What controls bone remodeling?

Bone remodeling is controlled by a combination of hormones, mechanical signals, and cellular communication. Estrogen, parathyroid hormone, and vitamin D play major hormonal roles. Mechanical stress from movement and weight-bearing activity tells your bones where new tissue is needed. Osteocytes within the bone itself coordinate when and where remodeling happens.

How often is the skeleton fully replaced through bone remodeling?

Your entire skeleton is replaced approximately every 10 years through bone remodeling, though the rate varies by bone type. Trabecular bone (the spongy bone inside vertebrae and joints) turns over faster — roughly every 3 to 4 years. Cortical bone (the dense outer layer) takes longer, around 10 years to fully renew.

Why is bone remodeling necessary?

Bone remodeling is necessary because your bones experience small amounts of damage every day from normal movement and stress. Without remodeling, microscopic cracks would accumulate and bones would weaken. Remodeling also releases stored calcium when your body needs it, maintains bone strength, and helps repair fractures.

When does bone remodeling occur?

Bone remodeling occurs continuously throughout your entire life, though the rate changes with age. It is most active during childhood and adolescence when bones are growing. After about age 30, when you reach peak bone mass, remodeling continues but the balance shifts gradually toward more bone loss than formation, particularly after menopause.

How does exercise affect bone remodeling?

Exercise — especially weight-bearing and resistance training — directly stimulates bone remodeling in your favor. Mechanical loading activates osteoblasts (bone-building cells) and quiets osteoclasts (bone-removing cells). It also tells your bone marrow stem cells to become bone rather than fat, which protects against age-related bone loss.

How does osteoporosis affect bone remodeling?

In osteoporosis, the bone remodeling cycle becomes unbalanced — osteoclasts remove bone faster than osteoblasts can replace it. Over time, this imbalance reduces bone density and weakens bone structure. The result is bones that are more porous, more fragile, and more likely to fracture, even from minor falls or stresses.

What is Bone Remodeling and Repair?

Did you know your bones are constantly rebuilding themselves? This amazing process, called bone remodeling, works around the clock to keep your skeleton strong and healthy. When everything’s working properly, your bones can handle everyday stress and recover from injuries without any special treatment.

In this post, we’ll explore four key topics:

How the bone remodeling cycle works.
What can throw this natural process off balance.
What causes bone loss.
How you can keep your bones in top shape.

To help us understand the bone remodeling process, I spoke with Dr. Theresa Guise from the MD Anderson Cancer Center in Houston. Dr. Guise is a professor in the Department of Endocrine Neoplasia and Hormonal Disorders, and an expert in skeletal health.

What is Bone Remodeling?

Inside each bone lies a complex network of cells and essential components known as the bone microenvironment. This specialized environment serves as the foundation for bone remodeling, the natural process of bone formation and bone resorption that keeps our bones healthy and strong. In the next section, we will discuss the bone microenvironment (and specifically each of these bone cells) in detail.

How Osteoblasts and Osteoclasts Remodel Bone

The process of bone remodeling relies on three specialized cell types, each performing distinct but interconnected roles in maintaining bone health. Here’s how each type functions:

Osteoclasts: The Cells That Remove Bone

Osteoclasts are large cells that originate in the bone marrow. Their primary function is bone resorption, the process of breaking down and removing old or damaged bone tissue. While this may sound destructive, osteoclasts play an essential role in bone health. They not only clear away old bone tissue but also stimulate bone-forming activity and help maintain a balanced remodeling process.

Osteoblasts: The Bone Formation Cells

Osteoblasts are responsible for bone formation, the process of creating new bone tissue. These cells develop from mesenchymal stem cells and typically remain active for about two weeks. During their lifecycle, some osteoblasts take on a unique role: instead of dying off, they embed themselves within the bone matrix they’ve created. These embedded cells then release enzymes that help maintain healthy bone tissue and transform into a third cell type called osteocytes.

