Kienböck disease is a condition of uncertain etiology that results in osteonecrosis of the carpal lunate.[1, 2] In 1843, Peste presented the initial description of lunate collapse in the French literature. Nearly 70 years later, the Viennese radiologist Robert Kienböck introduced the term lunatomalacia to describe the condition that now bears his name. Kienböck believed that traumatic rupture of the ligaments and vessels around the lunate produced lunate fracture with subsequent collapse.
In 1928, Hulten noted an association between Kienböck disease and the presence of negative ulnar variance. He advanced the progress of treatment by advocating shortening of the radius. Shortly thereafter, Persson presented the option of lengthening the ulna to restore normal ulnar variance.
The true natural history of this condition is not well understood, and this has hampered the determination of the ideal treatment. As with many conditions that affect the wrist, the clinical condition of the patient does not necessarily correlate well with the radiographic appearance.
NextForce transmission studies have formed an important part of the understanding of the pathophysiology of Kienböck disease. In the normal wrist in neutral alignment, 80% of the axial load through the wrist is transmitted through the radiocarpal joint, while the remaining 20% goes through the ulnocarpal joint.
Two-dimensional theoretical models of force transmission in patients with Kienböck disease have demonstrated that in the early stages of the disease (II and IIIa), the normally positioned scaphoid prevents excessive forces on the lunate. However, as the scaphoid assumes its flexed position in stage IIIb, loads across the lunate are increased. These excessive loads may further accelerate the process of fracture and fragmentation leading to collapse.
The etiology of Kienböck disease has not been clearly determined. Most likely, it occurs as a result of repeated loads to a "lunate at risk" by virtue of its unique vascular or mechanical environment. Although the underlying etiology of this condition is not known, the final results of fragmentation and collapse are secondary to osteonecrosis. Intrinsic and extrinsic factors have been implicated.
Vascular supply
The vascular supply of the lunate has been well studied by Gelberman.[3, 4] It consists of both extraosseous and intraosseous vessels running in the dorsal and volar radiocarpal ligaments. Three vessel patterns of intraosseous supply have been noted. In 70% of lunates, multiple vessels enter either volarly or dorsally (X or Y pattern). In the remaining 30% (I pattern), only a single vessel is present palmarly and dorsally, which theoretically places these lunates at increased risk of losing vascular supply.
Kienböck disease has not been reported following perilunate dislocations where the vascular supply has been damaged completely. Early signs of osteonecrosis (eg, increased radiodensity on plain radiographs) may be seen but have not been followed by progression to collapse. Increased intraosseous pressure has been shown to occur in lunates with Kienböck disease, but it is unclear whether this is a primary or secondary finding.
Lunate and distal radius geometry
Zapico classified lunate geometry into three types: Type I lunates occur in ulnar-negative wrists, while type II and III lunates are seen in ulnar-neutral or ulnar-positive wrists. His thesis was that the weakest trabecular pattern was seen in the type I lunate, which helped explain the relation between the ulnar-minus variant and the disease. Later work by Tsuge, however, failed to show an association between lunate geometry and Kienböck disease. Mirabello demonstrated that patients with Kienböck disease with decreased radial inclination developed the disease at an earlier age. The exact biomechanical effect of de-novo decreased radial inclination has not been determined.
Relation between radii of curvature of lunate and capitate
Compressive axial forces are concentrated on the distal articular surface of the lunate because the radius of curvature of the capitate is less than that of its articulating surface on the lunate. As the capitate settles proximally later in the disease process, it can act as a wedge to split the lunate into dorsal and volar halves.
Repetitive trauma
Although no specific data support a causal relation, a history of repetitive microtrauma is often noted in patients with Kienböck disease.[5]
Ulnar variance
A statistical relation between negative ulnar variance and Kienböck disease appears evident, though it is not currently thought to be a causal one. In Hulten's original work, he noted that 23% of the general population has negative ulnar variance, while 74% of his patients with the disorder were ulnar-minus. The ulnar-minus variant has been shown experimentally to cause an abnormal increase in the force transmitted across the lunate. In addition, the triangular fibrocartilage complex (TFCC) is thicker in these patients, and the differential loading between it and the ulnar edge of the radius is increased.
De Smet, however, countered that true correlation between the ulnar-minus variant and Kienböck disease has not been proved when appropriate sex- and age-matched controls and radiographs have been used.[6]
Kienböck disease usually affects the dominant wrist of men aged 20-40 years.
The natural history has not been well elucidated, primarily because few reported series focus exclusively on nonoperative treatment. Kristensen monitored 49 patients nonoperatively for an average of 20.5 years and found that 80% of the patients had no pain or had pain only with heavy labor.[7] Most patients reported a gradual lessening of symptoms over time. This benign clinical picture was not mirrored by radiographic findings, as degenerative changes in the wrist were common and every lunate was deformed.
