Journal of the American Academy of Orthopaedic Surgeons 128 In 1910, Robert Kienböck, a Viennese radiologist, reported a series of 16 cases of “traumatic malacia” of the lunate. 1 Although others had de- scribed similar anatomic findings in cadaveric specimens, Kienböck’s was the first clinical report of osteo- necrosis 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, occasion- ally with fragmentation, and felt that this condition was caused by “a disturbance in the nutrition of the lunate caused by the rupture of liga- ments and blood vessels during contusions, sprains, or subluxa- tions.” 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 fre- quently 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 pa- tients 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 mo- tion 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 compro- mise. Bone necrosis results in trabec- ular fractures and sclerosis. Un- treated, the process continues, with collapse and fragmentation of the lunate. At this stage, carpal height is decreased, the capitate migrates proximally, and the scaphoid hyper- flexes (Fig. 1). Abnormal carpal mo- tion, particularly related to scaphoid rotation, 3,4 leads to degenerative changes throughout the carpus and the radiocarpal joint. Patients in early stages of the dis- ease rarely seek medical attention. Therefore, the true incidence and the natural history are not known with certainty. Nevertheless, the apparent common pathway in- volves osteoarthritic changes and debilitating pain, which has led to the development of a large and con- fusing array of treatment options. Dr. Allan is Assistant Professor, Department of Orthopaedics, University of Washington Medical Center, Seattle. Dr. Joshi is Resident, John Peter Smith Health Network, Fort Worth, Texas. Dr. Lichtman is Professor and Chair- man, Orthopaedic Residency Program, John Peter Smith Health Network, Fort Worth. Reprint requests: Dr. Allan, Department of Orthopaedics, Box 356500, 1959 NE Pacific Street, Seattle, WA 98195. Copyright 2001 by the American Academy of Orthopaedic Surgeons. Abstract Kienböck’s disease, or osteonecrosis of the lunate, can lead to chronic, debilitat- ing wrist pain. Etiologic factors include vascular and skeletal variations com- bined with trauma or repetitive loading. In stage I Kienböck’s disease, plain radiographs appear normal, and bone scintigraphy or magnetic resonance imaging is required for diagnosis. Initial treatment is nonoperative. In stage II, sclerosis of the lunate, compression fracture, and/or early collapse of the radial border of the lunate may appear. In stage IIIA, there is more severe lunate collapse. Because the remainder of the carpus is still uninvolved, treat- ment in stages II and IIIA involves attempts at revascularization of the lunate—either directly (with vascularized bone grafting) or indirectly (by unloading the lunate). Radial shortening in wrists with negative ulnar vari- ance and capitate shortening or radial-wedge osteotomy in wrists with neutral or positive ulnar variance can be performed alone or with vascularized bone grafting. In stage IIIB, palmar rotation of the scaphoid and proximal migra- tion of the capitate occur, and treatment addresses the carpal collapse. Surgical options include scaphotrapeziotrapezoid or scaphocapitate arthrodesis to correct scaphoid hyperflexion. In stage IV, degenerative changes are present at the midcarpal joint, the radiocarpal joint, or both. Treatment options include proximal-row carpectomy and wrist arthrodesis. J Am Acad Orthop Surg 2001;9:128-136 Kienböck’s Disease: Diagnosis and Treatment Christopher H. Allan, MD, Atul Joshi, MD, and David M. Lichtman, MD Christopher H. Allan, MD, et al Vol 9, No 2, March/April 2001 129 The clinical condition of Kienböck’s disease, therefore, remains challeng- ing to both patient and physician. Etiology Many direct or indirect causes of Kienböck’s disease have been pro- posed. The local vascular and os- seous 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 con- tributions from branches entering both dorsally and palmarly. How- ever, the lunate was supplied by only a single palmar artery in 7% of wrists in one study. 6 In addition, in- traosseous branching patterns vary, with 31% of specimens in one study showing a single path through the bone without significant arboriza- tion (Fig. 2). 