How does the Trapeziometacarpal joint really function ? Anatomy and Biomechanics of the thumb

The basal thumb joint or trapeziometacarpal (TMC) joint is crucial for the high mobility of the thumb. Its particular configuration has been described as a saddle joint with two principal axes of motion allowing extension-flexion and abduction-adduction. In addition, the thumb can rotate around its long axis, a movement also referred to as pronation-supination. During opposition of the thumb, which is typically used to score thumb mobility and functionality (i.e. Kapandji score), flexion, adduction and pronation are combined. With its unique configuration diplaying high intrinsic mobility and limited intrinsic stability, osteoarthritis (OA) of the TMC joint is highly prevalent, making this joint the most common hand site for surgical joint reconstruction. Painful TMC OA is a highly disabling, age-related joint disorder with a large socioeconomic impact which is only expected to increase with the aging of the population. This major public health problem strengthens the need for further research in the field.

The state of knowledge shows a lack of consistency, robustness and evidence for the TMC joint ligaments anatomy and function. Available anatomical studies do not agree on the identification, nomenclature and stabilizing role of the ligaments. Early publications pointed the anterior oblique ligament (AOL) as the key stabilizing structure, while the dorsoradial ligament (DRL) has been put forward as the main TMC joint stabilizer in some more recent studies. This may have an important impact on the functional outcome of the available surgical procedures that were developed on early AOL-based concepts. Another major point in thumb function is that an accurate quantification of the kinematics of the TMC joint, but also of the more proximal joint, namely the scaphotrapezial (ST) joint, remains lacking. This is largely due to the fact that the existing body of literature on healthy and OA conditions only describe the first metacarpal (MC1) kinematics with either a fixed trapezium or trapezium-based coordinate system. Despite the high value of these studies in elucidating the TMC joint kinematics, the motion of the trapezium as well as of the scaphoid remain excluded from the analyses. Furthermore, many in vitro studies have been performed in the past years to understand the contact biomechanics of the TMC joint, with a strong inconsistency when comparing their respective results. One of the main limitations of these studies is the use of highly invasive techniques, only applicable on cadaver specimens. To date, experimental studies have not yet been able to define the behaviour of the MC1 and trapezium articular surfaces during in vivo thumb motions, and the evolution of the contact biomechanics from a healthy to a diseased TMC joint. Another surprising fact is that, since over 40 years, TMC joint arthroplasty for OA has been performed using ball-and-socket implants inspired from hip implant concepts to replace a saddle-shaped joint, without any kinematical studies on the effect total joint replacement on the three-dimensional (3D) motion capability of the TMC joint.

This state of knowledge raises many questions. Where is the truth on TMC joint stabilizing ligaments? What about ligament reconstructive surgeries based on an earlier contested concept? What are we, as surgeons, supposed to do with these ligaments? Which ligaments to reconstruct? How do bones and joints move during thumb motions in daily activities? What is the pressure distribution inside the TMC joint? Is a ball-and-socket implant able to restore the native thumb mobility? Why do ball-and-socket implants work successfully and why do they fail?

To address all these questions, we designed several studies, starting with the basics, i.e. ligament anatomy, then focusing on in vivo kinematics and contact biomechanics of the MC1, trapezium and scaphoid. Understanding the thumb joints anatomy and function is of primordial importance in optimizing surgical procedures and treatment strategies, as well as our knowledge on OA pathogenesis.