ArticleJournal of translational medicine2023
Parathyroid hormone stimulates bone regeneration in an atrophic non-union model in aged mice.
Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Correlation between Biochemical Parameters and Radiographic Healing Score in Tibial Fractures.Journal of orthopaedic case reports · 2025Article
- Modern Approaches and Emerging Biological Therapies to Treat Fracture Nonunion.Pharmaceutics · 2025Review
- Cortisol stress response after musculoskeletal surgery: a narrative review.EFORT open reviews · 2025Review
- Fortified Withaferin A accelerates the transition from fibrovascular to bone remodeling phase during endochondral bone formation to promote ossification.Frontiers in endocrinology · 2025Article
- NovelPathology oncology research : POR · 2025Article
- Correction to: Parathyroid hormone stimulates bone regeneration in an atrophic non-union model in aged mice.Journal of translational medicine · 2024Article
- Injective hydrogel loaded with liposomes-encapsulated MY-1 promotes wound healing and increases tensile strength by accelerating fibroblast migration via the PI3K/AKT-Rac1 signaling pathway.Journal of nanobiotechnology · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNon-union formation still represents a major burden in trauma and orthopedic surgery. Moreover, aged patients are at an increased risk for bone healing failure. Parathyroid hormone (PTH) has been shown to accelerate fracture healing in young adult animals. However, there is no information whether PTH also stimulates bone regeneration in atrophic non-unions in the aged. Therefore, the aim of the present study was to analyze the effect of PTH on bone regeneration in an atrophic non-union model in aged CD-1 mice.
methodsAfter creation of a 1.8 mm segmental defect, mice femora were stabilized by pin-clip fixation. The animals were treated daily with either 200 µg/kg body weight PTH 1-34 (n = 17) or saline (control; n = 17) subcutaneously. Bone regeneration was analyzed by means of X-ray, biomechanics, micro-computed tomography (µCT) imaging as well as histological, immunohistochemical and Western blot analyses.
resultsIn PTH-treated animals bone formation was markedly improved when compared to controls. This was associated with an increased bending stiffness as well as a higher number of tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts and CD31-positive microvessels within the callus tissue. Furthermore, PTH-treated aged animals showed a decreased inflammatory response, characterized by a lower number of MPO-positive granulocytes and CD68-positive macrophages within the bone defects when compared to controls. Additional Western blot analyses demonstrated a significantly higher expression of cyclooxygenase (COX)-2 and phosphoinositide 3-kinase (PI3K) in PTH-treated mice.
conclusionTaken together, these findings indicate that PTH is an effective pharmacological compound for the treatment of non-union formation in aged animals.
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