The Association Between Obesity and Knee Osteoarthritis: A Review of Mechanical and Metabolic Mechanisms

Abstract

Introduction: Knee osteoarthritis (OA) is the most common form of arthritis and a primary cause of chronic disability. Obesity is recognized as the most significant modifiable risk factor for knee OA, a link historically explained by increased mechanical load on the joint.

Literature Review: A review of the pivotal scientific literature confirms that while mechanical overload is a major factor, the pathogenesis is more complex. Evidence has established that obesity also promotes knee OA through systemic metabolic and inflammatory pathways. Epidemiological studies showing an association between obesity and OA in non-weight-bearing joints provided the first clue for a systemic link. Subsequent research characterized adipose tissue as an active endocrine organ that secretes signaling molecules called adipokines. Pro-inflammatory adipokines, particularly leptin, were found in elevated levels in obese individuals and were shown to directly exert catabolic, cartilage-degrading effects within the joint. Furthermore, the chronic, low-grade systemic inflammation that characterizes obesity is now understood to contribute to local synovial inflammation, further accelerating the degenerative process.

Conclusion: The body of evidence reviewed has reshaped the understanding of the relationship between obesity and knee osteoarthritis. It confirms that obesity acts via a dual-pathway, promoting joint degeneration through both excessive mechanical stress and adverse metabolic and inflammatory signaling. This reframes OA as a disease with a major metabolic component.