In a retrospective study comparing surgical treatment with nonsurgical treatment for patients with Kienböck disease, Delaere noted that surgical management did not appear to show superiority over nonsurgical treatment at 5 years of follow-up.[8] Care should be taken in interpreting these results, however, because scaphotrapeziotrapezoid (STT; triscaphe) fusions were performed in the majority of those treated surgically. This procedure has not been shown to produce long-lasting good results. In addition, patients who had more advanced disease were more likely to undergo surgery.
Mikkelsen noted that 15 of 25 patients treated conservatively had daily problems with the wrist.[9] He concluded that nonoperative treatment was not indicated for Kienböck disease. In the early stages of Kienböck disease, a short trial of casting may alleviate symptoms and obviate the need for surgery. These patients should be monitored closely so that surgery, if necessary, can be performed when radial shortening is still feasible.
Although initial success was seen with the use of a silicone spacer following lunate resection, this implant is no longer indicated. Alexander presented a 5-year follow-up of a group of 10 patients with silicone lunate replacements and noted 50% unsatisfactory results.[10] Sixty percent of patients who had radiographs at final follow-up demonstrated evidence of silicone particulate synovitis.
Lunate excision is not commonly recommended, because of concerns of progression of carpal collapse. A fascial or palmaris anchovy replacement has had variable success in preventing subsequent collapse, though Carroll reported long-term (>10 years) success in a series of 10 patients treated with a fascial implant following lunate excision. He noted no evidence of carpal collapse, and all patients had unrestricted use of their hands.
Radial shortening remains a mainstay of treatment. It is a reliable, reproducible procedure with good results. Weiss and Quenzer presented large series of radial shortenings,[11, 12, 13] noting decreased pain in about 90% of patients, as well as improved motion and grip strength at 4-year follow-up. Weiss also demonstrated that good results can be obtained in patients with stage III disease who have evidence of lunate collapse.
Despite good clinical outcomes, radiographic signs of continued collapse and degeneration are common. Although ulnar lengthening has demonstrated similar clinical outcomes, it is also associated with a higher complication rate. For this reason, radial shortening is the preferred joint-leveling method.
Watson reported on the use of STT (triscaphe) fusion for stage III disease and noted nearly 80% of his patients had good or excellent pain relief at 51-month follow-up.[14] Caution should be used in evaluating these results, in that nearly 40% of his patients required additional procedures to achieve this outcome. Compared with STT fusion, scaphocapitate (SC) fusion has demonstrated similar pain relief rates but slightly decreased motion. Currently, no long-term results are available on the use of capitate shortening with or without capitohamate arthrodesis.[15]
In a series of 51 patients who underwent vascular bundle implantation, 98% showed a reduction or resolution of pain at long-term follow-up. Again, these encouraging clinical results were not mirrored by radiographic improvement: 20% had further degeneration and 10% had frank fragmentation. Results of the newer technique of distal radial vascular bone pedicle were noted previously.
The expected outcome following proximal row carpectomy (PRC) is 75° in the flexion-extension arc and grip strength of 75% of the opposite side. Pain relief has been demonstrated in 80% of patients who underwent PRC for Kienböck disease. As noted, a PRC can be converted successfully to wrist arthrodesis.
Several other options for treatment have been reported. Ruby performed cancellous bone grafting supplemented by postoperative external fixation and found good pain relief in 80% of patients.[16] In patients with stage III disease and mechanical symptoms, arthroscopic debridement was found to decrease pain and increase motion. Wrist denervation is a simple, safe option that can also be combined with other procedures to aid in postoperative pain reduction. In fact, denervation itself may provide much of the perceived pain reduction in cases where the dorsal capsule is incised to perform the index procedure.
Gay et al evaluated the use of a simple capitate osteotomy without arthrodesis, through a dorsal medial approach and fixed with staples, in 11 patients with mild forms (stage I to IIIA, Lichtman classification) of Kienböck disease.[15] At final follow-up (mean, 67.4 months), the mean visual analogue scale score was 1.7 (range, 0-7). There were six good results, two fair results, and three poor results. Compared with the healthy side, mean strength improvement was 25%. In two cases, revision surgery was necessary.[15]
Takahara et al reported on 13 patients (6 with stage II, 4 with stage IIIA, and 3 with stage IIIB) who responded to a DASH (Disabilities of the Arm, Shoulder and Hand) questionnaire regarding previous radial osteotomy for Kienböck disease (mean follow-up, 21 years).[17] Mean DASH score was 8 points (range, 0-23), and patient satisfaction was high. The DASH scores tended to be worse in patients with stage IIIB disease.
Follow-up radiographs revealed that the Lichtman stage had progressed in six of the 12 patients.[17] Compared with the contralateral wrist, mean range of motion was 81% in flexion and 82% in extension; mean grip strength was 88%. Clinical results were considered excellent in six patients, good in five, and moderate in one.
Clinical Presentation
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