Immobilization of Denosumab on Titanium Affects Osteoclastogenesis of Human Peripheral Blood Monocytes.
Cell Differentiation
/ drug effects
Denosumab
/ pharmacology
Humans
Macrophage Colony-Stimulating Factor
/ pharmacology
Male
Monocytes
/ cytology
Nanoparticles
/ chemistry
Osteogenesis
/ drug effects
RANK Ligand
/ pharmacology
Solubility
Tartrate-Resistant Acid Phosphatase
/ metabolism
Titanium
/ pharmacology
denosumab
implant
nanofunctionalization
osteoclast
titanium
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
26 Feb 2019
26 Feb 2019
Historique:
received:
21
12
2018
revised:
01
02
2019
accepted:
21
02
2019
entrez:
1
3
2019
pubmed:
1
3
2019
medline:
19
6
2019
Statut:
epublish
Résumé
Immobilization of proteins has been examined to improve implant surfaces. In this study, titanium surfaces were modified with nanofunctionalized denosumab (cDMAB), a human monoclonal anti-RANKL IgG. Noncoding DNA oligonucleotides (ODN) served as linker molecules between titanium and DMAB. Binding and release experiments demonstrated a high binding capacity of cDMAB and continuous release. Human peripheral mononuclear blood cells (PBMCs) were cultured in the presence of RANKL/MCSF for 28 days and differentiated into osteoclasts. Adding soluble DMAB to the medium inhibited osteoclast differentiation. On nanofunctionalized titanium specimens, the osteoclast-specific TRAP5b protein was monitored and showed a significantly decreased amount on cDMAB-titanium in PBMCs + RANKL/MCSF. PBMCs on cDMAB-titanium also changed SEM cell morphology. In conclusion, the results indicate that cDMAB reduces osteoclast formation and has the potential to reduce osteoclastogenesis on titanium surfaces.
Identifiants
pubmed: 30813507
pii: ijms20051002
doi: 10.3390/ijms20051002
pmc: PMC6429431
pii:
doi:
Substances chimiques
RANK Ligand
0
Denosumab
4EQZ6YO2HI
Macrophage Colony-Stimulating Factor
81627-83-0
Titanium
D1JT611TNE
Tartrate-Resistant Acid Phosphatase
EC 3.1.3.2
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Deutsche Forschungsgemeinschaft
ID : MA 5158/1-1
Organisme : Promotionsstudium LMU
ID : No
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