Kienböck’s disease is a condition of the wrist involving the death of the lunate bone, one of the eight carpal bones. This process is called avascular necrosis, meaning the bone tissue dies due to a lack of blood supply. The lunate is a central bone important for joint movement and stability. While the precise cause often remains unknown (idiopathic), it is understood to be multifactorial. Multiple variables, including blood supply, skeletal structure, and external stresses, combine to interrupt necessary blood flow.
The Underlying Physiological Mechanism
Bone tissue requires a continuous supply of blood to deliver oxygen and nutrients. When this flow is interrupted, bone cells become starved and die, leading to avascular necrosis. The lunate bone is particularly vulnerable because of its precarious blood supply. Unlike many bones, the lunate is largely covered in cartilage, leaving only small areas for nutrient vessels to enter.
The internal arrangement of these vessels varies, with a single vessel supply present in about 30% of people. The internal vascular patterns are categorized, and the Type I pattern, which features a single intraosseous vessel, is believed to be the most susceptible. Disruption of these vessels, whether from trauma or chronic compression, starves the bone. This dead, brittle bone hardens (sclerosis) and cannot withstand normal wrist forces, leading to fragmentation, collapse, and progressive deformity.
The lack of blood supply may also be exacerbated by a failure of venous outflow. This failure increases pressure within the bone, further compromising arterial inflow.
Anatomical and Structural Predispositions
A significant factor is anatomical variations that increase mechanical loading on the lunate. The most common is negative ulnar variance, where the ulna is shorter than the radius. This length discrepancy causes a disproportionate amount of force to be shunted through the radiolunate joint. Negative ulnar variance is found in up to 78% of Kienböck’s disease cases.
Variations in the shape and size of the lunate bone also play a role. Some lunates have an irregular, often triangular appearance, associated with a weaker internal structure. This abnormal morphology forces the lunate to carry a larger axial load or concentrates stress onto a smaller area. These structural issues increase the likelihood of microfractures and mechanical irritation, which can compress limited blood vessels and initiate the disease.
Acute Trauma and Repetitive Stress Triggers
While anatomical predispositions create a vulnerable environment, external events often act as direct triggers for vascular compromise. A single, acute trauma, such as a severe fall, can immediately damage the lunate’s blood vessels, potentially causing a fracture or tearing surrounding ligaments.
Far more common is repetitive microtrauma, where smaller, repeated impacts gradually damage the bone and its vascular network. This is frequently observed in young adult males involved in heavy manual labor or occupations exposing the wrist to chronic vibration. The cumulative mechanical stress can lead to stress fractures, violating internal blood vessels and causing localized swelling.
Systemic Factors
Certain systemic conditions can act as accelerating factors by affecting overall blood flow and bone health. These include connective tissue disorders like lupus, blood disorders such as sickle cell anemia, and the long-term use of corticosteroids. These factors independently compromise the delicate blood supply, tipping an at-risk lunate into avascular necrosis.