1. Introduction

Avascular osteonecroses (AVNS) are nonspecific de- structions of focal skeletal areas with necrosis of medullary and osseous tissue [2,9]. So far it has not been possible to describe a uniform etiopathogenesis of this entity. AVN at the wrist is mainly seen in the lunate and the proximal fragment of the scaphoid nonunion. The specific vascularization pattern of both the proximal areas of the lunate and scaphoid has to be regarded as predisposition to AVNs [7,8]. These areas are supplied by terminal arterial branches without suffi- cient collaterals. Both the AVN of the lunate and the scaphoid proceed via bone condensation resulting in reduced height of the proximal carpal row and finally, carpal collapse with secondary osteoarthritis (SLACwrist) [31,33]. AVNs of other carpal, metacarpal and phalangeal bones are rare.

Similar to osteonecrosis of the femoral head, the classical concept of AVN which is based on avital; aregenerational tissue [29] was revised. According to more recent results, which are in part based on MR tomography, osteonecrosis is accompanied by reparation processes having their origin in the normal adjacent tissue [2,5,9,26].

Often carpal AVNs get to definitive imaging findings only after longstanding clinical and conventional diagnostic procedures. However, according to current results it is possible to diagnose these lesions at a stage where the medullary and osseous tissue is not yet irreparably damaged [15,17,25]. In addition, computed tomography (CT) and magnetic resonance imaging (MRI) provide a more detailed imaging of the reparation processes and therefore, more accurate staging of disease.

The aim of diagnostic imaging in AVN has to be the visualization of all pathomophological details including the state of local marrow perfusion in the damaged areas. Our own findings are based on the evaluation of 65 examinations of the lunate (37 CT, 28 MRI), 118 examinations of the scaphoid (87 CT, 29 MRI) and different case observations at other carpal bones.

2. Clinical entities

Due to the unclear etiology of Kienbock's disease several predisposing conditions and initiating as well as modulating factors are up to now, controversially discussed. Mainly in manual workers chronic repetitive trauma is considered to damage supplying arteries of the lunate (1,11,16]. The vascular pattern of the lunate is regarded as an AVN predisposition: arteries entering the lunate from the dorsal and palmar pole form an intraosseous vascular network with the proximal pole supplied by terminal arteries only [7]. Another theory of compression or avulsion fractures as the primary cause of lunatomalacia (281 is nowadays rejected by many authors. According to an observation by Hulten (101, lunatomalacia is associated with a negative ulnar variance in 78% of the test population. Due to inadequate force transmission from the ulna to the wrist, the lunate is exposed to an increased axial load in the radiolunate articular cornpartnient. Most recently, the possibility of venous congestion is discussed as a cause of lunatomalacia with intraosseous measurements showing significantly higher pressures (241.

In Kienbock's disease, a dynamic process of bone remodelling is found in pathoanatomical studies [2,5,30]. Due to the effect of initiating and modulating factors, the remaining areas of viable osseous tissue facilitate reparation and revascularization processes. In- creased perfusion causes zonal osteopenia which is regarded as the basis of pathological fracture [2]. Subsequent fibrovascular tissue in the fractured area cannot be transformed into osseous tissue-point of no return. Separation and osteonecrosis result in bone collapse. Collapse of the lunate is followed by carpal instability and decreasing height of the proximal carpal row. The instability is characterized by proximal n-iigration of the capitate and rotatory subluxation of the scaphoid (dorsal subluxation, pahnar rotation). The resulting malarticulation leads to osteoarthritis mainly in the radiocarpal joint compartments [331.

Macroscopically the lunatomalacia consists of three different layers [2]:

o The maximum osteonecrosis is located at the proximal aspect of the lunate, being the origin of pathoanatomical changes. Unsuccessful reparation leads to increased bone sclerosis.

• The mid layer consists of zonal reparation with fibrovascular tissue (granulation tissue of repair), areas of deminerauation, fractured trabeculas, as well as phagocytosis of fibrous and bony tissue. This region is similar to the gap in a nonunion filled with fibrous tissue.

• The distal region of the lunate preserves bone and marrow tissue the longest and is included in the process of osteonecrosis at the end.

