In the skeleton, osteoblasts and osteoclasts synchronize their activities to maintain bone homeostasis and integrity. Investigating the molecular mechanisms governing bone remodeling is critical and helps understand the underlying biology of bone disorders. Initially, we have identified the ubiquitin‐specific peptidase gene (Usp53) as a target of the parathyroid hormone in osteoblasts and a regulator of mesenchymal stem cell differentiation. Mutations in USP53 have been linked to a constellation of developmental pathologies. However, the role of Usp53 in bone has never been visited. Here we show that Usp53 null mice have a low bone mass phenotype in vivo. Usp53 null mice exhibit a pronounced decrease in trabecular bone indices including trabecular bone volume (36%) and trabecular number (26%) along with an increase in trabecular separation (13%). Cortical bone parameters are also impacted, showing a reduction in cortical bone volume (12%) and cortical bone thickness (15%). As a result, the strength and mechanical bone properties of Usp53 null mice have been compromised. At the cellular level, the ablation of Usp53 perturbs bone remodeling, augments osteoblast‐dependent osteoclastogenesis, and increases osteoclast numbers. Bone marrow adipose tissue volume increased significantly with age in Usp53‐deficient mice. Usp53 null mice displayed increased serum receptor activator of NF‐κB ligand (RANKL) levels, and Usp53‐deficient osteoblasts and bone marrow adipocytes have increased expression of Rankl. Mechanistically, USP53 regulates Rankl expression by enhancing the interaction between VDR and SMAD3. This is the first report describing the function of Usp53 during skeletal development. Our results put Usp53 in display as a novel regulator of osteoblast–osteoclast coupling and open the door for investigating the involvement of USP53 in pathologies. © 2023 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).

This research explored the development of a new haptic device for wrist rehabilitation therapy. Specifically, the therapy requires providing resistive forces against the adduction/abduction, flexion/extension of the wrist and pronation/supination of the forearm. The new haptic device employs a spherical magnetorheological brake (MR-brake). This brake was developed by our research group for a previous study and is the only one of its kind. It resembles a typical ball-joint with 3 degrees of freedom (DOF). It can apply high levels of variable resistive force in a very compact single actuator. The new device was coupled to the spherical MR-brake via linkages so that the virtual center of rotation was placed at the center of the patient’s wrist. Compared to similar devices that use motors, conventional rotary MR-brakes or hybrid MR-motor actuators, our device has the advantage of using just a single compact actuator to control all 3 DOF. The interface is inherently safe in such a rehabilitation application as the MR-brakes are passive devices. Details of the design, the MR-brake and a series of experiments to characterize the device are presented. The experimental results indicate minimal backlash in the linkages and the device can provide easily controllable resistive forces in its range of motion. Such a haptic interface is promising since it can enable a computer-controlled and -monitored rehabilitation therapy with a virtual training environment.

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