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(v) Capsular shrinkage of the shoulder
Current Orthopaedics (2002) 16, 41^ 48
c 2002 Published by Elsevier Science Ltd. doi:10.1054/ycuor.237, available online at http://www.idealibrary.com on
MINI-SYMPOSIUM: SHOULDER PROBLEMS
(v) Capsular shrinkage of the shoulder I.T. Jones,* U. Hansenw and A. LWallace* *Imperial College of ScienceTechnology and Medicine, Charing Cross Campus, Fulham Palace Rd, Hammersmith, London W6 8RF, UK and w Department of Mechanical Engineering, Imperial College, Exhibition Rd, South Kensington, London SW7, 2BX
INTRODUCTION Since the days of cautery of bleeding wounds, the use of heat in surgery has been commonplace.With the advent of modern methods to deliver controlled doses of energy, heat energy has been used as a therapeutic tool in a range of surgical disciplines. In orthopaedic surgery, laser light and radiofrequency (RF) electrical energy have been used in this context. These sources facilitate the regulated heating of tissues to induce structural changes in the matrix leading to shrinkage. By controlling the amount of heat generated, ablation or burning can be avoided. Recent technological advances have increased interest in this technique for arthroscopic surgery. To date, the main orthopaedic application has been in the management of the unstable shoulder, although it may have a role in instability of other joints such as the knee and ankle.To a certain extent, the clinical use of thermal shrinkage has preceded an understanding of the basic science involved. This review will attempt to explain the fundamentals of heat application to the shoulder capsule by consideration of the ultrastructural changes in the tissue as well as discussion of the mechanical and biological responses to heat. Finally, the clinical application and results of this treatment will be evaluated.
LIGAMENT STRUCTURE AND THE THERMAL STABILITYOF COLLAGEN Most skeletal ligaments contain two-thirds water by weight, while nearly three-quarters of their dry mass is made up of collagen.Greater than 90% of this collagen is Type 1, with a few per cent of Type III. The remainder of the ligament is composed of elastin, glycosaminoglycans and cellular elements. Each collagen molecule is composed of three polypeptide chains (a chains), arranged as a triple helix. Each a chain is linked to another by heat-labile hydrogen bonds between adjacent glycine residues reinforced by hydrogen bonding based on the side chains of hydroxyproline Correspondence to: ALW.Tel.: +20 - 8383- 8837; Fax: +20 - 8383- 8835; E-mail: [email protected]
residues. Each collagen molecule (three a chains) is linked to another in a quarter-stagger array to form a linear polymer. This structure is stabilized in turn by covalent cross-links that are heat stable.These are predominantly derived from lysine residues. As tissue ages, these bonds are replaced with irreducible cross-links.1 It has long been suspected that the thermal contraction of collagen led to tissue shrinkage as the regular triple helical structure underwent a phase transition from a crystal lattice to a random coil, analagous to melting.The swelling and shrinkage of collagen bundles with heat is secondary to unwinding of the triple helix (dissociation of H bonds between a chains) with maintenance of the heat stable intermolecular cross-links.2 Denatured collagen is susceptible to degradation by the proteolytic enzyme trypsin, while native collagen molecules in the triple helical con¢guration are resistant to trypsin. Hayashi et al. found that heat (created by laser energy) exposed cleavage sites for trypsin on the collagen molecule by unwinding the triple helical structure. Nontreated collagen was not susceptible to such degradation by trypsin.3 The temperature at which this unwinding occurs is critical. Stringer et al. in 1964 coined the term ‘shrinkage temperature’ after their work on eye collagen.4 Studies using heated saline baths have shown that collagen starts to unwind at approximately 60 ^ 651C.5,6 Various factors a¡ect this shrinkage temperature. It has been shown that the shrinkage temperature of collagen increases with the age of the animal, possibly due to an increase in the number of heat stable irreducible crosslinks.7 The second important variable is the biochemical composition of the ligament. It is known that puri¢ed collagen I ¢lms demonstrate shrinkage at a much lower temperature (42^ 451C). This di¡erence has been attributed to the stabilizing e¡ect of matrix proteoglycans in the intact tissue. Other factors may in£uence the way in which di¡erent ligaments respond to heat. Rodeo et al.8 demonstrated that the composition of joint capsule from patients with shoulder instability patients was di¡erent to that in normal controls. There were di¡erences in stable and reducible bonds as well as
42
collagen ¢bre diameter, cystein content and elastin content.
METHODS OF DELIVERING THERMAL ENERGY There are two main modalities of energy delivery in current clinical use; laser light and radiofrequency electrical current. Laser light is a collimated beam of ¢nite wavelength, usually in the infrared region of the electromagnetic spectrum for clinical use. This wavelength of light is transmitted into the joint via optical ¢bres, and is absorbed strongly by water molecules within well-hydrated capsular tissues. Absorption of infrared photons causes molecular vibrations, or heating, of the water molecules within the tissues. Tissue shrinkage occurs when the thermal energy is su⁄cient to initiate denaturation of the collagen ¢bres. The control of lesion size is dependent on the power of the laser, the duration of application and the area irradiated. The distance from the probe tip from the tissue, and colour of tissue are also important The holmium: yttrium aluminium garnet laser (Ho:YAG ) is the laser of choice in the clinical context described above. Limitations arise because there is no feedback mechanism to determine the temperature within the tissue or the extent of tissue shrinkage. Using ovine glenohumeral capsule, Osmond et al.9 found that with the laser set at10 W and a distance of1.5 mm from the tissue surface, the surface temperature was 62.6710.61C, an optimal temperature for thermal shrinkage. However 3 mm deep to the surface, the temperature was still high enough to cause denaturation of enzymes (47.575.771C). Therefore with laser energy, the depth of e¡ect may be excessive, posing a risk to deeper structures such as the axillary nerve. Radiofrequency energy generates heat by the £ow of an alternating current. Currently, monopolar and bipolar probes are available for arthroscopic use. A monopolar probe uses an alternating current between the application probe (‘active electrode’) and the ground plate (‘return electrode’). This current density produces molecular friction within the tissues between the electrodes and results in tissue heating. Frictional or resistive heating of tissues around the probe tip is the primary source of heat, rather than the probe itself. In contrast, energy produced by a bipolar probe follows the path of least resistance through the tissues in immediate contact with the ‘active electrode’, the irrigating solution and the ‘return electrode’ at the tip. Probes used for shrinkage must not be confused with those used for ablation and coagulation. With electrical energy, the degree of damage depends on the power and waveform; damping and se-
CURRENT ORTHOPAEDICS
paration of wave trains results in tissue destruction or coagulation. In the radiofrequency probe, very high frequencies of 350KHz to1MHZ are used resulting only in a heating e¡ect. When using an RF probe the extent of the lesion depends on the power of RF energy used, treatment duration, electrode size and shape and ¢nally the temperature at the electrode tissue interface.10 ^13 The interface temperature is itself a¡ected by the cooling e¡ect of the irrigating £uid, blood £ow in the tissue and the varying pressure of the probe on the tissue. Aware of the problems with feedback associated with a laser, manufacturers have attempted to incorporate a temperature control feedback loop into their probes. This ensures that the temperature at the probe tip is kept constant by adjusting the power. Thus at higher power settings, the probe will heat to 651C rapidly and any tendency to a further increase in temperature results in a reduction in power delivery.14 It has been proposed that temperature monitoring could be a method to control lesion size. Most studies in ligament tissue have shown that the actual tissue temperature is lower than that indicated in the probe and this has been attributed to the cooling e¡ect of the irrigating £uid.15 There is usually a latency period between the probe temperature tip being measured and the actual rise in tissue temperature. By changing the other variable, the power, and keeping the maximum probe tip temperature constant a strong correlation was observed between power and depth of lesion.14 At 10 W, with the temperature set at 651C, the lesion depth was 0.9571.2 mm at low power but 4.7571.3 mm at 30 W power. Using a bipolar probe, it was demonstrated that as power was increased tissues at a deeper plane were heated in a predictable manner. However, as with the laser, care should be taken since at 4 mm depth, with a power setting of 20 W (typical settings for clinical use) the denaturation of enzymes could still occur (44.972.81C).16 Variables such as probe contact pressure, irrigation temperature and velocity of probe over the surface are hard to control in the clinical setting, but may also a¡ect lesion size.17
