An Anatomical Study of the Lunate Bone in Kienbock's Disease

Orthopedics ◽  
1985 ◽  
Vol 8 (4) ◽  
pp. 483-487
Author(s):  
Beddie H Fu ◽  
Joseph F Imbriglia
Keyword(s):  
Anatomical Study ◽  
Lunate Bone ◽  
Kienböck’S Disease ◽  
Kienböck's Disease ◽  
Kienbock’S Disease

THE ETIOLOGY OF KIENBÖCK'S DISEASE — A HISTOPATHOLOGICAL STUDY

Hand Surgery ◽  
1998 ◽  
Vol 03 (01) ◽  
pp. 63-69 ◽  
Author(s):  
H.-G. Simank ◽  
M. Schiltenwolf ◽  
W. Krempien
Keyword(s):  
Femoral Head ◽  
Blood Supply ◽  
Primary Lesion ◽  
Histopathological Study ◽  
Arterial Blood Supply ◽  
Lunate Bone ◽  
Kienböck’S Disease ◽  
Kienböck's Disease ◽  
Arterial Blood ◽  
Kienbock’S Disease

The etiology of the necrosis of the lunate bone is still unclear. In today's theories, the necrosis is explained by impairment of the arterial bone circulation or fracture following mechanical overloading. In this study, six specimen in different stages of the disease were investigated histologically. In all the specimens, focal necrosis was detected, but also signs of regeneration, i.e. immature bone formation. No signs of fracture were seen in all stages of the disease. These findings are not compatible with sudden interruption of arterial blood supply or fracture of the lunate bone as a primary lesion. Comparable histological patterns are known in the necrosis of the femoral head. The etiological model of necrosis of the femoral head is well investigated and postulates primary marrow hypertension, induced by impairment of the venous drainage. Our results are contradictory to the etiological theories of fracture or breakdown of the arterial blood supply as a primary lesion in Kienböck's disease, and support the assumption that the model of intraosseous hypertension is transferable to the necrosis of the lunate bone.

Ulnar Variance in Kienböck’s Disease

1986 ◽  
Vol 11 (2) ◽  
pp. 258-260
Author(s):  
S. S. KRISTENSEN ◽  
E. THOMASSEN ◽  
F. CHRISTENSEN
Keyword(s):  
Bone Formation ◽  
Mean Value ◽  
Observation Time ◽  
Ulnar Variance ◽  
X Rays ◽  
Lunate Bone ◽  
Kienböck’S Disease ◽  
Kienböck's Disease ◽  
The Mean ◽  
Kienbock’S Disease

Forty four patients with forty seven wrists suffering from Kienböck’s disease were re-examined. The mean observation time was 20.5 years. In all forty seven wrists the treatment had been immobilization. Using a standard X-ray projection, and a reliable method of ulnar variance measuring, the ulnar variance was determined by three observers independently. Comparing the result with the ulnar variance in normal wrists we found the so-called “ulnar minus variant” overrepresented in patients with Kienböck’s disease. However, comparing X-rays taken at the time of diagnosis with X-rays at re-examination, we found in eight out of forty seven wrists that a subchondral bone formation in the distal radius opposite the lunate bone had taken place. This bone formation will tend to enhance the negative value of ulnar variance measurements, and suggests an explanation of the overrepresentation of “ulnar minus variants” in Kienböck’s disease. Excluding these eight wrists from the material and comparing the mean ulnar variance value in the remaining thirty nine wrists with the mean value in normal wrists no statistical difference was shown. Based on these observations it seems unlikely that the “ulnar minus variant” has any bearing on the cause of Kienböck’s disease.

Histopathology of Kienböck’s Disease

1996 ◽  
Vol 21 (1) ◽  
pp. 89-93 ◽  
Author(s):  
H. HASHIZUME ◽  
H. ASAHARA ◽  
K. NISHIDA ◽  
H. INOUE ◽  
T. KONISHIIKE
Keyword(s):  
Early Stage ◽  
Granulation Tissue Formation ◽  
Bone Necrosis ◽  
Lunate Bone ◽  
Kienböck’S Disease ◽  
Kienböck's Disease ◽  
Magnetic Resonance Imaging Mri ◽  
Reactive Interface ◽  
Histopathological Studies ◽  
Kienbock’S Disease

Histopathological studies of extracted whole lunate bones obtained from 10 patients with Stage 3 Kienböck’s disease at surgery for tendon-ball replacement were correlated with magnetic resonance imaging (MRI), computed tomography (CT) and tomography images made prior to surgery. A reforming zone, or a reactive interface between the reactive new bone and granulation tissue formation, and new vascularization were observed surrounding the bone necrosis area showing empty lacunae, fatty necrosis, and disappearance of osteoid. Findings of CT, tomography and microradiography of slices of extracted lunate bone confirmed that fractures of the articular cartilage and the subchondral bone occurred secondarily by overloading, and showed the extent of the collapsed area of the lunate. MRI showed complete loss of signal intensity in T1 images of the lesion of the lunate in advanced Stage 3 Kienböck’s disease. MRI is at present unable to distinguish bone necrosis, the histological reactive interface or surrounding hyperaemia in detail. However, the low-intensity arc, or the reactive interface present on MRI in early Stage 3, sometimes correlates with the histological findings of osteoid and granulation zones.

scholarly journals Stage III Kienböck’s disease treated with hyperbaric oxygen: the role of an unusual approach to a rare condition

2018 ◽  
pp. bcr-2018-226090
Author(s):  
Paulo Jorge Figueira ◽  
Diogo Alpuim Costa ◽  
Nunzio Barbagallo ◽  
Francisco Gamito Guerreiro
Keyword(s):  
Hyperbaric Oxygen ◽  
Rare Condition ◽  
Experimental Treatment ◽  
Aseptic Necrosis ◽  
Once Daily ◽  
Lunate Bone ◽  
Kienböck’S Disease ◽  
Kienböck's Disease ◽  
Kienbock’S Disease

