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Kienböck’s Disease: Diagnosis and Treatment

Allan, Christopher H. MD; Joshi, Atul MD; Lichtman, David M. MD

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Journal of the American Academy of Orthopaedic Surgeons: March 2001 - Volume 9 - Issue 2 - p 128-136
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In 1910, Robert Kienböck, a Viennese radiologist, reported a series of 16 cases of “traumatic malacia„ of the lunate.1 Although others had described similar anatomic findings in cadaveric specimens, Kienböck’s was the first clinical report of osteonecrosis of the lunate. He provided radiographic evidence of isolated changes beginning in the proximal portion of the lunate and affecting the radiolunate articulation, with other areas spared. He described the collapse of the lunate, occasionally with fragmentation, and felt that this condition was caused by “a disturbance in the nutrition of the lunate caused by the rupture of ligaments and blood vessels during contusions, sprains, or subluxations.„ He recommended excision of the bone in the event of severe pain and disability.

Kienböck’s disease occurs most commonly in men aged 20 to 40.2 It is rarely bilateral, and patients frequently have a history of wrist trauma. The initial symptoms of pain over the dorsum of the wrist in the region of the lunate accompanied by limited wrist motion may have been present months to years before the patient seeks medical attention. Some patients with radiographic evidence of severe destruction are relatively asymptomatic; however, most have increasing reactive synovitis and limitation of wrist motion, swelling, grip weakness, and pain with motion and eventually at rest.

Isolated or repetitive trauma to a lunate predisposed to injury due to any of several factors (e.g., bone geometry and vascularity) may lead to a fracture or to vascular compromise. Bone necrosis results in trabecular fractures and sclerosis. Untreated, the process continues, with collapse and fragmentation of the lunate. At this stage, carpal height is decreased, the capitate migrates proximally, and the scaphoid hyperflexes (Fig. 1). Abnormal carpal motion, particularly related to scaphoid rotation,3,4 leads to degenerative changes throughout the carpus and the radiocarpal joint.

Figure 1
Figure 1:
Radiographic wrist measurements.

Patients in early stages of the disease rarely seek medical attention. Therefore, the true incidence and the natural history are not known with certainty. Nevertheless, the apparent common pathway involves osteoarthritic changes and debilitating pain, which has led to the development of a large and confusing array of treatment options. The clinical condition of Kienböck’s disease, therefore, remains challenging to both patient and physician.


Many direct or indirect causes of Kienböck’s disease have been proposed. The local vascular and osseous anatomy may play a role. The patterns of lunate blood supply provide insight into some possible causes of osteonecrosis of this bone. There are multiple patterns of arterial supply,2,5 with the lunate in most cadaveric specimens receiving contributions from branches entering both dorsally and palmarly. However, the lunate was supplied by only a single palmar artery in 7% of wrists in one study.6 In addition, intraosseous branching patterns vary, with 31% of specimens in one study showing a single path through the bone without significant arborization (Fig. 2).6 A lunate with a single vessel and minimal branching may be at increased risk of osteonecrosis after hyperflexion or hyperextension injuries or a minimally displaced fracture. Of interest, Takami et al7 reported that severe injuries, such as lunate dislocation, can occur without the development of osteonecrosis or with only a transient appearance of this condition. This is because the lunate usually dislocates palmarly, with a flap of palmar capsule still attached. All specimens examined in that study had at least one palmar vessel; therefore, the intact flap probably transmits sufficient vascular supply to maintain lunate viability.7

Figure 2
Figure 2:
Patterns of intraosseous arterial branching in the lunate. (Adapted with permission from Gelberman RH, Bauman TD, Menon J, Akeson WH: The vascularity of the lunate bone and Kienböck’s disease. J Hand Surg {Am[ 1980;5:272–278.)

Disruption of venous outflow has also been suggested as a cause of Kienböck’s disease. In one study,8 in vitro intraosseous pressure measurements within normal and necrotic lunates showed marked increases in pressure in the necrotic bones, a finding more consistent with venous stasis than with arterial compromise. It is unclear whether this is a cause or a result of the disease process (the authors of that study point out that these findings may be due solely to collapse of the lunate), but traumatic disruption of venous outflow may be another factor in lunate osteonecrosis.

