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Despite the clinical significance of acetabular dysplasia, there is a paucity of small animal models to investigate structural and functional changes that mediate morphology of the dysplastic hip and drive the subsequent OA cascade. Utilizing a novel murine model developed in our laboratory, 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\u2010weeks post\u2010injury. C57BL6 mice were used to develop titrated levels of hip instability (i.e., mild, moderate, and severe instabillity or femoral head resection) at weaning. Joint shape, acetabular coverage, histomorphology, and statistical shape modeling were used to assess quality of the hip following 8 weeks of destabilization. Acetabular coverage was reduced following severe, but not moderate, instability. Moderate instability induced lateralization of the femur without dislocation, whereas severe instability led to complete dislocation and pseudoacetabulae formation. Mild instability did not result in morphological changes to the hip. Removal of the femoral head led to reduced hip joint space volume. These data support the notion that hip instability, driven by mechanical loss\u2010of\u2010function of soft connective tissue, can induce morphometric changes in the growing mouse hip. This work developed a new mouse model to study hip health in the murine adolescent hip and is a useful tool for investigating the mechanical and structural adaptations to hip instability during growth. \u00a9 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. 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