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Exogenous parathyroid hormone (1-34) attenuates knee osteoarthritis in mice through activating the TGF-β/Smad

Peng Sun1, Haoran Jin1, Qirui Ding1

  • 1Department of Orthopedics, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huai'an City, 223300, Jiangsu Province, China.

Hormones (Athens, Greece)
|January 21, 2026
PubMed
Abstract

Insights

Parathyroid hormone (PTH) treatment was found to significantly reduce knee osteoarthritis (OA) progression in mice. This was achieved by promoting chondrocyte proliferation and activating the TGF-β/Smad signaling pathway, thereby protecting articular cartilage.

Area of Science:

  • Orthopedics and Sports Medicine
  • Cell Biology
  • Molecular Biology

Background:

  • Osteoarthritis (OA) is a degenerative joint disease with limited treatment options.
  • Parathyroid hormone (PTH) has shown potential in delaying OA progression, but its underlying mechanisms are not fully understood.
  • The transforming growth factor-beta (TGF-β)/Smad signaling pathway is crucial for chondrocyte function and OA pathogenesis.

Purpose of the Study:

  • To investigate the therapeutic effects of PTH on knee osteoarthritis (KOA) in a mouse model.
  • To elucidate the molecular mechanisms by which PTH influences KOA, particularly focusing on the TGF-β/Smad signaling pathway.

Main Methods:

  • Knee osteoarthritis was induced in mice using anterior cruciate ligament transection (ACLT).
  • Mice were treated with PTH (1-34) or a vehicle control.
  • Knee joint phenotypes were assessed using radiography, micro-computed tomography (micro-CT), and histology.
  • The expression of key proteins and mRNA related to cartilage metabolism and signaling pathways was quantified using immunohistochemistry and quantitative real-time polymerase chain reaction (qRT-PCR).

Main Results:

  • PTH (1-34) treatment significantly attenuated OA phenotypes in ACLT mice, reducing Mankin's and OARSI scores.
  • PTH enhanced the synthesis of type II collagen and inhibited the expression of type X collagen and matrix metalloproteinase-13 (MMP-13) in articular cartilage.
  • PTH increased the expression of parathyroid hormone receptor 1 (PTH1R), p-cAMP response element binding protein (p-CREB), proliferating cell nuclear antigen (PCNA), TGF-β receptors (TβRI, TβRII), and Smad2/3 proteins and mRNA.

Conclusions:

  • PTH (1-34) effectively attenuates knee OA induced by ACLT in mice.
  • PTH promotes chondrocyte proliferation, inhibits hypertrophy and maturation, and reduces articular cartilage degradation.
  • The therapeutic effects of PTH involve the activation of the TGF-β/Smad signaling pathway.
Keywords:
Anterior cruciate ligament transectionOsteoarthritisParathyroid hormone (1–34)TGF-β/Smad signaling pathway

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