The pathogenesis of osteonecrosis.
Although numerous studies concerning the pathogenesis of osteonecrosis have been published, the pathophysiologic mechanisms that may be involved continue to be debated. In the early 1980s, the concept of accumulative cell stress was advanced, which is a theory that proposes that bone cells are exposed to multiple insults or stresses, the effects of which accumulate to the point that the cells cannot sustain themselves and die. Technologic advances have led scientists to a better understanding of cell and molecular biology, and recent studies of osteonecrosis and its risk factors have indicated that this concept should be revisited. It now appears that using the term "necrosis" may be incorrect and that apoptosis may play a significant role. Research on osteoporosis, fracture healing, bone graft incorporation, hematology, and genetics may lend insight into the etiology and pathogenesis of osteonecrosis. Several studies on osteoporosis have focused on the effect of exogenous glucocorticoids on the behavior of osteocytes, osteoblasts, osteocytes, and their precursors. Recent findings on osteonecrosis and bone biology are placed into the context of what has been previously reported.
Jones
Lynne C
LC
Center for Osteonecrosis Research and Education, Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Hungerford
David S
DS
D005270:Femur Head / Q000473:pathology; D006801:Humans; D059630:Mesenchymal Stem Cells / Q000502:physiology; D010006:Osteoblasts / Q000473:pathology; D010010:Osteoclasts / Q000473:pathology; D010020:Osteonecrosis / Q000453:epidemiology / Q000235:genetics / Q000503:physiopathology*; D020641:Polymorphism, Single Nucleotide; D012307:Risk Factors