Invited Speaker 23rd International Society of Magnetic Resonance Conference 2023

Recent data reveal a mismatch between dietary sodium intake and urinary sodium excretion over prolonged periods, and sodium retention without attendant weight-gain. Skin, as the largest organ in the body, has been proposed to serve as a reservoir for sodium by many researchers. We tested skin biopsies from patients with T2D (n=9) and euglycemic patients with no history of Diabetes Mellitus (n=8). To visualize stored sodium, ²³Na MRI GE protocol with spectroscopically optimised triple quantum filter (TQF) was used.  2D triple quantum-filtered with time proportional phase incrementation (TQ-TPPI) spectroscopy was used to determine sodium storage skin capacity in all studied skin biopsies. We provide the first evidence for stored sodium within the human dermis, co-locating to the GAG scaffold. We also provide evidence that T2D associates with diminishment of the dermal binding capacity for sodium^1,2.

Osteoarthritis is the most prevalent musculoskeletal disease, affecting 250 million people worldwide.  Articular cartilage is a dense extracellular matrix-rich tissue that degrades following chronic mechanical stress, resulting in osteoarthritis (OA). We hypothesised that sodium, sequestered within the aggrecan-rich matrix, was freed by injurious compression, thereby enhancing the bioavailability of pericellular growth factors. A flux in free matrix sodium upon mechanical compression of cartilage was visualised by ²³Na-MRI just below the articular surface and further quantified using ²³Na TQ-TPPI. Our results describe a novel intrinsic repair mechanism, controlled by matrix stiffness, and mediated by the free sodium concentration, in which heparan sulfate-bound growth factors are released from cartilage upon injurious load³.

In a separate study using human cartilage specimen, we revealed intriguing experimental results providing the evidence that the slow component of sodium triple quantum filtered relaxation is a marker for OA during compression/relaxation cycle.  Our data demonstrate that the compression/relaxation cycle subjects the cartilage tissue to undergo changes that result in the same relaxed state as the tissue was initially for the controls while in the case of OA the tissue never restores to its original pre-compression state. This indicates on a different mechanical response to the normal stress associated with the loss of glycosaminoglycans (GAGs) in the cartilage scaffold linked to OA progression⁴.