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Ann Thorac Surg 2004;77:537-543
© 2004 The Society of Thoracic Surgeons

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Original article: cardiovascular

Role of oral bacterial flora in calcific aortic stenosis: an animal model

^a Cardiothoracic Surgery Service, Brooke Army Medical Center, Fort Sam Houston, Texas, USA
^b Department of Pathology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA
^c Department of Surgery, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA
^d Department of Orthopedics, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA

Accepted for publication July 8, 2003.

^* Address reprint requests to Dr Cohen, Colonel Medical Corps, US Army, 15638 Dawn Crest, San Antonio, TX, USA 78248-1723
e-mail: david_j_cohen{at}hotmail.com

BACKGROUND: Calcific aortic stenosis is a major public health problem in the United States. The mechanism of calcification remains unclear. The hypothesis that low grade chronic or recurrent bacterial endocarditis with specific calcifiable bacteria is a cause of calcification of the aortic valves was investigated using an animal model. Such bacteria are typically present as part of the normal human oral flora.

METHODS: Forty New Zealand white rabbits were divided into four groups: group 1, control (1 ml of normal saline); group 2, Corynebacterium matruchotti 100,000 colonies; group 3, Streptococcus sanguis II 10 colonies; and group 4, C matruchotti 100,000 colonies plus S sanguis II 10 colonies. Animals were inoculated with bacteria through a flexible catheter placed through the aortic valve through a right carotid cut down. Inoculations were repeated every 3 days the first 2 weeks and then twice a week thereafter. At postmortem examination the aortic valves were harvested, embedded in paraffin, and stained with von Kossa stain. They were also examined by scanning and transmission electron micrography.

RESULTS: Group 4 had 93.3% large calcifications (confluent calcium densities that are easily recognized with minimal magnification) and 6.6% small microcalcifications (dustlike microscopic particles requiring a compound microscope to appreciate) of the aortic valves. Group 3 exhibited large calcification in 20% and small in 40% of the aortic valves. Group 1 and group 2 had no evidence of calcification.

CONCLUSIONS: These results suggest that recurrent low-grade endocarditis from calcifying oral bacteria, particularly when occurring with synergistic strains, may be one cause of calcific aortic stenosis.

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