Osteonecrosis of the knee is a debilitating disease that can progress to end-stage osteoarthritis. Spontaneous osteonecrosis of the knee (SONK or SPONK) is 1 of 3 categories that are used to substratify osteonecrosis, the other 2 being secondary and postarthroscopic. SONK has been described as a focal, superficial subchondral lesion. While several risk factors have been proposed (including female sex, age, cartilage degeneration, low bone mineral density [BMD] and medial meniscus posterior root tears), the precise etiology is unknown and the pathological mechanisms involved remain poorly characterized, making effective management challenging.
The etiology and pathogenesis of SONK and postarthroscopic osteonecrosis remain highly controversial, and many theories have been proposed. Historically, SONK has been thought to occur secondary to ischemia, resulting in necrosis. Recently, however, a theory has been popularized proposing this entity to be a subchondral insufficiency fracture in osteopenic bone with no evidence of necrosis. These insufficiency fractures are thought to lead to fluid accumulation in the bone marrow, resulting in edema with focal ischemia and eventual necrosis. Factors predisposing to insufficiency fractures may include meniscal tears or meniscectomy, which can alter the native biomechanics and increase contact pressures and stress concentration on weightbearing areas. Postarthroscopic osteonecrosis seems to follow a similar pathogenesis. Therefore, the purpose of this study was to perform a detailed systematic review of the literature to evaluate studies that suggest etiological mechanisms for SONK in order to establish an improved understanding. We hypothesized that the etiology of SONK would be multifactorial.