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What Happens to Older Cartilage During Bone Growth?

4 min read

Did you know that long bone development from cartilage typically ceases around age 25? However, the story of what happens to older cartilage during bone growth is far more nuanced, detailing cellular transformations that profoundly affect lifelong joint integrity and function.

Quick Summary

Mature cartilage, unlike its younger counterpart, is not replaced by new bone. Instead, with age, cartilage cells called chondrocytes become senescent, contributing to degeneration, reduced regeneration, and calcification that compromises overall joint health and function.

Key Points

  • Endochondral Ossification: Young cartilage in growth plates is actively replaced by bone, a process that stops during skeletal maturity.

  • Cellular Senescence: In older cartilage, chondrocytes enter a senescent state, reducing their ability to repair and maintain the cartilage matrix.

  • Inflammation and Damage: Senescent chondrocytes release inflammatory chemicals that contribute to cartilage degradation and increase the risk of osteoarthritis.

  • Calcification: As cartilage ages, it can undergo unwanted calcification and stiffening, distinct from the normal mineralization of bone growth.

  • Shift in Role: The primary function of older cartilage is maintenance and cushioning, not acting as a template for new bone, making joint health management a key focus for healthy aging.

  • Limited Repair: Unlike growing cartilage, mature cartilage has a very limited capacity for self-repair, making damage cumulative over a lifetime.

In This Article

The End of Growth: The Fate of the Epiphyseal Plate

During childhood and adolescence, our long bones grow through a process called endochondral ossification. At the epiphyseal plates, or growth plates, chondrocytes (cartilage cells) multiply and enlarge. As they mature, they calcify the surrounding matrix and then die, leaving behind a scaffold that is invaded by blood vessels and bone-forming cells (osteoblasts). This repeated cycle is what allows our bones to lengthen.

However, this process is finite. As an individual reaches skeletal maturity, typically between the ages of 18 and 25, the rate of chondrocyte proliferation slows dramatically. Eventually, all the cartilage in the growth plate is replaced by bone, and the epiphysis and diaphysis fuse. The growth plate, now just a remnant, becomes the epiphyseal line. At this point, the mechanism for bone growth from a cartilage template ceases. Therefore, the question of what happens to older cartilage during bone growth is primarily a misnomer in the context of growth plate activity, as the process of growing bone has concluded.

Cartilage Beyond the Growth Plate

For the rest of our lives, the cartilage that remains in our joints, known as articular cartilage, has a very different fate. Articular cartilage serves to cushion and protect bones, allowing for smooth, frictionless movement. Unlike growth plate cartilage, it is not destined to be replaced by bone. Instead, it faces the challenges of aging, wear and tear, and a limited capacity for self-repair.

Cellular Senescence and the Aging Cartilage

One of the most significant changes affecting older cartilage is cellular senescence. This is a state where cells, including chondrocytes, stop dividing and lose their normal function. Senescent chondrocytes accumulate with age, leading to a cascade of negative effects within the joint.

  • Inflammatory Responses: Senescent chondrocytes secrete pro-inflammatory molecules, a phenomenon known as the senescence-associated secretory phenotype (SASP). This creates a low-grade, chronic inflammatory environment within the joint, which further promotes cartilage degradation.
  • Impaired Matrix Production: Healthy chondrocytes continuously produce and maintain the extracellular matrix (ECM) of cartilage, which is composed primarily of collagen and proteoglycans. Senescent chondrocytes lose their ability to effectively produce and repair the ECM, leading to a breakdown of the cartilage structure.
  • Reduced Self-Repair: The normal turnover and repair processes in cartilage are significantly diminished. The body's ability to replace damaged or worn-out cartilage is greatly reduced, making older joints more susceptible to long-term damage.

Calcification and Structural Changes

While not part of a deliberate bone growth process, the aging of articular cartilage can involve unwanted calcification. The cartilage matrix can begin to mineralize, becoming stiffer and less flexible. This calcification is one of the key hallmarks of osteoarthritis and can disrupt the normal joint environment. As the cartilage deteriorates, the underlying bone can also be affected, leading to bone remodeling, the formation of osteophytes (bone spurs), and increased pain.