6 A lunate with a single vessel and minimal branching may be at increased risk of osteonecrosis after hyperflexion or hyperexten- sion injuries or a minimally dis- placed fracture. Of interest, Takami et al 7 reported that severe injuries, such as lunate dislocation, can oc- cur without the development of osteonecrosis or with only a tran- sient 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 Disruption of venous outflow has also been suggested as a cause of Kienböck’s disease. In one study, 8 in vitro intraosseous pressure mea- surements within normal and ne- crotic lunates showed marked in- creases 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 dis- ease 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 fac- tor in lunate osteonecrosis. Lunate geometry and local anat- omy may be important as well. Neg- ative ulnar variance, first identified as a factor by Hultén 9 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 al 10 found no statistically signifi- cant difference in ulnar variance when they compared 125 normal wrists with 52 wrists in patients with Kienböck’s disease. Several investigators from Japan 11,12 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 pre- dispose to Kienböck’s disease. 12,13 Watanabe et al 13 noted a tendency toward smaller lunates in their pa- tients with the disorder. Thus, neg- ative ulnar variance and flattened radial inclination may predispose certain patients to develop Kien- Figure 1 Radiographic wrist measurements. Figure 2 Patterns of intraosseous arterial branching in the lunate. (Adapted with per- mission 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.) Radial inclination Carpal height Ulnar variance Scapho- lunate angle Kienböck’s Disease Journal of the American Academy of Orthopaedic Surgeons 130 böck’s disease, but neither is likely to be the sole factor. Occasional occurrences of Kien- böck’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 war- rants screening when considering the diagnosis. 2,14 Thus, the etiology of Kienböck’s disease seems to involve the inter- play of multiple factors. Vascular and skeletal variations may lead to an at-risk lunate, which, when sub- jected to traumatic insult, repetitive mechanical loading, or some other factor, may develop osteonecrosis. It is still not clear whether the lu- nate fracture lines occasionally seen in early Kienböck’s disease repre- sent 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 dis- ease 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. Ten- derness over the dorsum of the lunate is a frequent finding. Grip strength may be markedly reduced. Wrist range of motion may be mini- mally or severely impaired. In 1977, Lichtman described a clinical and radiographic classifica- tion for Kienböck’s disease, which is now widely used to stage treatment and compare outcomes 2 (Table 1). Before the advent of magnetic reso- nance (MR) imaging, radionuclide scintigraphy was the next diagnos- tic study recommended after plain radiography. Hashizume et al 17 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 never- theless superior to plain radiog- raphy, tomography, or computed tomography, in defining the early stage of Kienböck’s disease (Licht- man stage I), when trabecular bone has not yet been destroyed. By con- trast, once lunate collapse has oc- curred, tomography or computed tomography best reveals the extent of necrosis and trabecular destruc- tion. 17 Quenzer et al 18 reported that tri- spiral tomography makes possible more accurate staging than stan- dard tomography or plain radiogra- phy. 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 tri- spiral tomography is not routinely available, plain radiography and MR imaging (Fig. 3) remain the most common tools for staging Kienböck’s disease. In stage I, plain radiographs are either normal or occasionally dem- onstrate a linear fracture without sclerosis or collapse of the lunate (Fig. 4). No changes are seen else- where in the carpus. The early-flow Table 1 Stages of Kienböck’s Disease Stage I Normal radiographs or linear fracture, abnormal but nonspecific bone scan, diagnostic MR appearance (lunate shows low signal intensity on T1-weighted images; lunate may show high or low signal intensity on T2-weighted images, depending on extent of disease process) Stage II Lunate sclerosis, one or more fracture lines with possible early collapse of lunate on radial border Stage III Lunate collapse IIIA Normal carpal alignment and height IIIB Fixed scaphoid rotation (ring sign), carpal height decreased, capitate migrates