The role of NPY in obesity-induced bone loss

Abstract

p = 0.0352). Concentrations of NPY in advanced stage group of KOA patients has no significant difference compare with middle stage group of KOA patients (p= 0. 2175). Concentrations of HA in middle and advanced stage groups of KOA patients were significantly lower than early stage group of KOA patients (early stage 217.2 ± 35.4 μg/L, middle stage 163.6 ± 31.1 μg/L, advanced stage 111.1 ± 43.8 μg/L) (p= 0.0300, p = 0.0719). Concentrations of HA in advanced stage group of KOA patients has significant difference compared with middle stage group of KOA patients (p= 0. 4009). According to Hideo Watanabe's pain score, 100KOApatientsweredivided into5 subgroups: no pain (n= 12), mild pain (n= 25), moderate pain (n= 37), strong pain (n= 19) and severe pain (n= 7). Within the KOA group, significantly higher concentrations of NPYwere found in each subgroup as pain intensified (no pain 81.4 ± 11.7 pg/mL, mild pain 99.1 ± 23.2 pg/mL, moderate pain 119.9 ± 31.5 pg/mL, strong pain 171.2 ± 37.3 pg/mL and severe pain 197.3 ± 41.9 pg/mL). Meanwhile, within the KOA group, significantly lower concentrations of HA also were found in each subgroup as pain intensified (no pain 235.5 ± 58.3 μg/L, mild pain 173.8 ± 38.1 μg/L, moderate pain 147.6 ± 37.2 μg/L, strong pain 121.4 ± 46.6 μg/L and severe pain 97.8 ± 50.8 μg/L). Conclusions: This study demonstrated the presence and variation of concentrations of NPY and HA in the KOA joint fluid, suggesting a role for NPY and HA as a putative regulator of structural severity of KOA and KOA pain.