Makarand V. Risbud

This paper describes a standardized protocol for creating mouse models of bisphosphonate-related and radiation-induced jaw osteonecrosis using minimally invasive surgical and irradiation techniques.

The paper identifies bone lymphatic endothelial cells as a distinct population that drives skeletal repair and shows that their dysfunction contributes to mandibular diseases.

The paper redefines skeletal endothelial heterogeneity by showing the proposed type R population is part of a venous continuum and includes fatty acid-handling endothelial cells.

This study shows that a human hip OA-associated Chadl variant causes intervertebral disc degeneration in mice, with changes in ECM and biomechanics.

This study shows that activating SIRT6 with MDL-800 improves intervertebral disc health in aged mice by enhancing autophagy, reducing senescence, and improving matrix quality.

This study shows that SDC4 deletion protects against disc degeneration in mice under increased spinal flexion by preserving notochordal features and modulating proteomic pathways.

The paper shows that skull bone marrow is vulnerable to age-related decline, contradicting previous claims of resilience, and highlights its role in blood and immune health.

This study shows that OPA1 maintains mitochondrial structure and metabolic functions in NP cells and chondrocytes, preventing age-related degeneration in mouse intervertebral discs and knee joints.

This study identifies SM/J mice as a model for spontaneous disc herniations and shows neuroimmune changes drive chronic discogenic pain.

This study shows that lactate transfer via MCT1 between nucleus pulposus and endplate cells is essential for intervertebral disc health, as its absence leads to degeneration.

This study shows oral K3Citrate reduces disc calcification in LG/J mice without affecting bone structure or locomotion, suggesting Ca2+ chelation as a potential mechanism.

This study shows that SIRT6 loss in mice leads to intervertebral disc degeneration by promoting senescence and SASP through changes in histone modifications, DNA accessibility, and autophagy.

This study shows that increased HIF-2α activity in nucleus pulposus cells accelerates intervertebral disc degeneration in aging mice.