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Exploring the Calcitonin Receptor Relationship With Bone Resorption in Odontogenic Cysts.

Maria Luiza Diniz de Sousa Lopes1, Débora Frota Colares1, Tiago João da Silva Filho2

  • 1Department of Oral Pathology, Federal University of Rio Grande do Norte, Natal, RN.

Applied Immunohistochemistry & Molecular Morphology : AIMM
|April 13, 2026
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Summary

Calcitonin receptor (CTR) is linked to the development of odontogenic cysts (OCs). This study found associations between CTR, RANKL, and TNF-α in radicular, residual, and dentigerous cysts, suggesting their role in cyst pathogenesis.

Keywords:
bone resorptioncalcitonin receptorodontogenic cystsreceptor activator of nuclear factor-κBtumor necrosis factor-α

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Area of Science:

  • Oral pathology
  • Bone metabolism
  • Immunohistochemistry

Background:

  • Odontogenic cysts (OCs) are common jaw lesions.
  • Understanding their pathogenesis is crucial for developing effective treatments.
  • Calcitonin receptor (CTR) plays a role in bone metabolism and has been implicated in gnathic bone lesions.

Purpose of the Study:

  • To investigate the association between CTR and bone resorption markers, specifically receptor activator of nuclear factor kappa B ligand (RANKL) and tumor necrosis factor alpha (TNF-α), in different types of OCs.
  • To explore the potential role of these factors in the pathogenesis and biological behavior of OCs.

Main Methods:

  • Immunohistochemical analysis was performed on epithelial and capsular tissues from radicular cysts (RCs), radicular residual cysts (RRCs), and dentigerous cysts (DCs).
  • Expression levels of CTR, RANKL, and TNF-α were quantified.
  • Statistical analyses were used to assess correlations between these markers and cyst types.

Main Results:

  • RANKL expression was significantly higher in the epithelial lining of RCs and RRCs compared to DCs.
  • Significant positive correlations were observed between epithelial RANKL and capsular CTR in RCs.
  • Interactions between CTR, RANKL, and TNF-α were identified in all studied cyst types, with varying patterns across RCs, RRCs, and DCs.

Conclusions:

  • CTR is implicated in the pathogenesis of RCs, RRCs, and DCs.
  • RANKL and TNF-α are involved in the biological behavior of these odontogenic cysts.
  • The interplay between CTR, RANKL, and TNF-α may influence osteolytic or osteogenic activity within the cystic microenvironment.