Lunate biomechanics: application to Kienböck's disease and its treatment

Abstract Kienbock's disease was initially considered as lunate osteomalacia due to lesions of its nutrient arteries during carpal ligament tears. It has also been suggested following primary fractures, or because of repeated microtrauma. It is only in the past 20 or 30 years that it has appeared as aseptic necrosis. Based on Hulten's hypothesis that a negative radioulnar index was the cause of Kienbock's disease, equalization osteotomies (shortening of the radius or lengthening of the ulna) were developed. The observation of Kienbock's disease in subjects with a positive index and the risk of ulnar abutment after osteotomy led to the introduction of new osteotomies to get around these difficulties, still in the hope of treating the cause of Kienbock's disease. While it has been confirmed that a negative radioulnar index promotes lunate fracture, it clearly does not induce the pathology in the form of necrosis. In this scenario, perilunar osteotomies produce durable decompression, limiting the risk of lunate fracture in case of necrosis by removing the compressive constraints. After comparing the different osteotomies used to treat Kienbock's disease, it seems that the Camembert osteotomy for radius shortening, combined with selective shortening of the ulnar head as described by Sennwald, decompresses the lunate maximally, and protects it long enough for potential natural revascularization to occur.