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Kienbock’s Disease: Osteonecrosis of the Lunate

Kaleigh Petekavich

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Abstract

Kienbock’s disease is a rare disease that affects the lunate of the wrist. It is a

progressive disease by nature eventually causing a necrosis of the lunate, which will lead

to a complete collapse of the lunate, as well as a malalignment of the carpal bones.

Though the disease was discovered in 1910 by Robert Kienbock, its specific etiology is

still unknown. There are many different factors that are believed to contribute to the

development of the disease, but none have given a precise reasoning behind the actual

origin. Kienbock’s disease is primarily diagnosed through the use of the imaging

modalities: diagnostic radiography, magnetic resonance imaging (MRI), and computed

tomography (CT). Each imaging modality plays a specific role in the diagnosis and

staging of the disease. Initial treatment of Kienbock’s disease is typically nonsurgical by

immobilization. If immobilization is not effective and the disease continues to progress

and cause discomfort, there are many different treatments available depending on the

stage of the disease. The treatments appear to be highly effective resulting in an overall

satisfying prognosis for the patient.

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In 1910 an Australian radiologist by the name of Robert Kienbock discovered

numerous cases of people that suffered from malacia of the lunate, or osteonecrosis of the

lunate, which is now known today as Kienbock’s disease.1 Kienbock’s disease is a

slowly progressive disorder that will eventually lead to a collapse of the lunate, causing

an alteration of the carpal bones surrounding it; it can also be referred to as lunatomalacia

or osteochondrosis of the lunate bone.2 Kienbock’s disease is so rare that it affects less

than 5 in 10,000 people.3 Even though it was discovered over 100 years ago, it still has

an unknown etiology. Over the years some possible theories have developed regarding

the origin. There are many different treatments depending on the stage of the disease; this

disease has the possibility of being debilitating, but many of the treatments can be very

successful. The way this disease is diagnosed is primarily through the use of the imaging

sciences: diagnostic radiography, magnetic resonance imaging and computed

tomography.

Methods

A report was conducted on the causality, imaging and treatment of Kienbock’s

disease. For this study there were four electronic databases used: Cinahl, Medline-

EBSCO, Medline-Pubmed and Google Scholar. Terms associated to Kienbock’s disease

were posted into each of the databases. The terms included “Kienbock’s disease”,

“Kienbock’s disease imaging”, and “Kienbock”. Only resources that were within the past

10 years were utilized and articles that had free access from the databases. Twenty

resources were obtained for this study.

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Etiology

The etiology for Kienbock’s disease appears to be multifactorial. Researchers

believe there are some predisposing factors that may put a person at risk for developing

the disease, these include: ulnar variances, morphology, vascularization, trauma,

trabeculae and systemic conditions. Ulnar variance refers to the length of the radius and

ulna at the distal end of the bones on articulating surfaces (see Figure 1).

Figure 1 (on the left) Normal Wrist, (on the right) Wrist with Kienbock’s disease, ulna is

shorter than the radius.13

The lengths can be measured using radiographs and what is known as the

perpendicular method. The perpendicular method utilizes a posteroanterior radiograph of

the wrist, then at the ulnar point of the distal articular surface of the radius, a line is

drawn that is perpendicular to the long axis of the bone. The distance is measured

between this point and the ulnar dome to determine the ulnar variance in millimeters.4

Positive ulnar variance demonstrates the articular surface of the ulna protruding more

distally, while a neutral ulnar variance will have both of the articular surfaces of the

radius and ulna at an equal level. A negative ulnar variance exhibits the surface of the

ulna more proximally and occurs in 78% of all Kienbock’s disease cases.5 The

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morphology of the lunate may influence the chances of developing Kienbock’s disease,

they tend to be square or rectangular in shape, such as type one or two of the Antuna

