Kienbo ̈ ck Disease

                               Dr. KS Dhillon

Lunate collapse secondary to osteonecrosis was first described in 1910. Robert Kienbo ̈ ck, an Austrian pioneer in the field of radiology was the first to describe the clinical and radiographic changes of lunate osteonecrosis [1-3]. In his series of patients with lunate osteonecrosis, the patients were largely male laborers presenting with wrist pain in their third and fourth decade of life. Initially, he postulated that the changes in the lunate structure and shape could be secondary to congenital anomaly, compression fracture, infection, or inflammatory arthritis.

However later he attributed it to “a disturbance in the nutrition of the lunate

caused by rupture of the ligaments and blood vessels during contusions, sprains, or subluxations”. He called it “lunatomalacia” [4].

In 1925, Goldsmith was the first to describe an idiopathic lunate fracture without preceding trauma [2]. He agreed with Kienbo ̈ ck that lunate subluxation with spontaneous reduction was responsible for disruption to the dorsal ligaments and lunate nutritional supply [5]. In his case series of 3 patients, he described 4 clinical stages of Kienbo¨ck disease. These include (1) joint irritation stage following trauma, (2) an asymptomatic stage, (3) a symptomatic disease stage, and (4) a stage of moderate disability [6].

In 1928, Hulte’n was the first to describe the normal distribution of ulnar wrist variance in the Swedish population. He identified a significant correlation between ulnar negative variance and the development of Kienbo¨ck disease [7]. In his radiographic analysis of 400 wrists, he found that ulnar variance was distributed in a bell shape curve. Most individuals were ulnar neutral (61%), followed by ulnar negative (23%) and ulnar positive (16%) [5]. In his series, a subsequent analysis of 23 patients with Kienbo¨ck disease revealed that 17 (74%) had ulnar negative wrists and 6 (26%) had ulnar neutral wrists. No patients with Kienbo¨ck disease had ulnar positive variance.

This anatomic observation that ulnar negative variance was associated with the development of Kienbo¨ck disease led to the development of joint leveling procedures that redistributed forces across the lunate and limited the progression of the disease.

 In 1945, Persson reported his series of 19 corrective osteotomies, 3 radial shortening, and 16 ulnar lengthening for the treatment of Kienbo¨ck disease in patients with ulnar negative variance [5,8]. The study showed a 50% improvement in lunate structure following the corrective osteotomy [5].

Kienbo¨ck’s belief that a dorsal ligamentous injury caused a disruption in the vascular supply to the lunate was later challenged by Stahl in 1947 [9]. He performed arteriograms of the wrist and found that the volar circulation was the dominant blood supply to the lunate. He postulated that injury to these small vessels may be the cause of Kienbo¨ck disease [5]. He was also the first to propose a radiographic staging system for Kienbo¨ck disease. The staging endured until subsequent revision by Lichtman 30 years later [10,11]. 

In Stahl’s original staging system, there were 5 stages [5]:

Stage 1- Kienbo¨ck disease began as a radiodense lunate fracture.

Stage 2- Secondary bony resorption with development of a rarefaction line.

Stage 3- Diffuse lunate sclerosis.

Stage 4- Secondary fractures with fragmentation.

Stage 5- Arthrosis.

Lichtman’s revised classification system added details provided by computed tomography and MRI. It demonstrated disease progression from lunate edema to sclerosis, fracture, and collapse, followed by carpal instability and arthritis [11,12].

The controversy surrounding the dominant blood supply to the lunate was resolved in 1980 when Gelberman published his cadaveric study that detailed the extensive intraosseous and extraosseous lunate vascular anatomy [13]. Gelberman found that the extraosseous vascular supply was constituted by a system of 2 to 3 dorsal vessels and 3 to 4 volar vessels feeding carpal vascular plexuses over the dorsal and volar poles of the lunate [13]. The nutrient vessels were found to enter the lunate through distinct foramina [13,14]. In 1993, Jensen confirmed the decreased vascularity of the lunate in patients with Kienbo¨ck disease using technetium 99m-methylene diphosphonate scintigraphy [15]. 

