Bone homeostasis is characterized by a continuous process of remodeling, which relies on the balance of bone resorption by osteoclasts and bone formation by osteoblasts. Osteoclasts are highly specialized multinucleated cells with the unique ability to resorb bone. The current concept suggests that osteoclasts arise from two sources of progenitors, the embryonic yolk sac-derived erythromyeloid extramedullary progenitors and hematopoietic stem cell-derived myeloid progenitors. In addition to physiological differentiation factors, the inflammatory cytokine network is also able to induce pathological osteoclast differentiation, causing excessive bone resorption. Studies have demonstrated that chronic inflammatory autoimmune diseases are frequently associated with bone destruction. As such, bone loss and fracture risk are commonly observed in inflammatory joint diseases such as rheumatoid arthritis and ankylosing spondylitis as well as in systemic lupus erythematosus and inflammatory bowel disease. In addition, increased osteoclast activity and bone resorption are associate with inflammation cause by infection, injury or metastatic tumors.
Despite the numerous breakthroughs made in osteoimmunology research over more than last twenty years in revealing the interaction of the immune system and bone cells, and the importance of inflammatory environment for enhancement of bone resorption, many parts of the exact mechanisms remain to be yet elucidated. Moreover, pharmacological treatments, including biological therapy, often do not completely correct the pathological bone resorption in autoimmune and inflammatory diseases. Thus, a more in-depth understanding of the mechanisms involved in bone pathology associated with chronic inflammatory or infection diseases (like rheumatic diseases, periodontitis, inflammatory bowel diseases, psoriasis, and osteomyelitis) could possibly lead to earlier intervention and to the identification of alternative therapeutic approaches. In addition, elucidation of the immune and bone cell interactions in the inflammatory conditions may help to reveal processes involved in the progression of bone metastasis.
This Research Topic aims to gather Original Research articles, Reviews and Mini-Reviews that will further the current knowledge on regulation of osteoclast differentiation in autoimmune and inflammatory diseases. Potential topics include, but are not limited to:
1) Characterization of osteoclasts’ origin, differentiation and phenotype in autoimmune and inflammatory diseases
2) Role of cytokines and other pro-inflammatory molecules in the process of inflammation-induced bone loss
3) Role of immune cells in inflammation-induced bone loss and identification of inflammatory bone microenvironment
4) Ex vivo and in vivo models to investigate mechanisms of enhanced osteoclast activity and inflammation-induced bone loss
5) Novel potential approaches to suppress osteoclast differentiation and function, and to treat inflammation-induced bone loss.
Bone homeostasis is characterized by a continuous process of remodeling, which relies on the balance of bone resorption by osteoclasts and bone formation by osteoblasts. Osteoclasts are highly specialized multinucleated cells with the unique ability to resorb bone. The current concept suggests that osteoclasts arise from two sources of progenitors, the embryonic yolk sac-derived erythromyeloid extramedullary progenitors and hematopoietic stem cell-derived myeloid progenitors. In addition to physiological differentiation factors, the inflammatory cytokine network is also able to induce pathological osteoclast differentiation, causing excessive bone resorption. Studies have demonstrated that chronic inflammatory autoimmune diseases are frequently associated with bone destruction. As such, bone loss and fracture risk are commonly observed in inflammatory joint diseases such as rheumatoid arthritis and ankylosing spondylitis as well as in systemic lupus erythematosus and inflammatory bowel disease. In addition, increased osteoclast activity and bone resorption are associate with inflammation cause by infection, injury or metastatic tumors.
Despite the numerous breakthroughs made in osteoimmunology research over more than last twenty years in revealing the interaction of the immune system and bone cells, and the importance of inflammatory environment for enhancement of bone resorption, many parts of the exact mechanisms remain to be yet elucidated. Moreover, pharmacological treatments, including biological therapy, often do not completely correct the pathological bone resorption in autoimmune and inflammatory diseases. Thus, a more in-depth understanding of the mechanisms involved in bone pathology associated with chronic inflammatory or infection diseases (like rheumatic diseases, periodontitis, inflammatory bowel diseases, psoriasis, and osteomyelitis) could possibly lead to earlier intervention and to the identification of alternative therapeutic approaches. In addition, elucidation of the immune and bone cell interactions in the inflammatory conditions may help to reveal processes involved in the progression of bone metastasis.
This Research Topic aims to gather Original Research articles, Reviews and Mini-Reviews that will further the current knowledge on regulation of osteoclast differentiation in autoimmune and inflammatory diseases. Potential topics include, but are not limited to:
1) Characterization of osteoclasts’ origin, differentiation and phenotype in autoimmune and inflammatory diseases
2) Role of cytokines and other pro-inflammatory molecules in the process of inflammation-induced bone loss
3) Role of immune cells in inflammation-induced bone loss and identification of inflammatory bone microenvironment
4) Ex vivo and in vivo models to investigate mechanisms of enhanced osteoclast activity and inflammation-induced bone loss
5) Novel potential approaches to suppress osteoclast differentiation and function, and to treat inflammation-induced bone loss.