Zapico classification of the lunate (see Figure2).5

Figure 2: Antuna Zapico’s classification of the lunate bone.5

In addition to the shape of the lunate, variations of the capitate morphology relates

to a change in the lunate anatomy.6 The lunate is supplied with nutrient rich blood

through the volar and dorsal poles.7 There are a few scenarios in which a decreased flow

of blood in these areas could result in this disease, such as a lack of collateral vessels,

existence of only one palmar vessel or issues with venous outflow. When there is

suboptimal arterial supply, trauma can impede on this more, causing a higher risk of

developing the disease. Trauma by itself will not cause avascular necrosis of the lunate,

it’s always in conjunction with other factors.8

A recently explored predisposing factor is the trabeculae of the bone. The

trabeculae of lunates were 2.67 times denser and 1.84 thicker in patients with Kienbock’s

disease than unaffected lunates.6 Trabeculae are not randomly arranged, they are carefully

constructed by the body to support the areas that experience the most stress. As a person

moves, they create stress on the trabeculae and it can grow and change shape and

direction in order to give them the support they need to have an active life. So loss of

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blood supply that will occur with this disease will create the fragmentation, or fracture, in

the lunate; it will then have a subchondral collapse with loss of radially arranged

trabeculae, which becomes thick as a remodeling to withstand the stress.9 Finally there is

a slight correlation between Kienbock’s disease and systemic conditions such as

autoimmune disease and sickle cell anemia.10

Symptoms

Some cases of Kienbock’s disease can actually be asymptomatic, but most exhibit

symptoms. It is often difficult to diagnose, especially the beginning stages, because the

symptoms mimic other conditions. Some of the more frequent symptoms observed with

this disease is dorsally located central wrist pain and tenderness, especially around the

lunate. As well as inflammation of the synovial membrane that can lead to weakness,

limited mobility and a loss of grip strength, and even at times the development of carpal

tunnel syndrome.5 Flexion and extension also tend to be restricted. See Table I below

for a demonstration of the changes in a patient’s range of movement and strength in his

affected right wrist.11

Table I. Functional evaluation

Right Left

Range of movement

Flexion 30 85

Extension 10 55

Radial deviation 0 10

Ulnar deviation 20 55

Pronation 70 80

Supination 80 75

Strength (kg)

Grip 9 16

Pinch 9.5 8.5

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Kienbock’s disease has 4 stages, with stage 3 being subdivided. In Stage 1 of the

disease, activities may aggravate it, causing minor pain especially when in extension

under an axial weight; this stage tends to mimic symptoms of a wrist sprain. Stage 2

shows signs of swelling from synovitis, inflammation of the synovial membrane, and

pain becomes continual often even at night. Stage 3 the pain becomes more constant and

symptoms mimic that of early degenerative arthritis. Stage 4 the wrist becomes stiff and

mimic the symptoms of advanced degenerative arthritis.12 For morphological evaluation

of the lunate to be made, use the Lichtman classification to determine the extent of the

disease. The Lichtman classification uses findings of CT, diagnostic radiography and

MRI to help stage the disease, as well as using the shape of the lunate and the density of

the bone itself. The most common stage at initial appearance for Kienbock’s disease is

stage III. The symptoms of the disease may not also correspond with the radiographic

severity, which makes it even more difficult to evaluate the natural history of the

ailment.6

Imaging

Diagnostic Radiography

Diagnostic radiography is the first imaging modality utilized to diagnose

Kienbock’s disease in an effort to assess the extent of the disease. Diagnostic

radiography by itself is not sufficient in confirming later stages IIIB and IV. It is also

used to assess pertinent anatomy of the wrist useful in diagnosing and staging – ulnar

variance, radial inclination, carpal height, radioscaphoid angle, and lunate size and

morphology.6 Stage I will appear normal in shape on a radiograph with no sign of

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disease. Stage II will appear normal in shape, but with slight sclerosis. Sclerosis can be

seen on an image as an increase in bone density in comparison with the other carpals.

Stage III-A, the lunate collapses entirely but the carpal alignment remains stable and the

radioscaphoid angle is less than 60 degrees. Stage III-B, the lunate collapses entirely and

there is instability in the carpal bones and the radioscaphoid angle is greater than 60

degrees. This stage can be demonstrated by a cortical ‘ring sign’ on a posteroanterior

radiograph.2 Stage III-C, the lunate collapses entirely and often a coronal lunate fracture

is present. Stage IV will show radiocarpal and midcarpal degenerative arthritis as well as

widening of volar and dorsal end of lunate. See Figure 3 for visualization of the different

stages of Kienbock’s disease on radiographs.

