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Testosterone regulates bone response to inflammation.

J P Steffens1, B S Herrera2, L S Coimbra1

  • 1Department of Physiology and Pathology, School of Dentistry at Araraquara - UNESP, São Paulo State University, -Araraquara, SP, Brazil.

Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme
|February 15, 2014
PubMed
Summary
This summary is machine-generated.

Both low and high testosterone levels exacerbate inflammatory bone loss in male rats. The proresolving mediator Resolvin D2 (RvD2) shows potential in mitigating these effects on osteoblast function.

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Area of Science:

  • Endocrinology
  • Periodontology
  • Osteology

Background:

  • Testosterone levels significantly influence bone metabolism and periodontal health.
  • Alveolar bone loss is a hallmark of periodontal disease, often exacerbated by hormonal imbalances.
  • Understanding the interplay between testosterone, inflammation, and osteoblast function is crucial for developing targeted therapies.

Purpose of the Study:

  • To evaluate the impact of varying testosterone concentrations on alveolar bone response and periodontal inflammation.
  • To investigate the effect of Resolvin D2 (RvD2) on testosterone-modulated osteoblast activity.
  • To elucidate the mechanisms underlying testosterone's influence on bone remodeling markers and inflammatory mediators.

Main Methods:

  • In vivo study utilizing male rats with experimentally induced periodontal inflammation and varying testosterone levels (sub-physiologic, normal, supra-physiologic).
  • In vitro study involving primary osteoblasts treated with different testosterone concentrations and RvD2.
  • Analysis of bone loss using micro-computed tomography and assessment of inflammatory markers (IL-1β) and bone remodeling markers (alkaline phosphatase, osteocalcin, RANKL, OPG).

Main Results:

  • Both sub-physiologic and supra-physiologic testosterone levels significantly increased alveolar bone loss compared to normal levels.
  • Low testosterone heightened gingival IL-1β expression, while high testosterone increased the RANKL:OPG ratio in osteoblasts.
  • RvD2 partially reversed the suppressive effects of low-dose testosterone on osteocalcin, RANKL, and OPG in osteoblasts.

Conclusions:

  • Altered testosterone levels (both low and high) promote inflammatory alveolar bone loss in male rats.
  • Low testosterone predominantly exacerbates inflammation, whereas high testosterone favors an increased osteoblast-derived RANKL:OPG ratio.
  • The proresolving mediator RvD2 demonstrates a potential therapeutic role in ameliorating testosterone's adverse effects on osteoblast function and bone metabolism.