EXTENTOF SHRINKAGE WITH THERMALTREATMENT Although it is established that heating collagen leads to denaturation and shrinkage, several questions remain. How do temperature changes a¡ect shrinkage? By how much does ligament tissue shrink, and does the e¡ect persist long-term in vivo? The most important factors are the temperature and duration of application. Vangsness et al.18 reported approximately 70% shrinkage of fresh frozen human Achilles tendon with 701C saline bath. Osmond et al.9
CAPSULAR SHRINKAGE OF THE SHOULDER
demonstrated, with both a laser and radiofrequency probe, that by keeping the tissue temperature between 651C and 751C, approximately 45% shrinkage could be attained. Again with saline baths, Naseef et al.5 demonstrated in bovine knee capsule that after shrinkage began at 601C, 30% shrinkage could be attained after 5 min. However, by increasing the temperature to 651C, a 55% reduction in length could be attained after only 1min. Most investigators have found that above 75^ 801C, there is no further increase in shrinkage irrespective of duration of application.5,6,19 The relationship between shrinkage and temperature therefore appears not to be a linear one but rather a sigmoid curve, with a sharp increase in shrinkage at 65^701C, and a £attening of the curve above 801C.5,17,18 The relationship between shrinkage and duration of application is also sigmoidal, with longer application periods resulting in steeper sigmoidal curves.20 In vivo experiments demonstrate that this initial shrinkage may be reduced but not necessarily maintained. In a rabbit patella tendon, a mean shrinkage of only 6.6% was observed after laser treatment. Subsequently, under physiological loads the patella tendon began to stretch at 4 weeks, so that at 8 weeks it was 5% longer than the original length.15 Some of the discrepancies between in vitro and in vivo e¡ects may be explained by the fact that in the living subject the ligament is held within the constraints of its normal bony attachments, limiting shrinkage.15 Therefore, shrinkage of a ligament structure which is already at a physiologically appropriate length and tension may not serve as a relevant model. In previous studies, we21 developed a model of ligament laxity in the rabbit medial collateral ligament. After monopolar radiofrequency treatment, the lax ligament had shrunk by 12%. At 12 weeks after treatment, the ligament had stretched out under physiological loading so that they were only 6% shorter than pre-treatment lengths.
STRUCTURAL PROPERTIES Although heat appears to shrink ligaments, what is the physical quality of the resultant tissue? The mechanical properties of a ligament may be described in terms of the of load vs deformation relationship. When tested in tension, the gradient of the linear part of the load^ deformation curve is the sti¡ness (which is the inverse of tissue compliance), while the apex of the curve, the point of failure of the ligament, de¢nes both the strength, and the elongation to failure. However, most ligaments are probably loaded to only 10 ^20% of their tensile strength in vivo. The behaviour of tissue under low loads is therefore of interest. Viscoelasticity is a measure of the time-dependent properties of the tissue when subjected to a load. This is usually
43
characterized as stress relaxation (how the load decreases over time when subjected to a constant deformation) or creep (the extent of deformation over time when subjected to a constant load). Immediately after treatment most investigators have found that sti¡ness is reduced (the tissue has become more compliant).3,22^25This reduction appears to be similar after laser- or radiofrequency-induced shrinkage. Surprisingly, Selecky et al.26 found no changes in tissue sti¡ness immediately after treatment in their experiment with cadaveric shoulders. However, the mean age of the specimens was 82 years, and the reduction in shrinkage and sti¡ness with age, due to morphological change in aged ligament may have in£uenced this result. Most studies have shown that sti¡ness is reduced even further during the next few weeks after thermal treatment.23,15,27,25 The timescale for recovery of normal sti¡ness has not been well de¢ned. Schaefer et al.15 found that laser-treated rabbit patellar tendons were 19% less sti¡ than controls after 9 weeks.Others have found sti¡ness to be the same as control values at 2,22 623 and 12 weeks.27 In comparison, Frank et al.28 found that surgically transected ligaments (which heal by a bridging scar) were still less sti¡ than controls at 40 weeks. Sti¡ness also appears to be related to the degree of shrinkage. Wall et al.20 demonstrated that progressive shrinkage of tendons heated in a saline bath resulted in them becoming more extendable (less sti¡).They postulated that the maximal shrinkage before signi¢cant material property changes occurred was between 15% and 20%. Ultimate failure stress or strength of the ligament immediately after treatment has been tested in a few cases. It is important to di¡erentiate between the material and structural properties of the ligament. The structural properties incorporate the size and shape of the material being tested. The material properties re£ect the intrinsic properties of the tissue itself. Many, measuring the structural properties of the ligament, report little to no detrimental e¡ect on the strength of the ligament.3,22,23,26,29 Wallace et al.21 however, measured the material properties of the scar and found that 25% of their RF-treated ligaments failed at loads corresponding to 5% of ultimate tensile strength of normal MCL. Schultz et al.25 found that the material properties of laser-treated lapine retinacular specimens were approximately 30% less strong than controls immediately after treatment. These ¢gures suggest that the thickened, shrunken ligament as a whole, has similar high-load characteristis to untreated ligament. The intrinsic high-load properties of the thermal scar, however, appear inferior. In vivo studies suggest that there is a loss of strength (structural and material) that persists for some time. In two experiments using a rabbit knee model, Sandusky et al.27,25 found that ultimate stress was reduced almost
44
50% at 6 weeks, returning towards control values at 12 weeks. In another rabbit model,21 57% of specimens failed at less than 5% of the strength of intact ligament at 3 weeks after treatment. Hecht et al.23 demonstrated signi¢cantly weaker tissues at 2 weeks relative to 12 weeks. The e¡ects on viscoelastic properties are important, since the time-dependent behaviour under low ‘physiological’ loads and deformations is relevant to the maintenance of joint stability. Several authors using laser shrinkage and testing stress relaxation have found no adverse e¡ects.3,22,24,26 Using an RF probe, Hecht et al.23 found that stress relaxation was increased initially, returning to normal between 6 and 12 weeks after treatment (as did strength and sti¡ness). Sandusky et al.27 found similar results with normal properties returning by 6 weeks.Wallace et al.21 found that thermal treatment conferred an increased susceptibility to creep, changes which were still far from normal at 12 weeks. Using a similar model, it had been demonstrated previously30 that healing ligament scars crept more than intact non-injured ligaments. In order to put some of these mechanical ¢ndings into a more relevant clinical setting, passive translation has been measured in human cadaver shoulder joints after thermal capsulorrhaphy. Standardized loads were applied, and the translation measured before and after treatment, giving an indication of reduction in joint laxity. Using either a laser or radiofrequency probe in a cadaveric shoulder, there was a statistically signi¢cant reduction in anterior joint translation when tested under ‘physiological’ loads.31,32 In summary, the biomechanical data available indicate that although signi¢cant alterations in length of capsular and ligamentous tissues may be achieved at the time of thermal treatment in vitro and to a lesser extent in vivo, the shrinkage may not be maintained once physical activity resumes. During the early stages of healing and remodelling, there is a reduction in sti¡ness and strength as well as an increase in potential to creep.This may explain the apparent ‘stretching-out’ under physiological loads seen in some studies. It should also be remembered that these biomechanical investigations have been based on normal tissues, which are likely to behave quite di¡erently from the tissues found in pathologically unstable joints or joints subjected to previous surgery.
