Miyata T, Iida Y, Notoya K, Taketomi S, Maeda K
Beta-2-microglobulin modified with advanced glycation end products enhances osteoclast-induced bone resorption: Role in the pathogenesis of dialysis-related amyloidosis
33rd Congress of the Eur Dial Transplant Assoc
Nephrol Dial Transplant (Jun) 11:A240 1996

Advanced glycation end products (AGEs) are present in amyloid fibril beta2-Microglobulin (beta2M) of patients with dialysis-related amyloidosis (DRA), one of the characteristic features of which is an accelerated bone resorption around amyloid deposits.

The aim of the study was to investigate whether AGE-beta2M enhances osteoclast-induced bone resorption by pit formation assay, using an unfractionated bone cell culture system containing osteoclast and osteoblasts from newborn mice. When the cells were cultured on dentin slices, both AGE-beta2M purified from urine of long-term hemodialysis patients and in-vitro prepared AGE-beta2M (beta2M incubated with glucose for 60 days) increased the number of resorption pits formed by osteoclasts, whereas normal beta2M did not enhance bone resorption. AGE-beta2M, however, did not increase the number of tar/rate-resistant acid phosphatase-positive cells, i.e., mature osteoclasts. Enhanced bone resorption was also observed by AGE-BSA or when the cells were cultured on AGE-modified dentin slices. AGE-induced bone resorption was effectively inhibited by calcitonin and ipriflavone at the therapeutic doses.

Comment: In conclusion, these data suggest the AGEs enhance bone resorption, not by promoting differentiation of osteoclast precursor cells into mature osteoclasts, but by activating mature osteoclasts probably in concert with osteoblasts. Thus, the bone resorption in dialysis related amyloid might be the combined result of excessive accumulation of AGEs in amyloid deposits linked to a heightened cellular (monocyte/macrophage and osteoclast/osteoblast) response to these deposits (Carlo Basile, M.D., Taranta, Italy).

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33rd Congress of the Eur Dial Transplant Assoc
CRF by organ system : Joint disease, beta-2 microglobulin
CRF by problem area : Bone disease/aluminum