Bone loss occurs when more bone tissue is removed from bones than is added.

This imbalance in the bone remodeling process can result from various factors, hormonal changes caused by natural aging, and prescription drugs’ side effects.

Today, we will explore core mechanisms behind shifts in the bone remodeling process that lead to bone loss: the energy metabolism of osteoclasts and age-related oxidative stress on osteoblasts.

The Engine Of Bone Remodeling

Bones continually undergo a process of change and renewal. That process, called bone remodeling, has two primary parts: bone resorption and bone deposition.

Old bone is resorbed by cells called osteoclasts and new bone is deposited by cells called osteoblasts. When bone remodeling is balanced, bones stay strong and healthy. An imbalance that favors bone resorption causes bone loss, leading to osteoporosis.

A study published in the journal Frontiers has determined that osteoclast overactivity is tied to changes in osteoclasts' cellular energy metabolism.

The energy metabolism of osteoclasts allows them to function properly. Metabolic disruptions can destabilize the bone remodeling process, resulting in too much bone resorption.

Under normal conditions, osteoclasts are synthesized to increase bone resorption, and then a secondary system limits their actions to prevent imbalance. The researchers refer to this limiting action as “compensatory regulation”.

Bone loss occurs when the systems that generate osteoclasts activate but the compensatory mechanism meant to limit their actions fails. Oxidative stress is one source of damage to cellular processes like this compensatory mechanism. Increasing antioxidants can help to maintain the bone remodeling process, including healthy osteoclast function.

The researchers reached a clear conclusion about the possibilities that follow from this new understanding.

“If this compensatory mechanism can be restored in a targeted manner when osteoporosis develops, the curative effect is presumed to be significant and the side effects will be eliminated instead of blindly stimulating bone formation and inhibiting bone resorption.”¹

Synopsis

A study determined that osteoclast overactivity is linked to osteoclasts' cellular energy metabolism. Metabolic disruptions lead to overactivity of osteoclasts and the failure of compensatory mechanisms that are meant to limit bone resorption.

Maintaining Cellular Metabolism For Bone Remodeling

A study published earlier this year determined how normal aging affects bone metabolic pathways in mice.

Researchers studied the bones of the mice over time and observed osteoblasts from the mice in the lab. Older mice experienced dramatic bone loss and there were significant differences between the metabolic profiles of osteoblasts between younger and older mice.² Osteoblasts are the cells responsible for depositing new bone.

The researchers linked aging related changes in metabolic function to the upregulation of oxidative stress genes and the down-regulating of osteoblast-related genes.²

This connection between aging, oxidation, and reduced osteoblast function helps explain the age-related imbalance in bone remodeling.

Synopsis

A study of mice and their osteoblasts over time found that as the mice aged their oxidative stress genes were upregulated, and their osteoblast-related genes were down-regulated.

Reducing Oxidation To Maintain Cellular Metabolism

Oxidative stress occurs when a radical oxygen species (ROS) molecule, also called a free radical, damages another molecule by stealing an electron from it. Cellular metabolism is one of the processes that can be harmed by oxidative damage.

Reducing oxidative damage protects cellular function throughout the body. The studies above indicate the importance of cellular metabolic function for proper bone remodeling and how oxidative damage can harm metabolic function and create imbalance in the bone remodeling process.^1,2

Preventing oxidative damage is key to protecting bone health. One direct way to help reduce oxidative damage is a diet rich in antioxidants. A healthy and balanced diet additionally provides all of the nutrients your body needs to maintain these complex systems. The study on osteoclasts notes that one of the impacts of anorexia is increased osteoclast activity.¹

Not only do antioxidants protect osteoblasts so they can deposit new bone, but they prevent oxidative damage from undermining the compensatory regulation system that keeps osteoclasts in check.

Synopsis

Oxidative stress damages cells that maintain healthy bone remodeling. An antioxidant-rich diet can help protect your osteoblasts, osteoclasts, and the regulatory processing that help maintain their actions balanced.

What This Means To You

Protect the metabolic function of your osteoblasts and osteoclasts by reducing oxidative damage. The Osteoporosis Reversal Program offers an in depth explanation of how radical oxygen species drive the process of oxidation and how through diet and supplementation you can reduce oxidative stress.

Remarkably, the choices we make every day trickle down through the many systems that govern our body until they ultimately impact us on the cellular level. The deeper our understanding of these intricate relationships, the better we can make choices that serve our bones and our health.

References

¹ https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2021.675385/full

² https://pubmed.ncbi.nlm.nih.gov/37548937/