Publications by authors named "Keshia E Mora"

Article Synopsis
  • Tendons typically face longitudinal tensile forces, but they also experience transverse forces from bone impingement, which affects both normal and abnormal tendon function.
  • A study using mouse hindlimb explants and advanced imaging techniques revealed that impingement leads to significant transverse compression in the extracellular matrix and alters cell shape and compression in the pericellular matrix.
  • The findings, supported by a finite element model, indicate that the stresses and strains from impingement can greatly exceed those from normal tension, and these effects are influenced by the spacing between cells, highlighting their relevance in understanding tendon injuries.
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Article Synopsis
  • Tendon impingement creates a multiaxial strain environment leading to fibrocartilage changes, including increased glycosaminoglycan (GAG) matrix and altered collagen structure, which are linked to tendinopathy.
  • Although fibrocartilage is normal in areas of healthy tendons, excessive GAG and collagen disorganization indicate tendinopathy, and impingement is recognized as a key factor in its development.
  • The research introduces a new murine hind limb model that replicates the conditions of tendon impingement in its natural anatomy, allowing for more accurate studies of how mechanical strains influence tendon health over time.
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Immediately prior to inserting into bone, many healthy tendons experience impingement from nearby bony structures. However, super-physiological levels of impingement are implicated in insertional tendinopathies. Unfortunately, the mechanisms underlying the connection between impingement and tendon pathology remain poorly understood, in part due to the shortage of well-characterized animal models of impingement at clinically relevant sites.

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Despite the requirement for -lineage (Scx) cells during tendon development, the function of Scx cells during adult tendon repair, post-natal growth, and adult homeostasis have not been defined. Therefore, we inducibly depleted Scx cells (ScxLin) prior to tendon injury and repair surgery and hypothesized that ScxLin mice would exhibit functionally deficient healing compared to wild-type littermates. Surprisingly, depletion of Scx cells resulted in increased biomechanical properties without impairments in gliding function at 28 days post-repair, indicative of regeneration.

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