Kienböck’s disease is a rare condition characterised by avascular necrosis of the lunate bone. Its natural history and aetiopathogenesis have not yet been clarified, nor are its triggering factors identified. We present a case of a 17-year-old male gymnast, without relevant medical/family history, with stage IIIA Kienböck’s disease diagnosed in 2016. Initially, submitted to conservative treatment that proved to be insufficient. Consequently, surgical treatment was proposed, but refused. The patient instead underwent experimental treatment with hyperbaric oxygen (120 sessions, 100% oxygen at 2.5 atm, for 70 min periods, once daily, five times per week). In April 2018, a favourable clinical and radiological evolution was observed, with an improvement in the patterns of pain, motion and strength and an almost complete involution of the process of aseptic necrosis of the semilunar. To the best of our knowledge, this is the first report of Kienböck’s disease treated with hyperbaric oxygen.

Biomechanical effect of isolated capitate shortening in Kienböck’s disease: an anatomical study

2012 ◽  
Vol 38 (5) ◽  
pp. 500-507 ◽  
Author(s):  
K.-D. Werber ◽  
R. Schmelz ◽  
C. A. Peimer ◽  
S. Wagenpfeil ◽  
H.-G. Machens ◽  
...  
Keyword(s):  
Pressure Sensors ◽  
Anatomical Study ◽  
Kienböck’S Disease ◽  
Kienböck's Disease ◽  
Average Decrease ◽  
Physiological Loading ◽  
Before And After ◽  
Biomechanical Changes ◽  
Biomechanical Effect ◽  
Kienbock’S Disease

Multiple operations have been proposed to slow the progression of osteonecrosis and secondary carpal damage in Kienböck’s disease. To assess the biomechanical changes after capitate shorting, we inserted pressure-testing devices into the carpal and radiocarpal joints in an anatomical study. Pressure sensors were placed into eight thawed non-fixated human cadaver arms to measure the forces transmitted in physiological loading. Longitudinal 9.8 N and 19.6 N forces were applied before and after capitate shortening. After capitate shortening, significant load reduction on the lunate was evident in all specimens. An average decrease of 49% was seen under a 9.8 N load and 56% under a 19.6 N load. The load was transferred to the radial and ulnar intercarpal joints. More relief of pressure on the lunate after isolated capitate shortening is achieved with a shallow angle between the scaphoid and capitate in the posteroanterior radiograph.

Existing or Worsening Symptoms of Kienböck’s Disease after Distal Radius Fracture: Two Case Reports

2018 ◽  
Vol 23 (04) ◽  
pp. 585-588
Author(s):  
Takeshi Ogawa ◽  
Shunsuke Asakawa
Keyword(s):  
Distal Radius Fracture ◽  
Distal Radius ◽  
Case Reports ◽  
Combined Therapy ◽  
Compression Fracture ◽  
Radius Fracture ◽  
Lunate Bone ◽  
Kienböck’S Disease ◽  
Kienböck's Disease ◽  
Kienbock’S Disease

We report two rare cases of existing or worsening symptoms due to Kienböck’s disease after distal radius fracture (DRF). During examination, radiographs show changes in the lunate bone; there was persistent wrist pain after treatment for DRF. In each case, surgeries were performed: A combined therapy (bone marrow transfusion, bone peg graft, external fixation, and low intensity pulsed ultrasound) for one, as well as carpal coalition for another. The etiology of these case presentations suggest that a compression fracture of the lunate due to a DRF resulted in softening and sclerosis.

Metaphyseal Core Decompression of the Distal Radius for Early Lunate Necrosis

2019 ◽  
Vol 24 (03) ◽  
pp. 276-282
Author(s):  
Christoph U. Schulz
Keyword(s):  
Distal Radius ◽  
Core Decompression ◽  
Stage I ◽  
Lunate Bone ◽  
Kienböck’S Disease ◽  
Kienböck's Disease ◽  
Mayo Wrist Score ◽  
Lunate Necrosis ◽  
Kienbock’S Disease

Background: Metaphyseal core decompression of the distal radius (MCD) is clinically effective in early lunate necrosis without changing individual wrist mechanics. Its concept is based on the induction of physiologic mechanisms known as physiologic fracture healing response. However, this biological concept does not yet have its place in the historically developed mechanical concepts about Kienböck’s disease and requires more detailed clarifications to understand when a change of individual wrist mechanics might be unnecessary. Methods: Thirteen consecutive cases, Lichtman stage I (n = 1) or II (n = 12), confirmed by conventional MRI, were treated by MCD. Time off work, changes in magnetic resonance imaging of the lunate, as well as clinical outcome using modified Mayo wrist score were evaluated at final follow-up. Results: Return to work was at six (1–10) weeks after surgery. MRI controls at short-term generally demonstrated stop of progression and signs of bone healing. Independently from ulna variance complete signal normalization was observed in six and a distinct, yet incomplete decrease of lunate bone marrow edema and zones of fat necrosis was confirmed in further six cases after a mean of 21 (13–51) weeks. One patient had radiographic controls only, stating normal healing at 56 months. After a mean follow-up of 37 (12–70) months the clinical outcomes were excellent in eleven and good in two cases (mean 95% in modified Mayo wrist score). Conclusions: In stage I and II lunate necrosis MCD stops disease progression, it improves clinical symptoms and induces normalization of lunate bone signal alterations in MRI. Findings suggest that stage I and II lunate necrosis can be effectively treated without alterations of individual wrist mechanics. Future studies are necessary to readjust common concepts regarding Kienböck’s disease, especially focusing on conservative therapy.

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