Oxidative metabolism is impaired by phosphate deficiency during fracture healing and is mechanistically related to BMP induced chondrocyte differentiation.

Prior studies of acute phosphate restriction during the endochondral phase of fracture healing showed delayed chondrocyte differentiation was mechanistically linked to decreased bone morphogenetic protein signaling. In the present study, transcriptomic analysis of fracture callus gene expression in three strains of mice was used to identify differentially expressed (FDR = q ≤ 0.05) genes in response to phosphate (Pi) restriction.

Clinical Presentation and Outcomes of Patients With a Lumbar Far Lateral Herniated Nucleus Pulposus as Compared to Those With a Central or Paracentral Herniation.

Study Design: Retrospective cohort study.

Objectives: Examine pre- and postoperative outcomes between patients presenting with a central/paracentral versus a far lateral herniated nucleus pulposus (HNP) and assess whether significantly worse postoperative outcomes, assessed via patient self-reported survey, are associated with far lateral disc herniations.

Methods: We performed a retrospective cohort analysis of patients who underwent primary lumbar decompression between January 2008 and December 2015.

Hypophosphatemia Regulates Molecular Mechanisms of Circadian Rhythm.

Transcriptomic analysis showed that the central circadian pathway genes had significantly altered expression in fracture calluses from mice fed a low phosphate diet. This led us to hypothesize that phosphate deficiency altered the circadian cycle in peripheral tissues. Analysis of the expression of the central clock genes over a 24-36 hour period in multiple peripheral tissues including fracture callus, proximal tibia growth plate and cardiac tissues after 12 days on a low phosphate diet showed higher levels of gene expression in the hypophosphatemia groups (p < 0.