Adiposity and Osteoarthritis

           

Special thanks to DPT students Kelly Gabbett, Sarah Glazewski, Mark Abrams, Victoria Bensinger (Widener University Class of 2024)

          We all know that carrying excessive weight has a negative impact on our joints but the magnitude of that impact goes beyond the compression forces.  When an individual is overweight or obese, the weight bearing joints experience excessive loads during functional activities and can result in joint stresses and pain. It makes sense that weight loss can help decrease these factors but did you know the loss of one kilogram of body weight has been shown to reduce the force on the knee by as much as four-fold?

          Yet the impact of carrying excessive weight also has a plethora of physiologic effects.  Adipose tissue releases a wide variety of bioactive peptides, some of which are molecules related to the immune system and inflammatory mediators. These chemicals are referred to as either “adipokines” or “adipocytokines.”  They include Leptin, Adiponectin, and many more. Their purposes include vascular homeostasis, metabolism, and immunity.  They apply strong modulatory effects onto cartilage, bone, synovium, and immune cells. Much like everything else in the human body, adipokines must be maintained within a given homeostatic range.

          However, adipocyte size is directly related to the dysregulation of the production of adipokines. The hypertrophy of adipocytes in overweight and obese individuals results in an increase of the proinflammatory mediators released by adipocytes. Therefore, a patient with larger adipocytes will experiences a greater number of inflammatory symptoms.

          Leptin is a hormone your adipose tissue (body fat) releases that helps  maintain your normal weight. It does this by regulating hunger by providing the sensation of feeling full (satiety).  The level of leptin in your blood is directly related to your amount of body fat.  However, Leptin resistance causes you to feel hungry and eat more even though your body has enough fat stores. Studies have shown that Leptin prevents several physiologic processes that results in an increase of proinflammatory cytokines. This produces a cascade of events stimulating chondrocyte apoptosis, one of the pathogenic factors of osteoarthritis (OA).   Leptin also directly targets osteoblasts. It has been found that subchondral osteoblasts in OA patients produce twice the amount of Leptin than cells of a non-OA effected joint. Although BMI (body mass index) does not represent the composition of the body, studies have demonstrated that the Leptin levels in the blood serum and plasma levels in knee OA patients were positively correlated with BMI.  3D-MRI studies have also shown that Leptin levels are positively correlated with cartilage loss. Therefore, the higher an individual’s body fat percentage, the greater amount of Leptin their body produces and thus the greater the amount of cartilage degeneration an individual may experience within their joints.

          Adiponectin is a fat-derived hormone that appears to play a crucial role in protecting against insulin resistance/diabetes and atherosclerosis.  Decreased adiponectin levels are thought to play a central role in the development of type 2 diabetes, obesity and cardiovascular disease in humans.  Higher body fat percentages are also correlated with low levels of Adiponectin.  Since adiponectin has been found to have anti-inflammatory properties, the lower Adiponectin levels caused by one’s increased body fat ultimately results in increased inflammatory activity and thus potentially increased tissue destruction.

          Thus, prevention of osteoarthritis is multi-factorial.  Exercise can do more than increase muscle strength.  The reduction in body fat can significantly alter the cascade of physiologic events to restore homeostasis.

 

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If you would like to learn more about the Mobil–Aider Arthrometer to quantify joint mobility, please visit:  https://mobil-aider.com/

 

References

• Achari AE, Jain SK, Adiponectin, a therapeutic target for obesity, diabetes, & endothelial dysfunction. International Journal of Molecular Science. 2017 June;18(6):1321
• Azamar-Llamas D, Hernández-Molina G, Ramos-Ávalos B, Furuzawa-Carballeda J. Adipokine Contribution to the Pathogenesis of Osteoarthritis. Mediators Inflamm. 2017;2017:5468023. doi:10.1155/2017/5468023
• Cleveland Clinic https://my.clevelandclinic.org/health/articles/22446-leptin  Accessed May 29, 2022
• Georgiev T, Angelov AK. Modifiable risk factors in knee osteoarthritis: treatment implications. Rheumatol Int. 2019; 39:1145–1157. https://doi.org/10.1007/s00296-019-04290-z
• Rai MF, Patra D. Pathobiology of Osteoarthritis. Pathobiology of Human Disease, 2014.