In his case series of 10 patients, he was able to measure intraosseous lunate pressure using a transducer and compared the values to the adjacent capitate and radial styloid pressure measurements [15]. He found that in patients with Kienbo¨ck disease, the lunate pressures were significantly higher than the capitate and radial styloid pressures. The precise etiology of Kienbo¨ck disease remains unknown. It is now believed that predisposing factors such as repetitive lunate microtrauma, vascular insufficiency, elevated intraosseous pressure, and anatomic factors such as negative ulnar variance, increased uncovering of the lunate, abnormal radial inclination, and a trapezoidal lunate shape all play a role in the development of Kienbo¨ck disease [14,15].

Epidemiology

The true prevalence of Kienbo¨ck disease is not known as the early stages of the disease are often asymptomatic. The timing of disease progression is highly variable. Kienbo¨ck disease is considered a rare disease. It currently affects less than 200,000 people in the United States [16,17,18].

Previous studies have estimated that the prevalence of asymptomatic disease is between 1% and 2% in African and Japanese populations, respectively [15,16].

A large retrospective analysis of over 51,000 American patients who received wrist radiographs for other reasons than suspected Kienbo¨ck disease found an overall incidence of Kienbo¨ck disease to be 0.27% [19]. The study also found that younger patients with a mean age of 43 years with more advanced carpal collapse were more likely to be symptomatic as compared to older patients with a mean age of 54 years who were in the precollapse stages of the disease [19]. In Kienbo¨ck original series, most patients were male laborers between the ages of 20 and 29 years [5]. There are larger studies that have found a male predominance with a male to female ratio of 2 to 4:1[1].

Recent studies have suggested that there is a possible genetic component to Kienbo¨ck disease. Kazmers et al [20] have identified familial enrichment and an increased relative risk of Kienbo¨ ck disease among first-degree relatives. The specific genetic mutations, however, remain unknown. In the study, the risk factors that correlated with the development of Kienbo¨ck disease included diabetes, alcohol and tobacco use, and prolonged corticosteroid use [20].

Manual laborers have been found to have the highest incidence of Kienbo¨ck disease. In 1920, Walter Mueller coined the term “occupational lunatomalacia” to describe the pathologic changes to the lunate bone in Kienbo¨ck disease from repetitive overload [21]. This was later supported in a larger series by Stahl in 1947 and Therkelson in 1949 where over 97% of patients with Kienbo¨ ck disease were found to be manual laborers [22,23].

Individuals with cerebral palsy (CP) also have a relatively high incidence of Kienbo¨ck disease. This is believed to be due to spasticity, habitual wrist flexion, and subsequent volar vascular injury [24]. In a series of adult CP patients living in an assisted living facility, Rooker and colleagues found that 5 of 53 (9%) residents with CP at the assisted living facility had radiographic evidence of Kienbo¨ck disease [24]. There are other reports that have shown the incidence of Kienbo¨ck disease in patients with CP to be between 2% and 10%. Bilateral involvement as well as unilateral Kienbo¨ck disease affecting the non-dominant hand has been seen in patients with CP [25,26].

Another population group that has a higher predilection for developing Kienbo¨ck disease is athletes. Nakamura et al [27] investigated the difference in age and sex distribution, symptoms, and radiographic findings in 91 cases of Kienbo¨ck disease related to sports and manual labor. They found that athletes participating in tennis, handball, and Asian martial arts had similar clinical and radiographic findings as manual laborers but the athletes had a significantly shorter period of insult before the onset of symptoms (5 vs 9 years on average).

Clinical Presentation

The classical Kienbo¨ck disease patient is a manual laborer with unilateral activity-related complaints affecting the dominant wrist [8]. There may or may not be a history of known previous traumatic event. The symptoms are nonspecific and include generalized central wrist pain, dorsal wrist swelling, pain with grip and loading, and decreased range of motion [1]. Grip strength can be reduced by up to 50% of the contralateral side [28]. The dorsal wrist pain is often worse with wrist extension. Percussion of the third metacarpal can elicit pain over the lunate [5].

