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Normal hematopoietic stem and progenitor cells slow the regeneration of their niche after injury to minimize leakage from the niche vasculature.

Interplay between AML and stromal cells can initiate a mechanism involving gap junctions where ROS is transferred from cancer cells to stromal cells which then produce acetate which can in return be absorbed/utilised by the cancer cells.

Single-cell sequencing of the alveolar bone marrow of apical periodontitis reveals the cellular and molecular composition of the microenvironment and highlights an osteogenic potential within mesenchymal stem cells of inflammatory-related bone diseases.

Senescent cells accumulate in the fracture callus and a reduction in the number of these cells accelerates fracture healing in mice.

Age-stratified comparisons of gene expression in progeria patient fibroblasts reveals disruption of mesenchymal lineage pathways and points to a deficit in chondrogenic commitment in early development and a depletion of the mesenchymal lineage stem cell pool.

A comprehensive review focusing on the role of osteoclasts as active regulators of bone homeostasis by influencing osteoblast function explores the currently known mechanisms and coupling factors involved in osteoclast–osteoblast communication and their potential as treatments for bone diseases.

Genetically determined type 2 diabetes (T2D) may not increase the risk of fracture, but managing T2D-related risk factors is crucial to prevent fracture in patients with T2D.

A novel secondary adipogenesis pathway is defined that is unique to the bone marrow and is activated with age and in states of metabolic stress.

Osterix, a transcription factor regulating osteoblast differentiation and bone formation, is expressed in subsets of CAFs with osteogenic features and marks tumor infiltrating immune populations enriched in immune suppressive markers.

A newly identified adipose lineage cell population, MALP, regulates marrow vasculature and osteogenesis in bone.