Subchondral Bone and Cartilage Disease

Abstract

The role of subchondral bone in the pathogenesis of cartilage damage has likely been underestimated. Subchondral bone is not only an important shock absorber, but it may also be important for cartilage metabolism. Contrary to many drawings and published reports, the subchondral region is highly vascularized and vulnerable. Its terminal vessels have, in part, direct contact with the deepest hyaline cartilage layer. The perfusion of these vessels accounts for more than 50% of the glucose, oxygen, and water requirements of cartilage. Bony structure, local metabolism, hemodynamics, and vascularization of the subchondral region differ within a single joint and from one joint to another. Owing to these differences, repetitive, chronic overloading or perfusion abnormalities may result in no pathological reaction at all in one joint, while in another joint, these same conditions may lead to osteonecrosis, osteochondritis dissecans, or degenerative changes. According to this common etiological root, similar pathological reactions beginning with marrow edema and necrosis and followed by bone and cartilage fractures, joint deformity, and insufficient healing processes are found in osteonecrosis, osteochondritis dissecans, and degenerative disease as well.

MRI follow-up of subchondral signal abnormalities in a selected group of chronic low back pain patients

“…It has been suggested that they may represent different consecutive phases of the degenerative process in the subchondral marrow [3,17]. The importance of the endplate [21,22] and subchondral bone [8] for the integrity of the intervertebral disc has been pointed out. An injury to the vertebral body endplate has been found to provide a potent mechanical stimulus for disc degeneration [20] and tissue trauma following fracture has been suggested to cause accelerated intervertebral disc degeneration [10].…”

“…A microtrauma to the endplate has been suggested to be the initiating event for a progressive deteriorating process with inflammatory or autoimmune effects, by allowing a contact between the noxious substances in the degenerative disc and cells in the bone matrix via the injured endplate [1,20]. An endplate defect may also develop as a non-specific reaction to an insufficient healing process, beginning with bone marrow edema and necrosis [8]. An inflammatory process in endplates with M1 subchondral signal changes has been suggested to be induced by tumor necrosis factor (TNF) [18].…”

Osteoarthritis revisited—again!

“…But, is this so? The work of Imhof and others has shown our classical teaching of the impermeable osteochondral junction is not correct [26]. By revisiting the histology of this region, the conclusion is drawn that the terminal vessels in the richly supplied subchondral zone of normal mature bone directly contact the deepest hyaline cartilage layer.…”

Low Level Laser Therapy in the Treatment of Temporomandibular Joint Arthritis: Questions and Answers

“…Only 1-3% of load forces are attenuated by cartilage while the normal subchondral bone is able to attenuate about 30% of the load through the joints. (Imhof, Sulzbacher et al, 2000) The subchondral bone protects the articlar cartilage from damage caused by excessive loading. The condylar ear and the articular fossa receive their blood supply from arteries supplying the underlying bone.…”