THE EFFECTS OF THERMAL TREATMENTON THE MORPHOLOGY OF LIGAMENT Immediately following application of heat, shrinkage along the long axis of the collagen ¢bres causes an increase in transverse thickness.9,6,15 and a visible change in surface colour, from the tissues normal shiny white to
CURRENT ORTHOPAEDICS opaque, occurs.22,9,23 The increase in thickness correlates with temperature and the degree of shrinkage,9 and can be explained by histological observations. Under transmission electron micrography (TEM), collagen ¢brils are seen to be enlarged and to have blurred edges with loss of the normal longitudinal cross striations.3,22,6,23,33 These changes represent the denaturation of collagen and contribute to the swelling.2 This is also demonstrated on light microscopy as hyalinization of the collagen. Further examination reveals necrotic ¢broblasts, synovial cells and thrombosed and necrotic vessels.3,22,6,5,23,33 In keeping with the mechanical data and our knowledge of the thermal stability of collagen, the hyalinization and denaturation of collagen do not start until the shrinkage temperature is attained (60 ^ 651C).5,6 With increased energy, more collagen ¢brils in the capsule or ligament undergo conformational change.20 If the heating is continued it may be conducted to deeper layers causing necrosis of muscles and nerves.34 As stated previously, the severity of tissue damage is commensurate with the amount of energy transferred even if the temperature of the probe is kept constant.14 In one of the few studies examining the in vivo response of human capsular tissue to laser, tissues at this stage showed exactly the same histological response as in animal models.35 In surgically transected ligaments a marked in£ammatory response is seen during the ¢rst week.36 However, from the limited data available, it appears that the in£ammation after thermal treatment is not as great as after transection. In an ovine patello-femoral joint capsule treated with laser there was only a mild cellular response with synovial resurfacing at 3^7 days, and in£ammatory cells were not predominant at any time after laser treatment. Within the hyalinized collagen there were no viable cells.22,23,33 Only when power was su⁄cient to cause deep muscle damage (3^5 mm depth of lesion) was a £orid in£ammatory response observed.14 The intermediate phase is characterized by cellular proliferation. From the surrounding untreated zones there is capillary sprouting, further proliferation of synovial cells and ¢broblastic in¢ltration. Hyalinized regions are gradually resorbed and by day 60 are replaced with new, small-diameter collagen ¢brils. These small ¢brils surround the ¢broblasts and replace the normal bimodal distribution of predominantly large and small ¢brils found in normal tissue.22,23,15,33 This pattern suggests that the hyalinized collagen acts as a framework for migration and matrix synthesis.15 Such a homogenous population of small ¢brils is characteristic of scar tissue.37 Controversy exists about the extent of scar formation and ligament regeneration in the remodelling phase. In an ovine model at 6 months following laser shrinkage the ligament appeared ‘normal’ macroscopically and on light microscopy. However, the unimodal distribution of small diameter ‘scar’-type collagen persisted on TEM.22
CAPSULAR SHRINKAGE OF THE SHOULDER
In a sample of laser treated human glenohumeral ligament, at 12 months the normal crimp pattern (the regular wavy undulation of cells and matrix seen in thin histological sections) had returned.35 Levy et al.38 however, examined tissue specimens from radiofrequency-treated patients requiring revision at 5^10 months.They found a population of large diameter ¢brils with normal cross striations. This may represent either insu⁄cient initial treatment or an increase in size of the ¢brils due to load. Several papers have suggested that collagen ¢brils can increase in diameter to counter increasing loads.8,39,40 Interestingly, Lu et al.41 found that the treatment pattern can a¡ect rate and pattern of tissue repair. Monopolar RF energy was applied to sheep knee capsule in a commonly practiced ‘paint brush’ pattern. In a separate group, the energy was applied as a grid pattern where viable tissue was preserved between the treated zones. Tissue shrinkage was similar in both groups but in the grid pattern group, the rate of repair was signi¢cantly faster. This was attributed to greater cellular in¢ltration from the surrounding untreated tissue, and was correlated with a more rapid recovery of mechanical properties. In summary, it appears that as the hyalinized collagen is removed and replaced with new collagen the mechanical properties improve, though may not fully recover.23,15,42 Whether the resultant tissue behaves like ‘normal’ scar or ligament is unclear.
CLINICAL STUDIES The evolution of the arthroscope from its early days as a diagnostic tool, to a therapeutic surgical instrument has occurred rapidly. The advantage of minimally invasive surgery over conventional open procedures has led to the use of arthroscopic thermal shrinkage in a range of conditions ranging from resolving capsular redundancy in unstable shoulders to the tightening of lax cruciate ligament grafts in the knee.This enthusiasm, however, has been tempered by a lack of agreement on the way stability is restored and somewhat variable clinical results. Arthroscopic repair of the detached labrum appears to be a viable option in those patients diagnosed with symptomatic unidirectional instability. Unfortunately despite good short-term results,43 long-term follow-up revealed a failure rate of around 20 ^30%44 ^ 46 with some as high as 50%.47 This has been attributed to a failure to address the plastic deformation of the anterior capsule.45,48 Reducing excess laxity in the capsule has proven to be di⁄cult, but thermal capsular shrinkage may be a useful method to achieve this. Unfortunately there are only few published series49^51 that have observed outcome, mainly in the short term, after surgery and therefore few conclusions can be drawn with certainty.