Osteocytes: Cells That Manage The Regulation of Bone

Osteocytes function as the bone’s monitoring system. They manage bone formation and bone resorption. These long-lived cells can survive for up to 25 years within the bone matrix. Their primary role is to detect microscopic damage and stress in bone tissue. Upon detecting these changes, osteocytes send signals to both osteoclasts and osteoblasts, coordinating their activities to maintain proper bone structure and strength.

The Bone Matrix

The bone microenvironment also includes the mineralized bone matrix, the hard outer portion of bone that gives bone its strength. This matrix is built primarily from type 1 collagen, a special protein that forms strong fibers. Beyond providing structural support, the bone matrix serves another vital function: it acts as a storage depot for growth factors, which are important proteins that help maintain bone health.

The Bone Resorption and Formation Process

Your bones are continuously renewing themselves through a remarkable process that involves bone formation and bone resorption. Every time you move, jump, or make sudden movements, you create tiny stress points in your bones that can develop into microscopic cracks, called microfractures.

Bone Resorption

As we mentioned above, special cells called osteocytes act as the bone’s surveillance system and regulate bone formation and bone resorption. They detect stress points and locate these microfractures in your bones. When damage is found at a remodeling site, osteocytes signal another type of cell, called osteoclasts, to remove the damaged bone tissue.

Bone Formation

After the osteoclasts (that originate from your bone marrow) finish removing damaged bone, they signal yet another type of bone cell, called osteoblasts, to begin their work. These cells arrive at the site and build new, healthy bone tissue to replace what was removed.

This continuous cycle of removal and rebuilding keeps your entire skeleton healthy and strong. The complete process takes about 120 days and occurs simultaneously throughout all parts of your skeleton.

What Happens During Bone Remodeling?

During bone remodeling, osteoclasts break down old or damaged bone tissue in a process called resorption, then osteoblasts move in and form new bone in the same location. Osteocytes coordinate the entire process by detecting microscopic damage and signaling the other cells. The full cycle takes approximately 120 days.

Growth Phase and Bone Remodeling

Your bones are living, changing parts of your body that grow and transform throughout your life. Let’s look at how they change as you age.

From birth until about age 18, your long bones (like those in your arms and legs) gradually get longer. This growth doesn’t happen at a steady pace, sometimes it speeds up, like during growth spurts, and other times it slows down.

Osteoblasts make and lay down bone while the osteoclasts break bone down. The two cell types work in concert.

Peak Bone Mass

Your bones also get wider and their walls grow thicker until you’re about 30 years old when you achieve your peak bone mass. Think of it like a tree trunk getting thicker over time. At the same time, your bones are becoming denser as they pack in more minerals, especially calcium. This process peaks when you’re in your late twenties to early thirties.

How Adulthood Affects Bone Remodeling

While your bones stop getting longer by your early adult years, they never completely stop changing. Think of it like a tree, even though it might reach its full height, its trunk can still get thicker over time.

Throughout your entire life, your bones continue to adapt their shape and structure based on how you use them, like how exercise can make them stronger or how lack of activity can make them weaker. After that peak, bone density naturally starts to decrease, especially in women after menopause. [1]

How Mechanical Stress Impacts Bone Remodeling

When you engage in strength training, your muscles contract against the weight you’re lifting. All skeletal muscles are connected to your bones, either directly or through tendons. Each muscle contraction sends a mechanical signal to your bones that triggers two responses: it activates bone-building cells (osteoblasts) while reducing the activity of bone-removing cells (osteoclasts).

This physical stress also stimulates special cells called mesenchymal stem cells. These remarkable cells can develop into different types of tissue, including muscle, bone, cartilage, and ligaments. They respond particularly well to physical movement and mechanical forces. [2]

Bone Remodeling As We Age

As we age, two significant changes occur: we naturally lose muscle mass and the connections between our muscles and nerves become less efficient. This combination results in weaker muscles, which in turn leads to weaker bones.

