Related Experiment Video

Updated: Jun 27, 2025

Evaluation of Injury-induced Senescence and In Vivo Reprogramming in the Skeletal Muscle
09:14

Evaluation of Injury-induced Senescence and In Vivo Reprogramming in the Skeletal Muscle

Published on: October 26, 2017

9.6K

Senolytics ameliorate the failure of bone regeneration through the cell senescence-related inflammatory signalling

Xinchen Wang1, Yue Zhou2, Chuyi Luo3

  • 1Hospital of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Guanghua School of Stomatology, Institute of Stomatological Research, Sun Yat-sen University, Guangzhou, Guangdong, China; Department of Orthodontics, Osaka Dental University, 8-1 Kuzuhahanazonocho, Hirakata, Osaka 573-1121, Japan.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|April 26, 2024
PubMed

Insights

Dasatinib and quercetin senolytics (DQ) enhance bone formation by clearing senescent cells in contaminated bone implants. This study shows DQ reduces inflammation and improves bone regeneration, offering therapeutic potential for bone defects.

Area of Science:

  • Biomaterials Science
  • Regenerative Medicine
  • Cellular Biology

Background:

  • Stress-induced premature senescent (SIPS) cells impair tissue function.
  • Senolytics, like dasatinib and quercetin (DQ), eliminate senescent cells.
  • Bone infection hinders bone regeneration, particularly with implants like α-tricalcium phosphate (α-TCP).

Purpose of the Study:

  • To investigate if DQ administration ameliorates impairments in bone repair caused by inflammation and contamination via SIPS cell elimination.
  • To explore DQ's mechanisms in improving bone formation in Lipopolysaccharide (LPS)-contaminated implants within maxillofacial bone defects.

Main Methods:

  • Implantation of α-TCP and LPS-contaminated α-TCP into rat calvaria bone defects.
  • Oral administration of DQ with assessment of bone formation using micro-computed tomography and histology.
  • Analysis of senescent cell markers (p21, p16), inflammation, macrophages, reactive oxygen species, and tartrate-resistant acid phosphatase.

Main Results:

  • DQ administration significantly enhanced bone formation at the defect site.
  • DQ treatment reduced senescent cell markers, inflammation, macrophage infiltration, reactive oxygen species, and osteoclast activity.
  • In vitro, DQ partially alleviated senescence markers and senescence-associated secretory phenotypes.

Conclusions:

  • LPS-contaminated α-TCP biomaterials induce cellular senescence and impede bone regeneration.
  • Senolytics (DQ) demonstrate significant therapeutic potential in mitigating infection-related adverse effects on bone formation.
  • DQ improves bone regeneration capacity in contaminated bone defect models.
Keywords:
BiomaterialBone formationBone infectionDasatinib and quercetinSenescenceSenolytics

More Related Videos

SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs07:39

SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs

Published on: June 28, 2019

23.9K
Improved Methodology for Studying Postnatal Osteogenesis via Intramembranous Ossification in a Murine Bone Marrow Injury Model05:10

Improved Methodology for Studying Postnatal Osteogenesis via Intramembranous Ossification in a Murine Bone Marrow Injury Model

Published on: February 7, 2025

334

Related Concept Videos

Bone Remodeling01:40

Bone Remodeling

Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
38.3K
Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
2.9K