First Author | Philbrick KA | Year | 2018 |
Journal | Sci Rep | Volume | 8 |
Issue | 1 | Pages | 14790 |
PubMed ID | 30287858 | Mgi Jnum | J:295600 |
Mgi Id | MGI:6454100 | Doi | 10.1038/s41598-018-33173-9 |
Citation | Philbrick KA, et al. (2018) Leptin Increases Particle-Induced Osteolysis in Female ob/ob Mice. Sci Rep 8(1):14790 |
abstractText | Particles generated from wear of prosthesis joint bearing surfaces induce inflammation-mediated periprosthetic bone resorption (osteolysis). Morbidly obese leptin-deficient ob/ob mice are resistant to polyethylene particle-induced bone loss, suggesting that leptin, a hormone produced by adipocytes that circulates in concentrations proportional to total body adiposity, increases osteolysis. To confirm that particles induce less osteolysis in leptin-deficient mice after controlling for cold stress (room temperature)-induced bone loss, ob/ob mice on a C57BL/6 (B6) background and colony B6 wildtype (WT) mice housed at thermoneutral temperature were randomized to control or particle treatment groups (N = 5/group). Polyethylene particles were implanted over calvaria and mice sacrificed 2 weeks later. Compared to particle-treated WT mice, particle-treated ob/ob mice had lower osteolysis score, less infiltration of immune cells, and less woven bone formation. To determine the role of leptin in particle-induced osteolysis, ob/ob mice were randomized into one of 4 groups (n = 6-8/group): (1) control, (2) particles, (3) particles + continuous leptin (osmotic pump, 6 mug/d), or (4) particles + intermittent leptin (daily injection, 40 mug/d). Leptin treatment increased particle-induced osteolysis in ob/ob mice, providing evidence that the adpiokine may play a role in inflammation-driven bone loss. Additional research is required to determine whether altering leptin levels within the physiological range results in corresponding changes in polyethylene-particle-induced osteolysis. |