45 Savoie and Field49 used a radiofrequency device in 30 patients with signs of multidirectional instability. Postoperatively an initial period of immobilization for 1^3 weeks was followed by an active rehabilitation protocol protocol until week 8. There was a gradual introduction of resistance strengthening until, at around 4 months, normal activity was allowed. No passive stretching of the capsule was allowed. At a mean follow-up of 26 months, 94% of patients had a satisfactory result on all outcome scales, which included return to sporting activity. Fanton50 similarly treated 54 patients, with a mean follow-up of 2 years. He documented a 90% success rate. Tyler et al.51 reviewed 75 patients 3 years after surgery. Almost all had a strict period of immobilization followed by muscle strengthening exercises that were designed to protect the anterior capsule. There were ¢ve failures (6%), three of which were in patients who had not received this capsular protective physiotherapy. The authors did not describe the return to sporting activity. Conversely, Miniaci52 conducted a 2-year prospective review of 19 multidirectional instability patients treated with monopolar radiofrequency. Patients were immobilised for 3 weeks after treatment. Nine patients had recurrence of their instability occurring on average 9 months after treatment. Interestingly, all those with predominantly posterior instability failed. Levy et al.53 had failure rates of 24% and 36% for RF and laser capsulorrhaphy, respectively. However, this cohort of MDI patients included some who had had previous failed open procedures and all had relatively unrestrained postoperative mobilization. Other studies with much shorter followup periods have emphasized the importance of this controlled return to activity.54,55 Experience of thermal shrinkage in other joints is even more limited.Ola¡ et al.56 applied radiofrequency shrinkage to the stabilization of chronic anterolateral ankle instability. In their retrospective review of10 patients, with a relatively short mean follow-up of 9.675.44 months, they found that all ankles were stable. This was supported by a statistically signi¢cant reduction in talar translation (as seen in the anterior draw test) and improvement in stability score (subjective, retrospective review). Postoperative management focused on the immobilization and protection of the treated ligament for 6 weeks.Thabit57 treated lax anterior cruciate ligaments (ACL), and ACL grafts with monopolar radiofrequency energy. Short-term results (18 months) were excellent in 23 out of 25 patients, although one sustained spontaneous rupture 2 months following surgery (attributed to a lack of patient compliance), and another had increased laxity. Long-term results are not known. Bailie et al.58 recount 17 patients who had radiofrequency treatment to lax ACL grafts (7) and ligaments (10). Ten ACL cases failed after an average of 4 months. Of the seven successful patients (at short time follow-up), six were native ligaments.
46
Few complications of capsular shrinkage have been reported to date. Of concern, however, are the recent reports of autolysis of treated tissue. Perry and Higgins59 recount a case of radiofrequency treatment of a slightly lax cruciate ligament graft following cruciate reconstruction. At arthroscopy, 5 months after thermal shrinkage, they found an empty notch with friable stumps. Sekiya et al.60 describe a similar case where a lax cruciate graft had been treated as above. Three weeks later after a trivial injury they found ‘no remnant of the previous hamstring autograft.’ It is possible that using too much power, too long a contact period, and failure to protect the treated tissue, may have caused these ¢ndings, although Sekiya et al. proposed a possible autoimmune reaction. Axillary neuropraxia is clearly a risk in the shoulder, in view of the nerves proximity to the inferior recess of the joint. Fanton50 described one case of axillary neuropraxia and one case of adhesive capsulitis after thermal shrinkage of 54 shoulders. Miniaci52 described a transient neuropraxia in 21% of his patients. Greis et al.61 recommended reducing the power and moving the probe continually whilst in the axillary recess. The exact mechanism of restoring joint stability by thermal shrinkage remains unclear. It seems unlikely to be a purely mechanical e¡ect, since as isolated structures shoulder ligaments are not strong enough to prevent dislocation.Ligaments are also sites of proprioceptive nerve endings.62,63 Savoie has postulated that in the unstable patient the lax capsule provides inappropriate proprioception for the rotator cu¡. By tightening this redundant capsule, we allow the cu¡ to regain a more normal ¢ring pattern, thereby restoring normal function.38,49,64 Exactly how this may occur is unclear, since the temperature required to shrink collagen is also likely to destroy proprioceptive nerve endings.
CONCLUSION From the information available thermal shrinkage of lax ligamentous tissue appears to be an e¡ective method of reducing the volume of redundant capsule. The reduction of intracapsular volume is probably limited by the linear extent of shrinkage achieved (15^20%). A grid-type pattern of application seems to confer a more rapid histological and mechanical recovery. During the early postoperative period the treated tissue is less sti¡, not as strong and more prone to ‘stretch out’, under physiological loads. The treated tissue appears to be replaced by a form of scar tissue, the mechanical properties of which approach those of the non-treated capsule at around 3 months after surgery.The exact mechanism of restoring joint stability is still unknown, but may partly be due to proprioceptive changes in the cu¡ and capsule.
CURRENT ORTHOPAEDICS
The clinical data so far are limited in number and in the extent of follow-up. However, early results of glenohumeral ligament shrinkage are promising and in some cases comparable to conventional surgery. In view of the basic scienti¢c evidence a conservative rehabilitation protocol seems prudent following either laser or radiofrequency shrinkage. The application of thermal shrinkage outside the shoulder is still controversial, particularly in view of the reported cases of autolysis of wholly intraarticular ligaments or grafts. Further work is required to overcome several technical di⁄culties, such as controlling lesion size, depth and the e¡ects of various treatment patterns.
REFERENCES 1. Smith, S H, Judge M D. Relationship between pyridinoline concentration and thermal stability of bovine intramuscular collagen. J Anim Sci 1991; 69: 1989–1993. 2. Allain J C, Le Lous M, Cohen-Solal L et al. Isometric tension developed during the hydrothermal swelling of rat skin. Connect Tissue Res 1980; 7: 127–133. 3. Hayashi K, Peters D M, Thabit G, III, Hecht P, Vanderby R Jr, Fanton G S, Markel M D. The mechanism of joint capsule thermal modification in an in-vitro sheep model. Clin Orthop 2000; 370: 236–249. 4. Stringer H, Parr J. Shrinkage temperature of eye collagen. Nature 1964; 1307. 5. Naseef G S, Foster T E, Trauner K, Solhpour S, Anderson R R, Zarins B. The thermal properties of bovine joint capsule. Am J Sports Med 1997; 25: 670–674. 6. Hayashi K, Thabit G III, Massa K L, Bogdanske J J, Cooley A J, Orwin J F, Markel M D. The effects of thermal heating on the length and histological properties of the glenohumeral joint capsule. Am J Sports Med 1997; 25: 107–112. 7. Horgan D J, King N L, Kurth L B, Kuypers R. Collagen cross links and their relationship to the thermal properties of calf tendons. Arch Biochem Biophys 1990; 281: 21–26. 8. Rodeo S A, Suzuki K, Yamauchi M, Bhargava M, Warren R. Analysis of collagen and elastic fibres in shoulder capsule in patients with shoulder instability. Am J Sports Med 1998; 26: 634–643. 9. Osmond C, Hecht P, Hayashi K, Hansen S, Fanton G S, Thabit G III, Markel, M D. Comparative effects of laser and radiofrequency energy on joint capsule. Clin Orthop 2000; 375: 286–294. 10. Cosman E R, Nashold B S, Bedenbaugh P. Stereotactic Radiofrequency lesion making. Appl Neurophysiol 1983; 46: 160–166. 11. Erez A, Shitzer A. Controlled destruction and temperature distributions in biological tissues subjected to monoactive electrocoagulation. J Biomech Eng 1980; 102: 42–49. 12. Haines D E. The biophysics of radiofrequency catheter ablationin the heart. Pace 1993; 16: 586–591. 13. Nath S, Haines D E. Biophysics and pathology of catheter energy delivery systems. Prog Cardiovasc Dis 1995; 37: 185–204. 14. Hecht P, Hayashi K, Cooley A J, Lu Y, Fanton G S, Thabit G III, Markel M D. The thermal effect of monopolar radiofrequency energy on the properties of joint capsule. An in vivo histologic study using a sheep model. Am J Sports Med 1998; 26: 808–814. 15. Schaefer S L, Ciarelli M J, Arnoczky S P, Ross H E. Tissue shrinkage with the holmium:yttrium aluminum garnet laser. A postoperative assessment of tissue length, stiffness, and structure. Am J Sports Med 1997; 25: 841–848.