The radiographic workup involves 3 views of the wrist i.e AP, lateral, and 45 oblique. In the ulna-positive wrist, ulnar variance views are also important to assess for possible ulnar impaction syndrome. Ulnar negative variance has historically been associated with Kienbo¨ck disease. Its exact role in the etiology of Kienbo¨ck disease is now more controversial [29]. 

Radial shortening in ulnar-negative patients with early Kienbo¨ck disease remains popular since studies have shown consistently reduced radiolunate contact pressure and improved healing [30,31].

Radiographs are usually normal in the early stages of the disease. The radiographs help to differentiate between other sources of dorsal wrist pain, including fractures, ulnolunate impaction, carpal instability, and arthritis. The earliest finding of the disease on radiographs is sclerosis of the lunate.  In the later stages, radiographs will reveal progression of lunate collapse, fracture, scaphoid flexion, loss of carpal height, and carpal arthritis [1].

Advanced imaging is sometimes needed for accurate staging and surgical planning. CT scans provide better detail of the bone structure and are able to detect subtle lunate fractures and collapse.

Han et al [32] found lunate changes in patients with advanced Kienbo¨ck disease to result in thicker, denser, and flatter trabeculae in response to internal stress. This plate-like microstructure is hypothesized to limit reparative mesenchymal stem cell migration.

MRI scans are useful for diagnosis in the early stages of the disease where plain radiographs are normal. Early findings on MRI include diffuse hyperintensity of the lunate on T1 imaging. Later diffuse hypointensity of the lunate on T1 and T2 sequences is seen, indicating decreased vascularity. This helps to distinguish Kienbo¨ck disease from ulnolunate impaction syndrome. Impaction syndrome is typically hyperintense on T2 sequences secondary to bone edema at the point of impaction in the proximal lunate. Gadolinium-enhanced MRI scans are a helpful adjunct to T1 fat-suppressed imaging. They have been shown to improve diagnostic accuracy and assist in surgical planning [1,33].

Areas of increased gadolinium enhancement are thought to represent neovascular tissue with increased reparative potential whereas areas of decreased enhancement are thought to represent bone edema [33,34].

Wrist arthroscopy is an additional diagnostic tool to assess the integrity of the chondral surface of the lunate as well as its adjacent carpal articulations [35]. During arthroscopy, loose osteochondral fragments, flaps, and synovitis are debrided [36]. Functional articulations are identified for later reconstruction [36].

Proponents of wrist arthroscopy have found that articular damage is underestimated on plain imaging. Findings during arthroscopy often lead to a change in the management plan. Some patients have an intact chondral surface despite subchondral compromise on imaging [35,36]. This has led to the development of the arthroscopy-based Bain and Begg classification system of Kienbo¨ck disease (table 1). This classification system helps surgeons determine the appropriate surgical treatment plan where “nonfunctional articular surfaces” can be bypassed or excised to reduce pain and maintain functional wrist movement [35].

Table 1

Bain and Begg arthroscopic classification of Kienbo¨ck disease

Grade             Nonfunctional Articulation

0                     None

1                     Lp

2A                  Lp/R

2B                  Lp/Ld

3                    R/Lp/Ld

                      C is typically spared

4                    R/Lp/Ld/C

Abbreviations: C, proximal capitate articular surface; Ld, distal lunate; Lp, proximal lunate; R, lunate facet of radius.

Treatment

The treatment of Kienbo¨ck disease has been largely conservative.  Kienbo¨ck in 1910 advocated splint immobilization for symptom control in most patients. Lunate excision is reserved for patients with advanced disease who have recalcitrant pain [5]. Hulten’s elucidation in 1928 [7] that negative ulnar variance was associated with Kienbo¨ck disease led to the emergence of joint leveling procedures such as radial shortening and ulnar lengthening [37]. 

