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Updated: May 3, 2026

Osteoclast Derivation from Mouse Bone Marrow
Published on: November 6, 2014
Massive accumulation of osteoclastic giant cells in rapid destructive hip disease
Sebastian Seitz1, Jozef Zustin, Michael Amling
1Department of Orthopaedics, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany.
Insights
Rapid destructive hip disease (RDHD) causes rapid femoral head destruction. Histological analysis reveals increased giant osteoclasts and granulomas, suggesting an unknown trigger for bone loss in this rare coxarthropathy.
Area of Science:
- Orthopedics
- Rheumatology
- Bone Biology
Background:
- Rapid destructive hip disease (RDHD) is a rare coxarthropathy.
- The etiology and pathogenesis of RDHD remain largely unknown.
- RDHD is characterized by rapid femoral head destruction over weeks to months.
Purpose of the Study:
- To define the histological and histomorphometric hallmarks of RDHD.
- To elucidate the underlying mechanisms of rapid bone loss in RDHD.
- To establish a basis for understanding RDHD pathogenesis.
Main Methods:
- Histological and histomorphometric analyses were performed on 15 RDHD patients.
- Samples included bone marrow and synovium.
- RDHD findings were compared to controls with primary osteoarthritis (OA).
Main Results:
- RDHD showed severe bone resorption with increased, morphologically altered giant osteoclasts.
- Giant cell granulomas were observed in bone marrow and synovium.
- Increased osteoblast numbers and osteoid were noted, but insufficient to counteract bone resorption.
Conclusions:
- RDHD involves massive osteoclast activation, likely due to an unknown stimulus.
- A reactive increase in osteoblast activity occurs but is insufficient to prevent rapid hip destruction.
- Further research should focus on identifying stimuli upstream of osteoclast activation in RDHD.
Abstract:
The term rapid destructive hip disease (RDHD) designates a rare coxarthropathy characterized by a rapid destruction of the femoral head within a few weeks to several months. The etiology and pathogenesis of RDHD are not understood. The goal of this study was to define the histological and histomorphometric hallmarks of RDHD to provide a basis for a deeper understanding of the underlying mechanisms. Fifteen consecutive RDHD patients (mean age 78.9 ± 6.4 years, 14 females) demonstrated the characteristic radiographic appearance of vanishing femoral head bone stock without signs of reactive anabolic changes. Histologic and histomorphometric analyses revealed severe bone resorption with significantly increased numbers of morphologically altered giant osteoclasts, the formation of giant cell granulomas both in bone marrow and the synovium and significantly increased osteoblast numbers and osteoid as compared to controls with primary osteoarthritis (OA). These results suggest that in RDHD, an unknown stimulus leads to a massive activation of osteoclasts and this in turn provokes a reactive increase in osteoblast activity that is too weak to counteract the rapid destruction of the hip, thus providing a rationale for a prospective systematic search for the stimuli upstream of the massively increased osteoclast activation in RDHD.
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