Direct Bone Destruction by Neutrophils in Collagen-induced Arthritis Treated with Bisphosphonates

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  • NAKAYAMA Mayuko
    Department of Oral Anatomy and Developmental Biology, Showa University School of Dentistry Department of Orthodontics, Showa University School of Dentistry
  • YAGI Hideki
    Cell Biology Laboratory, Kinki University School of Pharmaceutical Science
  • ENDO Yasuo
    Department of Molecular Regulation, Tohoku University Graduate School of Dentistry
  • MAKI Koutaro
    Department of Orthodontics, Showa University School of Dentistry
  • NAKAMURA Masanori
    Department of Oral Anatomy and Developmental Biology, Showa University School of Dentistry

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To identify the direct destruction of bone by neutrophils in collagen-induced arthritis treated with powerful anti-osteoclastic bone resorptive agents, bisphosphonates, we designed the experiments to examine whether the bone destruction induced by collagen-induced arthritis (CIA) was inhibited by nitrogen-containing bisphosphonates (NBPs) or not, and examined histologically and ultrastructually to detect the cells directly related to bone destruction. One of the representative NBPs, alendronate (1.6 µmol/kg), was injected once a week from one week before the onset of the first sensitization with type II collagen. Flow cytometric analysis indicated the enhanced granulopoiesis in both BP-treated and non-treated CIA mice. Severe bone destruction was detected in both saline-group and alendronate-group. Although many active osteoclasts were developed on the destructive bone in saline-group, almost no active osteoclasts were detected in alendronate-group, where many neutrophils were accumulated. Some of neutrophils accumulated on the destructive bone were ruptured and cytoplasmic granules were scattered extracellularly, where collagen fibers were no longer detected. These results indicated that the bone destruction in CIA mice was not prevented by the injection of NBP and suggested that neutrophils in addition to osteoclasts might directly have the capacity for the bone destruction.

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