Wrist Biomechanics as Applied to the Lunate and Kienböck’s Disease

Abstract

Negative ulnar variance, a high lunate uncovering index, and angulated lunate trabeculae are anatomic variants that predispose to Kienböck’s disease. These conditions induce abnormal internal lunate stress, encourage progression of incomplete fractures, and cause progressive lunate collapse and localized trabecular osteonecrosis. Conversely, type II lunates appear to be protective against coronal fractures and scaphoid flexion deformities (which increase stress on the lunate). Lichtman stage IIIb Kienböck’s disease and scapholunate dissociation appear to have different patterns of carpal collapse, particularly with respect to radioscaphoid joint congruity. Unlike scapholunate dissociation, stage IIIb Kienböck’s disease does not involve dorsal subluxation of the proximal scaphoid proximal pole and congruity of the radioscaphoid joint is retained. Radial shortening or ulnar lengthening of 2.5 mm decreases radiolunate pressure by 50 %. Radial wedge osteotomy or lateral closing wedge osteotomy does not actually decrease the total radiolunate load; however, it enlarges the radiolunate joint contact by allowing better coverage of the lunate, thereby decreasing its deleterious peak pressures. Among different types of surgical decompression procedures, the largest reduction of compressive forces on the lunate is obtained by capitate shortening. However, capitate shortening causes the scaphoid–trapezium joint to be greatly overloaded and, under such forces, the scaphoid progressively adopts an abnormal palmar flexed position and carpal collapse occurs. Carpal collapse following capitate shortening can be prevented by partial capitate shortening, which retains articular contact between the capitate and the scaphoid.