@entity130 can have systemic consequences, as the early inflammatory response after @entity130 can lead to tissue destruction at sites not affected by the @entity130 . This systemic catabolism may occur in the skeleton following traumatic injuries such as anterior cruciate ligament (ACL) @entity397 . However, @entity604 following injury at distant, unrelated skeletal sites has not yet been established. In the current study, we utilized a @entity19 @entity3331 model to determine whether @entity131 causes a mechanically significant trabecular @entity604 at a distant, unrelated skeletal site (L5 vertebral body). @entity3331 was noninvasively induced using either high-speed (HS; 500   mm/s) or @entity258 ( @entity258 ; 1   mm/s) tibial compression overload. @entity130 creates an ACL @entity397 by midsubstance tear, while @entity258 injury creates an ACL @entity397 with an associated @entity174 . At 10 days post-injury, vertebral trabecular bone structure was quantified using high-resolution microcomputed tomography ( CT), and differences in mechanical properties were determined using finite element modeling (FEM) and compressive mechanical testing. We hypothesized that @entity3331 would initiate a loss of trabecular bone structure and strength at the L5 vertebral body. Consistent with our hypothesis, we found significant decreases in trabecular bone volume fraction (BV/TV) and trabecular number at the L5 vertebral body in @entity258 injured @entity19 compared to sham (-8.8% and -5.0%, respectively), while HS injured @entity19 exhibited a similar, but lower magnitude response (-5.1% and -2.5%, respectively). Contrary to our hypothesis, this decrease in trabecular bone structure did not translate to a significant deficit in compressive stiffness or ultimate load of the full trabecular body assessed by mechanical testing or FEM. However, we were able to detect significant decreases in compressive stiffness in both HS and @entity258 injured specimens when FE models were loaded directly through the trabecular bone region (-9.9% and -8.1%, and 3, respectively). This finding may be particularly important for @entity3604 risk, as @entity16 has been shown to initiate within the trabecular bone compartment. Altogether, these data point to a @entity79 as a consequence of @entity174 or @entity130 , which may be an underlying mechanism contributing to increased risk of refracture following an @entity130 . This finding may have consequences for treatment of @entity85 and the prevention of future @entity79 .

Trabecular XXXX at a Distant Skeletal Site Following Noninvasive @entity3331 in @entity19 .

@entity3604 :: ('MESH:D058866', 'Disease') :: ['osteoporotic fracture'] @entity131 :: ('MESH:D001930', 'Disease') :: ['acute knee injury'] @entity174 :: ('MESH:D050723', 'Disease') :: ['avulsion bone fracture', 'fracture'] @entity19 :: ('10090', 'Species') :: ['mice', 'mouse'] @entity604 :: ('MESH:D016301', 'Disease') :: ['bone loss'] @entity3331 :: ('MESH:D007718', 'Disease') :: ['Knee injury', 'knee injury'] @entity16 :: ('MESH:D009422', 'Disease') :: ['damage within vertebral bodies'] @entity79 :: ('MESH:D001847', 'Disease') :: ['bone fragility', 'systemic trabecular bone loss'] @entity397 :: ('MESH:D012421', 'Disease') :: ['rupture'] @entity85 :: ('MESH:D009140', 'Disease') :: ['acute musculoskeletal injuries'] @entity258 :: ('MESH:D009800', 'Disease') :: ['LS', 'low-speed'] @entity130 :: ('MESH:D014947', 'Disease') :: ['traumatic musculoskeletal injury', 'HS injury', 'trauma', 'initial injury', 'Traumatic injuries']
@entity604 :: (MESH:D016301,Disease) :: ['Bone Loss']
