Kienbock's Disease Treatment: Past, Present, and Future

Abstract

There are various approaches to the management of Kienböck's disease, which differ depending on factors such as the patient's age, the stage of the disease, and the viability of the lunate. Treatment options have ranged from the correction of radioulnar dysmetria and lunate decompression in the early stages to lunate excision or even prosthetic placement in more advanced stages. Furthermore, alternatives such as revascularization with bone grafts or palliative techniques, including partial or total wrist arthrodesis, are considered. In this review article, we examine the different available treatment modalities and present our preferred treatment approach, informed by the current body of evidence, to enhance the management of Kienböck's disease.

 

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Keywords

Kienböck - treatment - arthroscopy

Introduction

Kienböck's disease (KD) is characterized by ischemic necrosis of the lunate bone, leading to wrist pain, limited mobility, and functional disability. Treatment strategies vary widely, influenced by the stage of the disease and individual anatomical and clinical considerations.[1] [2]

KD presents significant challenges due to its heterogeneous clinical presentation and the progressive nature of avascular necrosis of the lunate. Despite the variety of approaches, no method has been proven universally effective, emphasizing the need for personalized strategies based on disease stage and patient-specific factors.[1] [2]

 

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Etiology

Although the etiology and pathogenesis of KD are not yet fully understood, several potential causes have been postulated.[3]

There are factors traditionally considered precipitating factors, but these have not been proven. The analysis of 100 cases of KD, published in the doctoral thesis of one of the authors, reveals a wide variability in morphologies, which contradicts these classic associations. To date, they appear to play a role in the progression of KD once established, but they are not factors influencing its onset[4]:

• A) Short ulna. Authors such as the Swedish Hulten considered that a short ulna would cause the lunate to be subjected to greater load, leading to a compression fracture over time. Today, the majority of authors disagree with this assertion, as shown in the meta-analysis by Chung et al.[5]

• B) Type I lunate. In 1966, Antuña Zapico, in his doctoral thesis, described three morphological types of lunate, based on the angle of inclination formed by the articular facet for the scaphoid and the distal radius. In type I, this angle is equal to or greater than 135° and usually corresponds to a short ulna. In type II, the angle of inclination is less than 135° and usually corresponds to a neutral ulna. In type III, it presents two convergent articular facets and usually coexists with a long ulna. As S. Pombo Expósito pointed out in his doctoral thesis, based on the analysis of 100 cases of KD, the morphology of the SE could influence the evolution of KD, but it is not an influential factor in its onset. Therefore, the relationship between the morphology of the lunate and KD will remain controversial until the real cause or causes of the disease are known.[4] [6] ([Figure 1])

• C) Specific vascular patterns. The vascularization of the SE has been meticulously studied by authors such as Stahl (1947), Lee (1963), Gelberman et al. (1980), and Lamas (2000, 2007). To date, a direct relationship between vascular patterns and the development of KD has not been demonstrated.[7] [8]

• D) Repetitive trauma. Some authors have based the hypothesis of traumatic etiology on the appearance of pseudofractures on radiographs, which, in our opinion, are nothing more than fragmentation or collapse of the spinal cord that occurs in the advanced stages of the disease.

Fig. 1 Top row: Drawings in Antuña's Doctoral Thesis of the morphological types of SE. Second row: SE types 1–2–3. Third row: Cases of EK in SE types 1, 2, and 3.