Lunate geometry and local anatomy may be important as well. Negative ulnar variance, first identified as a factor by Hultén9 in 1928, was present in 78% of his patients with Kienböck’s disease, but in only 23% of the general population. Hultén suggested that a short distal ulna led to increased force transmission across the radiolunate articulation, contributing to an increased risk of osteonecrosis. However, D’Hoore et al10 found no statistically significant difference in ulnar variance when they compared 125 normal wrists with 52 wrists in patients with Kienböck’s disease. Several investigators from Japan11,12 have noted that negative ulnar variance occurs with equal frequency in patients with Kienböck’s disease and in the general population. A flattened radial inclination may predispose to Kienböck’s disease.12,13 Watanabe et al13 noted a tendency toward smaller lunates in their patients with the disorder. Thus, negative ulnar variance and flattened radial inclination may predispose certain patients to develop Kienböck’s disease, but neither is likely to be the sole factor.

Occasional occurrences of Kienböck’s disease have been reported in association with such conditions as septic emboli, sickle cell disease, gout, carpal coalition, and cerebral palsy, as well as corticosteroid use. However, there is no well-defined correlation with any systemic or neuromuscular process that warrants screening when considering the diagnosis.2,14

Thus, the etiology of Kienböck’s disease seems to involve the interplay of multiple factors. Vascular and skeletal variations may lead to an at-risk lunate, which, when subjected to traumatic insult, repetitive mechanical loading, or some other factor, may develop osteonecrosis. It is still not clear whether the lunate fracture lines occasionally seen in early Kienböck’s disease represent a primary event, or whether these fractures occur later in the process, after revascularization and resorption of necrotic bone cause structural weakness.15,16

Diagnostic Techniques and Staging

Kienböck’s disease can occur in patients of any age and either sex even if there is no history of prior wrist problems. Symptoms vary depending on the stage of the disease at presentation and may range from mild discomfort to constant, debilitating pain. Swelling over the carpus is common and may occur palmarly as well as dorsally. Tenderness over the dorsum of the lunate is a frequent finding. Grip strength may be markedly reduced. Wrist range of motion may be minimally or severely impaired.

In 1977, Lichtman described a clinical and radiographic classification for Kienböck’s disease, which is now widely used to stage treatment and compare outcomes2 (Table 1). Before the advent of magnetic resonance (MR) imaging, radionuclide scintigraphy was the next diagnostic study recommended after plain radiography. Hashizume et al17 have pointed out, however, that MR imaging cannot distinguish among osteonecrosis, the histologic reactive interface between living and dead bone, and reactive hyperemia. They suggest that MR imaging is nevertheless superior to plain radiography, tomography, or computed tomography, in defining the early stage of Kienböck’s disease (Lichtman stage I), when trabecular bone has not yet been destroyed. By contrast, once lunate collapse has occurred, tomography or computed tomography best reveals the extent of necrosis and trabecular destruction.17

Table 1
Table 1:
Stages of Kienböck’s Disease

Quenzer et al18 reported that trispiral tomography makes possible more accurate staging than standard tomography or plain radiography. In a study of 105 patients with Kienböck’s disease, they noted that 89% of patients with radiographic stage I disease actually met the tomographic criteria for stage II; this “up-staging„ was true as well for 71% of those with radiographic stage II disease and 9% of those originally considered to have stage III disease. Nevertheless, since trispiral tomography is not routinely available, plain radiography and MR imaging (Fig. 3) remain the most common tools for staging Kienböck’s disease.

Figure 3
Figure 3:
T1-weighted MR image reveals decreased signal intensity of the lunate in the wrist of a patient with Kienböck’s disease.

In stage I, plain radiographs are either normal or occasionally demonstrate a linear fracture without sclerosis or collapse of the lunate (Fig. 4). No changes are seen elsewhere in the carpus. The early-flow phase of bone scintigraphy may indicate reactive synovitis. In stage I, MR imaging is highly suggestive when there is uniformly decreased signal intensity on T1-weighted images in comparison with the surrounding normal bones. This change in signal intensity reflects reduced vascularity of the lunate.19 Caution must be exercised when partial T1 signal loss is noted, however. Disorders such as ulnar abutment, fractures, enchondromas, and osteoid osteoma can cause focal MR signal changes. In addition, transient ischemia may cause a generalized decrease in lunate signal intensity. T2-weighted images typically show low signal intensity in Kienböck’s disease, but will show increased signal if revascularization is occurring.20,21 For this reason, MR imaging may also be used to assess healing of the lunate after treatment. Symptoms in stage I resemble those of wrist sprains and early nonspecific synovitis.

