Obesity and its chronic inflammation as pain potentiation factor in rats with osteoarthritis

Obesity produces the accumulation of adipose tissue and a chronic inflammatory process, while osteoarthritis (OA) is also an inflammatory disorder.

to evaluate whether obesity associated to OA may be a factor that increases inflammation and pain.

Male animals (M) were divided into groups: control (CM), OA-induced pain (MP), obese (OM) and obese with OA-induced pain (OMP). Similarly, females (F) were divided into groups: control (CF), OA-induced pain (FP), obese (OF) and obese with OA-induced pain (OFP). All the groups except for control and obese groups were submitted to OA induction by sodium monoiodoacetate injection and monitored until day 65. Their adiposity index, thermal, mechanical and spontaneous pain nociceptive profile were investigated. At the end of the experiment (t = 65 days) hematological parameters, biochemical parameters, andcytokines were assessed.

Rats with obesity induction showed alterations in mechanical and thermal nociceptive profile, and increase in systemic inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-8 and leptin) with reduction in anti-inflammatory cytokines (adiponectin and IL-10). These profile changes were investigated by principal component analysis (PCA), in which the first two principal components explained near 90% of the data variability. Obesity, when present together with OA in OMP and OFP groups, yielded the highest levels of inflammatory cytokines and pain scores and the lowest levels on anti-inflamatory cytokines.

Obesity modified the nociceptive profile when inflammatory process is produced. When obesity occurs concomitantly with OA, inflammatory progression is intensified, yelding increase in pain scores.