INVITED COMMENTARYEtiology of Kienbock Disease ¨ Alex Lluch, MD* and Marc Garcia-Elias, MD, PhDw process is somehow related to its vascularity, biomechanics, osseous anatomy, and/or to the morphological features of the distal forearm and surrounding carpal bones. On the basis of this fact and from a comprehensive point of view, a differentiation has been made between mechanical and vascular factors for the development of Kienbock disease. These 2 ¨ theories should not be considered as mutually exclusive, as both share the concept of the lunate becoming ischemic at a certain stage. The essential difference between the vascular and mechanical theories is that the first attributes to the loss of lunate blood supply to primary circulatory problems or traumatic interference with vascularity, whereas most mechanical theories postulate that multiple osseous lesions due to repetitive trauma result in secondary vascular impairment. There are also reasons to believe that aside from mechanical and vascular factors, there are metabolic factors predisposing to the disease as well.4 Considering these different viewpoints, it is not clear whether the lunate fracture lines seen in advanced stages of Kienbock disease represent a primary event or occur later ¨ when revascularization and resorption of necrotic bone have caused structural weakness. More recently, attention has been paid to the so-called ‘‘biological’’ factors. These factors refer not only to immunemediated vasculitis5–7 or certain viral infections such as HIV,8 which is not common in patients with Kienbock disease, but to ¨ factors that could induce a reactive vascular impairment in the subchondral vessels of the lunate in predisposed individuals.9 Abstract: The etiology of Kienbock disease is still unknown and, ¨ consequently, the ideal treatment is in doubt. Many different hypotheses have been suggested. There are reasons to believe that there are mechanical, vascular, and metabolic factors predisposing to the disease, and probably some factors triggering the development of the process. Among mechanical factors, the short ulna has been thought to be the most relevant. However, presently there are insufficient data to support a significant association between negative ulnar variance and Kienbock ¨ disease. With regard to vascular factors, anatomical studies have shown consistent dorsal and palmar arteries entering the bone, and thus, the most likely site for vascular impairment may be at the subchondral level. Many triggering factors have been proposed during the past years, but until this is truly clarified, finding the real cause of Kienbock disease will continue ¨ to be a real challenge. Key Words: Kienbock disease, lunatomalacia, etiology ¨ (Tech Hand Surg 2011;15: 33--37) n 1910, Robert Kienbock, an outstanding radiologist from ¨ Vienna (Austria), published the first clinical series and radiologic features of the entity that he named lunatomalacia.1,2 Presently, 1 century later, the etiology of Kienbock ¨ disease remains unknown. Although the term Kienbock disease has been used since ¨ 1916, during many years it was also known as ‘‘aseptic necrosis of the lunate.’’ This is explained by the fact that during the 19th and the beginning of 20th centuries, osteonecroses were diseases usually with a septic origin, but no positive culture was obtained from the necrotic lunate specimens.3 In other locations, such as the femoral head, the term ‘‘avascular necrosis’’ is now widely used. Contrary to common belief, the term is not strictly correct because all necrosis are, by definition, avascular. Many hypotheses have been proposed for Kienbock ¨ disease during these decades, but what can be deduced from multiple experimental and clinical studies that have been published is that the pathogenesis of the disease cannot be attributed to 1 single cause. It seems more likely that a combination of risk factors is required for the condition to appear, and some factors triggering the development of the disease process have to participate. In any case, why a healthy bone, without an obvious reason, undergoes a process of ischemia, necrosis, fragmentation, and final collapse is still beyond our current understanding. The fact that the lunate is almost the only bone of the carpus that may undergo complete necrosis suggests that the I MECHANICAL FACTORS Several mechanical factors have been theorized to contribute to the development of Kienbock disease. These factors include ¨ those that arise from the local anatomy of each wrist and could result in a prolonged uneven distribution of forces being transferred across the lunate and those that are related to a particular lunate geometry implying less ability to tolerate axial loading. Watson10 named the first type of factors, the ones that derive not from features of the lunate itself but from adjacent structures, as extrinsic factors. In contrast, he coined the term intrinsic anatomical factors for the second group. Extrinsic Factors Ulnar Variance Among all the risk factors considered in Kienbock disease, ¨ negative ulnar variance is by far the most frequently mentioned and has long been thought to play a determinant role in the development of lunatomalacia (Fig. 1). Olle Hulten,11 in 1928, was the first to establish a statistical ´ correlation between negative ulnar variance (a short ulna) and Kienbock disease. In his study, a short ulna was present in 74% ¨ of his 23 patients with Kienbock disease, but only in 23% of a ¨ sample of 400 wrists of the general Swedish population. A few years later, he was also the first to suggest the possibility of lunate fracture, after which necrosis develops, being the result of an uneven distribution of forces within the wrist.12 www.techhandsurg.com | From the *Institut Kaplan, Hand Unit, Vall d’Hebron Hospital, Orthopaedic Surgery, Universitat Autonoma de Barcelona; and wInstitut Kaplan, ` Barcelona, Spain. Supported by none. Address correspondence and reprint requests to Marc Garcıa-Elıas, MD, ´ ´ PhD, Institut Kaplan, Paseo Bonanova 9, 2-2, Barcelona 08022 Spain. E-mail:
