Osteoporosis: When there are holes in my bones

The difference between healthy and osteoporotic spongy bone. — Photos: Dr LEE TZE YAN

“I never feel back pain or knee pain. I can move around freely. I do not think there is anything wrong with my bones.”

This is a common response whenever mass bone health screening is conducted for those living in the Klang Valley.

Yet, the screening result often leaves them gasping in surprise.

“Gosh! I can’t believe I am at risk for a fracture! What should I do now?”

For some participants, it is the first time they would have heard of the word “osteoporosis”.

Osteoporosis is a Latin word that translates to “porous bone”.

As the name implies, osteoporosis is characterised by a reduction in bone mass and the degeneration of skeletal structure, leading to a porous appearance.

This condition develops without any symptoms.

In a recent survey, 16.1% of the female participants and 8.4% of the male were newly diagnosed as having osteoporosis.

They are lucky as nothing unfortunate has happened to them.

Most people only realise they have osteoporosis when they suffer a fragility fracture.

So, how does our seemingly impervious bone become porous and at risk for a fracture?

After all, isn’t it the only thing left when dead bodies decompose?

Faster destruction

Our bone is actually a reactive organ.

It changes its geometry and mineral content in response to various internal and external stimuli through a process called bone- remodelling.

This process is regulated by three types of cells in the bone: osteoblasts (the builder), osteoclasts (the destroyers) and osteocytes (the mediators).

Normally, damaged bone is knocked down by osteoclasts through a process called reabsorption.

Osteoblasts then rebuild the bone by depositing organic materials at the same site and mineralising it.

Osteocytes sense the mechanical stimuli from physical activity and coordinate the bone-remodelling process.

This “renovation” process occurs all time inside our body to maintain the strength of our skeletal system.

However, the bone-remodelling process can go askew as we age.

During menopause, the production of the female sex hormone, oestrogen, ceases.

The bone reacts to this hormonal change by increasing bone destruction activities by osteoclasts.

Osteoblasts will try to rebuild the bone, but they are not able to keep up with the rate of destruction, thus bone loss occurs.

A similar event can happen in men, but andropause is not universal among elderly men.

Therefore, postmenopausal women have a greater risk for osteoporosis.

Other external stimuli known to cause bone loss include nicotine from cigarettes/vaping, alcohol, glucocorticoids (a drug that suppresses our immune system) and a lack of physical activity.

Excessive bone loss will lead to skeletal fragility and fractures, even at minimal impact.

If an older person has a fracture due to a fall from a standing height, or even a severe cough, he or she could have osteoporosis.

Some of the common bone sites for fragility fractures include the hip, lumbar vertebra and wrist.

Many patients with bone fractures suffer decreased quality of life because they lose the ability to live independently.

Moreover, one fracture often leads to a second and increases the risk of death.

Treating osteoporosis

Although we obviously cannot stop the ageing process and menopause, we can slow it down.

Assoc Prof Chin does an ultrasound scan of a participant in a bone health screening test. Many such participants are often shocked to find out they actually have osteoporosis.

A balanced diet rich in calcium and vitamin D could prevent the acceleration of bone loss.

Calcium is the building block of our bones and vitamin D helps calcium absorption in the intestines.

Examples of such foods include milk, dairy products, fatty fish and green leafy vegetables.

Moderate sun exposure will help our body synthesise vitamin D.

Engaging in physical activities, especially weight-bearing ones, could help maintain our bone mass.

For those who already have osteoporosis, medications to stop bone resorption (like bisphosphonates) or increase bone formation (like teriparatide) are available.

However, most of these medications are not free from side effects.

That is why researchers around the globe are working on better drugs to reverse bone loss.

Indeed, Malaysian researchers have discovered that the ubiquitous oil palm produces a compound that could protect bone health.

Called tocotrienol, it is a variant of the vitamin E found in palm oil.

Consumption of tocotrienols is known to reduce oxidative stress and inflammation in the body.

It is also recognised for its cholesterol-lowering effects.

The bone-protective effects of tocotrienols were first identified by local pharmacologist Professor Dr Ima Nirwana Soelaiman.

She and her team supplemented castrated female rats, which resemble postmenopausal women, with palm tocotrienols and found that their bone mass was preserved despite oestrogen deficiency.

This observation has been replicated in many animal models in our laboratory, including osteoporosis induced by nicotine, alcohol, glucocorticoids, testosterone deficiency and metabolic syndrome.

Osteoporosis is also characterised by the destruction of skeletal architecture.

If you have experience preparing bone broth in the kitchen, you might have noticed that long bones from big animals like cows and lambs consist of two layers.

The inner layer is spongy bone, which is enveloped by a hard and compact outer layer, just like human bones.

Researchers have observed that the inner layer can diminish rapidly with the advent of osteoporosis.

This degenerative change leaves our bone hollow and reduces its strength.

In rats supplemented with palm tocotrienols, the destruction of this spongy bone is prevented, thus making their bones stronger.

Applicable to humans

How does tocotrienol achieve its skeletal protective effects?

It is observed that tocotrienols promote the formation of osteoblasts and their bone-building activities.

It also protects them from oxidative assaults, thus guaranteeing their survival and function.

Tocotrienols slow down the formation of osteoclasts and their bone-resorbing activities as well.

In addition, it directs the osteocytes to stop secreting proteins that inhibit bone formation.

Overall, tocotrienol supplementation produces a net bone gain in our body.

The cautious reader will question whether the findings of animal studies can translate into humans.

This is a valid concern as rats and humans are two different organisms after all.

However, the findings from animal studies provide a good rationale to perform a clinical trial in humans.

A team at Texas Tech University in the United States have been supplementing postmenopausal women suffering early osteoporosis with tocotrienols derived from annatto, a native South American plant.

The researchers reported that markers of bone formation increased and markers of bone resorption decreased in the women receiving tocotrienols, compared to the control group, who were receiving a placebo, after 12 weeks.

The oxidative stress level also decreased with supplementation.

Hopefully, these findings can be replicated among Malaysian patients with osteoporosis, using tocotrienols derived from oil palm.

However, implementing a randomised clinical trial investigating bone health is challenging.

It requires long-term investment from potential funders because bone takes a long time to show beneficial changes in response to medications.

Findings from the American research group showed indications for altered bone cell activities with tocotrienol supplementation, but they have not shown an increase in bone mass, which will take at least 12 months.

Furthermore, the composition of annatto tocotrienols is different from palm tocotrienols.

While we look forward to implementing such a trial in the future, there’s no harm in offering those you know who are at risk of osteoporosis, a capsule or a teaspoon of palm tocotrienols.

It may just save them from a fracture or two.

Dr Lee Tze Yan is a lecturer in molecular medicine at Perdana University School of Liberal Arts, Science and Technology, while Associate Prof Dr Chin Kok Yong is a lecturer in at Universiti Kebangsaan Malaysia’s Department of Pharmacology. This article is courtesy of Perdana University. For more information, email [e-mail]. The information provided is for educational and communication purposes only, and it should not be construed as personal medical advice. Information published in this article is not intended to replace, supplant or augment a consultation with a health professional regarding the reader’s own medical care. The Star disclaims all responsibility for any losses, damage to property or personal injury suffered directly or indirectly from reliance on such information.