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Clonal hematopoiesis driven by mutated DNMT3A promotes inflammatory bone loss.

Hui Wang1, Kimon Divaris2, Bohu Pan3

  • 1Department of Basic and Translational Sciences, Laboratory of Innate Immunity and Inflammation, Penn Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

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|June 5, 2024
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Summary

Clonal hematopoiesis of indeterminate potential (CHIP) linked to DNMT3A mutations promotes periodontitis and bone loss. This treatable condition involves maladaptive hematopoiesis and inflammation, suggesting therapeutic interventions.

Keywords:
DNMT3AT cellsarthritisbone marrowclonal hematopoiesis of indeterminate potentialhematopoietic stem and progenitor cellsinflammationneutrophilsosteoclastogenesisperiodontitis

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Area of Science:

  • Hematology
  • Immunology
  • Genetics

Background:

  • Clonal hematopoiesis of indeterminate potential (CHIP) involves aging-associated mutations in hematopoietic progenitors, leading to altered leukocytes.
  • CHIP with DNMT3A mutations is associated with increased periodontitis and gingival inflammation in adults.

Purpose of the Study:

  • To model DNMT3A-driven CHIP using mice with a heterozygous loss-of-function mutation (R878H) equivalent to human R882H.
  • To investigate the impact of DNMT3A-driven CHIP on periodontitis, arthritis, and related inflammatory pathways.

Main Methods:

  • Utilized mice with Dnmt3aR878H/+ mutation for bone marrow transplantation.
  • Assessed clonal expansion, osteoclastogenesis, inflammatory markers (IL-17), immune cell function (Tregs, neutrophils), and periodontitis/arthritis severity.
  • Evaluated the effect of rapamycin treatment on CHIP and associated conditions.

Main Results:

  • DNMT3A-driven CHIP led to clonal expansion of myeloid and lymphoid cells, increased osteoclast precursors, and promoted periodontitis and arthritis in mice.
  • CHIP induced IL-17-dependent inflammation, heightened neutrophil responses, and impaired regulatory T cell function.
  • Rapamycin treatment suppressed DNMT3A-driven CHIP, periodontitis, and related inflammatory bone loss.

Conclusions:

  • DNMT3A-driven CHIP is a treatable state of maladaptive hematopoiesis that promotes inflammatory bone loss through enhanced osteoclastogenesis and immune dysregulation.
  • Targeting CHIP and its downstream inflammatory effects offers a potential therapeutic strategy for periodontitis and related inflammatory conditions.