The etiology of kienböck’s disease

This chapter reviews the conceptual aspects of the etiology of Kienböck’s disease. The stress fracture model would account for many of the cases we see in clinical practice with the “at risk” lunate. The fracture commences on the proximal radial aspect of the lunate and corresponds to the shape of the distal radius. There can be a coronal fracture of the lunate due to the nutcracker effect. Abrasion and reabsorption of the medullary bone can lead to comminution and collapse of the lunate. Avascular necrosis is often considered to be a compartment syndrome of bone. Although it is common to be concerned about the arterial supply of the lunate in Kienböck’s disease, it is more likely to be a venous condition. Jensen has demonstrated increased intraosseous pressure within the Kienböck’s lunate compared to the normal lunate. Crock demonstrated that the subarticular venous plexus consists of wavy parallel venules that are precariously placed directly adjacent to the thin subchondral bone plate. We postulate that the venous condition could be a local condition secondary to the stress fracture. Alternatively it occurs as a extraosseous venous obstruction that produces a global venous ischemia. Finally there is a small group of patients who have a global ischemia, with sclerosis of the entire lunate, and often have a reactive enhancement of the lunate with gadolinium. These patients have a better prognosis.