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.
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