2.1.2. 1. Conventional radiography. Basis for exact radiographic analysis are radiographs in neutral positions of the forearm and hand. For the dorsopalmar projection, the forearm and hand are positioned on a special device in a plane level with the shoulder. The length of the ulna in relation to the radius (i.e. relative ulnar variance) depends on the actual position: In pronation the head of the ulna is in a distal position and in supination, a more proximal position to the radius. Therefore, only the standard projection in a neutral position is appropriate to measure the length of the ulna. In most cases, the distal part of the ulna head is in a plane level with the radial articular surface, whereby length differences up to + 2 mm are normal. Negative ulnar variance is diagnosed only, if the. ulna is more than 2 mm shorter than the radius.

Most commonly used is the staging classification by Decouix et al. [4] (Table 1):

In stage I of Kienbock's disease diffuse trabecular sclerosis is seen with regular shape of the lunate . Due to asymptomatic clinical presentation radio- graphical imaging of this stage I is rare.

In stage 11 intraosseously there are microcystic changes in addition to increased sclerosis, still with regular shape of the bone.

Stage III is characterized by fracture and progressive collapse of the lunate, on plain films often seen in

Table I

Staging classification of Kienbock's disease on radiological criteria.

Stage Conventional radiography

Diffuse spongiosal sclerosis

Spongiqsal sclerosis and pseudocystic inclusions

III (a) Fracture of the proximal aspect of the lunate with- out carpal instability

III (b) Progressive fracture of the proximal aspect of the shell-formed lunate and carpal instability (rotational subluxation of the scaphoid)

IV Progessive carpal collapse and ostcoarthritis (SLAC wrist)

Decoutx et al. [4]; modified after Lichtman et al. (14).

flattening, and condensation of the proximal aspect only. Cross sectional techniques such as conventional tomography [19] and high resolution CT [17] are more suitable to diagnose the fracture (Fig. 2). Lichtman and coworkers [14] have proposed a classification in stages III (a) and III (b) depending on presence of carpal instability. A reliable criterion of instability in stage III (b) is the so-called 'ring sip', the orthograde view on the distal pole of paimar tilted scaphoid. Decreased height of the lunate can be evaluated with the quotient of deformation [28], i.e. the relation of longitudinal and sagittal diameter of the lunate (normal 0.53). More commonly used is the carpal index of Youm [17], i.e. the relationship of the length of the carpus to the length of the third metacarpal bone (average 0.54 ± 0.03).

In stage IV there are signs Of Perilunar osteoarthritis (decreased width of interarticular spaces, subehondral sclerosis, manifestation of osteoPhYtes), and sometimes with articular loose bodies.

2.1.2.2. CT. In imaging of lunatomalacia, most suitable are sagittal CT views with a slice thickness Df I or 2 mm parallel to the long axis of the forearm .

Without disturbance by partial volume artefacts, this view best demonstrates the proximal aspect of the lunate, presence of carpal instability (rotatory subluxation of the scaphoid, DISI configuration of the mid carpal column) as well as initial osteoartmtis of the radiocarpal and mediocarpal joints.

In 65% (24 out of 37 cases) we have found a higher stage in CT when compared to conventional radiography [17). CT enables an earlier and snore extensive detection of pseudocystic inclusions within spongiosal sclerosis (stage 11), otherwise Occult Or typically shell- formed avulsion fractures at the proximal pole (stage III (a)) and signs of perilunar ostcoarthritis

(stage M [17,18,23]. Due to high resolution capability, imaging of sclerosis in lunatomalacia is more intensive by CT [6].

Table 2

Staging classification of carpal osteonecrosis on contrast enhanced MRI criterias.

Stage Signal in plain TI-w.sequence Enhancement after gadopentetate Pathology

I LOW Homogenous Edema

11 LOW Patchy-inhomogenous Partial necrosis

III Low Absent Complete necrosis

Schmitt et al., [25).

2.1.23. MRI. Technical requirements to diagnose carpal AVN include application of a surface coil, slice thickness of 2 or maximal 3 mm, as well as intravenous application of gadopentetate using a dose of 0.1-0.2 mmol/kg body weight tl7]. Recommended are fat saturated sequences, intrinsic fat saturation techniques (short tau inversion recovery (STIR)) as well as spectral fat saturating sequences , before and after application of contrast medium.

In the lunate every change in signal intensity leads to suspicion of a medullary or osseous lesions. Plain T1- weighted images show a decreased signal of bone mar- row, focal (proximal aspect) or in the whole bone [5,21,26,30]. Several pathoanatomic mechanisms are the basis of changed signal behavior in Kienbock's disease:

• In the early stage ischemia results in a bone marrow edema, reducing the marrow signal in T1-weighted, increasing it in T2-weighted sequences [26]. This stage is regarded as prognostic beneficial.

