Scott Cunningham, MD, PhD | March 30, 2022
Autoimmunity, as evidenced by the presence of anti-modified protein antibodies (AMPAs), has been reported to precede the clinical onset of RA by years.
Indeed, AMPA-positive patients without joint signs and symptoms are considered to be at-risk for developing RA, even though not all at-risk patients develop RA. Moreover, it is thought that anti-citrullinated protein antibodies (ACPAs) trigger osteoclast activity and ACPA-positive patients exhibit more severe bone changes than ACPA-negative patients.
Seventy-five AMPA- and ACPA-positive patients without joint swelling were enrolled in the study. The second metacarpal head of each patient was scanned using high-resolution peripheral QCT. Additional bone measurements included the total volumetric bone mineral density (vBMD), trabecular vBMD, and cortical vBMD.
Patients with broad AMPA-positivity had a greater number of microstructural bone changes than patients with narrow AMPA-positivity.
Specifically, there was a higher number of cortical microchannels per joint, and decreased total, trabecular, and cortical vBMD. In addition, the progression to RA was more rapid in patients with broad AMPA-positivity than narrow AMPA-positivity. Thus, microstructural bone changes herald the onset of RA in at-risk patients.
Consider these findings from similar research studies:
The increased cortical microchannels that occur in RA patients with broad-spectrum autoimmunity may reflect antibody-mediated osteoclastogenesis (Source).
Citrullinated vimentin induces autoantibody formation, which in turn directly induces bone loss (Source).