Metabolic activity of osteoarthritic knees correlates with BMIAvery L. Buchholz; Matthew C. Niesen; Elizabeth B. Gausden; David G. Sterken; Scott J. Hetzel; Samuel Z. Baum; Matthew W. Squire; Lee D. Kaplan
Osteoarthritis of the knee has consistently been linked to obesity, defined as a body mass index (BMI) > 30 kg/m 2. It has been hypothesized that obesity may lead to osteoarthritis through increased joint pressure, accumulated microtrauma, and disruption of normal chondrocyte metabolism. These changes in chondrocyte metabolism have not been thoroughly investigated, and it is the purpose of this study to identify a relationship between BMI and altered chondrocyte metabolism in osteoarthritic tissue. Articular cartilage was harvested from the femoral condyles of patients after total knee arthroplasty, and analyzed in explant and alginate models. Glycosaminoglycan (GAG) content was measured using a dimethylmethylene blue assay and normalized to DNA content using a PicoGreen® assay. Studies have reported GAGs to be a reliable measurement of chondrocyte metabolism and osteoarthritis progression. Our results show a significant linear relationship of increasing BMI and increasing GAG content in both alginate and explant models ( p < 0.001 and p = 0.001). Obese (BMI ≥ 30 kg/m 2) and non-obese (BMI < 30 kg/m 2) comparisons also demonstrated significant differences with higher GAG/DNA content in obese individuals compared to non-obese ( p = 0.001 and p = 0.015). The study results reveal significant relationships between GAG content and BMI in this population of osteoarthritic patients. The significant difference in GAG content between the obese and non-obese patients supports the connection between osteoarthritis and obesity previously reported. Higher patient BMI (> 30 kg/m 2) may be similar to dynamic compression injuries which cause increased GAG synthesis in response to cartilage damage.