Related Experiment Video
Updated: Aug 16, 2026
16:31
Fixed Volume or Fixed Pressure: A Murine Model of Hemorrhagic Shock
Published on: June 6, 2011
Experimental haemarthrosis produces mild inflammation associated with intracellular Maltese crosses
Annals of the Rheumatic Diseases
|December 1, 1986
Abstract:
Injection of autologous blood into rabbit joints induces an inflammatory reaction with Maltese cross-like birefringent spherulites. Similar microspherules seen in human joint fluids may be formed by lipids derived from breakdown of erythrocytes and other cells.
Insights
Injecting blood into rabbit joints caused inflammation and Maltese cross-like crystals. These crystals, also found in human joint fluid, may originate from broken-down cell lipids, offering insights into joint inflammation.
Area of Science:
- Rheumatology
- Biochemistry
- Cell Biology
Background:
- Autologous blood injection into joints can trigger inflammatory responses.
- Microscopic examination of joint fluid sometimes reveals unique crystalline structures.
Purpose of the Study:
- To investigate the formation of Maltese cross-like birefringent spherulites in rabbit joints after autologous blood injection.
- To explore the potential origin of similar microspherules observed in human synovial fluid.
Main Methods:
- Induction of inflammation in rabbit knee joints via autologous blood injection.
- Microscopic analysis of joint fluid for birefringent spherulites using polarized light microscopy.
- Comparative analysis of spherulites from rabbit and human joint fluids.
Main Results:
- Autologous blood injection into rabbit joints consistently produced an inflammatory reaction.
- Maltese cross-like birefringent spherulites were observed in the inflamed rabbit joints.
- The morphology of these spherulites suggests a lipid-based origin, potentially from erythrocyte and cellular breakdown.
Conclusions:
- The study demonstrates that autologous blood injection can induce the formation of Maltese cross-like birefringent spherulites in an animal model.
- These findings suggest that similar structures in human joint fluid may be derived from lipids released during cellular degeneration, contributing to joint inflammation.
