Kiaer T, Grønlund J, Sørensen K H
Department of Orthopaedic Surgery, Odense Sygehus, Denmark.
Clin Orthop Relat Res. 1988 Apr(229):149-55.
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.
原发性人类骨关节炎的发病机制尚不清楚。有人提出，软骨下血流减少所导致的缺氧在骨关节炎组织损伤的发展中起核心作用。本研究采用基于质谱的原位技术，对晚期单侧骨关节炎患者双侧股骨头及对侧正常髋关节的软骨下pO2和pCO2进行测量，以验证这一假说。记录骨内压，并测量从双侧股骨头采集的血样中的乳酸浓度和pH值。患侧髋关节的软骨下pO2显著低于正常髋关节（43托对63托）。患侧的骨内压显著高于正常髋关节。患侧髋关节的乳酸浓度增加了50%。两个部位的pCO2和pH值没有差异。