Repetitive microtrauma is not the primary cause of KD but rather an aggravating factor in pre-existing KD.[4] [9] [10]

Some lesser-known factors that should be added to the study of this pathology and that should continue to be studied in the future are:

• a) Familial association. Studies conducted in the Department of Genomic Medicine at the University of Santiago de Compostela with siblings and twins affected by KD in 2011 did not detect genetic abnormalities at the time, perhaps due to the limited resources available, at the time, but they paved the way for future research as genetic sequencing techniques improve. Authors such as Kazmers et al. published encouraging, though not definitive, findings in 2020.[4] [11]

• b) Causal biological factors. Other interesting studies have been conducted on the influence of causative biological factors, ranging from reactive arthritis to viral or bacterial infections, with the appearance of severe synovitis, which is still unknown whether it is a cause or consequence of the disease. Such synovitis is often a common finding in KD, even in younger patients and in its early stages; therefore, we consider it primary synovitis.[12]

• c) Atypical or secondary cases related to corticosteroid use, vasculitis, or other causes. These cases are not considered primary lunate necrosis, but should be considered as such when treating them from a pragmatic point of view.[4]

 

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Classification

The main factors to consider when proceeding with the treatment of KD are the stage of the disease and the clinical presentation at the time of diagnosis. There are multiple classifications for this staging, with the most common being the Litchman classification ([Table 1]), the arthroscopic classification described by Bain, and the 21st-century treatment algorithm.[13] [14] [15]

Table 1 Modified Litchman classification

Litchman classification
Stage I:	Normal radiographs. MRI intensity changes.
Stage II:	Lunate sclerosis without affecting its articular surface.
Stage III:	Collapse and deformity of the lunate joint surface.
-IIIA	Stable carpus.
-IIIB	Carpal instability.
-IIIC	Fragmentation of the lunate joint into two.
-IIID	Multifragmentation of the lunate joint.
Stage IV:	Appearance of radiocarpal or midcarpal osteoarthritis.

The Lichtman classification, proposed in 1977, has been the most widely used for over 50 years, focusing on plain wrist radiographs that detail the progressive stages of the disease. The use of gadolinium (GD) in MRI has allowed us to subdivide stage III. Depending on whether or not the signal intensity (SI) increases after GD injection, we differentiate a stage III GD+ from a GD-, with the positive having a better prognosis than the negative ([Figure 2]). The authors propose the addition of stage IIID to the Lichtman classification, consisting of multifragmentation of the lunate, which may occur without perilunar osteoarthritis having occurred, which does occur in stage IV. An example is attached in the[ Figure 3].[4] [9]

Fig. 2 Top row: Stage III Gd + . Bottom row: Stage III Gd–.

Fig. 3 Stage IIID is shown, with bone multifragmentation but still without arthropathy.

In 2006, Bain and Begg proposed an arthroscopic classification based on the state of the cartilage of the intercarpal and radiocarpal joints, and more recently, other authors have updated their proposal by incorporating clinical characteristics into a therapeutic algorithm.[14]

Furthermore, age at diagnosis has been another key factor in the decision to prescribe treatment. As Dr. Irisarri anticipated in 2004, depending on the age at which KD presents, we can distinguish a group of lunatomalacias with a highly variable prognosis, namely[3] [16]:

• ○ Infantile lunatomalacia (0–12 years)

• ○ Juvenile lunatomalacia (13–skeletal maturation)

• ○ Adult Kienböck's disease

• ○ Late Kienböck's disease (>65 years). More common in women and usually presents accidentally and asymptomatic in the context of other conditions.[17]

 

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Prognosis

In general, it could be summarized that in the early treatment of Kienböck's disease, the goal is to promote revascularization of the ES (although revascularization is almost never achieved, except in infantile and juvenile lunatomalacia, which have a better prognosis), while in advanced disease, the goal is to reduce the pain caused by synovitis while preserving maximum hand function.

For educational purposes, we could divide treatments according to whether they are aimed at treating an "at-risk lunate" or a "non-viable lunate." However, it would be a mistake to view the two as separate compartments, since by individualizing each case, we could consider therapeutic alternatives that are not included in the sections presented here.

There is still no reliable timeline for the rapidity of KD progression. In most cases, it is relatively slow, but in some young patients with high functional demands, progression is surprisingly rapid. In these cases, surgery should not be postponed. The appearance of the so-called "crescent line" indicates a worse prognosis ("lunate at risk") and can be considered a "point of no return", and is followed by a gradual collapse, in some cases in a very short period of time.

