Low-energy femoral stress fracture in long-term bisphosphonate use: conservative and surgical treatment

Bisphosphonates are commonly used for the treatment of osteoporosis and for reducing the risk of vertebra and hip fractures. The optimum length of therapy for their use has not been determined [1, 2]. In the literature, it is has been reported that alendronate is effective in reducing the risk of fracture [3]. Among the side effects of bisphosphonates are esophageal irritation, osteonecrosis of the jaw, atrial fibrillation, acute inflammatory response, and severe musculoskeletal pain. The effect of long-term alendronate use on bone metabolism is unclear [3, 4]. In animal experiments, bisphosphonate treatment is associated with the accumulation of microdamage and suppression of the turnover in cortical rather than spongious bone, resulting in reduced bone repair [5]. There are many studies about the potential link between prolonged bisphosphonate use and low-energy femoral subtrochanteric/diaphysis stress fractures. Specific radiographic description of these fractures, like a stress fracture pattern, show external cortical reaction, transverse fracture line, and medial cortical spike in the subtrochanteric area [6–10]. There are two types of stress fractures: fatigue fractures and insufficiency fractures. A fatigue fracture occurs when abnormal and repetitive stress is applied to the healthy bone. In contrast, an insufficiency fracture occurs when normal stress is placed on a deficient bone, in which prodromal thigh pain from the insufficiency changes may be present. Clinical features of these fractures are delayed healing, bilateral signs [11, 12] and symptoms, prodromal thigh pain prior to fracture and a history of minimal or no trauma [8]. The cases of five women with low-energy subtrochanteric or femoral shaft stress fractures while being on alendronate therapy for more than 5 years are reported in this study.