Swan neck deformity is a change in the finger’s resting position, causing it to resemble the curved neck of a swan. This condition is characterized by the middle joint, the proximal interphalangeal (PIP) joint, bending backward into hyperextension. To compensate for this overextension, the joint closest to the fingertip, the distal interphalangeal (DIP) joint, bends forward into flexion. This distinctive “S” shape is the physical result of underlying pathologies that disrupt the intricate balance of the hand’s tendons and ligaments.
Systemic Inflammatory Conditions
The most frequent cause of swan neck deformity is chronic inflammation stemming from systemic diseases. Rheumatoid Arthritis (RA) is the primary culprit, often affecting multiple fingers simultaneously. The chronic inflammation associated with RA causes synovitis, which is the swelling of the joint lining, particularly in the PIP joint.
This persistent swelling weakens and stretches the supportive soft tissues around the joint, including ligaments and tendons. This loss of stability allows the PIP joint to hyperextend uncontrollably. The deformity is seen in up to 50% of patients diagnosed with RA.
Other inflammatory arthritides can also lead to this condition through similar mechanisms of joint destruction. Examples include Psoriatic Arthritis and connective tissue diseases like Systemic Lupus Erythematosus (SLE) and scleroderma. These conditions cause soft tissue damage, weakening the structures that maintain finger alignment.
Localized Injury and Neurological Factors
Localized injuries can also initiate the process. Untreated trauma to the fingertip, such as a chronic mallet finger, can indirectly lead to the swan neck shape. Mallet finger involves an injury to the extensor tendon at the DIP joint, causing the fingertip to droop.
When the DIP joint cannot be straightened, the extensor mechanism’s force is redirected, causing the PIP joint to hyperextend. This imbalance creates the characteristic deformity over time. Other traumatic events, like a sprain, fracture, or a tendon laceration, can also damage the finger’s mechanics.
Neurological Factors
Neurological conditions that disrupt muscle control are another distinct cause. Issues like stroke, traumatic brain injury, or cerebral palsy can lead to muscle spasticity. This creates an imbalance between the flexor and extensor tendons, causing excessive tension that pulls the PIP joint into hyperextension.
Ligamentous Laxity
Generalized ligamentous laxity, often associated with connective tissue disorders, can also predispose an individual to the deformity. In conditions like Ehlers-Danlos syndrome, the naturally loose ligaments provide inadequate support to the PIP joint. The resulting joint instability allows the PIP joint to easily hyperextend, setting the stage for the compensatory DIP joint flexion.
The Mechanical Breakdown of the Finger Joint
Regardless of the initial cause, the swan neck deformity follows a specific mechanical pathway involving the failure of stabilizing structures. The primary event is the failure or stretching of the volar plate, a thick ligament on the palm side of the PIP joint. The volar plate normally prevents the PIP joint from bending backward excessively.
Once the volar plate is weakened by inflammation or trauma, the PIP joint is free to hyperextend. This structural failure leads to an imbalance in the extensor tendon system. The central slip of the extensor tendon, which attaches to the middle bone, is unopposed and pulls the PIP joint into further overextension.
The overextension causes the lateral bands—parts of the extensor mechanism—to shift upward (dorsally). This shift increases the extensor force on the PIP joint, locking it into the hyperextended position. The resulting laxity places tension on the oblique retinacular ligament, which connects the PIP and DIP joints.
This tension forces the DIP joint into flexion, as the flexor tendon becomes relatively unopposed. The combined hyperextension of the PIP joint and flexion of the DIP joint creates the unique “S” curve.