admin Age and Dupuytren’s: Why the Disease Gets More Common Over Time
Introduction
Age is one of the strongest predictors of Dupuytren’s contracture, often determining not only who develops the condition but also how quickly it progresses. While genetics, lifestyle, and environmental factors help set the foundation, the biological changes that occur as we get older create the perfect environment for fibrosis to take hold. Over time, the body’s repair systems become less efficient, cells accumulate oxidative damage, and connective tissues lose their natural elasticity. These shifts make the hands — especially the fascia of the palm — more vulnerable to the excessive collagen buildup that defines Dupuytren’s disease.
How Aging Affects Connective Tissue
As we age, the connective tissues throughout the body undergo predictable structural and biochemical changes. Fibroblasts — the cells responsible for producing and repairing collagen — begin to behave differently. Instead of maintaining a balanced cycle of collagen creation and breakdown, older fibroblasts tend to become less accurate in repair while simultaneously accelerating scar-like tissue production. This imbalance means that more collagen is laid down than is necessary, and much of it becomes excessively cross-linked. These cross-links act like tiny molecular “glue” bonds that stiffen the tissue.
In addition, aging reduces microcirculation. Blood vessels gradually narrow and stiffen, decreasing the amount of oxygen and nutrients delivered to tissues. Reduced blood flow slows natural healing processes and increases the chance of abnormal fibrosis. Over time, these changes collectively make the palmar fascia more prone to thickening, shortening, and forming nodules — the hallmarks of Dupuytren’s.
Cell Senescence and Fibrosis
Senescence is another crucial component of age-related fibrosis. Senescent cells are those that have stopped dividing but stubbornly refuse to die. Instead of remaining inert, they emit a cocktail of inflammatory molecules known as SASP (senescence-associated secretory phenotype). These molecules signal nearby fibroblasts to increase collagen production.
With decades of cumulative exposure to inflammation and oxidative stress, these senescent cells accumulate in tissues like the palm. Their chronic signaling gradually changes the tissue environment, making it more fibrotic and less capable of normal repair. This same mechanism plays a role in other age-related fibrotic conditions, including frozen shoulder, plantar fibromatosis, and even liver or lung fibrosis.
Research Findings
Modern research supports the link between aging, oxidative stress, and Dupuytren’s contracture. A study published in Aging Cell found that Dupuytren’s tissue in older adults shows significantly higher levels of oxidative damage and dysfunctional mitochondria — the cell’s energy factories. Mitochondrial dysfunction leads to inefficient energy production, which slows healing and disrupts normal collagen regulation. The same study also found elevated levels of senescence-associated proteins, reinforcing the role of aging biology in disease progression. These findings help explain why Dupuytren’s often advances more rapidly in older patients and why recurrence after treatment is common, even after successful surgery or enzyme injections.
Lifestyle Influences
While aging is unavoidable, certain lifestyle choices can help slow the fibrotic process and support healthier connective tissue:
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Eat antioxidant-rich foods such as berries, leafy greens, turmeric, nuts, and omega-3 fats. These help neutralize oxidative stress and support cellular repair.
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Stay physically active to stimulate blood flow, support collagen turnover, and maintain tissue flexibility.
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Avoid smoking and limit alcohol, both of which significantly increase oxidative stress and accelerate age-related tissue changes.
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Prioritize sleep and manage stress, as restorative sleep and lower cortisol levels enhance the body’s ability to repair and regulate inflammation.
These changes do not cure Dupuytren’s, but they may slow its progression and improve overall tissue health.
Emerging Therapies
Scientists are exploring advanced strategies to address the root causes of age-driven fibrosis. “Senolytic” therapies aim to selectively remove senescent cells, reducing the inflammatory signals that promote collagen overproduction. Other experimental treatments focus on restoring healthy mitochondrial function to improve cellular energy and reduce oxidative damage. While still in early research stages, these therapies offer promising avenues that may one day improve long-term outcomes for older Dupuytren’s patients.
Conclusion
Aging itself does not cause Dupuytren’s contracture, but it amplifies the biological processes underlying fibrosis. Declining cellular repair, oxidative stress, senescence, and reduced circulation all make connective tissues more vulnerable over time. By protecting cellular health through diet, lifestyle, and emerging technologies, it’s possible to support stronger, more flexible hands — and potentially slow Dupuytren’s progression — as the years go by.
Legal & Medical Disclaimer
This content is for informational purposes only and not a substitute for professional medical advice, diagnosis, or treatment. Always consult your healthcare provider. Dupuytren’s Solutions is an educational resource to support —not replace— professional care. Individual results may vary.
Call to Action
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Attribution
(CC BY 4.0) Adapted from Kirk T et al. Aging and Fibrosis in Dupuytren’s Contracture. Aging Cell. 2021; 20(4): e13312. Licensed under Creative Commons Attribution 4.0. Source.
