Poor trabecular microarchitecture at the distal radius in older men with increased concentration of high-sensitivity

T Rolland1, S Boutroy, N Vilayphiou

  • 1INSERM UMR 1033, Université de Lyon and Hospices Civils de Lyon, Lyon, France.

Insights

Low-grade inflammation, indicated by high-sensitivity C-reactive protein (hsCRP), increases fracture risk in older men. This risk is not explained by changes in bone microarchitecture, suggesting other mechanisms are involved.

Area of Science:

  • Bone biology and aging
  • Inflammation and chronic disease
  • Geriatric medicine

Background:

  • Low-grade inflammation, measured by serum high-sensitivity C-reactive protein (hsCRP), is linked to increased fracture risk, independent of bone mineral density.
  • The relationship between inflammation and bone health, particularly bone microarchitecture, requires further elucidation in aging men.

Purpose of the Study:

  • To investigate the association between hsCRP levels and bone microarchitecture using high-resolution peripheral quantitative computed tomography (pQCT).
  • To determine if bone microarchitecture mediates the relationship between hsCRP and fracture risk in men.

Main Methods:

  • Cross-sectional study of 1,149 men aged 19-87 years.
  • Measurement of serum hsCRP and bone microarchitecture at the distal radius and tibia via pQCT.
  • Statistical analysis adjusting for age, bone mineral density, and other confounders.

Main Results:

  • hsCRP levels increased with age until 72 years, then stabilized.
  • In men aged ≥72, higher hsCRP (>5 mg/L) was associated with poorer trabecular bone microarchitecture at the distal radius (lower density, number; higher spacing).
  • Fracture prevalence increased with hsCRP levels, and higher hsCRP remained an independent risk factor for fractures, even after adjusting for microarchitecture.

Conclusions:

  • Elevated hsCRP is associated with altered trabecular bone structure at the distal radius in older men (≥72 years).
  • Impaired bone microarchitecture does not appear to be the primary mechanism explaining the link between hsCRP and fracture risk.
  • Inflammation may contribute to fracture risk through pathways other than direct effects on bone microarchitecture.