proximally Stage IV Severe lunate collapse with intra-articular degenerative changes at midcarpal joint, radiocarpal joint, or both Figure 3 T1-weighted MR image reveals decreased signal intensity of the lunate in the wrist of a patient with Kienböck’s dis- ease. Christopher H. Allan, MD, et al Vol 9, No 2, March/April 2001 131 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, how- ever. Disorders such as ulnar abut- ment, fractures, enchondromas, and osteoid osteoma can cause focal MR signal changes. In addition, tran- sient ischemia may cause a general- ized decrease in lunate signal inten- sity. T2-weighted images typically Figure 4 Drawings and radiologic images illustrating staging of Kienböck’s disease, according to Lichtman. 2 In stage I, the trabecu- lar 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 den- sity 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.) Stage I Stage II Stage IIIA Stage IV Stage IIIB Kienböck’s Disease Journal of the American Academy of Orthopaedic Surgeons 132 show low signal intensity in Kien- böck’s disease, but will show in- creased 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. Radiographic findings in stage II Kienböck’s disease include in- creased density of the lunate on plain radiographs, frequently asso- ciated 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 fre- quently those of chronic synovitis. Increased density of the lunate can also occur as a transient finding, not associated with the typical pro- gressive changes of Kienböck’s dis- ease. 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 col- lapse. This stage can be divided into two categories. In stage IIIA, lu- nate collapse has occurred, but car- pal height is relatively unchanged. Lateral radiographs demonstrate a widened anteroposterior dimension of the lunate associated with short- ening in the coronal plane. Neither proximal migration of the capitate nor fixed hyperflexion of the scaph- oid (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 insta- bility 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 mid- carpal joint or both. Symptoms in stage IV are similar to those of de- generative arthritis of the wrist, with more severe swelling, pain, and limitation of motion. Treatment 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 pat- terns of success. These will be dis- cussed along with alternative pro- cedures for each stage of 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 dis- ease in the same way as stage II and stage IIIA disease. Nevertheless, for most clinicians, cast immobiliza- tion (or an equivalent form of wrist immobilization, such as with use of an external fixator) remains the first treatment option for stage I Kien- böck’s disease. The possibility of resolution of symptoms does exist; therefore, a trial of immobilization for as long as 3 months is appropri- ate. 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 al 22 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 dis- ease severity in the splinted group was one stage lower than that in the operatively treated group; thus, comparison was difficult. How- ever, in another series of 22 nonsur- Table 2 Options for Treatment of Kienböck Disease Stage of Disease Treatment I Immobilization (3 months) II and IIIA with negative Radius-shortening osteotomy; ulnar or neutral ulnar variance lengthening; capitate shortening II and IIIA with positive Direct revascularization + external fixation ulnar variance or temporary scaphotrapeziotrapezoid pinning (stage II only); radial-wedge or dome osteotomy; capitate shortening with or without capitohamate fusion; combination of joint-leveling and direct revascularization procedures IIIB Scaphotrapeziotrapezoid or scaphocapitate fusion with or without lunate excision with palmaris longus autograft; radius- shortening osteotomy; proximal-row carpectomy IV Proximal-row carpectomy; wrist arthrodesis; wrist denervation Christopher H. Allan, MD, et al Vol 9, No 2, March/April 2001 133 gically treated patients with vari- ous stages of disease, 2 17 showed progression, and 5 had no im- provement. When immobilization fails to reverse the avascular changes, the process will almost always have advanced to stage II. In this set- ting, analysis of ulnar variance is important. Stage II or IIIA With Neutral or Positive Ulnar Variance Stages II and IIIA are often con- sidered together, and treatment options are similar with one major exception. In stage II, lunate avas- cularity has developed, but the bone has not collapsed. Direct re- vascularization procedures have their greatest likelihood of success in this stage. A number of vascularized pedi- cle and/or bone grafting procedures have been described, including vas- cularized transfers of the pisiform bone, transfers of segments of the distal radius on a vascularized pedi- cle of pronator quadratus, and transfers of branches of the first, sec- ond, or third dorsal metacarpal arteries. 