TitleLeptin Increases Particle-Induced Osteolysis in Female ob/ob Mice.
Publication TypeJournal Article
Year of Publication2018
AuthorsPhilbrick, KA, Branscum, AJ, Wong, CP, Turner, RT, Iwaniec, UT
JournalSci Rep
Volume8
Issue1
Pagination14790
Date Published2018 Oct 04
ISSN2045-2322
Abstract
 

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 μg/d), or (4) particles + intermittent leptin (daily injection, 40 μg/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.

DOI10.1038/s41598-018-33173-9
Alternate JournalSci Rep
PubMed ID30287858
PubMed Central IDPMC6172200
Grant ListR03 AR054609 / AR / NIAMS NIH HHS / United States
AR 054609 / / U.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) /