Trigger finger (stenosing tenosynovitis) is a common condition affecting the tendons that bend the fingers and thumb toward the palm. It is characterized by a catching, snapping, or locking sensation when the affected digit moves. This mechanical issue arises from a problem within the hand’s intricate pulley system. This article explores the mechanics of trigger finger and the evidence surrounding genetic and acquired causes.
Understanding the Mechanics of Trigger Finger
The flexor tendons in the hand pull the fingers into a bent position and must glide smoothly for effortless movement. These tendons pass through fibrous tunnels, or pulleys, that keep them close to the bone, preventing “bowstringing.” The A1 pulley, located at the base of the finger where it meets the palm, is the structure most commonly implicated in trigger finger.
Trigger finger develops when there is a size mismatch between the tendon and the pulley, typically caused by thickening of the tendon sheath or the A1 pulley itself. This thickening restricts the smooth passage of the tendon, especially when a small, irritated nodule forms on the tendon’s surface. As the finger is straightened, the nodule catches on the narrowed A1 pulley, causing the characteristic painful pop or snap.
Symptoms often begin with stiffness and a sensation of clicking or catching, usually felt first thing in the morning. Over time, the condition can progress, leading to the finger becoming locked in a bent position that requires manual effort to straighten. Pain is usually localized to the base of the affected finger or thumb.
Genetic Influence and Familial Tendencies
Trigger finger is not classified as a purely hereditary disorder passed down through simple Mendelian patterns. However, recent genetic research suggests that a predisposition or susceptibility to the condition can be inherited. Genome-wide association studies (GWAS) have begun to identify specific genetic variants that increase the risk of developing trigger finger.
One study identified a genetic locus on chromosome 13, corresponding to the KLHL1 gene, that showed a significant association with the risk of trigger finger. A shared genetic variant has also been identified that links trigger finger with carpal tunnel syndrome, two conditions that frequently occur together. This variant may increase signaling through the Insulin-like Growth Factor 1 (IGF-1) pathway, contributing to the tissue changes seen in both conditions.
Familial tendencies are observed, where people with a close family history of the condition may be at a higher risk. It remains challenging for researchers to fully separate true genetic inheritance from the effects of a shared environment or similar occupational stress within a family unit. Despite this, the evidence points toward a polygenic model, meaning that multiple genes combine with external factors to determine who develops the condition.
Systemic and Acquired Risk Factors
While genetics may provide a background susceptibility, the most significant risk factors for trigger finger are systemic diseases and acquired mechanical stressors. Systemic conditions like Diabetes Mellitus are strongly associated with a significantly increased risk of developing the condition. People with diabetes have been found to have double the risk of developing trigger finger compared to those without the disease.
This increased risk is thought to be due to complications arising from high blood sugar levels over time. Hyperglycemia leads to the formation of advanced glycation end products (AGEs), which cause pathological cross-links in collagen. These cross-links accumulate in tissues such as tendons, leading to the thickening and decreased elasticity that restricts tendon gliding.
Other systemic conditions that increase risk include Rheumatoid Arthritis, Gout, and Hypothyroidism, all of which can cause inflammation or metabolic changes affecting the tendon sheath. Acquired factors, such as repetitive, forceful gripping or prolonged hand activity, also contribute to the mechanical stress that can initiate the inflammatory process.