Figure 4
Figure 4:
Drawings and radiologic images illustrating staging of Kienböck’s disease, according to Lichtman.2 In stage I, the trabecular bone has not yet been destroyed, and plain radiographs either are normal or demonstrate a linear fracture without sclerosis or collapse of the lunate. In stage II, findings include increased density of the lunate, frequently with one or more fracture lines; the entire lunate may be sclerotic, but lunate height is preserved. In stage IIIA there is lunate collapse, but carpal height is relatively unchanged. Stage IIIB is characterized by proximal migration of the capitate and fixed hyperflexion of the scaphoid (cortical “ring sign„). In stage IV, arthritic changes are apparent throughout the radiocarpal and/or midcarpal joint. (Reformatted coronal CT image depicts both radial styloid and radiolunate degenerative changes.)

Radiographic findings in stage II Kienböck’s disease include increased density of the lunate on plain radiographs, frequently associated with one or more fracture lines. Density changes in the lunate are often best appreciated on the lateral plain radiograph. The entire lunate may be sclerotic, but lunate height is preserved. There are no associated carpal abnormalities. Clinical findings in stage II are frequently those of chronic synovitis.

Increased density of the lunate can also occur as a transient finding, not associated with the typical progressive changes of Kienböck’s disease. This is a common finding after perilunate fracture-dislocations, and generally resolves with standard treatment of the initial injury.7

In stage III, the lunate shows collapse. This stage can be divided into two categories. In stage IIIA, lunate collapse has occurred, but carpal height is relatively unchanged. Lateral radiographs demonstrate a widened anteroposterior dimension of the lunate associated with shortening in the coronal plane. Neither proximal migration of the capitate nor fixed hyperflexion of the scaphoid (cortical “ring sign„) is present. In stage IIIB, these signs of carpal collapse do appear. In addition, there may be ulnar deviation of the triquetrum and either the dorsal or the volar intercalated segment instability pattern. Clinical findings are progressive stiffness in stage IIIA and signs of wrist instability in stage IIIB.

In stage IV Kienböck’s disease, arthritic changes are also apparent throughout the radiocarpal or midcarpal joint or both. Symptoms in stage IV are similar to those of degenerative arthritis of the wrist, with more severe swelling, pain, and limitation of motion.


The value of staging Kienböck’s disease lies in guiding the selection of treatment (Table 2), in predicting the results of treatment, and in comparing the results of different treatment regimens. There is a vast array of proposed treatments for Kienböck’s disease, but certain techniques have documented patterns of success. These will be discussed along with alternative procedures for each stage of disease.

Table 2
Table 2:
Options for Treatment of Kienböck Disease

Stage I

Many authors report poor results with prolonged immobilization as the primary treatment for stage I disease.22 For this reason, some clinicians elect to treat stage I disease in the same way as stage II and stage IIIA disease. Nevertheless, for most clinicians, cast immobilization (or an equivalent form of wrist immobilization, such as with use of an external fixator) remains the first treatment option for stage I Kienböck’s disease. The possibility of resolution of symptoms does exist; therefore, a trial of immobilization for as long as 3 months is appropriate. In addition, such a period may allow the restoration of vascularity in cases of transient osteonecrosis of the lunate, helping to distinguish this entity from Kienböck’s disease.

Delaere et al22 recently reported that night splinting during periods of discomfort for patients with stage I, II, or III Kienböck’s disease gave results equivalent to those obtained with surgical treatment. However, the average level of disease severity in the splinted group was one stage lower than that in the operatively treated group; thus, comparison was difficult. However, in another series of 22 nonsurgically treated patients with various stages of disease,2 17 showed progression, and 5 had no improvement.

When immobilization fails to reverse the avascular changes, the process will almost always have advanced to stage II. In this setting, analysis of ulnar variance is important.

Stage II or IIIA With Neutral or Positive Ulnar Variance

Stages II and IIIA are often considered together, and treatment options are similar with one major exception. In stage II, lunate avascularity has developed, but the bone has not collapsed. Direct revascularization procedures have their greatest likelihood of success in this stage.

