Correction to: Treatment strategy for atypical ulnar fracture due to severely suppressed bone turnover caused by long-term bisphosphonate therapy: a case report and literature review

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Treatment strategy for atypical ulnar fracture due to severely suppressed bone turnover caused by long-term bisphosphonate therapy: a case report and literature review

Background Atypical fractures may occur due to the combined effect of severely suppressed bone turnover (SSBT) caused by long-term bisphosphonate treatment and chronic repetitive bone microdamage. Atypical fracture of the ulna due to SSBT is a rare entity; there is no standardized treatment strategy for this condition. We successfully treated a patient with atypical fracture of the ulna. Herein, we present this patient, review the relevant literature, and discuss the treatment strategy. Case presentation An 84-year-old woman presented with atypical fracture of the left ulnar shaft due to SSBT. She had a history of bisphosphonate therapy (ibandronate and alendronate) since more than 10 years; her bone turnover was severely suppressed. We performed open reduction and internal fixation (ORIF) using dual plate with some additional treatments. These included drilling and decortication, use of autogenous bone graft, low-intensity pulsed ultrasound (LIPUS) treatment, and administration of teriparatide. Finally, bone union was observed at 11 months after surgery. Conclusions Based on the literature review and our experience with this case, ORIF alone may not be adequate to achieve bone union; drilling, decortication, and use of cancellus bone graft is important to achieve favorable outcomes. Administration of teriparatide and LIPUS may facilitate early bone union, although further studies are required to provide more definitive evidence. Furthermore, ORIF using dual plate may help avoid implant failure owing to the long time required for bone union.

BONE HISTOLOGY OF PATIENTS WITH ALENDRONATE-MEDIATED FRACTURED BONE — A NEW ENTITY OF ATYPICAL OSTEOMALACIA

Based on the pharmaco-physiology of the aminobisphosphonates, it could be speculated that bisphosphonates could induce not only the osteopetrotic bone disease because of their selective suppression of osteoclastic activity, but also could affect directly or indirectly the endocrine system, local factors, and also the bone metabolic turnover. Consequently, the bone fragility could be rather produced by long-term aminobisphosphonate therapy. Bisphosphonate-mediated bone disease was labeled by Odvina et al. in 2005 [Odvina CV, Zerwerth JE, Rao DS et al. Severely suppressed bone turnover; a potential complication of alendronate therapy. J Clin Endocrinol Metab 90: 1294–1301, 2005.] as the "severely suppressed bone turnover (SSBT)" on the metabolic turnover basis. However, such definition could contain various drug-induced bone diseases, and did not indicate any particular condition, induced by the bisphosphonate. The term "SSBT" is thought not solely to be based on its histology, and seems rather a clinical term applicable to the various drug-induced bone diseases. Therefore, the current authors attempted to characterize the bisphosphonate-mediated bone disease on the basis of the combined image and histological studies, and finally concluded that the prolonged bisphosphonate therapy could produce an atypical osteomalacic bone disease. (osteosclerosis of osteomalacia) which leads to fragility fracture. It is puzzling as to why malacia rather than petrosis develops in the skeleton.