However, there’s good news: your bones maintain their ability to strengthen themselves through physical activity at any age. This is why I strongly recommend staying active throughout your life. Whether you’re in your twenties or your sixties, your skeleton can still respond positively to regular exercise. [3]

But mechanical signals do something even more interesting than activating osteoblasts and quieting osteoclasts. They also influence the choices your stem cells make, choices that determine whether your bone marrow stays healthy or gradually fills with fat. This is one of the most important developments in bone research over the past decade, and it’s worth understanding. We cover this in the next section.

Bone and Fat: A Two-Way Conversation

Here’s something that surprises most people: the inside of your bones isn’t just bone. Your bone marrow contains fat, and as you age, it tends to contain more and more of it. This isn’t harmless. We now know that the gradual fattening of bone marrow is part of what makes osteoporotic bone weaker, not just an unrelated change that happens at the same time.

To understand why, we need to look at one of the most remarkable cells in your body: the bone marrow mesenchymal stem cell, or BMSC.

The Cell That Decides

A BMSC is a stem cell, a cell that hasn’t yet decided what it wants to be when it grows up. It can become several different things, but two of its most important options are:

An osteoblast (a bone-building cell), or
An adipocyte (a fat cell)

Think of each BMSC as standing at a fork in the road. One path leads to bone. The other leads to fat. In a healthy young person, plenty of BMSCs choose the bone path, and your skeleton stays strong.

But as you age, and especially after menopause, more and more BMSCs choose the fat path. The result is a slow shift inside your bones: less new bone being formed, more fat accumulating in the marrow. Over time, this contributes to the bone loss we call osteoporosis.

Bone and Fat Talk to Each Other

For a long time, scientists thought of bone and fat as two completely separate systems. We now know they’re in constant chemical conversation.

Your bones release signaling molecules, proteins like osteocalcin, osteopontin, and osteoprotegerin, that travel through your bloodstream and influence how fat tissue behaves. Your fat tissue, in turn, releases its own messengers, leptin, adiponectin, and others, that travel back and influence your bones.

Researchers call this back-and-forth communication bone-fat crosstalk. When the conversation is balanced, your bone marrow stays healthy and your bones keep rebuilding themselves. When the conversation breaks down, through aging, hormonal changes, inactivity, or disease, bone formation slows, marrow fat accumulates, and bones weaken.

This is why osteoporosis is now understood as more than just “thinning bones.” It’s a metabolic condition that affects the whole bone-fat system.

Why Exercise Is So Powerful

Here’s where this gets practical. Exercise, and specifically the kind of mechanical loading you get from weight-bearing and strength training, influences this entire system in three ways at once.

First, mechanical loading nudges BMSCs toward the bone path at that fork in the road. The same physical signals that activate your osteoblasts also tell your stem cells, “Become bone, not fat.”
Second, exercise prompts your bones and muscles to release messenger molecules that travel through your bloodstream and tell fat tissue to break down stored fat. So you’re not just building bone, you’re improving the metabolic environment your bones live in.
Third, exercise reduces the amount of fat already sitting in your bone marrow. Animal studies [5] have shown that even a few weeks of regular activity measurably decreases marrow fat and increases the markers of new bone formation.

No single medication targets all three of these mechanisms the way exercise does. This is why I keep coming back to the same recommendation, regardless of your age or starting point: the most powerful tool you have for protecting your bones is consistent, appropriately challenging physical activity.

The conversation between your bones and your fat tissue is happening whether you exercise or not. Exercise is how you join the conversation and tilt it in your favor.

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What Role Does Estrogen Play in Bone Remodeling?

Estrogen, an essential sex hormone, plays a crucial role in maintaining bone health by regulating how bones maintain and rebuild themselves. The most important form of estrogen for bone health, called estradiol, works in harmony with three types of bone cells:

Osteoblasts: the bone-building cells.
Osteoclasts: the bone-removing cells.
Osteocytes: the coordinating cells.

