Abstract

Previous studies have extensively examined the association between femoral insufficiency fractures and prolonged bisphosphonate therapy. However, alternative etiologies remain insufficiently characterized. This study aimed to analyze non-pharmacologic factors associated with femoral insufficiency fractures, with particular emphasis on paradoxical cortical hypertrophy and altered biomechanical load distribution. We reviewed three cases of femoral insufficiency fracture that were surgically treated at our institution between January 2018 and January 2022. None of the patients had a history of bisphosphonate use. Clinical histories—including underlying comorbidities, prior surgical procedures, and radiographic findings—were evaluated. Serial radiographs obtained before and after fracture occurrence were analyzed to characterize fracture morphology and associated cortical changes. Case 1 involved a patient with post-traumatic hip synostosis; case 2 involved a patient with osteogenesis imperfecta; and case 3 involved a patient who had previously undergone intramedullary nailing for an intertrochanteric fracture. Lateral femoral bowing and cortical hypertrophy preceded fracture development in two cases, whereas focal cortical hypertrophy at the distal locking screw site was observed in the third case. No history of bisphosphonate therapy was identified in any patient. Fractures developed at sites characterized by increased cortical remodeling and abnormal load concentration. Femoral insufficiency fractures can occur in the absence of bisphosphonate therapy. Paradoxical cortical hypertrophy and altered biomechanical force distribution appear to be important contributing factors. Level of evidence: IV.

• Keywords: Stress fracture; Osteoporosis; Diphosphonates; Bone remodeling