CAPSULAR SHRINKAGE OF THE SHOULDER
16. Shellock F G, Shields C L. Temperature changes associated with radiofrequency energy-induced heating of bovine capsular tissue: evaluation of bipolar RF electrodes. Arthroscopy 2000; 16: 348–358. 17. Obrzut S L. The effects of radiofrequency energy on the length and temperature properties of the glenohumeral oint capsule. Arthroscopy 1998; 14: 395–400. 18. Vangsness C T Jr, Mitchell W III, Nimni M, Erlich M, Saadat V, Schmotzer H. Collagen shortening. An experimental approach with heat. Clin Orthop 1997; 337: 267–271. 19. Spoerl E. Thermomechanical behavior of the cornea. Klin Monatsbl Augenheilkunde 1996; 208: 112–116. 20. Wall M S, Deng X H, Torzilli P A, Doty S B, O’Brien S J, Warren R F. Thermal modification of collagen. J Shoulder Elbow Surg 1999; 8: 339–344. 21. Wallace A L, Sutherland C A, Marchuk L L, Waddell M, Hollinshead R M, Shrive N G, Frank C B. Creep behaviour of a rabbit model of ligament laxity after electrothermal shrinkage in vivo. Am J Sports Med 2002. 22. Hayashi K, Hecht P, Thabit G III, et al. The biologic response to laser thermal modification in an in vivo sheep model. Clin Orthop 2000; 373: 265–276. 23. Hecht P, Hayashi K, Lu Y, Fanton G S, Thabit G III, Vanderby R Jr, Markel M D. Monopolar radiofrequency energy effects on joint capsular tissue: potential treatment for joint instability. An in vivo mechanical, morphological, and biochemical study using an ovine model. Am J Sports Med 1999; 27: 761–771. 24. Hayashi K, Markel M D, Thabit G III, Bogdanske J J, Thielke R J. The effect of nonablative laser energy on joint capsular properties. An in vitro mechanical study using a rabbit model. Am J Sports Med 1995; 23: 482–487. 25. Schulz M M. The healing effects on the biomechanical properties of joint capsular tissue treated with Ho;YAG laser: an in vivio rabbit study. Arthroscopy 2001; 17: 342–347. 26. Selecky M T, Vangsness C T Jr, Liao W L, Saadat V, Hedman, T P. The effects of laser-induced collagen shortening on the biomechanical properties of the inferior glenohumeral ligament complex. Am J Sports Med 1999; 27: 168–172. 27. Sandusky M D, Schulz M M, Mc Mahon P J, Tibone J E, Lee T Q. The effects of laser on joint capsular tissue F an in vivo rabbit study. 45th Annual Meeting, Orthopaedic Research Society, 1999; 366. 28. Frank C, Woo S L, Amiel D, Harwood F, Gomez M, Akeson W. Medial collateral ligament healing. A multidisciplinary assessment in rabbits. Am J Sports Med 1983; 11: 379–389. 29. Lopez M J, Hayashi K, Vanderby R, Jr, Thabit G III, Fanton G S, Markel M. D. Effects of monopolar radiofrequency energy on ovine joint capsular mechanical properties. Clin Orthop 2000; 274: 286–297. 30. Thornton G M, Frank C B, Shrive N G, Leask G P. Ligament scar creeps more than normal ligament in early healing. Trans Orthop Res Soc 1997; 22: 73. 31. Tibone J E, Mc Mahon P J, Black A D, Sandusky M D, Lee T Q. Glenohumeral translation after thermal anterior capsulorraphy; a comparison of appliction with laser and radiofrequency. Trans Orthop Res Soc 1998; 24: 735. 32. Orlevitch S, Alexander J, Noble P, Conditt M, Lowe W. Glenohumeral joint translation, rotation, and stiffness, after arthroscopic, anterior, thernal capsulorrhaphy with radiofrequency energy. Trans Orthop Res Soc 2000; 1: 116. 33. Hayashi K, Nieckarz J A, Thabit G III, Bogdanske J J, Cooley A J, Markel, M D. Effect of nonablative laser energy on the joint capsule: an in vivo rabbit study using a holmium:YAG laser. Lasers Surg Med 1997; 20: 164–171. 34. Pullin J G, Collier M A, Johnson L L, DeBault L E, Walls R. C. Holmium: YAG laser-assisted capsular shift in a canine model:
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intraarticular pressure and histologic observations. J Shoulder Elbow Surg 1997; 6: 272–285. Hayashi K, Massa K L, Thabit G III, Fanton G S, Dillingham M F, Gilchrist K W, Markel M D. Histological evaluation of the glenohumeral joint capsule after the laser-assisted capsular shift procedure for glenohumeral instability. The Am J Sports Medicine 1999; 27: 162–167. Frank C, Schachar N, Dittrich D. Natural history of healing in the repaired medial collateral ligament. J Orthop Res 1983; 1: 179–188. Frank C, McDonald D, Bray D, Bray R, Rangayyan R, Chimich D, Shrive N. Collagen fibril diameters in the healing adult rabbit medial collateral ligament. Connect Tissue Res 1992; 27: 251–263. Levy O, Copeland S. Thermal capsular shrinkage; the effects of radiofrequency energy on the ultrastructure of the human shoulder joint capsular collagen (in vivo study), and on shoulder proprioception. Trans SECEC 1999; 121–137. Frank C, McDonald D, Shrive N. Collagen fibril diameters in the rabbit medial collateral ligament scar: a longer term assessment. Connect Tissue Res 1997; 36: 261–269. Postacchini F, De Martino C. Regeneration of rabbit calcaneal tendon maturation of collagen and elastic fibers following partial tenotomy. Connect Tissue Res 1980; 8: 41–47. Lu Y, Hayashi K, Edwards R B III, Fanton G S, Thabit G III, Markel M D. The effect of monopolar radiofrequency treatment pattern on joint capsular healing. In vitro and in vivo studies using an ovine model. Am J Sports Med 2000; 28: 711–719. Sandusky M D, Schulz M M, Mc Mahon P J, Tibone J E, Lee T Q. The effects of laser on joint capsular tissue- an in vivo rabbit study. Trans Orthop Res Soc 1999; 24: 366. Wolf E M, Wilk R, Richmond J. Arthroscopic Bankart repair using suture anchors. Oper Tech Orthop 1991; 1: 184–191. Guanche