Although the accumulation of β
2-microglobulin (β
2-MG) appears to play a key role in the pathogenesis of hemodialysis related amyloidosis (HRA), the curious predilection of β
2-MG-amyloid (Aβ
2-MG) deposits for bone and joints is unexplained. The present animal study was undertaken to clarify whether the β
2-MG-Aβ
2-MG deposits are the cause or merely the results of arthropathy.
Eighteen heminephrectomised, male inbred DBA/1J mice were divided into 3 equal groups of 6 animals. In groups 1 and 2, arthritis was produced by intradermal injection of an emulsion of bovine collagen type II (C-II) and complete Freund's adjuvant with a subsequent i. p. booster injection of C-II. Group 3 mice did not receive C-II treatment and served as controls. After collagen induced arthritis (CIA) had developed in groups 1 and 2, human urine derived β
2-MG, 100 to 300μg, was given by s. c. injection to group 1 for up to 10 days. Human β
2-MG was also given to 6 mice without CIA in group 3 using the same schedule.
Regardless of the presence of CIA, human β
2-MG was deposited predominantly in the bone marrow, as well as synovia, of the human β
2-MG treated mice in groups 1 and 3. On the other hand, group 2 mice which had not been given human β
2-MG had no deposits of β
2-MG. Aβ
2-MG deposits were not seen probably because of too short observation period.
These findings suggest that if β
2-MG levels are high, β
2-MG is deposited in the articular structure as a primary event.
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