Mutations in sulfation-related genes, including SLC26A2, are associated with a number of human skeletal diseases. However, the precise function of sulfation in bone cells and its relevance to bone mass has remained unclear. New research reveals that SLC26A2 deficiency in osteoblasts affects the pericellular matrix and the mechanical regulation of bone mass, and highlights mechanotranduction pathways that could be targeted as a therapeutic strategy to prevent bone loss.