title: Local delivery of alendronate eluting chitosan scaffold can effectively increase osteoblast functions and inhibit osteoclast differentiation.
abstract: The aim of this study was to investigate the effect of alendronate released from chitosan scaffolds on enhancement of osteoblast functions and inhibition of osteoclast differentiation in vitro. The surface and cell morphologies of chitosan scaffolds and alendronate-loaded chitosan scaffolds were characterized by variable pressure field emission scanning electron microscope (VP-FE-SEM). Alendronate was released in a sustained manner. For evaluating osteoblast functions in MG-63 cells, we investigated cell proliferation, alkaline phosphatase (ALP) activity, and calcium deposition. Furthermore, for evaluating inhibition of osteoclast differentiation in RAW 264.7 cells, we investigated tartrate-resistant acid phosphatase (TRAP) activity, TRAP staining, and gene expressions. The in vitro studies revealed that osteoblasts grown on alendronate-loaded chitosan scaffold showed a significant increment in cell proliferation, ALP activity, and calcium deposition as compared to those grown on chitosan scaffolds. In addition, the in vitro study showed that osteoclast differentiation in RAW 264.7 cells cultured on alendronate-loaded chitosan scaffolds was greatly inhibited as compared to those cultured on chitosan scaffolds by the results of TRAP activity, TRAP staining, and gene expressions. Taken together, alendronate-loaded chitosan scaffolds could achieve the dual functions of improvement in osteoblast functions and inhibition of osteoclast differentiation. Thus, alendronate-eluting chitosan substrates are promising materials for enhancing osteoblast functions and inhibiting osteoclast differentiation in orthopedic and dental fields.
authors.affiliation: Department of Orthopedic Surgery and Rare Diseases Institute, Korea University Medical College, Guro Hospital, Seoul, Korea.
authors.forename: Sung Eun
authors.initials: SE
authors.lastname: Kim
authors.forename: Dong Hun
authors.initials: DH
authors.lastname: Suh
authors.forename: Young-Pil
authors.initials: YP
authors.lastname: Yun
authors.forename: Jae Yong
authors.initials: JY
authors.lastname: Lee
authors.forename: Kyeongsoon
authors.initials: K
authors.lastname: Park
authors.forename: Jun-Young
authors.initials: JY
authors.lastname: Chung
authors.forename: Deok-Won
authors.initials: DW
authors.lastname: Lee
mesh_terms: D000135:Acid Phosphatase / Q000235:genetics / Q000378:metabolism; D019386:Alendronate / Q000008:administration & dosage* / Q000494:pharmacology; D000818:Animals; D001483:Base Sequence; D050071:Bone Density Conservation Agents / Q000008:administration & dosage* / Q000494:pharmacology; D002454:Cell Differentiation / Q000187:drug effects*; D002460:Cell Line; D048271:Chitosan / Q000737:chemistry*; D017931:DNA Primers; D004337:Drug Carriers; D007527:Isoenzymes / Q000235:genetics / Q000378:metabolism; D051379:Mice; D008855:Microscopy, Electron, Scanning; D050778:NFATC Transcription Factors / Q000235:genetics; D010006:Osteoblasts / Q000166:cytology / Q000187:drug effects* / Q000201:enzymology; D010010:Osteoclasts / Q000166:cytology / Q000187:drug effects* / Q000201:enzymology; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D000071681:Tartrate-Resistant Acid Phosphatase
chemical_list: D050071:Bone Density Conservation Agents; D017931:DNA Primers; D004337:Drug Carriers; D007527:Isoenzymes; D050778:NFATC Transcription Factors; C494005:Nfatc1 protein, mouse; D012333:RNA, Messenger; D048271:Chitosan; D000135:Acid Phosphatase; C000605511:Acp5 protein, mouse; D000071681:Tartrate-Resistant Acid Phosphatase; D019386:Alendronate