Collagen induced arthritis is a commonly used mouse model of rheumatoid arthritis. Protocol to induce arthritis in C57BL/6 mice includes intradermal injection of the emulsion containing chicken collagen type II (CII) and complete Freund's adjuvant. After three weeks, immunization is boosted with an emulsion of CII and incomplete Freund's adjuvant. The pathogenesis of collagen induced arthritis is complex, comprising both autoinflammatory and autoimmune response. Initially, immunization induces myeloid expansion and cytokine production, and subsequent infiltration of joint with neutrophil and monocyte/macrophage cells, leading to joint impairment. Joint destruction exposes join-specific collagen antigens (CII) to anti-CII antibodies produced in response to xenogeneic CII by T and B lymphocyte mediated immune reaction. The aim of this study was to determine the dynamic of bone metabolism in local bone lesions, different sites of long bones and vertebrae in vivo following arthritis induction. Also, the number of osteoclast progenitors in various hematopoietic tissues and osteoblast progenitors in the bone marrow was assessed, as well as their osteoclastogenic and osteoblastogenic differentiation potential. Collagen induced arthritis in mice causes loss of subchondral and periarticular bone as well as systemic bone loss. Local inflammation (synovitis and osteitis) induces an increase in the number of osteoclast progenitors in bone marrow and their increased differentiation potential in vitro. Also, it promotes their functional ability to degrade subchondral and periarticular bone. We proposed that bone growth factors are released from the bone matrix as a result of bone resorption, leading to an increase in the number of osteoblast progenitors. On the other hand, highly expressed proinflammatory cytokines may inhibit the functional activity of osteoblasts. Chemokines CCL2 and CCL5, whose expression in the bone marrow, spleen and peripheral blood is increased in collagen induced arthritis, stimulate osteoclast progenitors to migrate from the bone marrow into the bloodstream. In arthritic mice, we observed higher proportion of peripheral osteoclast progenitors and their increased osteoclastogenic potential in vitro. Expansion of myeloid cell subpopulations in the bone marrow and peripheral blood contributes to the osteoresorptive environment by enhancing osteoclast differentiation from monocyte/macrophage and dendritic cells, and increasing the expression of proinflammatory cytokines. The net effect on bone remodeling is predominance of osteoresorption. With the duration of arthritis inflammation gradually attenuates allowing intensified bone formation, as evidenced by the increased volume of trabecular bone in the metaphyseal area of femur and lumbar vertebrae in the very late stage of arthritis. In general, we concluded that in a mouse model of rheumatoid arthritis there is an increase in the proportion and activity of most potent subpopulations of osteoclast progenitors within the bone marrow and in circulation. These mobilized progenitors can further home to bone tissue, as evidenced by an increased bone resorption. Consequently, bone degradation induces differentiation of mesenchymal progenitor cells toward osteoblast lineage. On the other hand, inflammatory environment may inhibit osteoblast differentiation in vivo by blocking Wnt-signaling pathway, so the final effect of arthritis is decreased bone formation. Complex changes in the proportions of hematopoietic and mesenchymal cell lineages are associated with changes in the expression of key proinflammatory cytokines and chemokines.