Kienböck’s disease is a complex and progressive wrist disorder involving the lunate, one of the eight small carpal bones. The condition is fundamentally defined as avascular necrosis (AVN) of this central wrist bone, meaning the bone tissue dies due to an interrupted blood supply. When the lunate loses its blood flow, its structure weakens, leading to bone collapse, fragmentation, and eventually, painful wrist arthritis. Experts conclude that Kienböck’s disease is not caused by a single event but rather by a convergence of multiple, pre-existing structural and vascular vulnerabilities.
The Role of Blood Supply
The physiological failure at the heart of Kienböck’s disease is the compromised circulation to the lunate bone. Unlike most bones, the lunate’s blood supply is often precarious and highly variable among individuals. It receives blood primarily from the dorsal and volar capsular networks, which branch off the wrist arteries and penetrate the bone at its poles.
The internal vascular architecture, known as intraosseous collaterals, is often sparse, making the lunate particularly vulnerable to any disruption of its external supply. Studies have identified different patterns of arterial blood entry, with some individuals having fewer penetrating vessels than others, increasing their risk for avascular necrosis. A significant vulnerability exists when the lunate is supplied by only a single major artery rather than the more common dual supply.
When the blood flow is interrupted, the bone cells suffer from ischemia, or lack of oxygen, which results in their death, a process called osteonecrosis. The dead bone tissue, unable to repair or maintain itself, begins to harden, or become sclerotic, as seen in early diagnostic images. This loss of living bone structure ultimately causes the bone to lose its mechanical integrity, leading to the collapse that characterizes the later stages of the disease.
Anatomical Predisposition
Structural variations within the wrist can significantly predispose an individual to Kienböck’s disease by altering the mechanical forces applied to the lunate. One of the most studied predisposing factors is ulnar variance, which describes the relative length of the two forearm bones, the radius and the ulna. A condition called negative ulnar variance occurs when the ulna is shorter than the radius, a finding present in a large percentage of Kienböck’s patients.
This length discrepancy shifts the load-bearing stress away from the ulna and onto the radius, increasing the compressive force exerted on the lunate. This excessive pressure from the radius on the lunate is believed to directly stress the lunate’s delicate blood vessels, contributing to the vascular compromise. Conversely, a positive ulnar variance, where the ulna is longer, is associated with a different wrist condition.
The inherent shape of the lunate bone, known as lunate morphology, also plays a role in disease risk and progression. The lunate is typically classified into two main types based on whether it has a small facet for articulation with the adjacent hamate bone. A Type I lunate lacks this medial facet, giving the bone a more triangular or trapezoidal shape.
Type I morphology is associated with a higher incidence of advanced disease at the time of diagnosis and a greater likelihood of suffering a coronal fracture within the lunate itself. The presence of the medial facet in a Type II lunate appears to offer a protective effect, possibly by distributing joint forces more evenly and stabilizing the lunate under mechanical load.
Mechanical Stress and Acute Injury
In a wrist already compromised by anatomical or vascular vulnerabilities, external mechanical forces can act as the final trigger for Kienböck’s disease. A single, significant acute trauma to the wrist, such as a fall onto an outstretched hand, can immediately disrupt the lunate’s limited blood supply. This sudden impact may tear the ligaments surrounding the lunate, including those that carry the nutrient arteries, leading to an abrupt onset of ischemia and necrosis.
Beyond acute injury, long-term, repetitive microtrauma is a common accelerating factor in individuals with pre-existing risk factors. Cyclical loading, often associated with heavy manual labor, the use of vibrating tools, or certain sports, causes cumulative damage to the bone structure. This chronic, repetitive strain leads to microscopic compression fractures and gradual inflammation.
The sustained mechanical stress can progressively impair the lunate’s microvascular system, causing chronic hypoperfusion that eventually culminates in avascular necrosis. This mechanism suggests that Kienböck’s disease often results from a predisposed wrist finally succumbing to the cumulative effect of occupational or environmental stressors.