Given the success of the previous collection, Bone Cell Differentiation in Health and Disease, and the new advances in the field, we are pleased to announce the launch of Volume II.
Bones have the unique ability to constantly undergo remodeling even after growth and modeling of the skeleton have been completed. These remodeling processes enable this tissue to respond and adapt to changing functional situations. Bone mass is controlled by the coordinated action of osteoblast and osteoclasts, which form and resorb bone, respectively. The actions of these two cell types as well as their differentiation is modulated by osteocytes. Mesenchymal stem cells have the ability to differentiate into one of the three cell types: osteoblasts, chondrocytes, or adipocytes.
It is now clear that hormones and growth factors produced by cells of other tissues are able to modulate bone modeling and remodeling by altering osteoblast, osteoclast, and osteocyte functions. The status of the bone represents the net result of a balance between the activity of osteoclast and osteoblast, which results compromised as a consequence of endocrine disorders. Thus, it is fundamental to identify new pathways and genes involved in osteogenesis. In certain circumstances, other cell types (e.g., smooth muscle cells, cancer cells) also undergo osteoblast-like differentiation to develop pathological calcification. Moreover, disseminated cancer cells also modulate the functions of bone resident osteoblast and osteoclast cells to deteriorate bone health. Similarly, obese adipocytes, high-cholesterol and diabetic situations disturb bone cell functions and bone health.
This article collection aims to discuss the pathways involved in osteogenesis in health and disease including but not limited to:
- Genes and proteins involved in mesenchymal stem cell differentiation;
- Hormones inhibiting or promoting osteogenesis;
- Pathways involved in osteogenesis impairment as a consequence of endocrine disorders;
- Bone cell response to other endocrine cells signals;
- Osteoblast, osteoclast, and osteocyte function in health and disease
- Atypical osteoblast-like differentiation and disease.
Authors are welcome to submit Original Research, Review, Mini Review, Methods, and Perspective articles to provide readers with up-to-date knowledge in the field of osteogenesis.
Given the success of the previous collection, Bone Cell Differentiation in Health and Disease, and the new advances in the field, we are pleased to announce the launch of Volume II.
Bones have the unique ability to constantly undergo remodeling even after growth and modeling of the skeleton have been completed. These remodeling processes enable this tissue to respond and adapt to changing functional situations. Bone mass is controlled by the coordinated action of osteoblast and osteoclasts, which form and resorb bone, respectively. The actions of these two cell types as well as their differentiation is modulated by osteocytes. Mesenchymal stem cells have the ability to differentiate into one of the three cell types: osteoblasts, chondrocytes, or adipocytes.
It is now clear that hormones and growth factors produced by cells of other tissues are able to modulate bone modeling and remodeling by altering osteoblast, osteoclast, and osteocyte functions. The status of the bone represents the net result of a balance between the activity of osteoclast and osteoblast, which results compromised as a consequence of endocrine disorders. Thus, it is fundamental to identify new pathways and genes involved in osteogenesis. In certain circumstances, other cell types (e.g., smooth muscle cells, cancer cells) also undergo osteoblast-like differentiation to develop pathological calcification. Moreover, disseminated cancer cells also modulate the functions of bone resident osteoblast and osteoclast cells to deteriorate bone health. Similarly, obese adipocytes, high-cholesterol and diabetic situations disturb bone cell functions and bone health.
This article collection aims to discuss the pathways involved in osteogenesis in health and disease including but not limited to:
- Genes and proteins involved in mesenchymal stem cell differentiation;
- Hormones inhibiting or promoting osteogenesis;
- Pathways involved in osteogenesis impairment as a consequence of endocrine disorders;
- Bone cell response to other endocrine cells signals;
- Osteoblast, osteoclast, and osteocyte function in health and disease
- Atypical osteoblast-like differentiation and disease.
Authors are welcome to submit Original Research, Review, Mini Review, Methods, and Perspective articles to provide readers with up-to-date knowledge in the field of osteogenesis.
