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Alterations in bone remodeling in the femur after medullary reaming and cemented hip arthroplasty in dogs.
Authors:B A VanEnkevort  M D Markel  P A Manley
Institution:Comparative Orthopaedic Research Laboratory, School of Veterinary Medicine, University of Wisconsin, Madison 53706, USA.
Abstract:OBJECTIVE: To determine whether medullary reaming alone, or followed by cemented hemiarthroplasty, influenced porosity, vascularity, and new bone formation in the proximal portion of the femur in dogs. ANIMALS: 12 adult mixed-breed dogs. PROCEDURE: Unilateral femoral head and neck excisions were performed, followed by femoral medullary reaming in 6 dogs and femoral medullary reaming and cemented hemiarthroplasty in 6 dogs; the contralateral femur was used as a control. All dogs were euthanatized 28 days after surgery, and femurs were harvested. Vascularity, porosity, and new bone formation were quantified for all femurs of dogs from both groups at 3 proximal-to-distal levels, 3 regions (periosteal, midcortical, and endosteal), and 4 quadrants (cranial, caudal, medial, and lateral) of the femur. RESULTS: Medullary reamed and cemented hemiarthroplasty femurs had significant increases in vascularity and porosity at all levels and in new bone formation at levels 2 and 3. Porosity was increased significantly in the periosteal region of the cemented hemiarthroplasty (9.7+/-0.7%), compared with control (2.3+/-0.2%) and medullary reamed (8.4+/-0.7%) femurs. Porosity was increased in the caudal and medial quadrants in the medullary reamed and cemented hemiarthroplasty femurs; vascularity results were similar. CONCLUSION: Increased porosity, vascularity, and new bone formation in reamed and cemented hemiarthroplasty-treated femurs supports the theory that surgical trauma associated with medullary reaming is an important factor in early cortical bone loss after hip arthroplasty. CLINICAL RELEVANCE: Femoral remodeling associated with reaming and broaching is appreciable but may be only a temporary response, whereas other factors may be responsible for chronic cortical bone loss.
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