• After complete marrow necrosis there is an intense loss of signal intensity Tl- and T2-weighted (21).

• Increased spongiosal sclerosis and beginning fragmentation result in further loss of signal intensity.

In our patient population with 28 individuals the residual perfusion was evaluated on ground of signal changes after application of gadopentetate [17] (Table 2):

* In MRI stage I there is homogenous, sometimes excessive, enhancement pathoanatomically bone marrow edema with intact perfusion .

o The MRI stage 11 shows an inhomogenous signal pattern with contrast enhancement of the reparation zone and the viable distally located tissue, but not of the necrotic proximal aspect of the lunate .

o In MRI stage III there is no enhancement after application of gadopentetate which corresponds to the pathoanatomical stadium of complete osteonecrosis . A longstanding Kienb5ck's disease may result in a synovialitic reaction visible in MRI after application of contrast agent .

Moreover, MRI is able to demonstrate an initial stage of Kienb5ck's disease with all conventional radio- graphic images being normal [5,21,26,30]. This 'stage O' (added to the Decoulx classification) correlates with marrow edema mainly in the proximal pole of the lunate. In such cases, MRI reveals focal areas of low signal in TI-weighted and high signal in T2- or T2*- weighted images [261. In our patient population we found seven patients with this sign , always presenting strong enhancement after injection of gadopentetate (MRI stage 1).

Z 1.3. Staging

The results of modem imaging are best summarized in the classification suggested by Lichtman and Ross

[15] (Table 3):

9 Stage I represents the earliest form of lunatomalacia which is detected by MRI only.

o Stage 11 complies of increased spongiosal sclerosis and infraction at the proximal pole.

o Stage III and IV represent Decoulx's classification, with clinical relevance of additional classification in stage III (a) (stable wrist) and III (b) (carpal instability). Additionally, the grade of residual lunate perfusion should be described by MRI stages 1-111.

2.1.4. Differential diagnosis

Differential diagnosis includes the rare fractures of the lunate without consecutive necrosis, the ulnolunar

impaction syndrome, and intraosseous ganglia originating from the scapholunar or lunotriquetral ligament.

2.2. 1. Etiology and pathogenesis

Scaphoid nonunion is the result of a non-healing scaphoid fracture. Recognized causes are the initially undiagnosed fracture, incomplete immobilization, severe fragment dislocation, concomitant carpal instability and proximal scaphoid fractures [25]. Similar to the lunate, nutritional arteries enter the distal pole of the scaphoid. The proximal pole is supplied by in- traosseous recurrent vessels and represents herewith an area of terminal vascularization [8]. This pattern of perfusion is the reason that scaphoid nonunion has to be expected in the scaphoid waist in 201/o and at the proximal pole in 36% of scaphoid fractures. For the

Table 3 Staging classification of Kienbock's disease on radiological and MRI criteria.

Stage MRI and conventional radiography

I Normal radiographic appearance,diagnosis by MRI only

11 Increased spongiosal sclerosis,initial fracture of the proximal pole possible

III (a) Lunate collapse without carpal instability

III (b) Progessive lunate collapse with carpal instability

IV Progessive carpal collapse and ostcoarthritis (SLAC wrist)

Lichtman and Ross [15).

Same reason the avascular osteonecrosis is almost exceptionally located at the proximal scaphoid fragment.

The scaphoid nonunion develops in different stages [22,29]. At first there is a zonal demineralization around the fracture cleft representing delayed union. In this stage bandlike areas of resorption within both fragments can be reversible under adequate therapy. There is no consolidation of the fracture and pseudo- cystic areas of resorption in both scaphoid fragments are signs of the developing irreversible nonunion. At last there is a progressive widening of the fracture cleft with sclerosis and osteophyte formation, changing into the gap of scaphoid nonunion. At the same time, ischemia of the proximal fragment can develop. Reparation processes are based on neovascularization over the nonunion gap filled with fibrovascular tissue. Manifest proximal ostenecrosis is the result of an unsuccessful reparation attempt.