Figure 3: Lichtman classification Stage 1: normal x-rays, Stage 2: the lunate appears to

be homogenously or heterogeneously denser (A); Stage IIA: lunate collapsed with non-

fixed adaptive severance of the carpus (B); Stage IIIB: lunate collapsed with fixed

adaptive severance of the carpus (C); Stage IV: osteoarthritis (D and E).14

Magnetic Resonance Imaging

MRI is the next best imaging modality to utilize after diagnostic radiography

whenever there is a suspicion of Kienbock’s disease. MRI is necessary in order to

properly diagnose stage I, since it cannot be diagnosed by diagnostic radiography or CT

alone. Contrast-induced MRI is also useful for helping to figure out the degree of

necrotic tissue in stages II and IIIA, because these stages tend to be the ones where there

a

b c d e

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could be changes in necrosis. Normally, on both T1 and T2 weighted images, a

consistently decreased signal intensity implies a marrow pathology that is typical of

avascular necrosis. Stage I the shape and density is the same, but there is edema

formation detected in the bone marrow, demonstrated by a decreased signal on the T1

weight image and a increased signal on the T2 weighted image (See Figure 4).2

Figure 4: MRI Images of Stage I (A) Lunate bone appears normal on radiograph (B)

Coronal T1-weighted image allows visualization of the hypointensity occurring in the

lunate bone.5

Stage II will still appear to have a normal shape, but the lunate will become

denser. T1 weighted images will have a low signal intensity. T2 weighted images will

have a variable signal intensity, mainly on the side of the lunate closest to the radius.

Stage III-A and stage III-B demonstrate the collapse of the lunate. Stage III-C also

demonstrates the collapse of the lunate, as well as a coronal lunate fracture. Stage IV

demonstrates a complete collapse of the lunate and osteoarthritic changes to the joint

spaces (See Figure 5).5

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Figure 5: MRI Images of Stage IV (A) A collapse of the lunate and osteoarthritic changes

are visualized in the radiolunate and midcarpal bones in the radiograph (B) Sagittal T1-

weighted MR image demonstrates a coronal fracture of lunate bone as well as elongation

(arrow) (C) Coronal T1-weighted MR image desmontrates a hypointensity of the lunate

bone as well as collapse and osteoarthritic changes in the radiolunate and midcarpal

joints (arrows).5

Computed Tomography

The best imaging modality to depict bone anatomy in Kienbock’s disease is

computed tomography (CT); it is also utilized to help stage more advanced stages of

disease. CT is good to utilize if the lunate has become fragmented or to detect any

fractures within the lunate. A common fracture demonstrated is a coronal lunate fracture,

which would result in volar and dorsal fragments. Stage I will appear normal in shape.

Stage II will also appear normal in shape, but have slight sclerosis. Sclerosis is

demonstrated in the image by the increase in bone density in comparison with other

carpal bones. Stage III-A the lunate collapses entirely, but carpal alignment still remains

the same and the radioscaphoid angle is less than 60 degrees. Stage III-B the lunate

collapses entirely and there is instability in the carpal bones and the radioscaphoid angle

is greater than 60 degrees. Stage III-C the lunate collapses and a coronal lunate fracture

can be seen on the image (See Figure 6). Stage IV will demonstrate radiocarpal or

midcarpal degenerative arthritis and widening of the volar and dorsal ends of lunate.15

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Figure 6: (A) A fracture in the midportion of the lunate bone ranging from both of the

articular surfaces can be seen on this initial sagittal view (arrow). (B) 1 month later

another sagittal view was done which revealed comminution and a further corrosion of

the lunate (arrow).16

Treatment

Treatments may vary during different stages based off the patient and their ulnar

variance. Extended immobilization is the first step, normally the length of 3 months, in

an effort to boost spontaneous revascularization as well as non-steroidal inflammatory

medications. Some of the immobilization techniques utilized are external fixation, cast,

or temporary intercarpal pinning. If revascularization is not successful or if it was

diagnosed late, it will require a more aggressive treatment; surgery is offered after six

months if their pain persists. Treatments often will either mechanically unload the lunate

or reestablish vascularity. There are many different treatments, the key to picking the

right one for that particular patient is to stage their disease and evaluate their anatomy at

the time of the diagnosis.2

Stage I Treatment

For stage I, no matter the ulnar deviance, the treatment is the same. First step is to

immobilize, but if it is not healing then capitate-shortening osteotomy or

revascularization of the lunate may be necessary. Dorsal distal radius pedicled

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vascularized bone grafting (VBGs) is one of the procedures suggested for this stage.

