established to improve bone density and structure.

Healthy bone has the ability to constantly remodel, rebuilding older bone areas that develop damage from use.  Osteoclasts remove bone from weakened areas and osteoblasts build new bone in these areas resulting in strong, healthy bone.  During the first half of life this activity is balanced maintaining bone density and strength.  Typically, between 50-60 years of age, there is a gradual shift in this balance with the osteoclasts becoming more active and the osteoblasts becoming less numerous and functional.  The net effect of this imbalance is ongoing bone loss.

While this shift in bone cell activity is accelerated as hormone levels decline in females/menopause and males/andropause, there are several other factors occurring during midlife which contribute.  These include decreasing weight bearing activity, higher levels of inflammation, decreased stem cell replenishment of osteoblasts and others.  Osteoporosis is caused by a collection of factors and the exact factors involved in a given case may vary.  The best outcome in each individual comes from a broad assessment of all factors and targeting the specific combination found.

Osteoclasts are activated by inflammation, something that has been shown to progressively increase with age.  Inflammation is an immune process that helps to fight infection and initiate repair in the early postinjury period.  The hallmark of inflammation in those two processes is that it is short term.  Chronic inflammation is a potent driver of osteoporosis.

There is a well-documented increase in inflammation that begins in midlife and further progresses with age.   This process has been called inflammaging and it also contributes to the development and progression of several other diseases that become progressively more common with age including arterial disease, diabetes, arthritis, neurodegenerative disease and many more.

Study into what drives inflammaging have isolated several pieces including:

Inflammation drives excessive bone resorption by activating the bone removal cells, osteoclast during midlife, while at the same time the bone building cells, osteoblasts, diminish.  The osteoblast population must constantly be replenished.  New osteoblasts are produced by mesenchymal stem cells (MSCs), cells that live primarily in bone marrow.  MSCs diminish in number and function during midlife leading to diminished re-population of osteoblasts.  Restoring bone marrow MSC numbers and their activity in osteoblast replenishment is key to effective osteoporosis treatment.

Significant research has shown that laser therapy of bone marrow increases MSC numbers and function.  Their migration to the bone area needed to produce osteoblasts is thought to be related to the secretion of bone morphogenic protein (BMP) by the remaining bone cells in that area.  This also can be increased by laser therapy to the weakened bone areas as well as by application of pulsed electromagnetic frequencies (PEMF).

Stem cells must get a signal as to what tissue to migrate to and what cells to replenish.  This homing signal in bone is from a proteins called bone morphogenic proteins (BMPs) which are released by the osteoblasts in bone needing replenishment. 

As the existing osteoblasts diminish, the release of BMPs declines diminishing the homing signal for stem cells.  Oral supplementation of BMPs can be used to enhance the bone repair process. BMPs have been used extensively in repairing large bone defects related to trauma.  More recently they have become available in an oral supplement.

Figure - Diminished mesenchymal stem cell numbers and activity in bone marrow seen with aging can be restored by laser therapy (1 + 2). PEMF to the osteoporotic bone area stimulates the release of BMPs by remaining osteoblasts (3). BMPs trigger MSC migration to the needed bone area to and their conversion into new osteoblasts (4 + 5).


In addition to the above-described therapies, additional treatments are added specific to the causative factors that are identified in the evaluation. These may include:

Osteoporosis is a heterogenous disorder which means it has a lot of pieces to it.  Some of these pieces are present in all cases while others are specific to an individual.  We concentrate on beginning with a comprehensive evaluation of all of the possible factors to develop an effective and specific program for each patient.

The therapies we use have been documented to enhance bone repair and improved bone mineral density (BMD).  For example, while medications used for osteoporosis have been shown to increase BMD by approximately 5% in the first year of use and 1-2% in the 2nd and 3rd years of use, laser therapy and PEMF have been shown to increase BMD 17% and 39% respectively in the first year.  Adding the other factors in a complete program promises even greater restoration.