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Novel preclinical murine model of trauma-induced elbow stiffness.
Moore-Lotridge SN, Oelsner WK, Ihejirika Y, Desai MJ, Gebhart SS, Schoenecker JG
Submitted Externally on 9/24/2018
Journal of experimental orthopaedics
Volume : Pages
5 : 36
Peri-articular injury may result in functional deficits and pain. In particular,
post-traumatic elbow stiffness is a debilitating condition, precluding patients
from performing activities of daily living. As such, clinicians and basic
scientists alike, aim to develop novel therapeutic interventions to prevent and
treat elbow stiffness; thereby reducing patient morbidity. Yet, there is a
paucity of pre-clinical models of peri-articular stiffness, especially of the
upper extremity, necessary to develop and test the efficacy of therapeutics. We
set out to develop a pre-clinical murine model of elbow stiffness, resulting
from soft tissue injury, with features characteristic of pathology observed in
these patients., A soft tissue peri-elbow injury was inflicted in mice using
cardiotoxin. Pathologic tissue repair was induced by creating an
investigator-imposed deficiency of plasminogen, a protease essential for
musculoskeletal tissue repair. Functional testing was conducted through analysis
of grip strength and gait. Radiography, microcomputed tomography, and
histological analyses were employed to quantify development of heterotopic
ossification., Animals with peri-elbow soft tissues injury in conjunction with
an investigator-imposed plasminogen deficiency, developed a significant loss of
elbow function measured by grip strength (2.387?±?0.136 N vs 1.921?±?0.157 N,
****, p 0.0001) and gait analysis (35.05?±?2.775 mm vs 29.87?±?2.075 mm, ***,
p 0.0002). Additionally, plasminogen deficient animals developed capsule
thickening, delayed skeletal muscle repair, fibrosis, chronic inflammation, and
heterotopic ossification; all features characteristic of pathology observed in
patients with trauma-induced elbow stiffness., A soft tissue injury to the
peri-elbow soft tissue with a concomitant deficiency in plasminogen, instigates
elbow stiffness and pathologic features similar to those observed in humans.
This pre-clinical model is valuable for translational studies designed to
investigate the contributions of pathologic features to elbow stiffness or as a
high-throughput model for testing therapeutic strategies designed to prevent and
treat trauma-induced elbow stiffness.
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the MMPC using the following text:
Financial support for this work was provided by the NIDDK Mouse Metabolic Phenotyping Centers (National MMPC, RRID:SCR_008997,
) under the MICROMouse Program, grants DK076169.
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