The clinical problem

Half of adults will experience knee pain at some point during their lives, resulting in approximately 4 million primary care office visits in the USA annually.1 The majority of these visits for knee pain evaluation are due to osteoarthritis (OA).2 As of 2015, it was estimated that 14 million people in the USA have symptomatic knee OA,3 and this number is expected to increase to up to 28 million over the next decade.4 One of the most common factors that can initiate the cascade of knee OA is meniscus tears.5

Meniscus root tears are a specific type of meniscal injury that have gained attention over the past 5 years and have been reported to account for 10%–21% of all meniscal tears, affecting nearly 100 000 patients annually.6–8 Untreated meniscal root tears have been reported to result in altered joint biomechanics and accelerated articular cartilage degeneration. In this regard, the ‘recently’ recognised pathology of meniscal root tears has been reported to precipitously worsen articular cartilage degeneration (figure 1), cause painful bone oedema and lead to progressive OA (figure 2) if left untreated.9–13 Furthermore, it is important to recognise the association of meniscal injuries leading to subchondral insufficiency and potentially spontaneous osteonecrosis of the knee (SONK). Previously, SONK was a pathology often diagnosed as an ‘idiopathic’ osteonecrosis of the knee prior to the recognition that this pathology was caused by a meniscal tear.9 13–15 However, the pathogenesis of SONK continues to be debated in the literature with many aetiologies, including certain meniscal tears and meniscectomy, reported to be the primary cause of insufficiency fracture development. It was recently reported that the term SONK is a misrepresentation of the aetiology and pathogenesis of the condition, and should be replaced with ‘subchondral insufficiency fractures of the knee’ (SIFK).16