 

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Treatment

The various surgical techniques applied to KD throughout history have experienced periods of initial popularity and subsequent obscurity.

Despite the wide range of treatments available, none has been proven to be truly and definitively curative.

Treatment of “At Risk” Lunate

Extra-articular techniques

These techniques are based on reducing loads on the lunate.

-Correction of radio-ulnar dysmetria

It includes lengthening the ulna (which carries a higher risk of nonunion and is technically more difficult) or shortening the radius.

Both techniques have faced technical challenges and mixed results, evolving as approaches and available osteosynthesis materials have improved. Their purpose is to reduce the loads borne by the lunate.

In radial shortening, the portion of the radius to be resected should be commensurate with the length of the ulna. The osteotomy will be transverse in patients with a short ulna, or wedge in patients with a zero or plus ulna, to avoid ulnocarpal impingement syndrome.

Angled osteotomies have been described in the radius, which do not aim to shorten, but rather to reduce the radioulnar inclination of the articular surface of the radius. However, existing biomechanical studies are contradictory. There is little data on the effect at the level of the distal radioulnar joint. Longer-term studies on their results are needed.[18] [19] [20] [21]

 

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-Shortening of the capitate bone

This procedure reduces loads across the lunate by 66%, at the expense of increasing loads on the trapezioscaphoid joint by 150%. One of the possible complications is necrosis of the proximal fragment, since its vascular supply comes from the distal portion.[22]

It is sometimes performed in conjunction with capitate-hamate fusion. The goal of this intervention is to prevent proximal migration of the capitate-third metacarpal axis into the defect created by the collapse of the lunate. This procedure would relieve the pressure exerted by the capitate bone on the lunate and allow for revascularization. In biomechanical studies, capitate-hamate fusion alone does not significantly reduce pressure on the lunate. However, the combination of this fusion with a shortening of the capitate bone is associated with decreased pressure transmission at the radiolunate joint, increasing pressure transmission at the radioscaphoid joint.[23] [24]

 

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Intra-articular Techniques

• Vascular stimulation and forage: Surgery for Kienböck's disease increases blood flow in the wrist and requires prolonged immobilization, which can relieve symptoms and explain the clinical-radiological dissociation between treatments. Illaramendi proposes metaphyseal decompression of the distal radius and ulna, with similar results to joint leveling, but with a lower risk of pseudoarthrosis, distal radioulnar incongruity, and ulnocarpal impingement. Techniques such as this or lunate perforation seek to improve blood flow, but lack conclusive evidence.[25]

• -Curettage and bone filling: In early stages (II and IIIA), curettage of the necrotic area and its filling with autologous bone grafts or substitute materials has been explored. The use of arthroscopy to perform this technique is being evaluated with promising initial results.[4] [26]

• -Intraosseous factors for osteogenesis: Experimental methods include intraosseous injection of stimulating factors, often assisted by arthroscopy, although these methods still lack extensive studies and long-term follow-up. Authors such as Ogawa have demonstrated the non-inferiority of bone marrow aspiration from the distal radius compared to that from the iliac crest, using them in conjunction with ultrasound and external fixation.[26] [27] ([Figure 4])

Fig. 4 (A) EK in a 24-year-old male. (B) Curettage of the SE. (C) Filling with cancellous bone chips. (D) X-ray 14 years after surgery.

Fig. 5 52-year-old male operated on by scaphoid–capitate arthrodesis with excision of the lunate.

