Tmem100- and Acta2-Lineage Cells Contribute to Implant Osseointegration in a Mouse Model.


Journal

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
ISSN: 1523-4681
Titre abrégé: J Bone Miner Res
Pays: United States
ID NLM: 8610640

Informations de publication

Date de publication:
05 2021
Historique:
revised: 18 01 2021
received: 26 06 2020
accepted: 26 01 2021
pubmed: 3 2 2021
medline: 10 8 2021
entrez: 2 2 2021
Statut: ppublish

Résumé

Metal implants are commonly used in orthopedic surgery. The mechanical stability and longevity of implants depend on adequate bone deposition along the implant surface. The cellular and molecular mechanisms underlying peri-implant bone formation (ie, osseointegration) are incompletely understood. Herein, our goal was to determine the specific bone marrow stromal cell populations that contribute to bone formation around metal implants. To do this, we utilized a mouse tibial implant model that is clinically representative of human joint replacement procedures. Using a lineage-tracing approach, we found that both Acta2.creERT2 and Tmem100.creERT2 lineage cells are involved in peri-implant bone formation, and Pdgfra- and Ly6a/Sca1-expressing stromal cells (PαS cells) are highly enriched in both lineages. Single-cell RNA-seq analysis indicated that PαS cells are quiescent in uninjured bone tissue; however, they express markers of proliferation and osteogenic differentiation shortly after implantation surgery. Our findings indicate that PαS cells are mobilized to repair bone tissue and participate in implant osseointegration after surgery. Biologic therapies targeting PαS cells might improve osseointegration in patients undergoing orthopedic procedures. © 2021 American Society for Bone and Mineral Research (ASBMR).

Identifiants

pubmed: 33528844
doi: 10.1002/jbmr.4264
pmc: PMC8715516
mid: NIHMS1766296
doi:

Substances chimiques

ACTA2 protein, human 0
Actins 0
Membrane Proteins 0
TMEM100 protein, human 0
Tmem100 protein, mouse 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1000-1011

Subventions

Organisme : NIAID NIH HHS
ID : R01 AI044938
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR055607
Pays : United States
Organisme : NIDCR NIH HHS
ID : R01 DE019420
Pays : United States

Informations de copyright

© 2021 American Society for Bone and Mineral Research (ASBMR).

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Auteurs

Alexander Vesprey (A)

Hospital for Special Surgery, New York, NY, USA.

Eun Sung Suh (ES)

Hospital for Special Surgery, New York, NY, USA.

Didem Göz Aytürk (D)

Hospital for Special Surgery, New York, NY, USA.

Xu Yang (X)

Hospital for Special Surgery, New York, NY, USA.

Miracle Rogers (M)

Hospital for Special Surgery, New York, NY, USA.

Branden Sosa (B)

Hospital for Special Surgery, New York, NY, USA.

Yingzhen Niu (Y)

Hospital for Special Surgery, New York, NY, USA.
Department of Joint Surgery, Hebei Medical University Third Affiliated Hospital, Shijiazhuang, China.

Ivo Kalajzic (I)

Department of Genetics and Genome Sciences, University of Connecticut, Farmington, CT, USA.

Lionel B Ivashkiv (LB)

Hospital for Special Surgery, New York, NY, USA.
Departments of Medicine and Immunology, Weill Cornell Medical College, New York, NY, USA.

Mathias Pg Bostrom (MP)

Hospital for Special Surgery, New York, NY, USA.
Department of Orthopaedic Surgery, Weill Cornell Medical College, New York, NY, USA.

Ugur M Ayturk (UM)

Hospital for Special Surgery, New York, NY, USA.
Department of Orthopaedic Surgery, Weill Cornell Medical College, New York, NY, USA.

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Classifications MeSH