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Updated: Jun 23, 2026

Methods for Analyzing the Impacts of Natural Uranium on In Vitro Osteoclastogenesis
Published on: January 30, 2018
Osteoclast-like multi-nucleated giant cells in uraemic tumoral calcinosis
Shunsuke Yamada1, Masatomo Taniguchi, Masanori Tokumoto
1Departments of Medicine and Clinical Science.
Insights
Tumoral calcinosis, a rare condition causing calcium deposits, can be linked to kidney disease. Osteoclast-like cells may play a role in resorbing these calcifications.
Area of Science:
- Nephrology
- Orthopedics
- Pathology
Background:
- Tumoral calcinosis is a rare condition characterized by massive calcification, often associated with metabolic disorders like chronic kidney disease.
- Patients undergoing long-term hemodialysis are at increased risk for developing tumoral calcinosis due to altered mineral metabolism.
Observation:
- A 46-year-old female on hemodialysis presented with severe hip pain and imaging revealed a calcified mass around the left femur head.
- Percutaneous biopsy confirmed calcium deposition, and surgical resection identified tumoral calcinosis associated with low bone turnover.
Findings:
- Immunohistochemistry of the resected tissue showed multinucleated giant cells expressing CD68, tartrate-resistant acid phosphatase, and calcitonin receptor, suggesting osteoclast-like activity.
- Treatment modification led to complete resolution of tumoral calcinosis lesions around the left knee within six months.
Implications:
- This case suggests that osteoclast-like cells may be involved in the active resorption of tumoral calcinosis.
- Understanding the cellular mechanisms of tumoral calcinosis could lead to novel therapeutic strategies for patients with chronic kidney disease.
Abstract:
A 46-year-old woman under 6-year haemodialysis was admitted for uncontrollable hip pain. An X-ray film revealed calcified mass around the 'left femur head', which was diagnosed as calcium deposition by percutaneous biopsy. Calcinotic tissues were removed surgically, and the resected specimen revealed tumoral calcinosis caused by low bone turnover. A complete resolution of calcinotic lesions around the 'left knee' occurred 6 months after treatment modification. Immunohistochemistry showed recruitment of multi-nucleated giant cells positive for CD68, tartrate resistant acidic phosphatase and calcitonin receptor, indicative of osteoclast-like features. We propose the involvement of osteoclast-like cells in active resorption of tumoral calcinosis.
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