Hip Stress Fracture on MRI & X-ray: Imaging Findings

Femoral neck stress fractures are classified by anatomical location because the mechanical environment differs fundamentally. Tension-side fractures occur on the superior femoral neck, where tensile forces act during weight-bearing. The superior cortex has less inherent resistance to tension, and fractures here carry a high risk of displacement, complete fracture, and subsequent avascular necrosis of the femoral head. Tension-side fractures extending more than 50% across the neck width or any that are complete are orthopedic emergencies requiring urgent surgical fixation. Compression-side fractures occur on the inferior femoral neck, where compressive forces are higher but the cortex resists them better. These fractures are intrinsically more stable and are generally managed with non-weight-bearing and progressive rehabilitation, provided close radiographic and MRI surveillance confirms no propagation.

Plain radiographs are normal in up to 50% of femoral neck stress fractures in the early stages, as cortical disruption and periosteal reaction require days to weeks to develop. MRI detects the periosteal and endosteal edema pattern within 24 to 72 hours of symptom onset with sensitivity approaching 100% on T2 fat-suppressed or STIR sequences. MRI also delineates fracture grade: bone marrow edema alone indicates a low-grade stress reaction, whereas a discrete low-signal fracture line through edema confirms a complete stress fracture and defines its location on the tension or compression side. This distinction directly determines whether the patient requires urgent surgery, protected weight-bearing, or activity restriction — decisions that cannot be made safely on clinical grounds or plain radiographs alone.

Relative energy deficiency in sport, formerly described in female athletes as the female athlete triad (inadequate energy intake, menstrual dysfunction, low bone mineral density), occurs when energy availability — the difference between dietary energy intake and exercise energy expenditure — is chronically insufficient to support normal physiological function. Low energy availability suppresses the hypothalamic-pituitary-gonadal axis, causing menstrual irregularity in women and reduced testosterone in men, which together with nutritional deficiencies impair bone accrual and remodeling. The result is reduced bone mineral density that increases stress fracture susceptibility well beyond what training load alone would predict. Management requires a multidisciplinary approach: sports medicine physician, registered dietitian, and psychologist addressing disordered eating behaviors, alongside bone-specific pharmacological treatment such as calcium, vitamin D, and sometimes bisphosphonates in severe cases.