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The pathogenesis of primary human osteoarthritis is unknown. It has been suggested that hypoxia caused by reduced subchondral blood flow plays a central role in the development of tissue damages in osteoarthritis. This hypothesis was investigated using an in situ technique based on mass spectrometry to measure subchondral pO2 and pCO2 in both femoral heads of patients with late stage unilateral osteoarthritis and the normal opposite hip. Intraosseous pressure was recorded and lactate concentrations and pH were measured in blood samples obtained from the two femoral heads. The subchondral pO2 in the diseased hip was significantly lower than pO2 in the normal hip (43 torr versus 63 torr). The intraosseous pressure was significantly higher in the diseased than in the normal hip. The lactate concentration showed a 50% increase in the diseased hip. There were no differences in pCO2 and pH between the two locations.
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