Biology subjects

Locke, R. C.

Publications and source records attributed to Locke, R. C..

2 recordsLinked to original sources

bioRxiv2018

Partial-Width Injuries of the Rat Rotator Cuff Heal with Fibrosis

PurposeThe purpose of this study was to identify the healing outcomes following a partial-width, full-thickness injury to the rotator cuff tendon-bone attachment and establish if the adult attachment can regenerate the morphology of the healthy attachment.\n\nHypothesisWe hypothesized that a partial-width injury to the attachment would heal via fibrosis and bone remodeling, resulting in increased cellularity and extracellular matrix deposition, reduced bone volume, osteoclast presence and decreased collagen organization compared to shams.\n\nMaterials and MethodsA biopsy punch was used to create a partial-width injury at the center one-third of the rat infraspinatus attachment, and the contralateral limb underwent a sham operation. Rats were sacrificed at 3- and 8-weeks after injury for analyses. Analyses performed at each time-point included cellularity (Hematoxylin & Eosin), ECM deposition (Massons Trichrome), bone volume (micro-computed tomography; microCT), osteoclast activity (Tartrate Resistant Acid Phosphatase; TRAP), and collagen fibril organization (Picrosirius Red). Injured and sham shoulders were compared at both 3- and 8-weeks using paired, two-way ANOVAs with repeated measures and Sidaks correction for multiple comparisons.\n\nResultsCellularity and ECM deposition increased at both 3- and 8-weeks compared to sham contralateral attachments. Bone volume decreased and osteoclast presence increased at both 3- and 8-weeks compared to sham contralateral limbs. Collagen fibril organization was reduced at 3-weeks after injury compared to 3-week sham attachments.\n\nConclusionsThese findings suggest that a partial-width injury to the rotator cuff attachment does not fully regenerate the native structure of the healthy attachment. The injury model healed via scar-like fibrosis and did not propagate into a full-width tear after 8-weeks of healing.

bioengineering↗

bioRxiv2018

A novel model for the induction of postnatal murine hip deformity

Acetabular dysplasia is a recognized cause of hip osteoarthritis (OA). A paucity of animal models exists to investigate structural and functional changes that mediate morphology of the dysplastic hip and drive the subsequent arthritic cascade. Utilizing a novel murine model, this study investigated the role of surgically-induced unilateral instability of the postnatal hip on the initiation and progression of acetabular dysplasia and impingement up to 8-weeks post-injury. Specifically, C57BL6 mice were used to develop titrated levels of hip instability (mild, moderate, severe, and femoral head removal) at 3-weeks of age, a critical time for hip maturation. Joint shape, acetabular coverage, histomorphology, immunohistochemistry, and statistical shape modeling were used to assess overall quality of joint health and three-dimensional hip shape following 8 weeks of titrated destabilization. This titrated approach included mild, moderate, severe, and complete instability via surgical destabilization of the murine hip. Acetabular coverage was reduced following severe, but not moderate, instability. Moderate instability induced lateralization of the femoral head without dislocation, whereas severe instability led to complete dislocation and formation of pseudoacetabula. Mild instability did not result in statistically significant morphological changes to the hip. Complete destabilization via femoral head removal led to reduced joint space volume and reduced bone volume ratio in the remnant proximal femur. Collectively, these results support the notion that hip instability, driven by loss of function, leads to morphometric changes in the maturing mouse hip. This model could be useful for future studies investigating the mechanical and cellular adaptations to hip instability during maturation.

pathology↗