In the case of primary fragment dislocation or unstable scaphoid nonunion, the whole wrist becomes unstable [121. Both lunate and proximal scaphoid fragment rotate into dorsal extension and the distal scaphoid fragment rotates into an opposite paimar flexion position. The result is the so-called DISI (dorsiflexed intercalated segment instability). Subsequent carpal osteoarthritis will follow. First degenerative manifestation occurs between the radial styloid process and distal scaphoid fragment while later stages include mediocarpal osteoarthritis between the lunate and the capitate head [31,33]. The final stage is carpal collapse with migration of the capitate to the radio- carpal joint, the so-called SLAC wrist (scapho-lunate advanced collapse).

2.2.2.1. Conventional radiography. Basic diagnostic imaging at the scaphoid are conventional radiographs of the wrist in neutral position. Additional scaphoid views should image the scaphoid with its long axis parallel to the film plane and therefore the whole extend of the scaphoid. Standard views are images with clenched fist and ulnarduction (Stecher's view), the so-called 'penholder position' (Schreck's view), mild dorsal extension (Bridgeman's view) and hyper- pronation.

The most commonly used staging classification of scaphoid nonunion was presented by Trojan and Jahna [29]. This concept consists of three stages: Stage I with areas of osseous resorption, stage 11 with manifestation of resorption cysts and stage III with sclerosis and edge smoothing adjacent to the nonunion gap. Due to the above mentioned patho- physiology it seems reasonable to add stage III (a) (no carpal instability), stage III (b) (manifest carpal

Table 4

Staging classification of scaphoid nonunion.

Stage Radiographic signs Reversibility

I Band-like resorption zones yes

If Resorptional cysts with marginal No sclerosis

III (a) Dilated fracture cleft, sclerotic No edges without carpal.instability

III (b) Dilated fracture cleft, sclerotic No edges, manifestation of carpal instability

IV Periscaphoidal osteoarthritis and No carpal collapse

After Trojan and Jahna 1291; modified by Schmitt et a]. (2@l.instability) and stage IV (periscaphoidal osteoarthritis) [25) (Table 4).

In stage I there are bandlike areas of resorption along the fracture cleft. The transparent areas of de- mineralization are symmetric in both fragments and appear somewhat blurred.

In stage 11 there are pseudocystic resorption lesions with marginal sclerosis, located in both fragments and neighbored to the fracture cleft.

In stage III both fragment sides near the nonunion gap are completely covered by dense lines of cortical sclerosis. The osseous borders in the transition zone from gap to articular surfaces are either rounded (at- rophic form) or osteophytic (hypertrophic form). In the dorsopalmar view signs of carpal instability are the so-called 'ring sign' (the orthograde projection of the tilted distal scaphoid pole) and the triangular shape of the dorsally rotated lunate. In' the sagittal view, the connecting line between radius, lunate, capitate and metacarpal III is disrupted and forms a zick- zack-configuration (DISI). The result of decreased carpal height can be quantified using the index of Youm (normal 0.54 + 0.03).

Periscaphoidal osteoarthritis of stage IV begins between the radial styloid process and the distal scaphoid fragment typically excluding the joint compartment between radius and the proximal scaphoid fragment. Later osteoarthritis extends to the medio- carpal joint between lunate and capitate head. Radio- graphically the articular space is narrowed and the subchondral osseous region is sclerosed. In the final stage, the so-called SLAC wrist, the capitate has migrated proximally along the dorsal aspect of the lunate showing increasing signs of osteoarthritis.

Radiological diagnosis of proximal fragment os teonecrosis can only be made in an indirect way on the basis of increased spongiosal sclerosis. The increased bone density is based on a distorted os teoclastic function. In case of significant scaphoid rotation, the degree of osteosclerrsis has to be evaluated with great caution in conventional radiography.

2.2.2.2. CT. Imaging the scaphoid the CT plane should be parallel to the long scaphoid axis-oblique-parasagittal in prone position, i.e. the arm of the patient elevated above the head [3,18,20,23,25]. In sequential scanning slice thickness should be I or 2 mm using a high-resolution reconstruction algorithm.

High-resolution CT enables a more precise staging of scaphoid nonunion. When compared to conventional radiography, CT of the scaphoid provides some advantages [18,23,25]:

• Earlier and more extensive identification of bone resorption along the fracture cleft and osseous pseudocystic lesions . Marginal sclerosis is often detectable by CT only.

• Earlier and safer detection of spongiosal sclerosis because of higher density resolution of CT and avoidance of projectional artefacts due to rotated scaphoid fragments .

• Safe detection of fragment dislocations, independent of their location and projection. Of eminent importance is the distortion of the anatomical long axis.

