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Understanding What Happens to Osteons as We Age

4 min read

Over 54 million Americans aged 50 and older have either osteoporosis or low bone mass, a decline that begins at the microscopic level. This article answers the question, what happens to osteons as we age, revealing the complex biological shifts that contribute to decreased skeletal strength.

Quick Summary

As we age, osteon remodeling becomes imbalanced, favoring resorption over formation, leading to smaller and more numerous new osteons, wider Haversian canals, and greater cortical porosity. Old osteons are replaced with structurally weaker tissue, reducing bone mass and increasing fracture risk.

Key Points

  • Imbalanced Remodeling: The cycle of bone formation and resorption skews toward resorption with age, accelerating bone loss.

  • Structural Weakening: Aged osteons are often less mineralized, have wider central canals, and are surrounded by more fragments, all of which compromise overall bone strength.

  • Increased Porosity: The enlargement of Haversian canals leads to greater cortical bone porosity, making the bone more fragile.

  • Cellular Decline: The function of bone-building osteoblasts slows down, while bone-resorbing osteoclast activity may remain high or even increase.

  • Proliferation of Small Osteons: Bone remodels more frequently but less effectively, resulting in a higher number of smaller, weaker osteons over time.

  • Lifestyle Intervention: Weight-bearing exercise and adequate calcium and vitamin D intake are crucial to slowing osteon degradation and supporting bone health.

In This Article

The Microscopic World of Your Bones

Our skeleton may seem like a static, unchanging structure, but it is in fact a living, dynamic tissue that is constantly undergoing a process of renewal called bone remodeling. This process involves the meticulous and coordinated efforts of specialized bone cells and is centered around tiny, cylindrical structures known as osteons, or Haversian systems. These microscopic units are the fundamental building blocks of compact (cortical) bone, which forms the dense outer layer of most bones.

At the heart of each osteon lies a central Haversian canal, which houses the blood vessels and nerves that supply the bone tissue. Concentric rings of bone matrix, called lamellae, surround this canal. Embedded within the lamellae are small, interconnected spaces called lacunae, which house mature bone cells called osteocytes. These osteocytes form a vast network of communication within the bone, sensing mechanical stress and directing remodeling efforts to repair microdamage.

The Imbalance of Bone Remodeling with Age

In younger adults, the rate of bone formation by osteoblasts perfectly balances the rate of bone resorption by osteoclasts, a process ensuring skeletal integrity and strength. However, with advancing age, this delicate balance shifts, and the scales tip in favor of resorption. The number of active remodeling sites may increase, but the amount of new bone laid down at each site is less than the bone removed. The following sections detail the specific ways this imbalance manifests in the osteons.

Increased Osteon Fragmentation and Number

One of the most noticeable changes at the microscopic level is the proliferation of osteon fragments. As existing osteons are resorbed and replaced by new ones, the process is not always perfectly clean. Remnants of the old osteons remain, scattered throughout the bone matrix. With age, the number of these interstitial lamellae increases, leading to a denser, more disorganized bone structure. This fragmentation effectively disrupts the organized, strong structure of the young bone matrix.

At the same time, the total number of osteons increases. This may sound like a positive change, but it is an indicator of more frequent but less complete remodeling cycles. Older bone is characterized by a higher density of these new, smaller osteons and their fragments, which contribute to the overall brittleness of the aging skeleton.

Changes in Osteon Structure and Mineralization

The structure and composition of individual osteons change significantly with age. For instance, the central Haversian canals of osteons tend to widen over time. This enlargement contributes to a greater overall porosity within the cortical bone, effectively hollowing out the dense outer layer and reducing its strength.

Furthermore, the quality of the new bone tissue produced by osteoblasts declines. Studies show that new osteons formed in older individuals are often less completely mineralized than those in younger bone. This means that the newly laid bone is not as hard or as strong as the older bone it replaces. The deficient mineralization leaves the bone more susceptible to stress and fracture, even under normal loads. This phenomenon is a key factor in age-related fragility fractures.

Cellular-Level Factors Affecting Osteons

Several underlying cellular and hormonal changes drive these microscopic alterations. Key among them is the reduced efficacy of bone-forming osteoblasts. The ability of mesenchymal stem cells to differentiate into osteoblasts decreases with age, while their tendency to become fat cells (adipogenesis) increases. This shift leads to both less bone formation and an accumulation of bone marrow fat.

