Persistent femoral neck non-union despite valgus intertrochanteric osteotomy: Relevance for secondary cam-type impingement.

Valgus intertrochanteric osteotomy is a well-established treatment in delayed union of femoral neck fractures as it converts shear forces into compression forces. Non-union of the femoral neck fracture may persist following valgus intertrochanteric osteotomy, and secondary femoroacetabular impingement (FAI) may be a contributing factor. Case: We report one case of persistent femoral neck non-union after treatment by valgus intertrochanteric osteotomy with concomitant secondary cam-type impingement from fracture callus as a possible cause for ongoing insufficient healing. Healing was achieved following surgical hip dislocation with corrective osteochondroplasty of the femoral head-neck junction. Two-year follow-up shows good clinical and radiological outcomes. Conclusion: In ongoing non-healing of femoral neck fractures following valgus intertrochanteric osteotomy, secondary cam impingement from fracture callus must be excluded.

Long-term loss of osteoclasts and unopposed cortical mineral apposition following limited field irradiation.

Late-onset fragility fractures are a common complication following radiotherapy for metastatic disease and soft tissue sarcomas. Using a murine hindlimb focal irradiation model (RTx), we quantified time-dependent changes in osteoclasts and mineral apposition rate (MAR). Mice received either a single, unilateral 5 Gy exposure or four fractionated doses (4 × 5 Gy). Osteoclast numbers and MAR were evaluated histologically at 1, 2, 4, 8, 12, and 26 weeks post-RTx. Radiation induced an early, transient increase in osteoclasts followed by long-term depletion. Increased osteoclast numbers correlated temporally with trabecular resorption; the resorbed trabeculae were not later restored. Radiotherapy did not attenuate MAR at any time point. A transient, early increase in MAR was noted in both RTx groups, however, the 4 × 5 Gy group exhibited an unexpected spike in MAR eight weeks. Persistent depletion of osteoclasts permitted anabolic activity to continue unopposed, resulting in cortical thickening. These biological responses likely contribute to post-radiotherapy bone fragility via microdamage accumulation and matrix embrittlement in the absence of osteoclastic remodeling, and trabecular resorption-induced decrease in bone strength. The temporal distribution of osteoclast numbers suggests that anti-resorptive therapies may be of clinical benefit only if started prior to radiotherapy and continued through the following period of increased osteoclastic remodeling.