During menopause, women experience a dramatic decrease in estrogen production. This decline disrupts normal bone maintenance by reducing the activity of osteoblasts, the cells responsible for building new bone tissue. When osteoblasts become less active, the delicate balance of bone renewal is disrupted, which can result in decreased bone density and strength.

While researchers have established estrogen’s importance in bone health, they continue to study the precise mechanisms behind this relationship. Current research suggests that estrogen may influence how certain stem cells develop into bone-building cells, though this theory requires further scientific verification.

Factors That Disrupt Bone Remodeling

Various factors can disrupt the natural process of bone remodeling. Hormonal changes significantly impact bone health, particularly in women. As mentioned the section above, the decline in estrogen levels during menopause is a major factor that can disturb this delicate process.

Similarly, when women experience amenorrhea, the absence of one or more menstrual periods, their bone remodeling process can be disrupted. When bone remodeling becomes unbalanced (the bone resorption and bone formation processes become uncoupled), it may lead to decreased bone density and, potentially, osteoporosis.

Fortunately, many factors affecting bone health can be managed through lifestyle choices. Two critical areas where positive changes can make a significant difference are:

Nutrition: The foods we eat, especially during our bone-building years, play a vital role in bone health. Poor nutritional choices during these crucial periods can have long-lasting effects on bone density.
Physical Activity: Regular exercise is essential for maintaining healthy bones. An inactive lifestyle fails to provide the necessary stimulation for bone building. Without consistent physical activity, the bone remodeling process becomes less effective.

Finally, cancer can disrupt bone remodeling and cause a decline in bone density. The next section discusses this in detail.

Cancer and Osteoporosis

Cancer and osteoporosis share a complex and significant relationship. When cancer cells invade the bone environment, they actively disrupt the natural bone remodeling process. These cells achieve this disruption either through direct invasion of the bone or by secreting substances that manipulate osteoclasts and osteoblasts, the cells responsible for bone maintenance.

Cancer cells initiate a destructive process by releasing factors that trigger excessive bone breakdown. As osteoclasts multiply on the bone surface, they accelerate bone destruction. Additionally, cancer cells can force osteoblasts to produce structurally weak bone tissue. This combination of accelerated destruction and compromised bone formation significantly increases fracture risk.

To put it simply, cancer cells commandeer healthy bone cells to serve their destructive purpose. This process becomes particularly dangerous when cancers like breast or prostate cancer metastasize to bone tissue, leading to rapid bone deterioration and eventual fractures.

Bone Matrix, Cancer, and Growth Factors

The mineralized bone matrix serves as a reservoir for crucial growth factors. When cancer triggers excessive bone destruction, it not only weakens the bone but also releases these stored growth factors. As osteoclasts break down bone tissue, the released factors create a dangerous cycle by stimulating cancer cells to grow more aggressively and produce additional bone-destroying factors.

This self-perpetuating cycle creates an environment where tumors thrive in bone tissue. Patients face severe consequences, including painful fractures, elevated blood calcium levels (hypercalcemia), and other serious complications resulting from disrupted bone remodeling.

Cancer Accelerates the Normal Bone Remodeling Process

Cancer dramatically speeds up bone remodeling, causing destruction that outpaces the body’s ability to form new bone tissue. While osteoblasts attempt to compensate, they cannot match the rate of destruction. The new bone they manage to create is structurally inferior, further compromising bone strength.

The impact extends beyond the bones themselves. Cancer cells in bone tissue trigger systemic effects throughout the body, with muscle weakness emerging as a particularly significant concern. This occurs through a specific mechanism: cancer cells stimulate factors that activate osteoclasts, which then release stored growth factors like transforming growth factor beta (TGF beta) from the bone matrix.