[email protected];
[email protected]. Copyright r 2011 by Lippincott Williams & Wilkins Techniques in Hand & Upper Extremity Surgery Volume 15, Number 1, March 2011 33 This increased loading between the capitate and ulnar parts of the radius that causes the radial part of lunate to suffer was named the ‘‘nutcracker effect. states that a short ulna cannot share axial loads with the radius. The fact is that the prevalence of the disease among workers using vibratory tools is not higher than among workers with sedentary jobs. Furthermore. Measured by the ‘‘radiolunate coverage index’’. The same results were reported by D’Hoore et al17 when comparing 52 cases of Kienbock disease with 125 normal wrists in Belgium. thereby increasing force transmission across the joint between the radius and the radial half of the lunate. 2). It has been shown that both wrists of the same individual are anatomically very similar. Type of Load Repetitive trauma was first suggested in 1920 by Walter Muller. when compared with 20% of the sample of general population (Fig. Certainly.9 Yet. Some others believe that good results are secondary to wrist denervation. Why this happens is still not known.10 Nevertheless. who coined the term ‘‘occupational lunatomalacia. another argument lies in the fact that Kienbock disease never develops after ulnar shortening ¨ or Darrach procedure is performed. which are the 2 parts that are subjected to different amounts of stress. or even to postoperative immobilization. Radial Inclination This is another anatomical feature that has been proposed to be a risk factor for Kienbock disease. They concluded that although the odds ratio of Kienbock disease ¨ was 3. there is evidence suggesting that by decreasing the radial tilt surgically (as performed in lateral closing wedge osteotomies).1 times more likely for those with a negative ulnar variance.19 Under these circumstances. there were insufficient data to support a significant association between negative ulnar variance and Kienbock ¨ disease. this has been supported by studies that reported a high percentage of manual workers suffering from Kienbock disease.techhandsurg. ¨ In a meta-analysis looking for the influence of negative ulnar variance in Kienbock disease published by Chung et al18 ¨ in 2001. On one hand. in which external pressure to the lunate is present. other investigators have found contradictory results: the incidence of negative ulnar variance in affected wrists was not significantly different from that in normal wrists.’’ Although the relationship between negative ulnar variance and Kienbock disease has been supported by some ¨ studies. developed based on Hulten ´ findings. only 3 of the 18 collected studies had enough data or a proper study design to meet the inclusion criteria. the statement by Hulten that ‘‘no wrist in which the ulna was longer than the ´ radius developed Kienbock disease’’ cannot be maintained ¨ nowadays. if ulnar variance or any other anatomical feature was such a relevant factor. the axial load across the lunate decreases whereas the radiolunate area of contact increases.13 r 34 | www. ¨ Some clinical observations should also be considered regarding the importance of ulnar variance.Garcia-Elias and Lluch Techniques in Hand & Upper Extremity Surgery Volume 15. Kienbock disease may be present in patients ¨ with ulna plus wrists (a long ulna).21 Radiolunate Coverage Index A reduced contact area between the radius and the lunate has also been said to play a role as a predisposing factor. it has been ¨ related in opposite ways. Number 1. Razemon22 found that 78% of the wrists with Kienbock disease presented an ulnar ¨ translation of more than one-fifth of the lunate width.16 after comparing the distal radioulnar relationship of 41 cases of Kienbock disease with 325 of the general ¨ Japanese population. Furthermore. stimulation of regional vascularization. did not find a significant correlation between negative ulnar variance and lunatomalacia. In the more frequent situation of an ulnar impaction syndrome due to a long ulna.23 This bias was avoided when data collected ¨ from general public hospitals were available. why there is no collapse and fragmentation in the portion of a lunate with a large intraosseous cyst?9 Moreover. Surprisingly. they also found that ulnar variance was lower for male patients and increased with age in the Japanese. good results are very often obtained after joint levelling operations. the compressed area becomes deformed but fragmentation and collapse never occur. if not equal.4.20 In contrast.com 2011 Lippincott Williams & Wilkins . As a consequence.’’ Since a long time. Another argument against the relevance of unbalanced loading in the lunate when a patient has a short ulna is that the lunate seldom fractures into radial and ulnar segments. if an overloading was an etiological factor. March 2011 FIGURE 1.13–15 Nakamura et al. bilateral presentations of lunatomalacia should have been more frequent than they are. The mechanical theory. Some surgeons consider that such acceptable results may be attributed to the fact that such levelling procedures create a positive alteration in pressure and force transmission across the avascular lunate. it has been reported that wrists with a flattened radial inclination may have a tendency toward having smaller lunates more predisposed to Kienbock ¨ disease than the ones with steeper radial inclinations. the lunate may undergo uneven high internal loads and predisposing stress fractures that would weaken the bone. Negative ulnar variance is the most frequently mentioned mechanical factor associated with Kienbock disease. ’’ and ‘‘X’’ are descriptive of the 3 major intraosseous vascular patterns.9 Persistently increased loading due to excessive muscle tone and continuous simultaneous muscular contraction.24 Intrinsic Factors Although more interest has been focused on extrinsic factors. in patients with rheumatoid arthritis.26 More recent anatomical studies. such as perilunate dislocations. 4A–C). implying severe disruption of the extraosseous vascular net. Severe ligament destruction is also seen in cases of rheumatoid arthritis. together with negative ulnar variance. From clinical observations we know that severe traumatic injuries. Number 1. a trabecular angulation of more than 135 degrees. In contrast. lunatomalacia almost never occurs. when it exceptionally appears. preferably at the subchondral level. ¨ The fact that the lunate has a spherical shape has suggested that it is more dependent on trabecular than cortical support. Once the vessels enter the bone. yet. ¨ It is without doubt that repetitive minor trauma may not be a primary cause of Kienbock disease. there are several patterns of arterial supply to the lunate. FIGURE 3. A major infarction secondary to traumatic obliteration of the external vessels is highly unlikely to happen. March 2011 Etiology Of Kienbock Disease ¨ FIGURE 2. and the different radii of curvature between capitate and radius are some other proposed mechanical factors for the development of Kienbock disease. the greater is the relative load placed on it.19 VASCULAR FACTORS As it has been widely described. whereas less active patients may only have mild clinical symptoms and seldom seek medical treatment. A normal radiolunate coverage index and a trabecular frame without angulation are supposed to be protective features against the development of Kienbock disease. and the second site would be at the level of the small vessels inside the bone. making the bone physiologically ballotable. As the intraosseous vessels anastomosed distally to the midportion of the bone. however. have been postulated as the etiological combination to explain the higher incidence of Kienbock disease among patients with cerebral palsy.10 ¨ From a theoretical point of view. ˜ Jose Manuel Antuna. no evidence of important www. The second situation is more likely to occur. Lunate’s spherical shape. 3). if it occurs in small intraosseous vessels. its cancellous structure. and associated with a negative ulnar variance are least able to tolerate axial loading. in 1 reported case of Kienbock disease in a patient with ¨ seronegative rheumatoid arthritis.4 a Spanish hand surgeon. it has also been said that anatomy of blood vessels plays little or no role in the genesis of Kienbock disease. If the impairment occurs in the extraosseous vessels. Classic studies mentioned that in r 7% to 26% of specimens. The size of the lunate bone has also been tried to be involved. and accordingly are at risk of Kienbock disease.25 Type I lunates. vascular impairment to the lunate may occur at 2 different levels. there are several morphological features of the lunate bone itself that are thought to play a role in the genesis of lunatomalacia. the affected wrist becomes more painful (and is then diagnosed) after strenuous use.com | 2011 Lippincott Williams & Wilkins 35 . there is only 1 single volar or 1 single dorsal vessel entering the bone. The letters ‘‘Y. The first site would be at the external vascular net that supplies the lunate. with a trapezoidal shape. because trabeculae within the lunate run perpendicular to the proximal and distal articular surfaces as and was confirmed recently.28 (Figs. the proximal region adjacent to the radial articular surface is supposed to be the least vascularized area. trabecular fractures could occur10 (Fig.’’ ‘‘I. described ´ 3 different types of lunate based on the external shape more than 50 years ago. He also found that the intraosseous trabecular frame was related to the external shape of the bone as well. usually increased density secondary to bony changes or to osteoporosis of the surrounding carpal bones. the first being the most common. microinfarctions at the proximal subchondral level may develop. The smaller the size. several intraosseous branching configuration patterns have been observed. Transient radiologic changes in the appearance of the lunate can be observed. radiologic and magnetic resonance imaging changes are different from those seen in Kienbock ¨ disease. but surely may appear ¨ as a factor that causes symptom aggravation of an already present disease. a major infarction pattern may result. Moreover. the number of vascular foramina being greater in the volar pole27.Techniques in Hand & Upper Extremity Surgery Volume 15. In a young heavy manual worker. probably because there are conditions that can be modified with surgery.techhandsurg. suggesting that it is a well-vascularized bone.15 It has been postulated that lunates that may have a single arterial nutrient or those with limited intraosseous branching patterns may be more susceptible to the development of osteonecrosis from acute or chronic repetitive trauma. If this ‘‘collapsibility’’ exceeds certain limits because of excessive loading. which in turn is dependent on the length of the ulna. seldom cause lunate necrosis. The ¨ initial thought that the permanent flexed position of the wrist could impair the volar blood supply has not been shown. Note in this ¨ injected specimen that several vascular spots can be seen in the lunate. In contrast. have shown that the lunate consistently has both dorsal and palmar nutrient arteries in all cases. During this process of revascularization. an ischemic threshold exists between reversible intraosseous hypoxia and irreversible osteonecrosis. and is the same phenomenon that explains how bone grafts are incorporated. as sickle cell anemia. as described by Aspenberg et al32 in their experimental model. Unfortunately. as described by Glueck et al.com 2011 Lippincott Williams & Wilkins . steroid-induced hypercoagulability. known as ‘‘creeping substitution. A–C. and dorsal views of the vascular supply to the lunate. in continuity with living bone. using latex injection and Spalteholz technique. Transverse. March 2011 ligamentous injury could be appreciated in radiology or magnetic resonance imaging.34 are well-known situations associated with osteonecrosis. the osteoclastic resorption of the subchondral bone can be seen in radiographs. What seems obvious is that osteoblasts and osteoclasts need a blood supply. Finally. as can be seen in a displaced femoral head fracture that has remained untreated. and increase in marrow fat cells are known mechanisms to produce interruption of intraosseous blood supply. else it has to undergo spontaneous revascularization. It has been suggested that more than 1 episode of ischemia is required for the development of osteonecrosis. Why these small vessels are affected is not known.33 whereas others think that return is impaired as a consequence of the transient synovitis seen at the initial stages of the disease. they are gradually invaded and replaced by new bone. Unfortunately. or inherited hypofibrinolysis and thrombophilia. but is doing it with an unbalanced process between osteogenesis and osteoclasia. Bone trabeculae do not need living bone cells to keep their strength.techhandsurg. this animal model is more comparable with lunate dislocation than with true Kienbock disease. The dead bone resorption and new bone deposition are balanced tasks carried out by osteoclasts and osteoblasts. especially during the last 2 decades.30 Once small areas of necrotic bone appear.’’ was introduced 80 years ago by Pheminster. an impaired venous return has also been thought to play a role. Consistently. the reason for the predominance of osteoclast activity over osteoblast activity is not known. palmar.Garcia-Elias and Lluch Techniques in Hand & Upper Extremity Surgery Volume 15. so that the lunate must still be at least partially vascularized. that Kenzora31 named ‘‘ubiquitous sign’’ because is present in avascular necrosis of any location. or as this theory postulates in the lunate. because they perform lunate ¨ excision and reimplantation. OTHER FACTORS Many other factors have been proposed for an increased risk of lunatomalacia. This means that if bone destruction is seen after ischemia in a femoral head. as it is postulated for the femoral head that a vascular impairment at the subchondral level occurs and causes small infarction areas and necrotic bone in the proximal lunate. Long-term steroid treatment is also related to avascular necrosis. Is is the well-known ‘‘crescent line’’ of the femoral head. It is interesting to note how sclerosis and lunate collapse may be a consequence of revascularization. 36 | www. and dead bone is usually as strong as living bone. This concept.29 It seems more logical. Coagulation disorders. it is because the living cancellous bone attempts to repair the necrotic area. Number 1. both dorsal and palmar nutrient arteries can be found. Some investigators sustain that coagulation could be activated during the acute phase reaction of any inflammatory process.35 r FIGURE 4. fat emboli due to abnormal lipid metabolism. and it is likely that most of these events are partial and reversible. Some investigators believe that impairment of venous drainage would be a primary risk factor and lunate should be considered as a venous bone at risk. Probably. The steroid-induced osteoporosis. The vascularity of the lunate bone and Kienbock’s disease. Kienbock himself was the first to mention. Chir Main. REFERENCES 1. Cooney WP. ¨ 1993. 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