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Related Experiment Video

Updated: Jun 23, 2026

Standardized Histomorphometric Evaluation of Osteoarthritis in a Surgical Mouse Model
07:32

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Published on: May 6, 2020

How aging causes osteoarthritis: An evolutionary physiology perspective.

David Gems1

  • 1Institute of Healthy Ageing, and Department of Genetics, Evolution and Environment, University College London, Gower Street, London, UK.

Osteoarthritis and Cartilage
|May 17, 2025
PubMed
Summary

The multifactorial model explains aging (senescence) as genetically programmed, non-adaptive mechanisms interacting with environmental factors. This model offers a new framework for understanding osteoarthritis (OA) etiology, focusing on futile developmental programs in cartilage.

Keywords:
Antagonistic pleiotropyChondrocyteEvolutionary medicineHyperfunctionOsteoarthritisProgrammatic theory

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Area of Science:

  • Evolutionary biology
  • Gerontology
  • Biomedical science

Background:

  • Late-life diseases, including osteoarthritis (OA), arise from senescence (aging), a process influenced by genetics.
  • The multifactorial model proposes that senescence results from evolved, non-adaptive genetic programs interacting with environmental disruptions.
  • Understanding the etiology of complex late-life diseases like OA requires exploring these underlying mechanisms.

Purpose of the Study:

  • To evaluate the utility of the multifactorial model in explaining osteoarthritis (OA) etiology.
  • To propose a cartilage-focused framework for understanding the development of OA.
  • To explore the evolutionary basis of OA, specifically the role of antagonistic pleiotropy.

Main Methods:

  • Conceptual analysis and theoretical exploration of the multifactorial model.
  • Application of the model to the complex disease of osteoarthritis (OA).
  • Development of a framework for OA etiology centered on cartilage biology.

Main Results:

  • The multifactorial model provides a useful framework for understanding OA etiology.
  • A core OA mechanism involves a futile program of endochondral ossification within articular cartilage chondrocytes.
  • Programmatic changes in chondrocytes, potentially driven by antagonistic pleiotropy, prime them for activation by secondary OA triggers like mechanical injury.

Conclusions:

  • The multifactorial model offers a comprehensive perspective on senescence and late-life diseases.
  • Osteoarthritis may stem from an evolved, non-adaptive developmental program in cartilage, exacerbated by environmental factors.
  • Antagonistic pleiotropy, favoring early-life benefits, may underlie the late-life costs observed in OA.