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Peer-reviewedCC BY-NC-NDInternational journal of oral science

Bone anabolic agents repair alveolar bone damaged by diabetes in mice.

  • Hakan Turkkahraman1
  • Carson Joseph Walton2
  • Yukiko Koizumi2,3,4
  • Tianli Zhu5
  • Nisreen Akel6
  • Xue Yuan7,8
  • Teresita M Bellido9,10
10 affiliations
  1. 1Department of Orthodontics and Oral Facial Genetics, Indiana University School of Dentistry, Indianapolis, IN, USA.
  2. 2Department of Otolaryngology-Head & Neck Surgery, Indiana University School of Medicine, Indianapolis, IN, USA.
  3. 3Department of Anatomy, Cell Biology & Physiology, Indiana University School of Medicine, Indianapolis, IN, USA.
  4. 4Indiana University School of Medicine, Indiana Center for Musculoskeletal Health, Indianapolis, IN, USA.
  5. 5Department of Biomedical Sciences and Comprehensive Care, Indiana University School of Dentistry, Indianapolis, IN, USA.
  6. 6University of Arkansas for Medical Sciences, Department of Physiology and Cell Biology, Little Rock, AR, USA.
  7. 7Department of Otolaryngology-Head & Neck Surgery, Indiana University School of Medicine, Indianapolis, IN, USA. [email protected].
  8. 8Indiana University School of Medicine, Indiana Center for Musculoskeletal Health, Indianapolis, IN, USA. [email protected].
  9. 9University of Arkansas for Medical Sciences, Department of Physiology and Cell Biology, Little Rock, AR, USA. [email protected].
  10. 10Central Arkansas Veterans Healthcare System, John L. McClellan, Little Rock, AR, USA. [email protected].
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Abstract

Type 2 diabetes (T2D) is a chronic metabolic disorder that significantly impacts skeletal health, including bones of the oral cavity, where alveolar bone is particularly susceptible due to its high remodeling rate and sensitivity to systemic metabolic changes. Using a mouse model of established T2D induced by high-fat diet and streptozotocin, we investigated the effects of the FDA-approved bone anabolic agents parathyroid hormone (PTH) and abaloparatide (ABL) on alveolar bone. In non-diabetic mice, PTH and ABL stimulated both bone formation and resorption, resulting in no net change in alveolar bone mass. In contrast, these agents selectively increased bone formation in T2D mice without further enhancing the already elevated resorption, leading to net alveolar bone gain. This anabolic effect involves suppression of sclerostin and Dickkopf-1 (Dkk-1) in osteocytes and activation of Wnt signaling in periodontal ligament cells. Studies using DMP1-Cre;PTH1Rfl/fl mice demonstrated that osteocytic PTH1R is essential for the anabolic effects but not for the bone resorption-promoting effects of PTH and ABL. These findings reveal a dual mechanism of PTH1R signaling in oral bone remodeling and suggest therapeutic strategies to restore alveolar bone and improve tooth retention and implant osseointegration in diabetic patients.

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Cite

BibTeXRIS
BibTeX
@article{turkkahraman2026bone,
  title = {{Bone anabolic agents repair alveolar bone damaged by diabetes in mice.}},
  author = {Hakan Turkkahraman and Carson Joseph Walton and Yukiko Koizumi and Tianli Zhu and Nisreen Akel and Xue Yuan and Teresita M Bellido},
  journal = {International journal of oral science},
  year = {2026},
  month = oct,
  doi = {10.1038/s41368-026-00470-3},
  url = {https://europepmc.org/article/MED/42957662},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Bone anabolic agents repair alveolar bone damaged by diabetes in mice.
AU  - Hakan Turkkahraman
AU  - Carson Joseph Walton
AU  - Yukiko Koizumi
AU  - Tianli Zhu
AU  - Nisreen Akel
AU  - Xue Yuan
AU  - Teresita M Bellido
PY  - 2026
DA  - 2026/10/29
JO  - International journal of oral science
DO  - 10.1038/s41368-026-00470-3
UR  - https://europepmc.org/article/MED/42957662
AB  - Type 2 diabetes (T2D) is a chronic metabolic disorder that significantly impacts skeletal health, including bones of the oral cavity, where alveolar bone is particularly susceptible due to its high remodeling rate and sensitivity to systemic metabolic changes. Using a mouse model of established T2D induced by high-fat diet and streptozotocin, we investigated the effects of the FDA-approved bone anabolic agents parathyroid hormone (PTH) and abaloparatide (ABL) on alveolar bone. In non-diabetic mice, PTH and ABL stimulated both bone formation and resorption, resulting in no net change in alveolar bone mass. In contrast, these agents selectively increased bone formation in T2D mice without further enhancing the already elevated resorption, leading to net alveolar bone gain. This anabolic effect involves suppression of sclerostin and Dickkopf-1 (Dkk-1) in osteocytes and activation of Wnt signaling in periodontal ligament cells. Studies using DMP1-Cre;PTH1Rfl/fl mice demonstrated that osteocytic PTH1R is essential for the anabolic effects but not for the bone resorption-promoting effects of PTH and ABL. These findings reveal a dual mechanism of PTH1R signaling in oral bone remodeling and suggest therapeutic strategies to restore alveolar bone and improve tooth retention and implant osseointegration in diabetic patients.
SN  - 1674-2818
SN  - 2049-3169
ER  -