W7 Arthroscopic Thermal Shrinkage for Scapholunate Ligament Injuries
The use of arthroscopic thermal shrinkage with radiofrequency (RF) for the treatment of scapholunate ligament injuries is a more recent technique, and the real effectiveness is undetermined.1–3 The ability of RF probes to débride and shrink tissues makes them an attractive alternative to the use of a mechanized resector for débridement of scapholunate ligament tears, and provides a means for stabilizing the scapholunate joint.
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, which is similar to melting, and the tissue tensile properties change.5 Typically, this thermal denaturation of collagen type I occurs at approximately 60°C to 65°C. The heat in ligamentous tissues is generated by a RF pulse, which results in the oscillation of molecules as their polarity changes (i.e., ohmic resistance). The RF probe imparts a high-frequency (350 kHz to 1 MHz) alternating current from an electrical generator to the tissue. This current 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 also is 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 increase in the tissue.6,7
Biological Response to Thermal Shrinkage
At time 0, after thermal shrinkage, under light microscopy there is evidence 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 produced new matrix. These newly arrived fibroblasts use the acellular “hyalinized” collagen as a scaffold for migration and matrix synthesis. At 3 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 7 months, the cell morphology and vascularity have returned to normal without evidence of any 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. Data are conflicting, however, 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 pertains 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°C 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 physiological loading immediately after surgery; and (5) leaving viable tissue between treated regions significantly improves the healing process.10
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 and the favorable results that were achieved after mechanical débridement of partial scapholunate ligament tears.11,12 We also were influenced by the biomechanical importance of the scapholunate ligament for stability of the carpus and the paucity of treatment methods for carpal instability, and the relative ease of performing an arthroscopic shrinkage of the scapholunate ligament. The scapholunate ligament (SL) is not a homogeneous structure. It is divided into three parts: dorsal, proximal, and palmar (Fig. W7-1). The dorsal part is the strongest subregion of the scapholunate ligament. It meets all the criteria for the definition of an articular ligament in that it is composed of collagen fascicles surrounded by connective tissue with intertwined neurovascular bundles.13–15 It has a thickness of 2 to 3 mm and a length of 4 to 5 mm (Fig. W7-2) and merges with the dorsal capsule (Fig. W7-3).