C A, Quick D C, Sodergren K M, Buss D D. Arthroscopic versus open reconstruction of the shoulder in patients with isolated Bankart lesions. Am J Sports Med 1996; 24: 144–148. Speer K P, Warren R F, Pagnani M, Warner J J. An arthroscopic technique for anterior stabilization of the shoulder with a bioabsorbable tack. J Bone Joint Surg Am 1996; 78: 1801–1807. Pagnani M, Warren R, Altchek D W, Wickiewicz T L, Anderson A F. Arthroscopic shoulder stabilization using transglenoid sutures. The Am J Sports Med 1996; 24: 459–467. Green M R, Christensen K P. Arthroscopic Bankart procedure: two- to five-year followup with clinical correlation to severity of glenoid labral lesion. Am J Sports Med 1995; 23: 276–281. Manta J P, Organ S, Nirschl R P, Pettrone F A. Arthroscopic transglenoid suture capsulolabral repair. Five-year followup. Am J Sports Med 1997; 25: 614–618. Savoie F H III, Field L D. Thermal versus suture treatment of symptomatic capsular laxity. Clin Sports Med 2000; 19: 63–75, vi. Fanton G S. Arthroscopic electrothermal surgery of the shoulder. Oper Tech Sports Med 1998; 6: 139–146. Tyler T, Calabrese G J, Parker R, Nicholas S. Electrothermally– assisted capsulorrhaphy (ETAC); A new surgical method for glenohumeral instability and its rehabilitation considerations. J Orthop Sports Phys Ther 2000; 30: 390–440. Miniachi A. Thermal capsulorrhaphy for the treatment of multidirectional instability of the shoulder. Trans Am Acad Orthop Surgeons 2001; 2: 617. Levy O, Wilson M, Williams H, Bruguera J A, Dodenhoff R, Sforza G, Copeland S. Thermal capsular shrinkage for shoulder instability. Mid-term longitudinal outcome study. J Bone Joint Surg Br 2001; 83: 640–645. Ellenbecker T S, Mattalino A J. Glenohumeral range of motion and rotator cuf strength following arthroscopic anterior stabilization
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with thermal capsulorraphy. J Orthop Sports Phys Ther 1999; 29: 160–167. Hardy P, Thabit G III, Fanton G S, Blin J L, Lortat-Jacob A, Benoit J. Arthroscopic treatment of recurrent anterior glenohumeral luxations by combining a labrum suture with holmium;YAG laser - assisted capsular shrinkage. Orthopa¨de 1996; 25: 91–93. Oloff L M, Bocko A P, Fanton G. Arthroscopic monopolar radiofrequency thermal stabilization for chronic lateral ankle instability: a preliminary report on 10 cases. J Foot Ankle Surg 2000; 39: 144–153. Thabit G III. The arthroscopic monopolar radiofrequency treatment of chronic anterior cruciate ligament instability. Oper Tech Sports Med 1998; 6: 157–160. Baliie David S. Thermal shrinkage of the anterior cruciate ligament. Trans Am Ac Orthopa Surgeons 2001; 2: 370. Perry J J, Higgins L D. Anterior and posterior cruciate ligament rupture after thermal treatment. Arthroscopy 2000; 16: 732–736.
60. Sekiya J K, Golladay G J, Wojtys E M. Autodigestion of a hamstring anterior cruciate ligament autograft following thermal shrinkage. A case report and sentinel of concern [In Process Citation]. J Bone Joint Surg Am 2000; 82–A: 1454–1457. 61. Greis P E, Burks R T, Schickendantz M S, Sandmeier R. Axillary nerve injury after thermal capsular shrinkage of the shoulder. J Shoulder Elbow Surg 2001; 10: 231–235. 62. Cooper D E, Arnoczky S P, O’Brien S J, Warren R F, DiCarlo E, Allen A. A. Anatomy, histology, and vascularity of the glenoid labrum. An anatomical study; J Bone Joint Surg [Am]. 1992; 74: 46–52. 63. Tibone J E, Fechter J, Kao J T. Evaluation of a proprioception pathway in patients with stable and unstable shoulders with somatosensory cortical evoked potentials. J Shoulder Elbow Surg 1997; 6: 440–443. 64. Warner J J, Lephart S, Fu F H. Role of proprioception in pathoetiology of shoulder instability. Clin Orthop 1996; 330: 35–39.
c 2002 Published by Elsevier Science Ltd. doi:10.1054/ycuor.237, available online at http://www.idealibrary.com on
MINI-SYMPOSIUM: SHOULDER PROBLEMS
(v) Capsular shrinkage of the shoulder I.T. Jones,* U. Hansenw and A. LWallace* *Imperial College of ScienceTechnology and Medicine, Charing Cross Campus, Fulham Palace Rd, Hammersmith, London W6 8RF, UK and w Department of Mechanical Engineering, Imperial College, Exhibition Rd, South Kensington, London SW7, 2BX
INTRODUCTION Since the days of cautery of bleeding wounds, the use of heat in surgery has been commonplace.With the advent of modern methods to deliver controlled doses of energy, heat energy has been used as a therapeutic tool in a range of surgical disciplines. In orthopaedic surgery, laser light and radiofrequency (RF) electrical energy have been used in this context. These sources facilitate the regulated heating of tissues to induce structural changes in the matrix leading to shrinkage. By controlling the amount of heat generated, ablation or burning can be avoided. Recent technological advances have increased interest in this technique for arthroscopic surgery. To date, the main orthopaedic application has been in the management of the unstable shoulder, although it may have a role in instability of other joints such as the knee and ankle.To a certain extent, the clinical use of thermal shrinkage has preceded an understanding of the basic science involved. This review will attempt to explain the fundamentals of heat application to the shoulder capsule by consideration of the ultrastructural changes in the tissue as well as discussion of the mechanical and biological responses to heat. Finally, the clinical application and results of this treatment will be evaluated.