23-25 Our preference has been to use the second dorsal inter- metacarpal artery and vein either as originally described 26 or as modi- fied by suturing it to a corticocancel- lous graft harvested from the distal radius. 24 Most of the recently de- scribed vascularized pedicle bone grafts have the advantage that the bone graft and vascular pedicle are harvested together, making the pro- cedure technically easier. The dor- sal aspect of the distal radius is sup- plied by several arterial branches, which enter the bone via septa be- tween the extensor compartments. When these are used, no vein is har- vested. Because of anatomic varia- tion, it is best to be aware of the location of several potential vascu- larized pedicle bone grafts before performing such a procedure. Ex- ternal 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 revasculariza- tion procedures are still being eval- uated. 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 capito- hamate fusion (Almquist proce- dure). 11,13,27 These may be consid- ered attempts to unload the lunate to improve its environment for re- vascularization through decreasing the shear stress across the radio- lunate 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 report 27 ). In addition, a recent biomechanical study showed that capitate shorten- ing with capitohamate fusion sig- nificantly (P<0.05) decreased the load across the radiolunate articula- tion. 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 Stage II or IIIA With Negative Ulnar Variance In patients with stage II or IIIA Kienböck’s disease and significant negative ulnar variance, a shorten- ing 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 neu- tral 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 discom- fort after surgery. Horii et al 30 described a two- dimensional wrist model in which they assessed the extent of unload- ing of the radiolunate joint after var- ious osteotomy procedures. They Figure 5 Capitate shortening with capitohamate fusion. Kienböck’s Disease Journal of the American Academy of Orthopaedic Surgeons 134 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 radio- scaphoid joint. Trumble et al 31 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 al 4 used a three-dimen- sional 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 per- formed on 68 patients demonstrated diminished pain in 93% at an average follow-up interval of 52 months. 32 One third of patients had radio- graphic signs of lunate revasculariza- tion. 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 iliac- crest bone graft and osteotomy heal- ing 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. Cor- recting 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 fur- ther carpal collapse, and stabilizes the midcarpal joint. 2,4,15 Some au- thors advocate proximal-row car- pectomy; others prefer joint-leveling procedures. A recent comparison between STT fusion and proximal- row carpectomy in advanced Kien- böck’s disease showed no statistical difference in grip strength, pain re- lief, or wrist range of motion. 33 In another comparison, radial short- ening led to better results than STT fusion in a group of 23 patients with late-stage Kienböck’s disease fol- lowed up for an average of 5 years. 34 In stage III, collapse and frag- mentation of the lunate may cause a significant synovial reaction. Exci- sion 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 re- placement of an excised lunate has been discontinued due to an un- acceptably high rate of particulate synovitis. 2 Naum et al 35 reported on the use of titanium implants for this pur- pose in 16 patients. At an average follow-up interval of 58 months, they recorded no loss of motion, an increase in grip strength, and pre- vention 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 rota- tion with loss of carpal height) are present, along with generalized de- generative changes throughout the midcarpal joint, the radiocarpal joint, or both. At this point, there is no value in attempting to revascu- larize or decompress the lunate, nor in attempting to arrest progression of palmar flexion of the scaphoid. 