Osteoarthritis is usually considered to be a primary disorder of chond
rocyte function with secondary changes in bones. However, a defect in
the subchondral bone resulting in loss of its shock absorbing capacity
could transfer the stress of loading directly to the articular cartil
age with secondary changes in the cartilage. Review of histomorphometr
ic and bone densitometric studies at sites of osteoarthritis at the hi
p or knee revealed that cartilage fibrillation could not be dissociate
d from bony changes even in the earliest stages of osteoarthritis and
that subchondral trabeculae are thickened and more spaced in osteoarth
ritis. Microfractures of subchondral trabecular bone were less frequen
tly seen in osteoarthritis compared to controls. Changes of the tidema
rk were found to be multiform and metabolically active in the osteoart
hritic process. Endochondral ossification depletes the calcified carti
lage at the cartilage/bone interface and the tidemark has been thought
of as a calcification front advancing in the direction of non-calcifi
ed cartilage. Duplication of the tidemark is cited as evidence of this
advancement. In the few experimental animal studies of subchondral bo
ne in osteoarthritis, thicker trabeculae which were closer together we
re found in guinea pigs already when only mild cartilage changes were
present. In the dog, with cruciate ligament transection, changes in bo
ne were later than in the cartilage, but the changes in bone could sti
ll contribute to the progression of osteoarthritis. To study if bone c
hanges may precede injury to the cartilage and if metabolic and system
ic influences can also alter the subchondral bone, rendering it less a
ble to withstand normal mechanical stresses, bone at different sites i
n the body has been studied extensively by the authors. Epidemiologica
l and case control studies have revealed that osteoarthritis cases hav
e more bone at all sites than expected and that bone in cases with gen
eralized osteoarthritis shows both quantitative and qualitative differ
ences, including increased contents of growth factors and hypermineral
ization. These findings suggest that a more generalized bone alteratio
n may be the basis of the pathogenesis of osteoarthritis. (C) 1997 Wil
ey-Liss, Inc.