Comparison of Young vs. Older Cartilage

To better understand the profound shift in cartilage's function and fate over a lifetime, consider the following comparison:

Feature Young, Growth Plate Cartilage Older, Articular Cartilage
Primary Function Template for bone lengthening Cushioning and joint lubrication
Cellular Activity Rapid proliferation and apoptosis Cellular senescence and reduced proliferation
Extracellular Matrix Rapidly synthesized and mineralized Slower synthesis, degraded by enzymes
Blood Supply Invaded by blood vessels Avascular, relying on diffusion for nutrients
End Result Replaced by new bone tissue Degeneration, calcification, and stiffening
Repair Capacity Excellent, part of the growth process Very limited; poor self-repair

The Health Implications of Aging Cartilage

The deterioration of older cartilage has significant health implications, particularly for seniors. The most well-known consequence is osteoarthritis (OA), a common and debilitating joint disease. In OA, the protective cartilage wears away, causing bone to rub directly on bone. The chronic inflammation and loss of cushioning lead to pain, stiffness, and reduced mobility.

Maintaining joint health is therefore a critical component of healthy aging. While we cannot reverse the aging process of our cartilage, we can take steps to slow its decline and manage its effects. This includes a combination of lifestyle choices and medical interventions.

Strategies for Healthy Joints as You Age

  • Stay Active: Low-impact exercises like swimming, cycling, and walking can help maintain joint mobility and strengthen the muscles that support the joints. Regular movement also promotes the circulation of synovial fluid, which nourishes cartilage.
  • Maintain a Healthy Weight: Excess body weight puts added stress on weight-bearing joints, such as the hips and knees. Maintaining a healthy weight can significantly reduce the load on your joints and slow cartilage wear.
  • Eat an Anti-Inflammatory Diet: Consuming foods rich in omega-3 fatty acids, antioxidants, and vitamins can help combat the chronic inflammation associated with aging cartilage. Examples include leafy greens, fatty fish, nuts, and berries.
  • Practice Good Posture and Biomechanics: Proper posture and movement patterns can minimize abnormal stress on joints. Correcting gait issues or using supportive footwear can make a difference.
  • Protect Your Joints: Avoid activities that place high, repetitive stress on your joints. Use protective gear during sports or when performing physically demanding tasks. Listen to your body and rest when needed.

Conclusion: A Shift from Growth to Maintenance

The fundamental shift in cartilage function from youth to old age is from active growth and replacement to passive maintenance and eventual decline. While the question of what happens to older cartilage during bone growth doesn't apply in the sense of skeletal lengthening, it's crucial to understand how age alters cartilage's cellular makeup and mechanical properties. A proactive approach to joint care, including sensible exercise, nutrition, and weight management, is the best strategy for promoting healthy aging and minimizing the impact of age-related cartilage changes. For more detailed information on cartilage aging and bone health, visit the National Center for Biotechnology Information.

Frequently Asked Questions

No, in healthy adults, cartilage at the joints does not typically turn into bone. The natural bone growth process, called endochondral ossification, concludes during skeletal maturation. Abnormal calcification can occur, but this is a sign of degeneration, not healthy growth.

Cellular senescence is a state in which chondrocytes (cartilage cells) stop dividing and lose their normal function with age. Senescent chondrocytes contribute to inflammation and the breakdown of the cartilage matrix, impairing the joint's health and function.

Aging cartilage becomes less resilient and more prone to degeneration. This loss of protective cushioning and increased stiffness can lead to pain, inflammation, and reduced range of motion, which are hallmark symptoms of osteoarthritis.

Currently, there is no way to fully reverse age-related cartilage damage. However, lifestyle changes like maintaining a healthy weight, regular low-impact exercise, and a healthy diet can help slow down the process and manage symptoms.

An epiphyseal plate is the site of bone lengthening in youth, where cartilage is actively replaced by bone. Articular cartilage is the permanent, flexible cartilage found at the ends of bones in joints, designed for cushioning and smooth movement.

Yes, moderate and low-impact exercise is crucial for maintaining healthy older cartilage. Movement helps circulate nutrient-rich synovial fluid within the joint, nourishing the cartilage and strengthening surrounding muscles to provide better joint support.

Inflammation, particularly the low-grade chronic inflammation caused by senescent cells, plays a significant role in older cartilage degeneration. It creates a hostile joint environment that promotes the breakdown of the cartilage matrix and accelerates damage.

References

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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.