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. A B Christopher H. Allan, MD, et al Vol 9, No 2, March/April 2001 135 Treatment options must be di- rected at the pancarpal arthritis. These include proximal-row carpec- tomy and wrist fusion, as well as wrist denervation. It should be noted that severe arthritic involve- ment of the capitate head is a con- traindication to proximal-row car- pectomy, although milder changes are accepted by some or can be addressed with an interposed flap of dorsal capsule between the capi- tate head and the lunate fossa. 36 Advocates for proximal-row carpec- tomy 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 compart- ment can be excised when perform- ing a proximal-row carpectomy to minimize postoperative wrist pain. More complete wrist denervation procedures have been described for the treatment of advanced Kien- böck’s disease. The concept is at- tractive, but these procedures offer little advantage in terms of results over the two former operations. 2,15,37 Authors have disagreed on the com- plete anatomic description of wrist innervation and therefore on the best method of denervation. 38 Summary 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 diagno- sis) and a greater understanding of the conditions leading to osteo- necrosis, 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 un- dertaken in lunates with a special predisposition to disease. Although arthroscopy has been used to diag- nose many wrist conditions, includ- ing 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 tech- nique in the near future. The use of ultrasound and electromagnetic fields has been extensively studied in fracture healing but not in Kien- böck’s disease. Dosage, method of application, and duration of treat- ment have not been addressed. Continued work defining avail- able vascularized bone grafts in the region of the lunate holds the prom- ise of increasing the ease with which direct revascularization of the lu- nate may be performed, as fewer steps are required to harvest a vas- cular 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) dur- ing revascularization is a creative extension of the use of external fixa- tors for the same purpose, and may find a place in the armamentarium of treatment options for Kienböck’s disease. Kienböck’s disease is an uncom- mon but potentially debilitating con- dition. The precise cause and opti- mal treatment continue to elude investigators. Nevertheless, increased attention to evaluation of outcomes has led to greater ease of decision making when faced with this diffi- cult problem. Accurate staging directs selection of appropriate treat- ment 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. References 1. Kienböck R; Peltier L (trans-ed): Con- cerning traumatic malacia of the lunate and its consequences: Degeneration and compression fractures [classic reprint]. Clin Orthop 1980;149:4-8. 2. Lichtman DM, Mack GR, MacDonald RI, Gunther SF, Wilson JN: Kienböck’s disease: The role of silicone replace- ment arthroplasty. J Bone Joint Surg Am 1977;59:899-908. 3. Iwasaki N, Genda E, Minami A, Kaneda K, Chao EYS: Force transmis- sion through the wrist joint in Kienböck’s disease: A two-dimension- al theoretical study. J Hand Surg [Am] 1998;23:415-424. 4. Iwasaki N, Genda E, Barrance PJ, Minami A, Kaneda K, Chao EY: Biomechanical analysis of limited intercarpal fusion for the treatment of Kienböck’s disease: A three-dimen- sional theoretical study. J Orthop Res 1998;16:256-263. 5. 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. 6. Panagis JS, Gelberman RH, Taleisnik J, Baumgaertner M: The arterial anato- my of the human carpus: Part II. The intraosseous vascularity. J Hand Surg [Am] 1983;8:375-382. 7. Takami H, Takahashi S, Ando M, Masuda A: Open reduction of chron- ic lunate and perilunate dislocations. Arch Orthop Trauma Surg 1996;115: 104-107. 8. Schiltenwolf M, Martini AK, Mau HC, Eversheim S, Brocai DRC, Jensen CH: Further investigations of the intra- osseous pressure characteristics in necrotic lunates (Kienböck’s disease). J Hand Surg [Am] 1996;21:754-758. 9. Hultén O: Über anatomische Varia- tionen der Handgelenkknochen. Acta Radiol Scand 1928;9:155-168. 10. D’Hoore K, DeSmet L, Verellen K, Vral J, Fabry G: Negative ulnar variance is not a risk factor for Kienböck’s disease. J Hand Surg [Am] 1994;19:229-231. 