Severely Suppressed Bone Turnover and Atypical Skeletal Fragility

2008 ◽  
Vol 93 (8) ◽  
pp. 2948-2952 ◽  
Author(s):  
Maja Visekruna ◽  
Deborah Wilson ◽  
Fergus Eoin McKiernan
2005 ◽  
Vol 90 (3) ◽  
pp. 1294-1301 ◽  
Author(s):  
Clarita V. Odvina ◽  
Joseph E. Zerwekh ◽  
D. Sudhaker Rao ◽  
Naim Maalouf ◽  
Frank A. Gottschalk ◽  
...  

Bone ◽  
2011 ◽  
Vol 49 (6) ◽  
pp. 1279-1289 ◽  
Author(s):  
Crystal K. Tjhia ◽  
Clarita V. Odvina ◽  
D. Sudhaker Rao ◽  
Susan M. Stover ◽  
Xiang Wang ◽  
...  

2015 ◽  
Vol 100 (2) ◽  
pp. 384-394 ◽  
Author(s):  
Gherardo Mazziotti ◽  
Elena Biagioli ◽  
Filippo Maffezzoni ◽  
Maurizio Spinello ◽  
Vincenza Serra ◽  
...  

Abstract Context: GH excess causes an increase in bone turnover, but the consequences in terms of skeletal fragility have long been uncertain due to the heterogeneity of studies dealing with this topic. Objective: We conducted a meta-analysis of studies examining the effects of acromegaly on bone turnover, bone mineral density (BMD), and fractures. Furthermore, we evaluated the effects of sex, gonadal status, and activity of disease on skeletal end-points in acromegaly. Data Sources: We conducted MEDLINE and EMBASE systematic searches up to December 31, 2013. Study Eligibility Criteria: Studies conducted in patients with acromegaly and reporting at least one determinant of skeletal fragility. Data Extraction and Analysis: Study design, patient characteristics, interventions, and outcomes were independently extracted by two authors. We calculated the standardized mean difference (SMD) of bone turnover and BMD differences, whereas fractures were presented as relative frequencies in acromegaly and odds ratios between patients and controls. Results: Forty-one studies fulfilled eligibility criteria and were therefore selected for data extraction and analysis. A total of 1935 patients were included (eight to 206 per study). Acromegaly patients had higher bone formation (SMD, 1.49; 95% confidence interval [CI], 0.97–2.01; P < .0001) and bone resorption (SMD, 1.57; 95% CI, 1.03–2.10; P < .0001) as compared to control subjects, without significant differences in lumbar spine BMD. BMD at the femoral neck tended to be higher in acromegaly patients vs control subjects (SMD, 0.67; 95% CI, 0.07–1.27; P = .03). Patients with acromegaly had high frequency of vertebral fractures (odds ratio, 8.26; 95% CI, 2.91–23.39; P < .0001), in close relationship with male gender, hypogonadism, and active acromegaly. Limitations: Limitations included heterogeneous study protocols with possible variability in the assessment of skeletal end-points. Conclusions: Skeletal fragility is an emerging complication of acromegaly.


2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Kensaku Abe ◽  
Hiroaki Kimura ◽  
Norio Yamamoto ◽  
Shingo Shimozaki ◽  
Takashi Higuchi ◽  
...  

Abstract 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.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Kensaku Abe ◽  
Hiroaki Kimura ◽  
Norio Yamamoto ◽  
Shingo Shimozaki ◽  
Takashi Higuchi ◽  
...  

An amendment to this paper has been published and can be accessed via the original article.


2014 ◽  
Vol 17 (03) ◽  
pp. 1450011
Author(s):  
Myung-Sang Moon ◽  
Ki-Tae Kwon ◽  
Chang-Won Ha ◽  
Sung-Soo Kim ◽  
Sung Sim Kim ◽  
...  

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.


Bone ◽  
2012 ◽  
Vol 51 (1) ◽  
pp. 114-122 ◽  
Author(s):  
Crystal K. Tjhia ◽  
Susan M. Stover ◽  
D. Sudhaker Rao ◽  
Clarita V. Odvina ◽  
David P. Fyhrie

2009 ◽  
Vol 105 (03) ◽  
pp. 125-133 ◽  
Author(s):  
M. J. Seibel ◽  
D. J. Baylink ◽  
J. R. Farley ◽  
S. Epstein ◽  
M. Yamauchi ◽  
...  

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