AbstractThe balance between bone forming osteoblasts and bone resorbing osteoclasts can
be disturbed in autoimmune diseases resulting in local and systemic bone loss.
It was long time believed that autoantibodies only indirectly contribute to bone
loss by fueling the overall inflammation. However, in the last decade, more and
more evidence emerged that autoantibodies and immune complexes directly activate
osteoclasts and pre-osteoclasts by binding to Fcγ receptors
(FcγRs) on the (pre)-osteoclast cell surface. This pro-osteoclastogenic
effect seems to be dependent on the absence of sialic acid in the IgG Fc glycan,
which is a typical feature of many autoantibodies. Clinical studies revealed the
importance of autoantibody-mediated bone loss mainly in rheumatoid arthritis,
but also in other diseases, such as celiac disease. In summary, the gained
knowledge about autoantibody-mediated bone loss helps to better understand bone
pathologies of autoimmune diseases. However, studies are still relatively
limited and more research is needed to fully understand the impact of
autoantibodies on bone and to develop future therapeutic strategies.
Bone Loss in Celiac Disease Is Related to Secondary Hyperparathyroidism
