Different predisposed risk factors have been implicated in the development of this Disease. The most commonly cited factors are the interruption of the blood supply to the lunate, negative ulnar variance, and the workplace environment. These factors, as well as how to minimize the risk for developing this disease will be discussed in the following paragraphs

Stahl believed that in a lunate with an already tenuous blood supply, traumatic compression fracture leads to avascular necrosis.

Lee found three vascular patterns in lunates from cadavers: a single vessel, either volar or dorsal, supplying the entire bone; several vessels at both volar and dorsal surfaces of the lunate without central anastomosis; and several vessels at both volar and dorsal surfaces of the lunate with central anastomosis. Therefore according to Lee, patients with the former two patterns are at greater risk for developing Kienbock's Disease.

In fresh specimens, Gelberman and associates also studied the extraossoeus and intraosseous blood supply of the lunate. They found that in intraosseous blood supply consisted from three patterns : Y in 59%, I in 31%, and X in 10%, with dorsal and volar anastomosis just distal to the center of the lunate. Evaluation of the terminal vessels in the lunate allowed Gelberman and associates to conclude that the proximal subchondral bone, adjacent to the radial articular surface, was least vascular. Because of the rich extraeossis blood supply, they discounted the theory held by some that interruption of vessels entering a single pole of lunate caused avascularity. Based on the work, Gelberman and co-workers suggested that it is intraosseous disruption of vascularity, owing to repeated trauma with compression fracture, that cause Kienbock's Disease.

Negative ulnar variance as a risk factor has received considerable attention from the research community. In 1928, Hulton noted that a short ulnar was present in 78% of his patients with Kienbock Disease, where as only 23% of normal patients had a short ulnar. He called this condition ulnar minus variant. Since the condition was first discovered, many authors have confirmed negative ulnar variance in patients with Kienbock's disease.

Theoretically, a short ulnar variance, relative to the distal articular surface of the radius, causes increased shear and compressive loads on the lunate. Elaborate studies by Werner and associates proved that altered load transmission through the radial carpal joint with ulnar minus variance predisposes the radiolunate articulation to increase loads. This is thought to be a contributing factor in the development of Kienbock's Disease.

Until recently, Hulton's findings have been confirmed by many investigators but has been questioned by others. To date, this controversy has not been resolved. To make matters more complicated accurate measurement of ulnar variance is not simple. As pointed out by Epner and Palmer, the apparent variance changes with the position of the arm.

With this in mind, Palmer and associates further standardized the method for determining ulnar variance. They found the position of the distal ulnar, in relation to the distal radial surface changes with varying degrees of forearm rotation and that the change in variance was least with the elbow fixed at 90 degrees, The standard view recommended is a poster anterior wrist radiograph obtained with the patient's shoulder abducted 90 degrees, the elbow flexed 90 degrees, and the forearm in neutral rotation. The importance of accurate measurement of ulnar variance is highlighted by the recent gain in popularity of ulnar lengthening and radial shortening techniques to treat Kienbock's Disease

It appears the effect of aging on ulnar variance supports the theory that negative ulnar variance is a predisposed risk factor in the development of this disease. It has been shown by several researchers that ulnar variance increase with age. The cause of the increase of ulnar variance with aging is unknown, but it might be due to shortening of the radius because the force of the forearm muscle is mainly transferred to the radius to developing Kienbock's Disease.

Although Kienbock's Disease mostly affects young, active males, usually in the 3rd or 4th decade of life, Yoshida reported that of a 127 cases reviewed, 15 patients were found with aged onset. Among these 15 cases women predominated. This is a striking difference from Kienbock's Disease in young adults. Other findings reported from that study revealed that symptoms in elderly are usually not so severe and conservative treatment is typically effective. It was also shown that the degree of negative ulnar variance was not as great as in the young effected population. Several other researchers have shown that the degree of negative variance is greater in males than in females. This supports the findings that males are more susceptible.

Besides the anatomical and biological factors, the workplace also has been implicated as a contributing factor to the advancement of this disease. Occupations which require the use of pneumatic tools such as a rivet gun and hammers are all at particular risk for the development of Kienbock's Disease. The increased impact loading upon the wrist is thought to be a catalyst for the disruption of the blood supply to the lunate ultimately leading to its demise. The etiology of Kienbock's disease is thought to be either repeated minimal trauma or by a single acute episode. The underlying theme behind the theory of repeated minimal trauma is repetition coupled with force. Both established Cumulative Trauma Disorders (CTD) risk factors have been recognized as potentially harmful elements to the musculoskeletal system. The other proposed etiology, a single acute episode, indicates that force may be of greater importance. In either case, ergonomist must evaluate these factors carefully when designing or redesigning the workplace.

Wrist posture has been indirectly implied as another possible risk factor for the development of Kienbock's Disease. In two separate studies, individuals with cerebral palsy were evaluated because they have a high muscle tone, which is essentially repeated trauma, and the radiocarpul joint is constantly exposed to considerably higher pressure than what is found in normal individuals. Rooker and Goodfellow found five cases of kienbock's Disease in a group of 53 adults with cerebral palsy. An abnormally flexed wrist posture was a common feature in all five cases. This suggested to them that this extreme posture compromised the blood supply to the lunate and was considered a contributing factor to the development of Kienbock's Disease. In a more recent study, Joji reported that there is increased pressure between the radius and lunate due to the dynamics conditions so excessive muscle tone characteristics of cerebral palsy. The resting posture of their subjects was predominantly ulnar flexion with one case of volar flexion. Joji and associates went on to conclude that it was unlikely that volar flexion was the cause of Kienbock's Disease. However, in both studies a resting deviated wrist posture was observed. It is therefore possible that deviated wrist postures, incorporated with other risk factors could lead to the development of Kienbock's Disease.

It appears that the dominant hand of the worker is at the greatest risk for developing Kienbock's Disease. This finding is consistent with the etiology. In fact, the majority of the time Kienbock's Disease is unilateral.

Like many other Cumulative Trauma Disorder's, Kienbock's Disease can be treated by various medical interventions. Many of these interventions will relieve symptoms but if the individual is returned to similar activities it is possible to see a reoccurrence of Kienbock's Disease.