Introduction

The use of arthroscopic thermal shrinkage with radiofrequency (RF) for the treatment of scapholunate (SL) ligament injuries is a recent technique, but the real effectiveness is undetermined.^1–3 The ability of RF probes to both debride and shrink tissues makes them an attractive alternative to the use of a mechanized resector for debridement of SL ligament tears, and provides a means of stabilizing the SL joint.

There is still uncertainty about the effectiveness of this technique in the wrist, which is also true with the use of thermal shrinkage in the shoulder or for ACL shrinkage. This may be because technology, rather than scientific clinical evidence, is often the driving force in orthopedic surgery today.

What Is Shrinkage?

Shrinkage is a physical phenomenon that occurs with heat modification of type I collagen in ligamentous tissue. When the collagen is heated to a critical temperature, the heat-labile intramolecular hydrogen bonds break.⁴ The protein undergoes a phase transition from a highly ordered crystalline structure to a random-coil state (similar to a melted state) and the tissue tensile properties change.⁵ Typically, this thermal denaturation of collagen type I occurs at approximately 60 to 65° C.

The heat in ligamentous tissues is generated by an RF pulse that results in the oscillation of molecules as their polarity changes (i.e., ohmic resistance occurs). The RF probe imparts a high-frequency (350 kHz to 1 MHz) alternating current from an electrical generator to the tissue. This creates an ionic agitation in the tissue as the ions attempt to follow the changes in direction of the alternating current. This ionic agitation results in frictional heating within the tissue. The current passes either between the probe tip and a grounding pad (monopolar) or between two points on the probe tip (bipolar).

Molecular Effects of Thermal Shrinkage

Transmission electron microscopy shows significant alterations in the collagen architecture. These changes are characterized by the loss of the classic 67-nm periodicity of the type I collagen fibril that is evidenced by the loss of the periodical cross-striations in the collagen fibril. There is also an increase in the cross-sectional area of the collagen fibril. The margins of the fibrils begin to lose their distinct edge, while maintaining their circular shape. These ultrastructural effects are caused by unwinding of the collagen triple-helix as a result of the temperature rise in the tissue.^6,7

Biologic Response to Thermal Shrinkage

At time 0, after thermal shrinkage there is evidence under light microscopy of diffuse hyalinization and fusion of the collagen fiber. By day 7, there is fibroblast proliferation around and within the hyalinized regions. By day 30, large fibroblasts have migrated into the region and have produced a new matrix. These newly arrived fibroblasts use the acellular “hyalinized” collagen as a scaffold for migration and matrix synthesis. At three months, active reparative changes are evident (with an increase in vascularity). The fibroblasts have now regained a more normal appearance under transmission electron microscopy. At seven months, cell morphology and vascularity have returned to normal—without evidence of permanent tissue injury or severe inflammation.^8,9

Biomechanical Effects of Thermal Shrinkage

The aim of thermal shrinkage is to improve joint stability when the ligaments or capsular tissue are lax or incompetent. There is, however, some conflicting data with regard to the biomechanical properties of thermally treated soft tissue. Some of these inconsistencies may be accounted for by differences in experimental protocols, which do not allow for direct comparison between studies. Only a few (but important) basic concepts may be extrapolated from these studies as they pertain to shrinkage of the scapholunate ligament.

Experimental studies have shown that (1) ligaments and joint capsular tissue can be modified significantly (shortened) by thermal energy at the temperature range of 70 to 80° C, (2) thermal energy causes immediate deleterious effects such as loss of the mechanical properties, collagen denaturation, and cell necrosis, (3) thermally treated tissue is repaired actively by a residual population of fibroblasts and vascular cells, with concomitant improvement of mechanical properties, (4) the shrunken tissue stretches with time if the tissue is subjected to physiologic loading immediately after surgery, and (5) leaving viable tissue between treated regions significantly improves the healing process.^10,11

Near- and long-term biomechanical effects of thermal energy treatment are different, and the result will depend on the final tissue composition of the scapholunate complex (ligament SL and dorsal capsular ligament). Thus, the postoperative program should maintain the surgically achieved stability for enough time for cellular invasion matrix formation and healing.

Rationale for Shrinkage of Scapholunate Ligament Injuries

Our concept for the use of thermal shrinkage for the treatment of instability of the carpus with scapholunate ligament injuries arose from previous published work on the use of thermal shrinkage on other articulations, as well as the favorable results that were achieved following mechanical debridement of partial SL ligament tears.^12,13 We were also influenced by the biomechanical importance of the SL ligament for stability of the carpus and the paucity of treatment methods for carpal instability, as well as the relative ease of performing an arthroscopic shrinkage of the SL ligament.

The SL ligament is not a homogeneous structure. It is divided into three parts: dorsal, proximal, and palmar (Figure 10.1). The dorsal part is the strongest subregion of the SL ligament. It meets all criteria for the definition of an articular ligament in that it is composed of collagen fascicles surrounded by connective tissue with intertwined neurovascular bundles.^14–16 It has a thickness of 2 to 3 mm and a length of 4 to 5 mm (Figure 10.2), and it merges with the dorsal capsule (Figure 10.3).

FIGURE 10.1 Lunate and SL ligament. (1) lunate, (2) midcarpal articular surface, (3) dorsal capsule, (4) SL ligament dorsal part, (5) SL ligament proximal part, (6) radioscapholunate ligament, and (7) long radiolunate ligament.

FIGURE 10.2 (1) Scaphoid, (2) lunate, (3) triangular area SL ligament.

FIGURE 10.3 Dorsal part of SL ligament merges with the dorsal capsule. (1) lunate, (2) scaphoid, (3) SL ligament, (5) dorsal capsule, (6) union of SL with dorsal capsule, and (7) l. testud.