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Exposed subchondral bone

normal articular cartilage joint capsule synovial membrane (subchondral) bone

osteoarthritis joint deformation cartilage destruction capsular fibrosis synovial hyperplasia (subchondral) bone remodeling and sclerosis osteophyte formation

Figure 1.3. Overview of the pathologic changes associated with OA. Apart from cartilage destruction, fibrosis of the synovial capsule, hyperplasia of the synovial membrane, subchondral bone remodeling, and osteophyte formation contribute to the disease. (Adapted from Aigner and Stove [4].)

osteoarthritis joint deformation cartilage destruction capsular fibrosis synovial hyperplasia (subchondral) bone remodeling and sclerosis osteophyte formation

Figure 1.3. Overview of the pathologic changes associated with OA. Apart from cartilage destruction, fibrosis of the synovial capsule, hyperplasia of the synovial membrane, subchondral bone remodeling, and osteophyte formation contribute to the disease. (Adapted from Aigner and Stove [4].)

studies of osteoblasts or of isolated chondrocytes [76]. It is not clear how factors released from osteoblasts can act on chondrocytes in vivo, inasmuch as the mineralized bone matrix constitutes a barrier to diffusion. Microdamage or microfracture could initiate vascular invasion [15,81], but healthy articular cartilage contains antiangiogenic factors [87], is resistant to vascular invasion, and is likely capable of repelling any invasion from the subchondral bone. However, OA cartilage has lost its antiangiogenic factors [39] and its resistance to vascular invasion [30,84]. This suggests that changes in the cartilage itself permit vascular invasion to take place. On balance, although the evidence for an association between OA and changes in osteoblasts and the subchondral matrix is strong, the inference that these are causes of OA is as yet controversial (for further details, see Chapter 2).

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Arthritis Relief and Prevention

Arthritis Relief and Prevention

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