Additionally, hormonal changes play a major role, particularly the decline in estrogen levels in postmenopausal women, which accelerates bone resorption. In both sexes, a decline in growth factors like IGF-1 can also impair osteoblast function. Chronic low-grade inflammation, a hallmark of aging, and increased oxidative stress can also negatively affect bone cell activity and compromise the remodeling process.

How Lifestyle Can Mitigate Age-Related Changes

While some aspects of bone aging are unavoidable, lifestyle factors can significantly influence the rate and severity of these changes. Regular, weight-bearing exercise is a powerful stimulus for bone formation. Activities like walking, jogging, dancing, and strength training place stress on the bones, signaling to the osteocytes to initiate localized remodeling that favors bone building. Conversely, a sedentary lifestyle promotes bone loss.

Adequate nutrition is equally vital. Consuming sufficient calcium and vitamin D is essential for proper bone mineralization. Calcium provides the raw material for bone matrix, and vitamin D is necessary for the body to absorb calcium. A balanced diet rich in these nutrients, along with other vitamins and minerals, supports optimal bone health throughout life.

Young vs. Aged Osteons: A Comparative Overview

Feature Young Osteon Aged Osteon
Number Fewer and larger More numerous and smaller
Mineralization Highly and more completely mineralized Less completely mineralized
Haversian Canal Narrower diameter Wider diameter, increasing porosity
Bone Matrix Organized, strong concentric lamellae Disorganized, with many interstitial fragments
Overall Strength Greater strength and elasticity Lower strength and more brittleness

Conclusion: A Microscopic View of Bone Health

The question of what happens to osteons as we age reveals a fascinating and critical aspect of the aging process. The shift from balanced, efficient remodeling to an imbalanced state of increased resorption and flawed formation is the microscopic root of age-related bone decline. These changes, including increased porosity, compromised mineralization, and structural disorganization, are key contributors to the rise in osteoporosis and fragility fractures. However, understanding this process also empowers individuals to take action. By adopting proactive measures such as regular weight-bearing exercise and a nutrient-rich diet, it is possible to support skeletal health and mitigate the impact of these age-related changes, building a stronger foundation for a healthier later life. For more on healthy aging, see the resources provided by the CDC: https://www.cdc.gov/healthy-aging/about/index.html.

Frequently Asked Questions

An osteon is the fundamental microscopic structural unit of compact bone. Its primary function is to organize the bone's matrix into a sturdy, weight-bearing structure while housing the central Haversian canal, which provides the necessary blood supply and nerves to the bone tissue.

As we get older, existing osteons are resorbed and replaced by new ones. Studies show that these newer osteons are generally smaller than those found in younger adults, a change that contributes to a less robust and more disorganized bone matrix.

Increased cortical porosity is primarily caused by the widening of the central Haversian canals within the osteons as a result of repeated, and often incomplete, remodeling cycles. This reduces the bone's density and strength, making it more brittle.

With age, bone-forming osteoblasts become less numerous and less active, while the resorptive activity of osteoclasts may remain constant or increase. This imbalance disrupts the remodeling process, leading to the formation of smaller, less mineralized osteons and an overall loss of bone mass.

No, osteon degradation is a microscopic process that is one of the key underlying mechanisms contributing to osteoporosis. Osteoporosis is the systemic disease characterized by significantly reduced bone mass and structural deterioration, which is the macro-level result of cumulative microscopic changes to osteons and other bone structures.

While exercise cannot fully reverse all age-related changes, consistent weight-bearing and resistance exercises are highly effective at stimulating osteocytes within the osteons. This signals to osteoblasts to increase bone formation, helping to slow bone loss and strengthen existing bone, thereby mitigating the negative effects of aging.

Proper nutrition is vital for supporting healthy osteons. Adequate intake of calcium and vitamin D is essential for the mineralization of new bone tissue laid down by osteoblasts. Without these key nutrients, the newly formed bone within the osteons will be weaker and less dense.

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Medical Disclaimer

This content is for informational purposes only and should not replace professional medical advice. Always consult a qualified healthcare provider regarding personal health decisions.