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Area of Science:

  • Rheumatology
  • Immunology
  • Bone Biology

Background:

  • Systemic sclerosis (SSc) is a chronic autoimmune disease characterized by fibrosis and vascular abnormalities.
  • Calcinosis, the deposition of calcium salts in soft tissues, is a common complication in SSc, particularly affecting the hands.
  • The underlying mechanisms driving SSc-associated calcinosis and its relationship with bone metabolism remain incompletely understood.

Purpose of the Study:

  • To investigate the association between radiographically confirmed hand calcinosis in SSc patients and osteoclastogenesis.
  • To explore potential biomarkers related to bone resorption and vascular function in SSc patients with and without calcinosis.

Main Methods:

  • Recruitment of 20 SSc patients (10 with calcinosis, 10 without) and 10 healthy controls.
  • Assessment of hand calcinosis severity using the Scleroderma Clinical Trials Consortium (SCTC) radiographic severity score.
  • In vitro culture of peripheral blood mononuclear cells (PBMCs) to quantify osteoclast formation.
  • Measurement of serum levels of RANKL, osteoprotegerin (OPG), and angiogenic factors (VEGF, angiopoietin-1, angiopoietin-2).

Main Results:

  • SSc patients with calcinosis exhibited significantly higher osteoclast formation from PBMCs compared to those without calcinosis and healthy controls (P = 0.001).
  • Calcinosis severity did not correlate with osteoclast number but was positively correlated with RANKL, RANKL/OPG ratio, and angiopoietin-2 levels.
  • Patients with calcinosis reported more digital ischemia than those without.

Conclusions:

  • Calcinosis in SSc is associated with an enhanced capacity of peripheral blood cells to differentiate into osteoclasts.
  • These findings highlight a potential role for osteoclastogenesis in SSc-associated calcinosis.
  • Targeting osteoclastogenesis may represent a promising therapeutic strategy for managing calcinosis in SSc.