 

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Treatment of “Non-Viable” Semilunar

Techniques Focused on the Lunate

• -Removal of the lunate: Although initially proposed, this technique causes severe carpal instability, leading to functional and radiological deterioration of the wrist. Options such as filling with tendon or capsular grafts have been ruled out over time due to inconsistent results.[4] [28]

• -Lunate prosthesis: Although widely studied, attempts have been made to prevent carpal instability resulting from lunate excision using different types of prostheses. These have evolved from the earliest silicone prostheses to more modern titanium or pyrocarbon prostheses. Despite these new prostheses, none have demonstrated consistent long-term results. For this reason, few surgeons continue to use them due to frequent complications.[29] [30]

• -Revascularization: This involves vascularized bone grafts, with variations including the use of the distal radius, medial femoral condyle, or pisiform bone. Despite its innovation, results have been inconsistent and limited by donor site morbidity and difficult reproducibility.[31] [32] [33]

 

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Palliative Techniques not Focused on the Lunate

• -Proximal row carpectomy (PRC). If the head of the capitate bone is wide, it allows for maintaining a high range of motion and acceptable strength, although its viability depends on the state of the head of the capitate bone, and of course, on the absence of osteoarthritis in the semilunar facet of the radius and the capitate bone.[34]

• -Partial carpal arthrodesis: There are several possibilities.

  • Triscaphoid arthrodesis (either preserving the SE or removing it and replacing it with a silastic prosthesis). This was initially the most commonly used technique. Watson justified it by reducing the load borne by the lunate. It has gradually fallen into disuse because it does not provide significant improvement in the lunate and instead causes radioscaphoid arthrosis, which, even when combined with a radial styloidectomy, ultimately generates disabling pain.[35]

  • Scaphoid-capitate arthrodesis , with or without lunate excision. Reported results have been highly variable in the past, but the availability of more effective screws has favored its widespread use. The number and orientation of screws has varied, depending on surgeon preference, although the latest results of Dr. Jorquera's review show very favorable results when performing lunate excision associated with arthroscopic scaphoid-capitate arthrodesis.36–38 ([Figure 5])

  • Carpal bone osteotomy proposed by Graner . In type I, he performed an E-SE-HG-Pi arthrodesis. In type II, he divided the capitate bone, moved its proximal fragment proximally, and placed a bone graft between the two fragments. Fixation was achieved with small cortical bone grafts. The results were unfavorable, which led to its progressive abandonment.[39]

• - Total radiocarpal arthrodesis. It is indicated in advanced stages in patients who are still young and have significant functional work demands. Often, friction between the plate and the extensor tendons can lead to the subsequent removal of the plate.[4] [13]

• Other surgical procedures:

• The list of surgical techniques for treating KD is not limited to those discussed. Some have fallen into disuse. Examples include carpal tunnel opening (Codega), lunate bone replacement with pisiform bone replacement according to Saffar, or osteosynthesis of bone fragments (Chou).[40] [41] [42]

 

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Conservative Treatment

It should be noted that orthopedic treatment for KD has been documented to lead to progressive radiographic deterioration toward carpal osteoarthritis, although this did not always correspond clinically with clinical deterioration in the studies conducted. Therefore, authors such as Saffar and Delaere recommended carefully assessing the indication for surgery in a disease such as KD after observing a significant percentage of patients whose clinical course is benign.[43] [44] [45]

Today, these concepts have fallen into disfavor for available therapeutic options, and studies focus more on surgical treatment of the disease. However, we always recommend discussing conservative treatment with the patient, especially as the older they are. It is a reliable alternative to consider in elderly patients with limited functional needs. In young patients who aim to lead a "normal" life, surgery is the standard option, but it should not be imposed by the surgeon.[45] [46]

 

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Proposed Therapeutic Algorithm and Choice of Authors

[Figure 6]

Fig. 6 Proposed therapeutic algorithm.

Techniques preferred by the authors:

-If the lunate is considered "at risk":

Metaphyseal radial shortening osteotomy, using a volar approach and with plate and screw synthesis.

The truth is that the theoretical basis for why this technique works is unclear. There is probably more than one explanation, with one finding meaning in lunate decompression, partial denervation, and indirect revascularization similar to that described by Illarramendi.

