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Trauma: S.-K. Goh, K. Y. Yang, J. S. B. Koh, M. K. Wong, S. Y. Chua, D. T. C. Chua, and T. S. Howe Subtrochanteric insufficiency fractures in patients on alendronate therapy: A CAUTION J Bone Joint Surg Br 2007; 89-B: 349-353 [Abstract] [Full text] [PDF]

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Authors' reply:

Seo-Kiat Goh, Tet Sen Howe   (17 May 2007)

Subtrochanteric insufficiency fractures in patients on alendronate therapy

Laurence E Dodd   (25 April 2007)

Alendronate therapy and insufficiency fractures

adel tavakkolizadeh   (20 April 2007)

Authors' reply: 17 May 2007
Seo-Kiat Goh, Orthopaedic Registrar Singapore General Hospital, Tet Sen Howe Send letter to journal: Re: Authors' reply: seokiat.goh{at}cantab.net Seo-Kiat Goh, et al.	Sir, We thank Dr Tavakkolizadeh and Dr Dodd for their interest in the subject of our paper and appreciate the various points raised. Almost all the patients in this cohort were started on alendronate by doctors outside our institution and presented to us only after the fractures had occurred. Hence, we are unable to establish the indication for which alendronate was started for most of the patients. We agree that in general, one of the causes of thigh pain could be degenerative joint disease of the hip. However, this is less likely in our study cohort for the following reasons. Firstly, degenerative joint disease of the hip is less common in our population. Secondly, those of our patients whose fracture healed no longer had pain. Osteoporotic subtrochanteric fractures are very rare in our population, and we could only identify very few patients with subtrochanteric fractures who were not on alendronate therapy to serve as controls. In our cohort of patients, we did not detect any significant lower limb malalignment. The possibility that the fracture in patient 8 was a metastatic one had been excluded with intraoperative histology, bone scan and biochemical investigations. We do not have a good explanation to account for her lack of response to the alendronate therapy. As for patient 4, it is likely that her osteoporosis had not responded well to bisphosphonate therapy due to concurrent steroid therapy for chronic ezcema. Based on the data available from this study, we are unable to address why the fracture had taken place in the subtrochanteric area. This study is also not designed to address the question of risk:benefit ratio of osteoporotic treatment with bisphosphonate. Finally, as we pointed out, a few patients in our series had cortical hypertrophy in the contralateral, unfractured femur. The objective of this paper is to raise the awareness of a possible association between the prolonged pharmacological bone-turnover and a hitherto undescribed low or atraumatic subtrochanteric fracture of the femur. As this series of patients is a small one, it is difficult to establish a causal relationship between the two. On the other hand, the morbidity of a subtrochanteric fracture is a serious one, and hence, we feel it is important for us to share this experience with the orthopaedic community at large. S.K. Goh, Orthopaedic Registrar, T.S. Howe, Singapore General Hospital, Singapore.
Subtrochanteric insufficiency fractures in patients on alendronate therapy 25 April 2007
Laurence E Dodd, Orthopaedic SpR Worthing Hospital, West Sussex, UK Send letter to journal: Re: Subtrochanteric insufficiency fractures in patients on alendronate therapy docdodd{at}doctors.org.uk Laurence E Dodd	Sir, I read this paper with interest. The authors comment on a potential link between the use of so-called bone protective drugs, and an increased incidence of subtrochanteric fragility fractures. My interest was sparked by this seeming paradox, however, there are a number of points I would like to raise. The authors reference Pauwels et al when describing the subtrochanteric region as the point of maximal stress, and therefore strength, in the femur. Do the authors therefore have any explanation as to why the fractures they have observed occur in this area, and not elsewhere? Furthermore, since the mid 1990s bisphosphonate therapy has become a major player in the pharmacological armoury, both to the orthopaedic surgeon and the elderly care physician. I would therefore assume that reports of nine fractures is not a fair representation of the population of patients receiving bisphosphonates as a whole. Can the authors comment on whether the risk:benefit ratio of bone protection is worthwhile given that a great number of users do not sustain fragility fractures? Indeed, is there any evidence to suggest the prodromal pain or cortical irregularities that they describe, exist in those patients on alendronate, but without fracture? L.E.Dodd, SpR Orthopaedics, Worthing Hospital, West Sussex, UK.
Alendronate therapy and insufficiency fractures 20 April 2007
adel tavakkolizadeh, orthopaedic SpR Kings college Hospital,london Send letter to journal: Re: Alendronate therapy and insufficiency fractures adeltav{at}hotmail.com adel tavakkolizadeh	Sir, I read this paper with interest. Firstly I must congratulate the authors on their instinctive observation that may well have significant implications. The authors suggest that there is a possible increased risk of insufficiency fractures in patients on long term alendronate. They have reached these conclusions cautiously recognising the limitations of their study. However, there are a number of points that have not been addressed in the study: Firstly, the indications for the alendronate therapy in this small group of patients are unclear. Only one patient had a definite diagnosis of osteoporosis with established T scores consistent with the World Health Organisation (WHO) definition with indication for treatment. Only four patients had osteopenia. Secondly, the authors have tried to differentiate the thigh pain from groin pain as a possible prodromal pain but in the selected group of published illustrations, there is radiological evidence of degenerative joint disease which could explain some of the pain described by the patients (Figures 1a,1b, 2b and 4). Thirdly, regarding the lateral cortical hypertrophy, this has been attributed to stress reaction on the tension side of the bone due to suppressed bone remodelling, but to do this any deformity of the femur or any significant mal-alignment of the lower limb needs to be excluded as a contributing factor, which has not been done in the study. Furthermore, in order to quantify the hypertrophy, a control group of radiographs of patients matched for age and sex and level of activity should have been used. Lastly in patient 8, despite five years of treatment with alendronate, the patient remained osteoporotic as confirmed by DEXA scan after the fracture. There is no obvious explanation for this and finally two of the patients had other medical conditions that are associated with insufficiency fractures (patients 4 and 8). In these cases the alendronate may have been only a confounding factor. A. Tavakkolizadeh, Orthopaedic SpR, Kings College Hospital, London, UK.