Intercarpal fusions came in the 1960s [38], capitate shortening in the 1980s [39,40], and radial wedge osteotomy in the 1990s [41] to decrease stress across the lunate and permit healing. 

Until 1970s, the treatment of advanced Kienbo¨ck disease remained problematic, because lunate excision was the only surgical option. This

frequently resulted in significant carpal shift and shortening. In 1970, Swanson tried to solve this problem by filling the void left after lunate excision with a silicone interposition arthroplasty. He achieved good long-term functional results in his patients [42,43]. This technique was later abandoned because the patients developed silicone associated synovitis. In 1970, Nahigian developed a dorsal flap interposition arthroplasty, which resulted in symptomatic improvement in all his 4 patients, and it prevented carpal migration [44].

In the 1990s and 2000s, new techniques were developed to restore lunate vascularity in early and more advanced disease. For early disease, both the distal radius and ulna core decompression [45], as well as direct lunate core decompression [46] were described to relieve increased intraosseous pressure and incite a local inflammatory/healing response.

Multiple techniques of pedicled corticoperiosteal vascularized bone flaps from adjacent bones were developed for use in patients without secondary arthritis [47]. This idea was based on work by Hori who demonstrated in a canine study that transplantation of a vascular bundle into necrotic bone resulted in neovascularization and bone growth [48]. Although these procedures did relieve pain in most patients and demonstrated modest improvements in wrist range of motion, they, however, are unable to reverse radiographic changes or replace degenerate cartilage [49]. This limitation of pedicled vascularized bone grafts inspired the application of free vascularized osteochondral flaps from the medial femoral trochlea for restoration of lunate height, vascularity, and chondral deficiency in advanced Kienbo¨ ck disease [49].

There are now over 20 procedures described for the treatment of Kienbo¨ck disease [16]. For early disease, the most popular treatments for Kienbo¨ck are splint/cast immobilization or radial shortening osteotomy [50]. There is a high acceptance rate (29%) of distal radius core decompression for stage I disease [51].

In patients with lunate collapse without fixed scaphoid rotation (stage IIIa), radial shortening osteotomy is performed in the setting of negative ulnar variance, and vascularized bone flap or capitate shortening osteotomy was performed in the setting of ulnar positive variance. For vascular bone grafting, a technique utilizing the fourth and fifth extensor compartment is most popular [51].

In patients with lunate collapse with fixed scaphoid rotation (stage IIIb), salvage procedures such as proximal row carpectomy or limited intercarpal arthrodesis are most commonly used.

When carpal collapse, as well as significant adjacent carpal arthritis (stage IV), is present, proximal row carpectomy or total wrist fusion is usually carried out [50].

Conclusions. 

The etiology of Kienböck’s disease remains poorly understood. Biomechanical factors are important at a certain stage of its evolution. This is suggested by the significant changes in mineralization of the distal radius [52,53]. The natural history is not well known and the symptoms do not often correlate with the radiological appearance. Surgical treatment has not been found to be superior to conservative treatment. Comparative retrospective studies have to be interpreted with caution, as patients with more advanced lesions are more likely to have undergone surgery. Radial shortening probably remains the best surgical option in symptomatic stages I to III-A in young manual workers with ulnar-minus variance, because in this procedure the carpus is left undisturbed, preserving its residual mobility. Bone healing should be obtained within a reasonable time span, and nonunion should be avoided. Autologous bone grafting should be done at the site of the osteotomy. 

Excision of the lunate with progressive lengthening of the capitate may be an excellent solution in stage III-B disease. In stage IV, arthrodesis of the wrist gives the most acceptable results, allowing many patients to return to their previous occupations with a painless ankylosed wrist.

Kienböck’s disease rarely occurs in children. A non-operative approach is recommended with prolonged immobilization in a cast as there is great potential for healing and remodeling at this age [54,55]. Radial shortening can occasionally be indicated in teenagers [56,57].

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