Biomechanics of the Acute Boutonniere Deformity

To demonstrate which structures of the extensor mechanism create a boutonniere deformity, when damaged, in a cadaver model. An analysis of how damage to these anatomical structures affects the biomechanical performance of the extensor mechanism was also performed.

We secured 18 fresh cadaveric hands onto an apparatus consisting of a computer-controlled motor and tensiometer attached in series to the extensor communis tendon of the ring and middle digits. The central slip, transverse, and oblique fibers of the interosseous hood and the triangular ligament were sequentially divided. After each structure was divided, the motors were activated to provide a constant tendon displacement force. The angular displacement at the proximal interphalangeal (PIP) and distal interphalangeal joints was recorded.

In all digits, detachment of the central slip from the middle phalanx produced a decrease in extension of the PIP joint. When the transverse and oblique fibers of the interosseous hood were also divided, extension at the PIP joint was further decreased. A boutonniere deformity occurred only when all 3 structures were damaged.

The boutonniere deformity requires subluxation of the lateral bands volar to the axis of rotation of the PIP joint. This study demonstrates that damage to the central slip alone does not cause the deformity. Combined injury of the central slip, triangular ligament, and transverse and oblique fibers of the interosseous hood causes a boutonniere deformity.

Division of the central slip leads to loss of extension at the PIP joint. A more substantial loss of extension after injury or development of a boutonniere deformity should alert clinicians that other structures of the extensor mechanism are also damaged.