Kienböck’s disease: Treatment implications of the wrist-joint tamponade hypothesis

Abstract

Kienböck’s disease, the cause of which is widely considered enigmatic, may be due to a wrist-joint tamponade. Urgently performed arthrocentesis reduces the intra-articular pressure and may thereby prevent osteonecrosis of the lunate and the development of the disease. However, by the time the patient usually seeks care, osteonecrosis has already occurred. On the other hand, if pharmacological inhibition of osteoclast activity is initiated at an early stage (while the anatomy of the necrotic lunate is still intact), it is possible that the lunate anatomy can be preserved and further development of Kienböck’s disease avoided. This hypothesis and the accompanying treatment implications deserve experimental and clinical corroboration.

Key Words: Osteonecrosis; Bone; Wrist; Fracture; Arthritis; Lunate; Kienböck’s disease; Wrist-joint tamponade

Core Tip: If pharmacological inhibition of osteoclast activity is initiated at an early stage (while the anatomy of the necrotic lunate is still intact), it is possible that the lunate anatomy can be preserved and further development of Kienböck’s disease avoided.

INTRODUCTION

After a nondisplaced scaphoid fracture, an intra-articular pressure of 10 kPa (76 mmHg) due to hemarthrosis was recorded and the hypothesis of wrist joint tamponade that may cause osteonecrosis of the carpal bones was put forward[1], since these bones are drained via capsular veins that are directly exposed to intra-articular pressure. The proposed mechanism is analogous to a muscle compartment syndrome, except that the increased pressure is confined within the joint capsule rather than a muscle fascia (Figure 1). Wrist-joint tamponade may explain both traumatic and non-traumatic cases of the disease and may also explain the long-standing mystery of why the disease rarely occurs after intercarpal dislocations and fracture-dislocations (none observed in 59 such cases[3] despite previous trauma to the wrist being reported in approximately 50% of Kienböck’s disease[4]): Because when the joint capsule ruptures in a displaced fracture, the intra-articular bleeding is drained and consequently no joint tamponade occurs. This paper identifies treatment implications arising from this hypothesis.

Figure 1 Schematic graph of a wrist-joint tamponade. A wrist-joint tamponade reduces the arteriovenous perfusion pressure and thus lunate blood flow, which can cause osteonecrosis of the lunate within a few hours. Note that the capsular vein pressure cannot be less than the intra-articular pressure, i.e. the higher the intra-articular pressure, the lesser the arteriovenous pressure perfusion. Urgently performed arthrocentesis reduces the intra-articular pressure and may thereby prevent osteonecrosis of the lunate. AV: Arteriovenous perfusion pressure. Adapted from Matsen[2].

FRAGMENTATION AND COLLAPSE

By the time the patient usually seeks care, the wrist tamponade has long since ceased, osteonecrosis has already occurred, and a slow process of spontaneous revascularization and concomitant resorption of necrotic trabecular bone has begun. The mechanism appears to be osteoclastic bone resorption at the periphery of the necrotic bone, leading to local stress concentration, micro-fractures, fragmentation, and ultimately collapse[5]. During this development, anatomical risk factors (such as ulnar variance, radial inclination, and lunate anatomy) can be expected to have a mechanical impact, through varying degrees of loading, on the weakened necrotic lunate. Current first-line treatments prior to fragmentation and collapse of the lunate include immobilization of the wrist (for at least three months) and decompression osteotomy in attempts to reduce the load on the lunate. This is the preferred treatment in adolescents and in older adults, but in active adults its chances of success are low[6].

MAINTAINING THE ANATOMY

Medical treatment should be aimed at maintaining the anatomy of the lunate as early as possible, i.e. preventing the resorption of necrotic trabecular bone while the anatomy of the lunate is intact. The resorption of necrotic bone can be inhibited pharmacologically with antiresorptive drugs such as bisphosphonates and denosumab that specifically inhibit osteoclast activity[7] without affecting bone formation, i.e. new bone is deposited on necrotic trabeculae during the healing period[5]—visible as sclerosis on radiographs (aka Lichtman stage II). If the pharmacological treatment is started at an early stage, it is likely that the necrotic lunate can be saved from fragmenting and collapsing (as has been shown for osteonecrosis of the femoral head[8,9]). The pharmacological treatment does, of course, not exclude simultaneous immobilization of the wrist and/or decompression osteotomy.

CONCLUSION

When Kienböck’s disease is detected radiographically, the wrist-joint tamponade may have ceased long ago, hence the long-standing difficulty in identifying this as the triggering mechanism. Urgently performed arthrocentesis of a tense joint effusion reduces the intra-articular pressure and may thereby prevent osteonecrosis, but when the patient usually seeks care osteonecrosis has already occurred. However, if pharmacological inhibition of osteoclast activity is initiated at an early stage (while the anatomy of the necrotic lunate is still intact), it is possible that the lunate anatomy can be preserved and further development of Kienböck’s disease avoided. In addition to the aforementioned femoral head, this approach can also be applied to other joints with osteonecrosis, e.g. carpal bones other than the lunate, such as the scaphoid (Preiser’s disease), and to the temporomandibular joint. The hypothesis of wrist-joint tamponade and the accompanying treatment implications deserve experimental and clinical corroboration, which have not yet been conducted (except for the femoral head).