Articular cartilage is bordered at its base by the subchondral bone plate, a very thin cortical bone structure that possesses an irregular surface to which the articular cartilage is anchored. Many arterial terminal branches are present in the subchondral bone plate and end in irregularly distributed sinusoids of uneven caliber. Because blood flow in subchondral bone is three to ten times higher than in trabecular bone , the blood flow to subchondral bone supplies approximately 50% of the glucose, oxygen, and water required by articular cartilage [112,141], whose oxygen consumption rate differs from that of other tissues. Indeed, chondrocytes consume much less oxygen than most other cell types. The oxygen supply to chondrocytes in adult cartilage is limited [21,218], so that these cartilage cells function under mainly hypoxic conditions. Microelectrode studies have shown that the oxygen gradient in cartilage is 7:1 from around 7% in superficial layers to 1% in deep zones [21,218]. However, a mathematical model suggests that the oxygen tension in normal cartilage is not likely to drop to 1%, except under abnormal conditions such as OA and rheumatoid arthritis. In fact, the oxygen supply from subchondral bone may be of particular importance forthe deep zone cartilage . Responses to hypoxia include initiation of angiogenesis from vessels within subchondral bone , inasmuch as cartilage itself contains no vascu-lature. Vascular penetration, a characteristic of OA, occurs through the tidemark, with vessels invading the more superficial, noncalcified articular cartilage [31,166]. However, it is uncertain whether this neovascularizationbrings more oxygen to the cartilage layers, because new vessels at the osteochondral junction are consistently associated with new bone formation in the form of osseous cuffs to the fibrovascular channels. Consequently, as the deep layers of articular cartilage become progressively ossified, the original osteochondral junction is obliterated [141,239]. It is likely this process leads to great variations in oxygen tension and modifies the adaptive responses of the chondrocyte, triggering either repair or degenerating processes.
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