LIGAMENT STRUCTURE AND THE THERMAL STABILITYOF COLLAGEN Most skeletal ligaments contain two-thirds water by weight, while nearly three-quarters of their dry mass is made up of collagen.Greater than 90% of this collagen is Type 1, with a few per cent of Type III. The remainder of the ligament is composed of elastin, glycosaminoglycans and cellular elements. Each collagen molecule is composed of three polypeptide chains (a chains), arranged as a triple helix. Each a chain is linked to another by heat-labile hydrogen bonds between adjacent glycine residues reinforced by hydrogen bonding based on the side chains of hydroxyproline Correspondence to: ALW.Tel.: +20 - 8383- 8837; Fax: +20 - 8383- 8835; E-mail: [email protected]
residues. Each collagen molecule (three a chains) is linked to another in a quarter-stagger array to form a linear polymer. This structure is stabilized in turn by covalent cross-links that are heat stable.These are predominantly derived from lysine residues. As tissue ages, these bonds are replaced with irreducible cross-links.1 It has long been suspected that the thermal contraction of collagen led to tissue shrinkage as the regular triple helical structure underwent a phase transition from a crystal lattice to a random coil, analagous to melting.The swelling and shrinkage of collagen bundles with heat is secondary to unwinding of the triple helix (dissociation of H bonds between a chains) with maintenance of the heat stable intermolecular cross-links.2 Denatured collagen is susceptible to degradation by the proteolytic enzyme trypsin, while native collagen molecules in the triple helical con¢guration are resistant to trypsin. Hayashi et al. found that heat (created by laser energy) exposed cleavage sites for trypsin on the collagen molecule by unwinding the triple helical structure. Nontreated collagen was not susceptible to such degradation by trypsin.3 The temperature at which this unwinding occurs is critical. Stringer et al. in 1964 coined the term ‘shrinkage temperature’ after their work on eye collagen.4 Studies using heated saline baths have shown that collagen starts to unwind at approximately 60 ^ 651C.5,6 Various factors a¡ect this shrinkage temperature. It has been shown that the shrinkage temperature of collagen increases with the age of the animal, possibly due to an increase in the number of heat stable irreducible crosslinks.7 The second important variable is the biochemical composition of the ligament. It is known that puri¢ed collagen I ¢lms demonstrate shrinkage at a much lower temperature (42^ 451C). This di¡erence has been attributed to the stabilizing e¡ect of matrix proteoglycans in the intact tissue. Other factors may in£uence the way in which di¡erent ligaments respond to heat. Rodeo et al.8 demonstrated that the composition of joint capsule from patients with shoulder instability patients was di¡erent to that in normal controls. There were di¡erences in stable and reducible bonds as well as
42
collagen ¢bre diameter, cystein content and elastin content.
METHODS OF DELIVERING THERMAL ENERGY There are two main modalities of energy delivery in current clinical use; laser light and radiofrequency electrical current. Laser light is a collimated beam of ¢nite wavelength, usually in the infrared region of the electromagnetic spectrum for clinical use. This wavelength of light is transmitted into the joint via optical ¢bres, and is absorbed strongly by water molecules within well-hydrated capsular tissues. Absorption of infrared photons causes molecular vibrations, or heating, of the water molecules within the tissues. Tissue shrinkage occurs when the thermal energy is su⁄cient to initiate denaturation of the collagen ¢bres. The control of lesion size is dependent on the power of the laser, the duration of application and the area irradiated. The distance from the probe tip from the tissue, and colour of tissue are also important The holmium: yttrium aluminium garnet laser (Ho:YAG ) is the laser of choice in the clinical context described above. Limitations arise because there is no feedback mechanism to determine the temperature within the tissue or the extent of tissue shrinkage. Using ovine glenohumeral capsule, Osmond et al.9 found that with the laser set at10 W and a distance of1.5 mm from the tissue surface, the surface temperature was 62.6710.61C, an optimal temperature for thermal shrinkage. However 3 mm deep to the surface, the temperature was still high enough to cause denaturation of enzymes (47.575.771C). Therefore with laser energy, the depth of e¡ect may be excessive, posing a risk to deeper structures such as the axillary nerve. Radiofrequency energy generates heat by the £ow of an alternating current. Currently, monopolar and bipolar probes are available for arthroscopic use. A monopolar probe uses an alternating current between the application probe (‘active electrode’) and the ground plate (‘return electrode’). This current density produces molecular friction within the tissues between the electrodes and results in tissue heating. Frictional or resistive heating of tissues around the probe tip is the primary source of heat, rather than the probe itself. In contrast, energy produced by a bipolar probe follows the path of least resistance through the tissues in immediate contact with the ‘active electrode’, the irrigating solution and the ‘return electrode’ at the tip. Probes used for shrinkage must not be confused with those used for ablation and coagulation. With electrical energy, the degree of damage depends on the power and waveform; damping and se-
CURRENT ORTHOPAEDICS
paration of wave trains results in tissue destruction or coagulation. In the radiofrequency probe, very high frequencies of 350KHz to1MHZ are used resulting only in a heating e¡ect. When using an RF probe the extent of the lesion depends on the power of RF energy used, treatment duration, electrode size and shape and ¢nally the temperature at the electrode tissue interface.10 ^13 The interface temperature is itself a¡ected by the cooling e¡ect of the irrigating £uid, blood £ow in the tissue and the varying pressure of the probe on the tissue. Aware of the problems with feedback associated with a laser, manufacturers have attempted to incorporate a temperature control feedback loop into their probes. This ensures that the temperature at the probe tip is kept constant by adjusting the power. Thus at higher power settings, the probe will heat to 651C rapidly and any tendency to a further increase in temperature results in a reduction in power delivery.14 It has been proposed that temperature monitoring could be a method to control lesion size. Most studies in ligament tissue have shown that the actual tissue temperature is lower than that indicated in the probe and this has been attributed to the cooling e¡ect of the irrigating £uid.15 There is usually a latency period between the probe temperature tip being measured and the actual rise in tissue temperature. By changing the other variable, the power, and keeping the maximum probe tip temperature constant a strong correlation was observed between power and depth of lesion.14 At 10 W, with the temperature set at 651C, the lesion depth was 0.9571.2 mm at low power but 4.7571.3 mm at 30 W power. Using a bipolar probe, it was demonstrated that as power was increased tissues at a deeper plane were heated in a predictable manner. However, as with the laser, care should be taken since at 4 mm depth, with a power setting of 20 W (typical settings for clinical use) the denaturation of enzymes could still occur (44.972.81C).16 Variables such as probe contact pressure, irrigation temperature and velocity of probe over the surface are hard to control in the clinical setting, but may also a¡ect lesion size.17
EXTENTOF SHRINKAGE WITH THERMALTREATMENT Although it is established that heating collagen leads to denaturation and shrinkage, several questions remain. How do temperature changes a¡ect shrinkage? By how much does ligament tissue shrink, and does the e¡ect persist long-term in vivo? The most important factors are the temperature and duration of application. Vangsness et al.18 reported approximately 70% shrinkage of fresh frozen human Achilles tendon with 701C saline bath. Osmond et al.9
CAPSULAR SHRINKAGE OF THE SHOULDER
demonstrated, with both a laser and radiofrequency probe, that by keeping the tissue temperature between 651C and 751C, approximately 45% shrinkage could be attained. Again with saline baths, Naseef et al.5 demonstrated in bovine knee capsule that after shrinkage began at 601C, 30% shrinkage could be attained after 5 min. However, by increasing the temperature to 651C, a 55% reduction in length could be attained after only 1min. Most investigators have found that above 75^ 801C, there is no further increase in shrinkage irrespective of duration of application.5,6,19 The relationship between shrinkage and temperature therefore appears not to be a linear one but rather a sigmoid curve, with a sharp increase in shrinkage at 65^701C, and a £attening of the curve above 801C.5,17,18 The relationship between shrinkage and duration of application is also sigmoidal, with longer application periods resulting in steeper sigmoidal curves.20 In vivo experiments demonstrate that this initial shrinkage may be reduced but not necessarily maintained. In a rabbit patella tendon, a mean shrinkage of only 6.6% was observed after laser treatment. Subsequently, under physiological loads the patella tendon began to stretch at 4 weeks, so that at 8 weeks it was 5% longer than the original length.15 Some of the discrepancies between in vitro and in vivo e¡ects may be explained by the fact that in the living subject the ligament is held within the constraints of its normal bony attachments, limiting shrinkage.15 Therefore, shrinkage of a ligament structure which is already at a physiologically appropriate length and tension may not serve as a relevant model. In previous studies, we21 developed a model of ligament laxity in the rabbit medial collateral ligament. After monopolar radiofrequency treatment, the lax ligament had shrunk by 12%. At 12 weeks after treatment, the ligament had stretched out under physiological loading so that they were only 6% shorter than pre-treatment lengths.
