Introduction: Leptin is a pleiotropic hormone that regulates food intake and energy homeostasis with enigmatic effects on bone development. It is unclear if leptin promotes or inhibits bone growth. The aim of this study was to characterize the micro-architecture and mechanical competence of femur bones of leptin-deficient mice.
View Article and Find Full Text PDFTraumatic brain injury (TBI) leads to skeletal changes, including bone loss in the unfractured skeleton, and paradoxically accelerates healing of bone fractures; however, the mechanisms remain unclear. TBI is associated with a hyperadrenergic state characterized by increased norepinephrine release. Here, we identified the β-adrenergic receptor (ADRB2) as a mediator of skeletal changes in response to increased norepinephrine.
View Article and Find Full Text PDFAims: Total knee arthroplasty (TKA) may provoke ankle symptoms. The aim of this study was to validate the impact of the preoperative mechanical tibiofemoral angle (mTFA), the talar tilt (TT) on ankle symptoms after TKA, and assess changes in the range of motion (ROM) of the subtalar joint, foot posture, and ankle laxity.
Methods: Patients who underwent TKA from September 2020 to September 2021 were prospectively included.
Background: The femoral neck system (FNS) was introduced as a minimally invasive fixation device for managing femoral neck fractures.
Objective: To compare radiographic, clinical, and patient-reported outcome measures (PROMs) of femoral neck fracture patients following FNS compared to dynamic hip screw (DHS) implantation combined with an anti-rotational screw.
Methods: Patients who underwent closed reduction and internal fixation of a femoral neck fracture between 2020 and 2022 were retrospectively included.
Traumatic brain injury (TBI) is associated with a hyperadrenergic state and paradoxically causes systemic bone loss while accelerating fracture healing. Here, we identify the beta2-adrenergic receptor (Adrb2) as a central mediator of these skeletal manifestations. While the negative effects of TBI on the unfractured skeleton can be explained by the established impact of Adrb2 signaling on bone formation, Adrb2 promotes neovascularization of the fracture callus under conditions of high sympathetic tone, including TBI and advanced age.
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