The aging of the population has been pronounced over the past 3-4 decades with the 45 and up age group growing 70% 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.

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.

The emphasis in non-drug therapy for bone loss has been on the simple 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. The reason simply supplying the nutrients that are needed in bone health has only minimal effect on osteoporosis, is that bone loss is primarily related to imbalance in the activity of the different cells in bone.

Healthy bone has the ability to constantly remodel, building more bone in areas of weight bearing stress and removing it from areas without this stress. When stress on bone changes, osteoclasts remove bone from non-stressed areas and osteoblasts build it in stressed areas. During the first half of life this activity is balanced. 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.

Any effective therapy should focus both on quieting osteoclasts and stimulating osteoblasts. Bisphophonates, such as Alendronate (Fosamax), are the first line drug therapy for bone loss. They only work on one side of the problem, slowing the activity of osteoclasts but not increasing the activity of osteoblasts. This is the likely mechanism of the complications seen with these drugs such as atypical fractures and osteonecrosis of the jaw.

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. Diseases associated with chronic inflammation such as rheumatoid arthritis are a known cause of osteoporosis.

There are two dominant causes of increased inflammation with age; higher numbers of poor functioning immune cells which have been termed “zombie cells” and a shift in the microbiome to an inflammatory producing pattern with age termed “dysbiosis”. The functional change in the immune system has been called inflammaging.

Immune cells which are highly involved in generating inflammation during acute events like infection, T cells, do not live as long as we do. They can age to the point where they can no longer replicate but have not yet died off. When an infection is encountered T cells must quickly replicate increasing the size of the army to fight. These zombie cells cannot replicate causing the weakening ability to fight infection with age.

These zombie T cells accumulate poorly functioning mitochondria, the cell organelles that produce energy. When these poorly functioning mitochondria incompletely process glucose and fatty acids, large amounts of free radicals are produced triggering inflammation. Many of these poorly functioning mitochondria can be eliminated by a process called autophagy or “self eating”. A metabolite produced in the gut by the microbiome, urolithin A. As we age the microbiome unfavorably changes (dysbiosis below) having more difficulty producing urolithin A. Supplements, however, of urolithin A are now available and can offset this weakness reducing inflammation.

The second common generator of inflammation and thus higher osteoclast bone removal with age, is a shift in the gut microbiome from one that helps reduce inflammation to one that causes it. This shift is termed dysbiosis. The healthy human microbiome is approximately 100 trillion organisms from across 1000 bacterial species. With age this often shifts to a population of a less diverse number of species and greater numbers of organisms that generate inflammation.

Dysbiosis is often accompanied by symptoms such as abdominal bloating, pain, indigestion, constipation/diarrhea. Interestingly, about a third of persons with it have no digestive symptoms to make that suspect except high systemic inflammation as the only indicator. This shift is thought to result from antibiotic use, antibiotic passthrough in food, and an imbalanced diet which provides the preferred foods for the dysbiotic bacteria and less for the preferred bacteria.

Dysbiosis is evaluated by stool microbiome testing. Once the imbalance is understood, restoration is possible with combination of herbal antimicrobials, probiotics and prebiotics reducing systemic inflammation.

On the other side of the problem of osteoporotic bone loss, diminished numbers and activity of osteoblasts which build bone, therapies are now understood which can restore this function. The osteoblast population must constantly be replenished. New osteoblasts are produced by mesenchymal stem cells, cells that live primarily in bone marrow of long bones and adipose or fat cells. 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 bone needing help.  

As the existing osteoblasts diminish, the release of BMPs declines diminishing the homing signal for stem cells. Two therapies can be used to restore BMPs signaling. The first is supplementation of BMPs. BMPs have been used extensively in repairing large bone defects related to trauma injecting them into bone implants. More recently they have become available in an oral supplement allowing targeting of broad areas of bone as seen in osteoporosis.

The second method to improve BPMs levels and increase stem cell migration to replenish osteoblasts is using infrared laser therapy to the weakened bone. Infrared laser has been shown to increase the release of BMPs in the remaining osteoblasts in osteoporotic bone. Infrared laser is also used over an accessible long bone area such as the blade of the tibia as it enhances stem cell release to respond to the homing signal of the BMPs.

One additional concern in restoring dense, strong bone is having adequate matrix. Matrix is the fibrous mesh that the minerals attach to. Literally, all body tissues have some sort of matrix. Most of it is collagen, and its generation also declines as part of the osteoporotic process. Supplementing with collagen is important, but it must be specific to the size on collagen found in bone. Collagen fibers come in a variety of sizes and that found in bone is relatively fine. Most collagen peptides have a molecular weight of 300 kDa. That in the walls of the white blood cell neutrophils is 75 kDa. Most of the matrix in bone is only 5 kDa so a general collagen supplement supplies very little of it. Fortunately, a bone specific collagen is available suited to bone matrix.

Osteoporotic/osteopenic bone loss is a complex problem. It would be great if simply taking high levels of the nutrient factors needed to make bone tissue such as minerals and vitamins D & K2, but this has proven largely ineffective. The use of the nutrients requires a balance in activity of the responsible cells, osteoclasts and osteoblasts. Too much osteoclastic activity and too little osteoblastic activity is at the core of the disorder. A program of addressing this cell activity balance is necessary for success. Fortunately, we are now understanding how to do that.