• Detection of the initial stages of carpal os- teoarthritis in the radiocarpal joint (radial styloid process vs. distal scaphoid fragment) and in the mediocarpal joint (lunate vs. head of the capitate) earlier than with conventional radiographs.

2.2.2.3. MRI. MRI allows the evaluation of medullary and osseous viability of the proximal scaphoid fragment and the characterization of fibrovascular tissue within the nonunion gap. Technical requirements are a surface coil, a slice thickness of 2 or 3 mm (5,321 and intravenous application of gadopentetate. In addition to standard views, oblique-parasagittal views analogous to CT diagnostics, are recommended (Fig. 8). For better visualization of enhancement after application of gadopentetate, an additional acquisition of fat saturation images is helpful [25). A T2*- weighted sequence (e.g. FLASH 2D 30') is necessary for cartilage evaluation in the diagnostic assessment of osteoarthritis.

The proximal fragment, the nonunion gap and in- variably the near fractured areas of the distal fragment, show a decreased signal in plain T1-weighted sequences [5,25,32]:

The intensity of signal enhancement in the proximal fragment is of prognostic relevance. An intact perfusion state leads to a shortening of the T1-relaxation time and thereby to an increase of medullary signal intensity after application of gadopentetate. Comparable to the lunatomalacia, we have found three patterns of enhancement [251 (Table 2). In MRI stage 1, representing a bone-marrow oedema, there is a homogenous, sometimes excessive enhancement in the proximal scaphoid fragment (Fig. 7). In MRI stage 11 a patchy inhomogenous enhancement correlates with co-existing osteonecrotic and viable areas of bone. In MRI stage 111, that is complete necrosis, there is no contrast enhancement in the proximal fragment (Fig. 8).

Direct visualization of fibrovascular tissue within the nonunion gap is possible with MRI only. In TI and T2-weighted sequences there is a hypointense band, which shows a focal (Fig. 7 (d)) or bandlike enhancement (Fig. 8 (e)), depending on the grade of vascularization [25]. A T2-weighted hyperintense effusion within the gap is a reliable sip of missing soft- tissue bridges.

In the early stages of scaphoid nonunion signal alterations are also seen in the distal scaphoid fragment. As a result of reparative. hypervascularization, the scaphoid waist often shows a zonal marrow edema of low signal in T1- and high signal in T2-weighted images [5,25,321, an increased enhancement after Gd- DTPA and is sometimes bordered by a bandlike sclerosis distally-'double-line sign'. The double-line- sign is regarded as representing an increased osteoblastic activity.

2.2.2.4. Postoperative diagnostic procedures. Fine osseous structures, such as trabecular spongiosa, marginal sclerosis at the edges of the nonunion gap or small bony bridges after Matti-Russe procedure can be visualized better with high-resolution CT when compared to MRI [3,20,23). Therefore, final postoperative assessment of osseous consolidation after shape- restoring surgery or Matti-Russe procedure can be made by CT only (Fig. 9). Removal of the plaster cast is not necessary. The same statement can be made for evaluation of ancylosis after limited arthrodesis.

2.3. 1. Idiopathic ostoneciosis of the scaphoid (Preiser's disease)

This idiopathic type is extremely rare when com- pared to the secondary osteonecrosis on the base of scaphoid nonunion. Mostly the etiology remains unclear. When in doubt, there has to be search after residual signs of an occult scaphoid fracture using CT [17]. The extend of osteonecrosis can be evaluated by contrast enhanced MRI. Rotational subluxations have been seen.

2.3.2 Osteonecroses of the capitate

This very rare posttraumatic condition affects the proximal pole of the capitate. In MRI, a zone of reparation is visible between the area of altered signal and the viable region of the capitate'@1311. Of differential diagnostic importance is the osteonecrosis of a capitate fragment after 180' rotation (the scaphoid- capitate-fracture-syndrome [27] and the capitate-fracture-syndrome), where the dividing layer consists of the hyaline cartilage of the capitate head pointing distally (Fig. 10).

2.3.3. Osteonecrosis of the hamate

The rare osteonecrosis of the proximal pole of the hamate, which is supplied by recurrent nutritional vessels, must be distinguished from the osteonecrosis of the fractured hamulus ossis hamati which is often undiagnosed in conventional radiograms. The radiological and MRI aspects are identical to the description above.

