Cargando…

Plasma <em>RANKL</em> level is not a reliable marker to monitor the bone destruction in mice model of osteomyelitis

OBJECTIVES: In this experimental study, we aimed to investigate the specific value of receptor activator of nuclear factor kappa-Β ligand (RANKL) plasma level in osteomyelitis to show the bone destruction and to determine its correlation with classical markers of infection in mice model of osteomyel...

Descripción completa

Detalles Bibliográficos
Autor principal: Şen, Hüsamettin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Bayçınar Medical Publishing 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9057532/
https://www.ncbi.nlm.nih.gov/pubmed/35361095
http://dx.doi.org/10.52312/jdrs.2022.537
_version_ 1784697918302715904
author Şen, Hüsamettin
author_facet Şen, Hüsamettin
author_sort Şen, Hüsamettin
collection PubMed
description OBJECTIVES: In this experimental study, we aimed to investigate the specific value of receptor activator of nuclear factor kappa-Β ligand (RANKL) plasma level in osteomyelitis to show the bone destruction and to determine its correlation with classical markers of infection in mice model of osteomyelitis. MATERIALS AND METHODS: Sixty Balb/c female mice (30 to 40 g weight, 3.5 to 4 month-old) were divided into two groups: Controls (n=15) and study group (n=45). All mice underwent tibial decortication and received an injection of sclerosing agent into the intramedullary cavity. The next process was proceeded in two steps to observe the detectability of osteomyelitis-induced bone destruction (step 1) and treatment response (step 2) using the variables examined in our study. In step 1, the study group received 1 mL solution containing Staphylococcus aureus (S. aureus) bacteria (2X108 per mL) into the intramedullary cavity. Five mice from each group were sacrificed every seven days for three weeks and tibia and blood samples were obtained. In step 2, the remaining 30 infected mice were further divided into two groups to investigate the possible value of RANKL plasma level as a marker of treatment response. Fifteen of these mice received teicoplanin 20 mg/kg for four weeks, while the rest did not receive antibiotics. Eight mice from each group were sacrificed at the end of the second week and the remaining 14 mice were sacrificed at the end of four weeks. Complete blood count, procalcitonin level, C-reactive protein (CRP), and RANKL concentrations were measured from blood samples of each sacrificed mouse. RESULTS: Median RANKL concentration of the control subjects was significantly higher than recipients of intervention at the first and third weeks in step 1 where bone destruction of osteomyelitis was examined. No significant changes occurred in groups receiving and not receiving antimicrobial treatment in terms of RANKL, CRP, and procalcitonin levels throughout four weeks in step 2. The RANKL concentration was significantly correlated with colony growth in subjects allocated to the S. aureus inoculation group (r=-0.547, p=0.035). CONCLUSION: The RANKL levels in mice with S. aureus osteomyelitis are not correlated with colony growth or other markers of inflammation and not useful for monitoring the response to antimicrobial treatment during osteomyelitis.
format Online
Article
Text
id pubmed-9057532
institution National Center for Biotechnology Information
language English
publishDate 2022
publisher Bayçınar Medical Publishing
record_format MEDLINE/PubMed
spelling pubmed-90575322022-05-04 Plasma <em>RANKL</em> level is not a reliable marker to monitor the bone destruction in mice model of osteomyelitis Şen, Hüsamettin Jt Dis Relat Surg Original Article OBJECTIVES: In this experimental study, we aimed to investigate the specific value of receptor activator of nuclear factor kappa-Β ligand (RANKL) plasma level in osteomyelitis to show the bone destruction and to determine its correlation with classical markers of infection in mice model of osteomyelitis. MATERIALS AND METHODS: Sixty Balb/c female mice (30 to 40 g weight, 3.5 to 4 month-old) were divided into two groups: Controls (n=15) and study group (n=45). All mice underwent tibial decortication and received an injection of sclerosing agent into the intramedullary cavity. The next process was proceeded in two steps to observe the detectability of osteomyelitis-induced bone destruction (step 1) and treatment response (step 2) using the variables examined in our study. In step 1, the study group received 1 mL solution containing Staphylococcus aureus (S. aureus) bacteria (2X108 per mL) into the intramedullary cavity. Five mice from each group were sacrificed every seven days for three weeks and tibia and blood samples were obtained. In step 2, the remaining 30 infected mice were further divided into two groups to investigate the possible value of RANKL plasma level as a marker of treatment response. Fifteen of these mice received teicoplanin 20 mg/kg for four weeks, while the rest did not receive antibiotics. Eight mice from each group were sacrificed at the end of the second week and the remaining 14 mice were sacrificed at the end of four weeks. Complete blood count, procalcitonin level, C-reactive protein (CRP), and RANKL concentrations were measured from blood samples of each sacrificed mouse. RESULTS: Median RANKL concentration of the control subjects was significantly higher than recipients of intervention at the first and third weeks in step 1 where bone destruction of osteomyelitis was examined. No significant changes occurred in groups receiving and not receiving antimicrobial treatment in terms of RANKL, CRP, and procalcitonin levels throughout four weeks in step 2. The RANKL concentration was significantly correlated with colony growth in subjects allocated to the S. aureus inoculation group (r=-0.547, p=0.035). CONCLUSION: The RANKL levels in mice with S. aureus osteomyelitis are not correlated with colony growth or other markers of inflammation and not useful for monitoring the response to antimicrobial treatment during osteomyelitis. Bayçınar Medical Publishing 2022-03-28 /pmc/articles/PMC9057532/ /pubmed/35361095 http://dx.doi.org/10.52312/jdrs.2022.537 Text en Copyright © 2021, Turkish Joint Diseases Foundation https://creativecommons.org/licenses/by-nc/4.0/This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
spellingShingle Original Article
Şen, Hüsamettin
Plasma <em>RANKL</em> level is not a reliable marker to monitor the bone destruction in mice model of osteomyelitis
title Plasma <em>RANKL</em> level is not a reliable marker to monitor the bone destruction in mice model of osteomyelitis
title_full Plasma <em>RANKL</em> level is not a reliable marker to monitor the bone destruction in mice model of osteomyelitis
title_fullStr Plasma <em>RANKL</em> level is not a reliable marker to monitor the bone destruction in mice model of osteomyelitis
title_full_unstemmed Plasma <em>RANKL</em> level is not a reliable marker to monitor the bone destruction in mice model of osteomyelitis
title_short Plasma <em>RANKL</em> level is not a reliable marker to monitor the bone destruction in mice model of osteomyelitis
title_sort plasma <em>rankl</em> level is not a reliable marker to monitor the bone destruction in mice model of osteomyelitis
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9057532/
https://www.ncbi.nlm.nih.gov/pubmed/35361095
http://dx.doi.org/10.52312/jdrs.2022.537
work_keys_str_mv AT senhusamettin plasmaemranklemlevelisnotareliablemarkertomonitorthebonedestructioninmicemodelofosteomyelitis