Recent research demonstrates that TGF beta can travel through the bloodstream to affect multiple organs, including muscles, heart, brain, and pancreas. The resulting muscle weakness occurs even before visible muscle wasting (cachexia) develops. This weakness increases fall risk, potentially leading to fractures and creating a cycle that increases patient suffering and mortality rates.

Medical science now recognizes the importance of blocking bone resorption not only to maintain bone strength but also to prevent systemic effects like muscle weakness. Research in mouse models shows promising results using bone-protective drugs to prevent muscle weakness, and human trials are on the horizon.

Breast cancer treatment introduces several unique challenges for postmenopausal women. These are covered, in detail, in our post on aromatase inhibitors and bone loss.

Cancer and Osteoporosis: Summary of Key Points

Cancer cells actively disrupt normal bone remodeling by manipulating bone-maintaining cells
This disruption creates a destructive cycle that weakens bones and promotes tumor growth
The effects extend beyond bone health, causing system-wide complications
Muscle weakness develops through the release of growth factors from damaged bone
Current research focuses on blocking bone destruction to prevent both skeletal and systemic effects

Bone Remodeling: Best Practices

While the hormonal changes of menopause and their effects on bone health are a natural part of aging for women, you can take proactive steps to maintain strong, healthy bones. A well-planned strategy can help keep your bone remodeling process functioning effectively.

Four key approaches can help protect your bone health:

First, following a comprehensive osteoporosis exercise program helps maintain bone strength.
Second, proper nutrition provides the essential building blocks your bones need to stay healthy.
Third, low intensity vibration therapy can assist the bone remodeling process by stimulating mesenchymal stem cells (MSEs) to produce osteoblasts, the cells responsible for bone formation.
For those whose bone density has decreased significantly, placing them at higher risk for fractures, medical professionals may recommend pharmaceutical treatments as a line of defence.

Conclusion and Summary

Bone remodeling is a remarkable and continuous process (involving bone resorption and bone formation) that keeps our skeleton strong and healthy throughout our lives. This complex system involves three main types of cells, osteoclasts, osteoblasts, and osteocytes, working together in a carefully orchestrated cycle of removing damaged bone tissue and building new bone.

While this process occurs naturally, various factors can influence its effectiveness. Age-related diseases and many medications can have a significant impact on bone remodeling. However, understanding these changes allows us to take proactive steps to maintain our bone health.

Through regular physical activity, proper nutrition, and medical intervention when necessary, we can support our body’s natural bone remodeling process and maintain strong, healthy bones at any age.

Whether you’re in your twenties or your sixties, it’s never too late to start taking care of your skeletal health. By making informed lifestyle choices and working with healthcare professionals when needed, you can help ensure your bones remain strong and resilient for years to come.

Remember: your bones are constantly rebuilding themselves, give them the support they need to do their job effectively.

Bone Remodeling FAQs

Margaret Martin

Margaret Martin is a Physical Therapist with 40 years of clinical experience. Her expertise is in the treatment and prevention of osteoporosis through exercise, safe movement and fall prevention. For the last 20 years, she has concentrated on bone health and has treated thousands of patients for their osteoporosis, osteopenia and low bone density.

References

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Rubin J, Styner M. The skeleton in a physical world. Exp Biol Med (Maywood). 2022 Dec;247(24):2213-2222. doi: 10.1177/15353702221113861. Epub 2022 Aug 19. PMID: 35983849; PMCID: PMC9899984.
National Cancer Institute. SEER Training Modules. Anatomy & Physiology. Skeletal System. https://training.seer.cancer.gov/anatomy/skeletal/growth.htm
Cheng CH, Chen LR, Chen KH. Osteoporosis Due to Hormone Imbalance: An Overview of the Effects of Estrogen Deficiency and Glucocorticoid Overuse on Bone Turnover. Int J Mol Sci. 2022 Jan 25;23(3):1376. doi: 10.3390/ijms23031376. PMID: 35163300; PMCID: PMC8836058.
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Bone Remodeling Explained: How Your Bones Rebuild Themselves

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