2.3.4. Osteonecrosis of all carpal bones (Caffey's disease) Radiological manifestation of the idiopathic osteone-

crosis of all carpal bones is ancylosis and homogeneous sclerosis of the whole carpus. Of differential diagnostic importance is the situation after osteomyelitis.

(Mauclaire's disease)

The etiology of this juvenile disease remains unclear. Radiologically, a flattening of the metacarpal heads, a widening of the interarticular space, and signs of os- teoarthritis are seen. Osteochondral fragments and periostitis with metaphyseal cortical thickening are typically found (17]. Growth disorders by premature fusion of the epiphysial plates have been observed.

(Thiemann's disease)

Affected is the proximal base of the first phalanx at the 11. and 111. finger. The radiological appearance is comparable to Mauclaire's disease.

2.3.7 Osteonecroses after trauma of the epiphyseal plates

At the growing hand, osteonecrosis of the epiphyseal region may be caused by epi-/meta-physeal fractures or epiphyseolysis, if the traumatic lesion involves vessels of the metaphyseal endplate .

3. Discussion

Because the imaging procedures of conventional radiography, CT and MRI are based on different physical and technical principles, carpal AVN must be judged with a differentiated and synoptical diagnostic view. On the basis of the presented staging classifications for Kienbock's disease and scaphoid nonunion and the resulting therapeutic decisions, we recommend the following diagnostic plan:

Static morphological pathology of the wrist is best evaluated by conventional radiography. Standard projections in neutral positions enable screening and exclusion of other carpal conditions.

If scaphoid nonunion of stage I to III (a) or lunatomalacia stage 11 or III (a) are to be diagnosed conventionally, the next step should be a high-resolution CT. As proven in our patient group, CT reveals that 5011/o of the cases have to be classified in a higher stage, mainly by imaging signs of initial osteoarthritis (stage IV). Therefore, CT delivers relevant information for the therapeutic decisions (shape-restoring or palliative surgical procedures). First choice would be the sagittal view at the lunate (17], and the oblique- parasagittal view at the scaphoid parallel to the long axis [3,23,251. We prefer these views in contrast to coronal views at the lunate as proposed by Friedman and coworkers [6]. Conventional trispiral tomograms [19] with slice intervals of 2 mm should be performed only if there is no high-resolution CT available.

Osteonecrosis of stages 11 or III (a) found with CT diagnostics is the indication for MRI to evaluate the viability of bone marrow before planning shape- restoring surgery. In normal bone tissue primarily the medullary fat cells only are responsible for the high MRI signal. Every change in signal intensity is highly sensitive for medullary and/or osseous pathology (5,17,21,25,26,30,32]. Pathoanatomical correlations have demonstrated that a changed signal intensity of the bone marrow is immediately correlated to an altered osseous metabolism [5].

Evidence of viable bone marrow and fibrosvascular tissue at areas of reparation is visualized by application of contrast enhanced sequences. In contrast to the results of other authors [5,21,26,301 we regard on the basis of our results, the direct imaging of perfusion by means of contrast enhanced MRI as more confident when compared to signal alterations in plain TI weighted sequences which are correlated with T2- or T2*-weighted sequences. We also prefer the contrast enhanced MRI examination compared to the STIR-sequence, which shows areas of edema with high signal and contrast. The prognostic value of fibrovascular tissue in the mid layer of lunatomalacia and within the nonunion gap of the scaphoid has to be evaluated in further MRI studies with histopathological correlation.

The diagnosis or exclusion of the initial stage of lunatomalacia is of important prognostic relevance. Stage I after Lichtman and Ross [15] can only be diagnosed by MRI which should be performed if conventional radiography is equivocal and there is clinical suspicion of a Kienbi5ck's disease (dorsal wrist pain, swelling and weakness). In stage I of lunatomalacia there is usually a focal signal alteration at the proximal aspect of the lunate with strong enhancement after application of gadopentetate.

In stages III (b) or TV of lunatomalacia or scaphoid nonunion no further imaging with CT or MRI is necessary. On one hand the therapeutic con- sequences in the advanced stages is limited by palliative procedures such as limited or extended wrist arthrodesis, salvage procedures or denervation [12,22]. On the other hand, in stages III (b) or IV, no significant enhancement after application of contrast agent was found.

The diagrams of Fig. 12 and Fig. 13 demonstrate the steps of a rational diagnosis of a carpal osteone- crosis. Furthermore, these tables definitely explain pathoanatomical and formal diagnostic similarities of Kienbock's disease and scaphoid nonunion.

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