A number of vascularized pedicle and/or bone grafting procedures have been described, including vascularized transfers of the pisiform bone, transfers of segments of the distal radius on a vascularized pedicle of pronator quadratus, and transfers of branches of the first, second, or third dorsal metacarpal arteries.23–25 Our preference has been to use the second dorsal intermetacarpal artery and vein either as originally described26 or as modified by suturing it to a corticocancellous graft harvested from the distal radius.24 Most of the recently described vascularized pedicle bone grafts have the advantage that the bone graft and vascular pedicle are harvested together, making the procedure technically easier. The dorsal aspect of the distal radius is supplied by several arterial branches, which enter the bone via septa between the extensor compartments. When these are used, no vein is harvested. Because of anatomic variation, it is best to be aware of the location of several potential vascularized pedicle bone grafts before performing such a procedure. External fixation to unload the lunate after revascularization has often been used, but temporary pinning of the scaphotrapeziotrapezoid (STT) joint or the scaphocapitate (SC) joint for the same purpose has also been described.24,25 Outcomes of the various direct revascularization procedures are still being evaluated.

Treatment options other than direct revascularization for patients with stage II or IIIA disease and positive ulnar variance include radial closing-wedge osteotomy, radial-dome osteotomy, and capitate shortening with or without capitohamate fusion (Almquist procedure).11,13,27 These may be considered attempts to unload the lunate to improve its environment for revascularization through decreasing the shear stress across the radiolunate joint. Capitate shortening (Figs. 5 and 6) is relatively simple, and good results have been reported (83% revascularization and healing of the lunate in one report27). In addition, a recent biomechanical study showed that capitate shortening with capitohamate fusion significantly (P<0.05) decreased the load across the radiolunate articulation.28 If this procedure is chosen, it is helpful to ensure that the hamate is not allowed to abut on the lunate after shortening of the capitate; if this appears to be the case, removal of the proximal tip of the hamate with a rongeur will correct the problem.29

Figure 5
Figure 5:
Capitate shortening with capitohamate fusion.
Figure 6 A,
Figure 6 A,:
Preoperative AP radiograph of the wrist of a patient with stage IIIA Kienböck’s disease. B, Postoperative radiograph shows fixation of the lunate fracture and vascularized bone grafting, in addition to capitate shortening.

Stage II or IIIA With Negative Ulnar Variance

In patients with stage II or IIIA Kienböck’s disease and significant negative ulnar variance, a shortening osteotomy of the radius may be performed in an effort to reduce forces on the lunate. Preoperative measurement of ulnar variance is made in order to plan the amount of radial resection; sufficient bone should be removed to result in neutral to 1-mm positive ulnar variance. Positive ulnar variance greater than 1 mm risks abutment of the ulna on the lunate or triquetrum, which is manifested by ulnar-sided discomfort after surgery.

Horii et al30 described a twodimensional wrist model in which they assessed the extent of unloading of the radiolunate joint after various osteotomy procedures. They found that shortening the radius or lengthening the ulna by 4 mm led to a 45% decrease in radiolunate load with only a moderate increase in force across the midcarpal or radioscaphoid joint.

Trumble et al31 assessed the effects on lunate loading after ulnar lengthening, radial shortening, STT fusion, and capitohamate fusion without capitate shortening in an in vitro model. They found that all but the capitohamate fusion significantly unloaded the lunate and that wrist motion was preserved in all except STT fusion.

In another biomechanical study, Iwasaki et al4 used a three-dimensional theoretical wrist model. They demonstrated reduced force across the radiolunate joint after STT or SC fusion but not after capitohamate fusion.

A report on radial shortening performed on 68 patients demonstrated diminished pain in 93% at an average follow-up interval of 52 months.32 One third of patients had radiographic signs of lunate revascularization. Range of motion was improved in 52% and worsened in 19%. Grip strength improved in 74% of patients. Thus, radial shortening is an effective option for either stage II disease or stage IIIA disease with negative ulnar variance. Ulnar lengthening has also been described, but this requires iliaccrest bone graft and osteotomy healing at two sites (each end of the graft) rather than one.