VBGs allow for primary bone healing as well as new bone formation by providing the

embedding of sustainable osteoclasts and osteoblasts.17 Radial shortening or ulnar

lengthening can also be performed to help to take some of the load off of the lunate (See

Figure 7).

Figure 7: Illustration demonstrating ulnar lengthening.18

Stage II Treatment

For stage II with partial necrosis the first step is to try 3 months of

immobilization. If immobilization is still not helping it to heal, the next step is to

perform joint leveling if the patient has ulnar negative deviance or revascularization of

the lunate if the patient has ulnar positive or neutral deviance. For stage II with complete

necrosis, the immobilization step is skipped and either the joint leveling for the ulnar

negative deviation patient or the radial-shortening osteotomy procedure for the ulnar

positive or neutral patient will be performed (See Figure 8). Dorsal distal radius pedicled

vascularized bone grafting (VBGs) are also recommended for this stage of the disease as

well.

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Figure 8: Illustration of radial shortening osteotomy 18

Stage III Treatment

For stage III-A with partial necrosis the first step is to try 3 months of

immobilization for all types of ulnar deviances. If the patient is not healing, it is

suggested to perform joint leveling if the patient has ulnar negative deviance or

revascularization of the lunate if the patient has ulnar positive or neutral deviance. For

stage III-A with complete necrosis, skip the immobilization step and perform either the

joint leveling for the ulnar negative deviance patient and the capitate-shortening

osteotomy procedure or revascularization for the ulnar positive or neutral patient. Stage

III-A is the final stage that a dorsal distal radius pedicled vascularized bone grafting

(VBGs) is recommended.

For stage III-B no matter the ulnar deviance, performing arthrodesis or a proximal

row carpectomy is the typical treatment route. For proximal row carpectomy to be

successful, the capitate head can’t have any degenerative changes yet. The purpose of

intercarpal arthrodesis is to relocate the scaphoid into a neutral (45 degree) position. By

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correcting this malalignment, it will slow or possible prevent the advancement of arthritis

within the midcarpal and radiocarpal joints.2

For stage III-C no matter the ulnar deviance, one of the following will be

performed: proximal row carpectomy or arthrodesis and excision of the lunate (See

Figure 9).

Figure 9: Illustration of proximal row carpectomy 18

Stage IV Treatment

For stage IV no matter the ulnar deviance, one of the following will be performed:

proximal row carpectomy, total wrist arthroplasty or total wrist fusion. Intercarpal fusion

tries to keep the scaphoid in its correct position as well as trying to preserve the carpal

height, to thwart the possibility of degenerative arthritis; if the lunate can be conserved it

will try to take some of the load off of it (See Figure 10). There is a significant loss of

movement in fusions as well as it may have complications such as nonunion or late

arthritis.19 Wrist denervation can also be performed in conjunction with other treatments

or by itself.

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Figure 10: Illustration of a wrist fusion 18

Prognosis

Ultimately all the treatments aim to relieve the pain, increase function and stop

the progression of the disease. Since Kienbock’s disease is a progressive disorder, if left

untreated, it could result in joint destruction.5 In a recent survey, patients who were

treated nonoperatively reported an improvement in their symptoms by 63% and patients

who were treated surgically reported between 72% and 90% no matter what procedure or

stage of disease.6 Below are some graphical representations of patients who have

undergone different treatments and their level of pain relief or absence (See Figure 11).

Figure 11: Graphical illustration of pain relief in the early stages (on the left). Graphical

illustration of pain relief in the late stages (on the right).20

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Conclusion

This paper describes the different theories proposed on the origin of this rare

disease, typical symptoms of the four stages, its presentation in different imaging

modalities and the many different treatments available for patients. Diagnostic

radiography, MRI and CT all play an important role in diagnosing, staging and

monitoring the disease. It is important for an imaging professional to be educated on

Kienbock’s disease so they know what to look for in order to give the patient the proper

care. Though it is difficult to catch in the beginning stages, improvements in medical

imaging, as well as continued research, help to increase the likelihood of a diagnosis at an

earlier stage, therefore stopping the progression of the disease by earlier intervention.

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