Osteoarthritis (OA) is a major cause of disability in the adult population. As a
progressive degenerative joint disorder, OA is characterized by cartilage damage,
changes in the subchondral bone, osteophyte formation, muscle weakness, and
inflammation of the synovium tissue and tendon. Although OA has long been viewed as a
primary disorder of articular cartilage, subchondral bone is attracting increasing
attention. It is commonly reported to play a vital role in the pathogenesis of OA.
Subchondral bone sclerosis, together with progressive cartilage degradation, is
widely considered as a hallmark of OA. Despite the increase in bone volume fraction,
subchondral bone is hypomineralized, due to abnormal bone remodeling. Some
histopathological changes in the subchondral bone have also been detected, including
microdamage, bone marrow edema-like lesions and bone cysts. This review summarizes
basic features of the osteochondral junction, which comprises subchondral bone and
articular cartilage. Importantly, we discuss risk factors influencing subchondral
bone integrity. We also focus on the microarchitectural and histopathological changes
of subchondral bone in OA, and provide an overview of their potential contribution to
the progression of OA. A hypothetical model for the pathogenesis of OA is
proposed.