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Rickert, M.

Publications and source records attributed to Rickert, M..

2 recordsLinked to original sources

Acoustic Prediction and Biomechanical Validation of Primary Stability in Uncemented Short-Stem Hip Prostheses: An In Vitro Study

BackgroundIn uncemented hip arthroplasty, achieving sufficient primary stability is essential for long-term implant success. However, objective intraoperative assessment of fixation quality remains challenging. Acoustic analysis of stem impaction sounds offers a promising tool for real-time evaluation, but its diagnostic accuracy and biomechanical correlation require further validation. MethodsTwelve formalin-fixed human femora were implanted with cementless Metha(R) short stems under three predefined anchorage conditions: loose, optimal (fit), and fracture-inducing press-fit. Impaction sounds were recorded using calibrated microphones and processed via frequency-domain analysis. Relative micromotions were quantified under torsional loading to biomechanically assess primary stability. ResultsSpectral markers reliably differentiated between anchorage states. The transition from loose to fit showed minimal spectral change, while fit-to-fracture was characterized by a significant increase in low-frequency energy (<2.5 kHz) and pronounced attenuation in high-frequency bands (>15 kHz). These acoustic signatures closely correlated with biomechanically measured micromotions, which showed a distinct hierarchy: fracture < fit < loose. Cluster permutation analysis confirmed statistically significant differences, particularly in the fracture group. ConclusionThis in vitro study demonstrates that frequency-based acoustic analysis can distinguish between stable, insufficient, and over-press-fit conditions during stem implantation. The findings support the potential of intraoperative acoustic monitoring as a real-time, objective tool to enhance implant safety and detect cortical compromise before it becomes clinically apparent.

bioengineering↗

Increased beta2-adrenergic signaling is a targetable stimulus essential for bone healing by promoting callus neovascularization

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. Mechanistically, norepinephrine stimulates the expression of Vegfa and Cgrp primarily in periosteal cells via Adrb2, both of which synergistically promote the formation of osteogenic type-H vessels in the fracture callus. Accordingly, the beneficial effect of TBI on bone repair is abolished in mice lacking Adrb2 or Cgrp, and aged Adrb2-deficient mice without TBI develop fracture nonunions despite high bone formation in uninjured bone. Pharmacologically, the Adrb2 antagonist propranolol impairs, and the agonist formoterol promotes fracture healing in aged mice by regulating callus neovascularization. Clinically, intravenous beta-adrenergic sympathomimetics are associated with improved callus formation in trauma patients with long bone fractures. Thus, Adrb2 is a novel target for promoting bone healing, and widely used beta-blockers may cause fracture nonunion under conditions of increased sympathetic tone. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=95 SRC="FIGDIR/small/548550v1_ufig1.gif" ALT="Figure 1"> View larger version (31K): org.highwire.dtl.DTLVardef@cea57corg.highwire.dtl.DTLVardef@d29642org.highwire.dtl.DTLVardef@186ea5aorg.highwire.dtl.DTLVardef@83eaae_HPS_FORMAT_FIGEXP M_FIG Artwork was created in BioRender. C_FIG

cell biology↗