Therapeutic Mechanisms of Action for Hyperbaric Oxygen on Femoral Head Necrosis

Abstract

Femoral head necrosis (FHN) is a disease process resulting from inadequate blood perfu- sion of subchondral bone. While the etiology of this disease is still not fully understood, there are multiple traumatic and atraumatic factors that are associated with the disease. Pathophysiology of the disease is characterized by the death of bone marrow and osteocytes. If left untreated, the disease may progress to joint collapse. While initial stages of the disease are asymptomatic, painful limitation of active and passive motion of the hip is eventually present. The current body of literature cannot identify an optimal treat- ment protocol for FHN. Postcollapse cases require surgical intervention, core decompression, or total hip arthroplasty. However, current strides in conservative management are being made. One of the possible conservative modalities that may effectively delay hip arthroplasty or even prevent the need for a surgical approach is hyperbaric oxygen (HBO 2 ) therapy. HBO 2 increases extracellular oxygen concentration and reduces cellular ischemia and edema by inducing vasoconstriction. Studies have reported radiographic improvement, reduction in pain, and increases in range of motion for early stages of the disease. Hyperbaric oxygen therapy has also been shown to stimulate angiogenesis and enhance osteoclast and osteoblast function for remodeling and repair.