The threshold stage for the use of radial osteotomies is still a matter of controversy. JM Botelheiro (Lisbon) advocates their use in all stages of stage III, acknowledging that occasionally the outcome is unfavorable, requiring a second joint operation as a rescue operation. Logically, the results are better the lower the stage of SE and the carpal instability, which Botelheiro considers adaptive rather than "true."[47] [48]

The authors recommend considering radial shortening osteotomy as a valid option up to stage IIIA, and even in some cases at stage IIIB, if the patient is young and has a low-demand profession.

- If the lunate is considered "non-viable":

In these cases, we believe that palliative alternatives offer more reproducible results, and within these, the choice should be individualized according to each patient's activity. The most established are proximal row carpectomy and scaphocapitate arthrodesis (preferably with arthroscopic assistance to ensure the good condition of the facet joints).

 

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Role of Arthroscopy in KD

Arthroscopy allows for a more precise assessment of the true condition of the lunate and the radiocarpal and midcarpal articular surfaces. Today, it is essential for therapeutic decision-making, helping to establish the appropriate definitive treatment, as it provides certainty about the stage of the patient's disease at the precise time of surgery. It sometimes leads to a change in therapeutic approach.[49] ([Figure 7])

Fig. 7 Cartilage detachment of the lunate bone during wrist arthroscopy in a case of EK. Arthroscopic correlation of the “crescent line. Left wrist. Radiocarpal view from the 3–4 portal.

As Bain and Begg proposed when publishing their arthroscopic classification, synovectomy should be performed at any stage, and arthroscopic surgery allows this to be performed with low morbidity and high precision. We would like to emphasize the value of this synovectomy, since synovitis is present even in the earliest cases. It is not known whether it is a cause or consequence of KD, but it is highly correlated with pain.[15]

Within the "curative" treatment strategies, such as stimulation of angiogenesis, forage or revascularization of the lunate, wrist arthroscopy has allowed performing with less morbidity techniques that were certainly aggressive when performed openly and often allows the combination of several techniques simultaneously without an increase in morbidity.

In cases where the lunate is no longer viable, open techniques such as PRC or arthroscopically assisted scaphocapitate arthrodesis have become popular with promising results.[38]

Radiological images often underestimate the joint damage observed at arthroscopy; however, we must be cautious when contraindicating a technique if a small chondral ulcer is seen in the arthroscopic view, which may not be clinically relevant. We must consider a joint surface affected when it presents significant joint damage throughout its entire length.[4]

 

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Conclusions

• - To date, the cause of KD remains unknown. Concrete evidence exists, such as the existence of infantile and juvenile lunatomalacia, which allows us to affirmthat the morphological factors traditionally considered to influence the onset of KD, such as having a short ulna or a type I lunate, are not necessary.

• - Although avascular necrosis, including KD, is still considered to be free of hereditary transmission, we believe it is important to continue investigating its genetic study, especially in cases of “familial” KD.

• - The emergence of arthroscopy has marked a turning point in assessing the stage of KD and making therapeutic decisions, as well as reducing the morbidity of surgical treatment.

• - KD remains a therapeutic challenge with no universally effective solution. Treatment choices should be individualized based on disease stage, patient age, and functional demands. Continued research is key to improving treatment options and the long-term prognosis of affected patients.

 

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Conflictos de Interés

Los autores no tienen ningún conflicto de interés que declarar. Todos los coautores han visto y están de acuerdo con el contenido del manuscrito, y no existe ningún interés económico que declarar. Certificamos que el artículo es un trabajo original y no está en revisión en ninguna otra publicación.

Acknowledgements

The authors wish to express their gratitude to Dr. Carlos Irisarri for his contributions to the study and dissemination of Kienböck's disease throughout his career, as well as for providing material and collaborating in the preparation of this article.

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Publication History

Received: 26 March 2025

Accepted: 02 May 2025

Article published online:
21 July 2025