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Right Ventricular Epicardial Fibrosis in Mice With Sternal Segment Dislocation
H A Adissu1, G A Medhanie2, L Morikawa3
1Centre for Modeling Human Disease, Toronto Centre for Phenogenomics, Toronto, ON, Canada Physiology & Experimental Medicine Research Program, The Hospital for Sick Children, Toronto, ON, Canada Department of Laboratory Medicine & Pathobiology, Faculty of Medicine, University of Toronto, Toronto, ON, Canada adissu@lunenfeld.ca.
Sternal segment dislocation in mice can lead to right ventricular fibrosis. This cardiac condition may result from direct injury by displaced sternal segments or associated callus formation.
Area of Science:
- Veterinary Pathology
- Cardiovascular Pathology
- Skeletal Pathology
Background:
- Routine histopathology in C57BL/6N mice revealed unexpected sternal segment dislocation.
- This finding prompted an investigation into potential cardiac consequences.
- The study aimed to understand the relationship between sternal defects and cardiac pathology.
Purpose of the Study:
- To determine if cardiac fibrosis is a pathological consequence of sternal segment dislocation in mice.
- To investigate the pathogenesis of coincident sternal and cardiac lesions.
- To assess the implications for interpreting phenotypes in mouse models.
Main Methods:
- Retrospective case series analysis of 1103 mice aged 4-16 weeks.
- Histopathological evaluation for sternal segment dislocation and cardiac fibrosis.
- Correlation analysis between sternal dislocation characteristics and fibrosis presence.
Main Results:
- Sternal segment dislocation identified in 4.6% of mice, predominantly in males, often at the fourth intersternebral joint.
- Regenerative cartilaginous callus surrounded dislocations in 82.4% of cases.
- Right ventricular epicardial fibrosis occurred in 43% of mice with sternal dislocation, but not in unaffected mice.
Conclusions:
- Right ventricular fibrosis is likely caused by direct sternal segment injury or intrathoracic callus.
- Sternal segment dislocation is a potential confounding factor in mouse models of cardiopulmonary and skeletal diseases.
- Findings highlight the importance of considering skeletal anomalies in cardiovascular phenotyping.
