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Endochondral Bone Formation in the Heart: A Possible Mechanism of Coronary Calcification

Departments of Internal Medicine (L.A.F.), Orthopedics (R.T.T.), and Physiology and Biophysics (E.R.R.), Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905

Address all correspondence and requests for reprints to: Lorraine A. Fitzpatrick, M.D., 5-194 Joseph, Endocrine Research Unit, Mayo Clinic and Mayo Foundation, 200 First Street SW, Rochester, Minnesota 55905. E-mail: fitz{at}mayo.edu.

During the atherosclerotic process, calcification occurs and is associated with a high likelihood of adverse events. Coronary calcification has been perceived as a passive precipitation of mineral. Recently, calcification associated with atherosclerosis has been found to be the result of an organized, regulated process that is similar to the process of calcification in bone. Mineralization in skeletal tissue can form by endochondral ossification in which mesenchymal cells differentiate into chondroblasts and produce a cartilage matrix which then degenerates and is remodeled to form bone. In this study, hearts from oophorectomized, aged female Sprague Dawley rats were found to contain areas of cartilage. Micro-computerized tomography radiogrammetry provided quantitative images of the architecture and confirmed the calcified tissue. Histological analysis revealed staining for several markers consistent with cartilage and bone tissue: acid phosphatase and bone matrix proteins, osteocalcin, osteopontin, osteonectin, and bone sialoprotein. In addition, cartilage types II, X, and procollagen type I were present.

The presence of chondrocytes in the aged rat heart provides insights into the process of calcification in coronary arteries. Many proteins associated with calcification in bone are present in the cartilage that is present in vascular tissue, suggesting that endochondral calcification is another possible mechanism by which calcification of vascular tissue may occur.

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