Rapid First-Year Proximal Femoral Bone Loss After Traumatic Transfemoral Amputation and Its Partial Reversal With Sequential Romosozumab and Antiresorptive Therapy: A Case Report
- 1Orthopaedic Surgery, Rehabilitation Medicine, Hyogo Prefectural Rehabilitation Center Central Hospital, Kobe, JPN
- 2Orthopaedic Surgery, Hyogo Prefectural Rehabilitation Center Central Hospital, Kobe, JPN
Abstract
Lower limb amputation causes early loss of bone mineral density (BMD) in the residual limb, and the loss is greater after transfemoral than after transtibial amputation. Densitometry is nevertheless rarely performed after amputation, and no report has described pharmacological treatment of this bone loss. A 37-year-old man underwent right transfemoral amputation after a road traffic injury; a concomitant left femoral shaft fracture was treated with an intramedullary nail. He was admitted to our hospital five months after the injury for prosthetic fitting and gait training, and dual-energy X-ray absorptiometry (DXA) was performed for the first time at that point. Three months later, during intensive inpatient gait training with progressive weight bearing, BMD had decreased at every site, and the magnitude of the decrease was graded according to loading condition: 1.9% at the lumbar spine, 8.7% at the non-amputated femoral neck, 15.6% at the amputated femoral neck, and 20.1% at the amputated total hip. Romosozumab 210 mg monthly was administered for 12 months, from 9 to 20 months after amputation, followed by denosumab and then zoledronic acid. Over 33 months of sequential treatment, BMD increased at every site relative to the value at treatment initiation, by 32.6% at the lumbar spine and 33.2% at the amputated femoral neck, but recovery was incomplete: BMD at the amputated total hip remained 2.5% below the value recorded five months after amputation. No fracture occurred, and the patient remains in employment. Rapid proximal femoral bone loss can therefore progress after transfemoral amputation despite prosthetic gait training and daily prosthesis use. This is an uncontrolled observation in a single patient: fracture healing, continuing rehabilitation, and progressively increasing physical activity coincided with pharmacotherapy, and the increase in BMD cannot be attributed to the medication. Whether early and repeated densitometry after lower limb amputation identifies this decline while it remains treatable and whether treatment reduces fractures require prospective evaluation.
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BibTeX
@article{toda2026rapid,
title = {{Rapid First-Year Proximal Femoral Bone Loss After Traumatic Transfemoral Amputation and Its Partial Reversal With Sequential Romosozumab and Antiresorptive Therapy: A Case Report}},
author = {Mitsunori Toda and Takashi Oshima},
journal = {Cureus},
year = {2026},
month = sep,
doi = {10.7759/cureus.116980},
url = {https://doi.org/10.7759/cureus.116980},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Rapid First-Year Proximal Femoral Bone Loss After Traumatic Transfemoral Amputation and Its Partial Reversal With Sequential Romosozumab and Antiresorptive Therapy: A Case Report
AU - Mitsunori Toda
AU - Takashi Oshima
PY - 2026
DA - 2026/09/26
JO - Cureus
DO - 10.7759/cureus.116980
UR - https://doi.org/10.7759/cureus.116980
AB - Lower limb amputation causes early loss of bone mineral density (BMD) in the residual limb, and the loss is greater after transfemoral than after transtibial amputation. Densitometry is nevertheless rarely performed after amputation, and no report has described pharmacological treatment of this bone loss. A 37-year-old man underwent right transfemoral amputation after a road traffic injury; a concomitant left femoral shaft fracture was treated with an intramedullary nail. He was admitted to our hospital five months after the injury for prosthetic fitting and gait training, and dual-energy X-ray absorptiometry (DXA) was performed for the first time at that point. Three months later, during intensive inpatient gait training with progressive weight bearing, BMD had decreased at every site, and the magnitude of the decrease was graded according to loading condition: 1.9% at the lumbar spine, 8.7% at the non-amputated femoral neck, 15.6% at the amputated femoral neck, and 20.1% at the amputated total hip. Romosozumab 210 mg monthly was administered for 12 months, from 9 to 20 months after amputation, followed by denosumab and then zoledronic acid. Over 33 months of sequential treatment, BMD increased at every site relative to the value at treatment initiation, by 32.6% at the lumbar spine and 33.2% at the amputated femoral neck, but recovery was incomplete: BMD at the amputated total hip remained 2.5% below the value recorded five months after amputation. No fracture occurred, and the patient remains in employment. Rapid proximal femoral bone loss can therefore progress after transfemoral amputation despite prosthetic gait training and daily prosthesis use. This is an uncontrolled observation in a single patient: fracture healing, continuing rehabilitation, and progressively increasing physical activity coincided with pharmacotherapy, and the increase in BMD cannot be attributed to the medication. Whether early and repeated densitometry after lower limb amputation identifies this decline while it remains treatable and whether treatment reduces fractures require prospective evaluation.
SN - 2168-8184
ER -