Stage IIIB

In stage IIIB Kienböck’s disease, in addition to lunate collapse, there is loss of carpal height along with hyperflexion of the scaphoid. Correcting the scaphoid position to its normal posture of 45 degrees of flexion followed by fusion to either the trapezium and trapezoid (STT fusion) or to the capitate (SC fusion) theoretically decreases load across the radiolunate joint, prevents further carpal collapse, and stabilizes the midcarpal joint.2,4,15 Some authors advocate proximal-row carpectomy; others prefer joint-leveling procedures. A recent comparison between STT fusion and proximalrow carpectomy in advanced Kienböck’s disease showed no statistical difference in grip strength, pain relief, or wrist range of motion.33 In another comparison, radial shortening led to better results than STT fusion in a group of 23 patients with late-stage Kienböck’s disease followed up for an average of 5 years.34

In stage III, collapse and fragmentation of the lunate may cause a significant synovial reaction. Excision of the lunate, performed in addition to a fusion procedure, may provide pain relief. Some authors interpose a rolled palmaris longus tendon to fill the dead space. The use of silicone prostheses for replacement of an excised lunate has been discontinued due to an unacceptably high rate of particulate synovitis.2

Naum et al35 reported on the use of titanium implants for this purpose in 16 patients. At an average follow-up interval of 58 months, they recorded no loss of motion, an increase in grip strength, and prevention of further carpal collapse. It should be noted that the stage of disease was not described, that associated intercarpal fusions were done in 7 of the 16 patients, and that one implant required reoperation for subluxation.

Stage IV

In stage IV Kienböck’s disease, all the findings of stage IIIB (lunate collapse and fixed scaphoid rotation with loss of carpal height) are present, along with generalized degenerative changes throughout the midcarpal joint, the radiocarpal joint, or both. At this point, there is no value in attempting to revascularize or decompress the lunate, nor in attempting to arrest progression of palmar flexion of the scaphoid.

Treatment options must be directed at the pancarpal arthritis. These include proximal-row carpectomy and wrist fusion, as well as wrist denervation. It should be noted that severe arthritic involvement of the capitate head is a contraindication to proximal-row carpectomy, although milder changes are accepted by some or can be addressed with an interposed flap of dorsal capsule between the capitate head and the lunate fossa.36 Advocates for proximal-row carpectomy claim that it preserves most of the already limited range of motion, is simple to perform, and leaves open the possibility of wrist fusion at a later date. A 1-cm segment of the posterior interosseous nerve within the fourth dorsal compartment can be excised when performing a proximal-row carpectomy to minimize postoperative wrist pain.

More complete wrist denervation procedures have been described for the treatment of advanced Kienböck’s disease. The concept is attractive, but these procedures offer little advantage in terms of results over the two former operations.2,15,37 Authors have disagreed on the complete anatomic description of wrist innervation and therefore on the best method of denervation.38


For the past 10 to 15 years, selection of treatment options for Kienböck’s disease has been primarily based on stage and ulnar variance. With advancements in diagnostic tools (and corresponding earlier diagnosis) and a greater understanding of the conditions leading to osteonecrosis, future treatment may be based on the underlying pathologic factors rather than the stage of Kienböck’s disease.

Treatment of a “lunate at risk„ might include revascularization or venous drainage before the actual onset of osteonecrosis. Corrections of bone anomalies can also be undertaken in lunates with a special predisposition to disease. Although arthroscopy has been used to diagnose many wrist conditions, including Kienböck’s disease, its use for treatment of this disorder has not been tested. Arthroscopic fusion, excision, or bone grafting may be reasonable applications of this technique in the near future. The use of ultrasound and electromagnetic fields has been extensively studied in fracture healing but not in Kienböck’s disease. Dosage, method of application, and duration of treatment have not been addressed.

Continued work defining available vascularized bone grafts in the region of the lunate holds the promise of increasing the ease with which direct revascularization of the lunate may be performed, as fewer steps are required to harvest a vascular pedicle with its attached bone graft. Outcomes data on these new techniques are eagerly awaited. The concept of temporary unloading of the lunate with temporary STT or SC pinning (rather than fusion) during revascularization is a creative extension of the use of external fixators for the same purpose, and may find a place in the armamentarium of treatment options for Kienböck’s disease.

Kienböck’s disease is an uncommon but potentially debilitating condition. The precise cause and optimal treatment continue to elude investigators. Nevertheless, increased attention to evaluation of outcomes has led to greater ease of decision making when faced with this difficult problem. Accurate staging directs selection of appropriate treatment and allows comparison of results with other investigators. New techniques continue to appear, holding promise for improvement in all phases of diagnosis, staging, and treatment.


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© 2001 by American Academy of Orthopaedic Surgeons