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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...
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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.
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Related Experiment Video

Updated: Feb 28, 2026

Isolation of Monocyte-Macrophage Lineage Cells from Rat Bones by Secondary Adherence Method
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Isolation of Monocyte-Macrophage Lineage Cells from Rat Bones by Secondary Adherence Method

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Lactate-Driven Reprogramming of Monocyte Bridges Bone Loss in Inflammatory Comorbidities.

Junbin Wei1, Zhiqian Ye1, Deqian Tang2

  • 1Hospital of Stomatology, Guanghua School of Stomatology, South China Center of Craniofacial Stem Cell Research, Guangdong Provincial Key Laboratory of Stomatology, Sun Yat-sen University, Guangzhou 510055, China.

Biomolecules
|February 27, 2026
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Summary

Elevated blood lactate links inflammation and bone loss in periodontitis and rheumatoid arthritis. Key genes SAT1, TET2, and HIF1A may serve as biomarkers for these inflammatory bone diseases.

Keywords:
inflammatory bone losslactate metabolismmachine learningperiodontitisrheumatoid arthritissingle-cell RNA sequencing

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Area of Science:

  • Immunometabolism
  • Bone Biology
  • Chronic Inflammatory Diseases

Background:

  • Inflammatory bone loss is common in periodontitis (PD) and rheumatoid arthritis (RA).
  • These distinct diseases share immune-mediated bone resorption mechanisms.
  • Understanding molecular drivers is crucial for treating comorbid inflammatory bone loss.

Purpose of the Study:

  • To identify molecular drivers of bone destruction in comorbid inflammatory diseases.
  • To investigate the role of lactate metabolism in PD and RA pathogenesis.
  • To find potential biomarkers for inflammation-related bone loss.

Main Methods:

  • Bioinformatic analysis and experimental validation using PD and RA models.
  • Single-cell RNA sequencing of PD and RA cohorts.
  • Machine learning to identify core lactate-related genes (SAT1, TET2, HIF1A).
  • In vivo and in vitro functional assays.

Main Results:

  • Elevated blood lactate levels correlated with disease severity in PD and RA models.
  • Lactate metabolism genes were upregulated in monocytes, linked to inflammation and osteoclastogenesis.
  • SAT1, TET2, and HIF1A showed diagnostic potential for both diseases.
  • Lactate reprogrammed monocytes, connecting immune activation to bone resorption.

Conclusions:

  • A lactate-driven immunometabolic axis connects immune responses and bone remodeling.
  • SAT1, TET2, and HIF1A are identified as potential biomarkers for inflammation-related bone loss.
  • Targeting lactate metabolism may offer therapeutic strategies for comorbid inflammatory bone diseases.