11. Nakamura R, Imaeda T, Miura T: Kienböck’s Disease Journal of the American Academy of Orthopaedic Surgeons 136 Radial shortening for Kienböck’s dis- ease: Factors affecting the operative result. J Hand Surg [Br] 1990;15:40-45. 12. Tsuge S, Nakamura R: Anatomical risk factors for Kienböck’s disease. J Hand Surg [Br] 1993;18:70-75. 13. Watanabe K, Nakamura R, Horii E, Miura T: Biomechanical analysis of radial wedge osteotomy for the treat- ment of Kienböck’s disease. J Hand Surg [Am] 1993;18:686-690. 14. Culp RW, Schaffer J, Osterman AL, Bora FW Jr: Kienböck’s disease in a patient with Crohn’s enteritis treated with corticosteroids. J Hand Surg [Am] 1989;14(2 pt 1):294-296. 15. Linscheid RL: Kienböck’s disease. Instr Course Lect 1992;41:45-53. 16. Aspenberg P, Wang JS, Jonsson K, Hagert CG: Experimental osteonecro- sis of the lunate: Revascularization may cause collapse. J Hand Surg [Br] 1994;19:565-569. 17. Hashizume H, Asahara H, Nishida K, Inoue H, Konishiike T: Histopathology of Kienböck’s disease: Correlation with magnetic resonance and other imaging techniques. J Hand Surg [Br] 1996;21: 89-93. 18. Quenzer DE, Linscheid RL, Vidal MA, Dobyns JH, Beckenbaugh RD, Cooney WP: Trispiral tomographic staging of Kienböck’s disease. J Hand Surg [Am] 1997;22:396-403. 19. Ficat RP: Idiopathic bone necrosis of the femoral head: Early diagnosis and treat- ment. J Bone Joint Surg Br 1985;67:3-9. 20. Sowa DT, Holder LE, Patt PG, Weiland AJ: Application of magnetic resonance imaging to ischemic necrosis of the lunate. J Hand Surg [Am] 1989;14: 1008-1016. 21. Desser TS, McCarthy S, Trumble T: Scaphoid fractures and Kienböck’s dis- ease of the lunate: MR imaging with histopathologic correlation. Magn Reson Imaging 1990;8:357-361. 22. Delaere O, Dury M, Molderez A, Foucher G: Conservative versus oper- ative treatment for Kienböck’s disease: A retrospective study. J Hand Surg [Br] 1998;23:33-36. 23. Sheetz KK, Bishop AT, Berger RA: The arterial blood supply of the distal radius and ulna and its potential use in vascularized pedicled bone grafts. J Hand Surg [Am] 1995;20:902-914. 24. Tamai S, Yajima H, Ono H: Revascu- larization procedures in the treatment of Kienböck’s disease. Hand Clin 1993;9:455-466. 25. Bochud RC, Büchler U: Kienböck’s disease, early stage 3: Height recon- struction and core revascularization of the lunate. J Hand Surg [Br] 1994;19: 466-478. 26. Hori Y, Tamai S, Okuda H, Sakamoto H, Takita T, Masuhara K: Blood vessel transplantation to bone. J Hand Surg [Am] 1979;4:23-33. 27. Almquist EE: Capitate shortening in the treatment of Kienböck’s disease. Hand Clin 1993;9:505-512. 28. Viola RW, Kiser PK, Bach AW, Hanel DP, Tencer AF: Biomechanical analy- sis of capitate shortening with capitate hamate fusion in the treatment of Kienböck’s disease. J Hand Surg [Am] 1998;23:395-401. 29. Hanel DP, Hunt TR: Capitate shorten- ing osteotomy: Kienböck’s disease. Atlas Hand Clin 1999;4:45-58. 30. Horii E, Garcia-Elias M, Bishop AT, Cooney WP, Linscheid RL, Chao EY: Effect on force transmission across the carpus in procedures used to treat Kienböck’s disease. J Hand Surg [Am] 1990;15:393-400. 31. Trumble T, Glisson RR, Seaber AV, Urbaniak JR: A biomechanical com- parison of the methods for treating Kienböck’s disease. J Hand Surg [Am] 1986;11:88-93. 32. Quenzer DE, Dobyns JH, Linscheid RL, Trail IA, Vidal MA: Radial reces- sion osteotomy for Kienböck’s disease. J Hand Surg [Am] 1997;22:386-395. 33. Nakamura R, Horii E, Watanabe K, Nakao E, Kato H, Tsunoda K: Proxi- mal row carpectomy versus limited wrist arthrodesis for advanced Kien- böck’s disease. J Hand Surg [Br] 1998; 23:741-745. 34. Condit DP, Idler RS, Fischer TJ, Hastings H II: Preoperative factors and outcome after lunate decompres- sion for Kienböck’s disease. J Hand Surg [Am] 1993;18:691-696. 35. Naum SC, VanGorp CC, DeHeer DH, Swanson AB: Titanium lunate implant arthroplasty for Kienböck’s disease: One to nine-year follow-up. Presented at the 52nd Annual Meeting of the American Society for Surgery of the Hand, Denver, September 11, 1997. 36. Salomon GD, Eaton RG: Proximal row carpectomy with partial capitate resec- tion. J Hand Surg [Am] 1996;21:2-8. 37. Buck-Gramcko D: Wrist denervation procedures in the treatment of Kien- böck’s disease. Hand Clin 1993;9: 517-520. 38. Ferreres A, Suso S, Foucher G, Ordi J, Lusa M, Ruano D: Wrist denervation: Surgical considerations. J Hand Surg [Br] 1995;20:769-772.