title: Bone density and osteoarthritis.
abstract: Osteoarthritis (OA) is a physiologic imbalance, a "joint failure" similar to "heart failure" in which mechanical as well as constitutional factors play a role. The initiation and progression of cartilage damage are distinct phenomena. One of the mechanisms of initiation of OA is subchondral bone stiffness, often a part of generalized inherited increased bone density. Evidence is accumulating that primary OA might initially be a bone disease rather than a cartilage disease. OA cases have a better preserved bone mass, even independent of body weight. Studies on iliac crest bone, a site far from load bearing forces, have shown differences in bone mass, biomechanical characteristics, biochemical composition, and mineralization profile according to the presence of OA in the hands. Women with OA had significantly more bone and the bone was significantly stiffer, they had higher compressive strength, higher osteocalcin, higher insulin-like growth factor I and II and transforming growth factor beta content, and a mineralization profile shifting to higher densities. These quantitative and qualitative differences in bone may produce disease by increasing subchondral bone stiffness and by making subchondral bone less deformable to impact leads. This stiff bone transmits more force to overlying cartilage, making it more vulnerable.
authors.affiliation: Arthritis and Metabolic Bone Disease Research Unit, University of Leuven, University Hospital, Pellenberg, Belgium.
authors.forename: J
authors.initials: J
authors.lastname: Dequeker
authors.forename: L
authors.initials: L
authors.lastname: Mokassa
authors.forename: J
authors.initials: J
authors.lastname: Aerssens
mesh_terms: D015519:Bone Density / Q000502:physiology; D005260:Female; D006801:Humans; D008297:Male; D010003:Osteoarthritis / Q000209:etiology / Q000503:physiopathology; D010024:Osteoporosis / Q000209:etiology / Q000503:physiopathology