STRUCTURAL PROPERTIES Although heat appears to shrink ligaments, what is the physical quality of the resultant tissue? The mechanical properties of a ligament may be described in terms of the of load vs deformation relationship. When tested in tension, the gradient of the linear part of the load^ deformation curve is the sti¡ness (which is the inverse of tissue compliance), while the apex of the curve, the point of failure of the ligament, de¢nes both the strength, and the elongation to failure. However, most ligaments are probably loaded to only 10 ^20% of their tensile strength in vivo. The behaviour of tissue under low loads is therefore of interest. Viscoelasticity is a measure of the time-dependent properties of the tissue when subjected to a load. This is usually
43
characterized as stress relaxation (how the load decreases over time when subjected to a constant deformation) or creep (the extent of deformation over time when subjected to a constant load). Immediately after treatment most investigators have found that sti¡ness is reduced (the tissue has become more compliant).3,22^25This reduction appears to be similar after laser- or radiofrequency-induced shrinkage. Surprisingly, Selecky et al.26 found no changes in tissue sti¡ness immediately after treatment in their experiment with cadaveric shoulders. However, the mean age of the specimens was 82 years, and the reduction in shrinkage and sti¡ness with age, due to morphological change in aged ligament may have in£uenced this result. Most studies have shown that sti¡ness is reduced even further during the next few weeks after thermal treatment.23,15,27,25 The timescale for recovery of normal sti¡ness has not been well de¢ned. Schaefer et al.15 found that laser-treated rabbit patellar tendons were 19% less sti¡ than controls after 9 weeks.Others have found sti¡ness to be the same as control values at 2,22 623 and 12 weeks.27 In comparison, Frank et al.28 found that surgically transected ligaments (which heal by a bridging scar) were still less sti¡ than controls at 40 weeks. Sti¡ness also appears to be related to the degree of shrinkage. Wall et al.20 demonstrated that progressive shrinkage of tendons heated in a saline bath resulted in them becoming more extendable (less sti¡).They postulated that the maximal shrinkage before signi¢cant material property changes occurred was between 15% and 20%. Ultimate failure stress or strength of the ligament immediately after treatment has been tested in a few cases. It is important to di¡erentiate between the material and structural properties of the ligament. The structural properties incorporate the size and shape of the material being tested. The material properties re£ect the intrinsic properties of the tissue itself. Many, measuring the structural properties of the ligament, report little to no detrimental e¡ect on the strength of the ligament.3,22,23,26,29 Wallace et al.21 however, measured the material properties of the scar and found that 25% of their RF-treated ligaments failed at loads corresponding to 5% of ultimate tensile strength of normal MCL. Schultz et al.25 found that the material properties of laser-treated lapine retinacular specimens were approximately 30% less strong than controls immediately after treatment. These ¢gures suggest that the thickened, shrunken ligament as a whole, has similar high-load characteristis to untreated ligament. The intrinsic high-load properties of the thermal scar, however, appear inferior. In vivo studies suggest that there is a loss of strength (structural and material) that persists for some time. In two experiments using a rabbit knee model, Sandusky et al.27,25 found that ultimate stress was reduced almost
44
50% at 6 weeks, returning towards control values at 12 weeks. In another rabbit model,21 57% of specimens failed at less than 5% of the strength of intact ligament at 3 weeks after treatment. Hecht et al.23 demonstrated signi¢cantly weaker tissues at 2 weeks relative to 12 weeks. The e¡ects on viscoelastic properties are important, since the time-dependent behaviour under low ‘physiological’ loads and deformations is relevant to the maintenance of joint stability. Several authors using laser shrinkage and testing stress relaxation have found no adverse e¡ects.3,22,24,26 Using an RF probe, Hecht et al.23 found that stress relaxation was increased initially, returning to normal between 6 and 12 weeks after treatment (as did strength and sti¡ness). Sandusky et al.27 found similar results with normal properties returning by 6 weeks.Wallace et al.21 found that thermal treatment conferred an increased susceptibility to creep, changes which were still far from normal at 12 weeks. Using a similar model, it had been demonstrated previously30 that healing ligament scars crept more than intact non-injured ligaments. In order to put some of these mechanical ¢ndings into a more relevant clinical setting, passive translation has been measured in human cadaver shoulder joints after thermal capsulorrhaphy. Standardized loads were applied, and the translation measured before and after treatment, giving an indication of reduction in joint laxity. Using either a laser or radiofrequency probe in a cadaveric shoulder, there was a statistically signi¢cant reduction in anterior joint translation when tested under ‘physiological’ loads.31,32 In summary, the biomechanical data available indicate that although signi¢cant alterations in length of capsular and ligamentous tissues may be achieved at the time of thermal treatment in vitro and to a lesser extent in vivo, the shrinkage may not be maintained once physical activity resumes. During the early stages of healing and remodelling, there is a reduction in sti¡ness and strength as well as an increase in potential to creep.This may explain the apparent ‘stretching-out’ under physiological loads seen in some studies. It should also be remembered that these biomechanical investigations have been based on normal tissues, which are likely to behave quite di¡erently from the tissues found in pathologically unstable joints or joints subjected to previous surgery.
THE EFFECTS OF THERMAL TREATMENTON THE MORPHOLOGY OF LIGAMENT Immediately following application of heat, shrinkage along the long axis of the collagen ¢bres causes an increase in transverse thickness.9,6,15 and a visible change in surface colour, from the tissues normal shiny white to
CURRENT ORTHOPAEDICS opaque, occurs.22,9,23 The increase in thickness correlates with temperature and the degree of shrinkage,9 and can be explained by histological observations. Under transmission electron micrography (TEM), collagen ¢brils are seen to be enlarged and to have blurred edges with loss of the normal longitudinal cross striations.3,22,6,23,33 These changes represent the denaturation of collagen and contribute to the swelling.2 This is also demonstrated on light microscopy as hyalinization of the collagen. Further examination reveals necrotic ¢broblasts, synovial cells and thrombosed and necrotic vessels.3,22,6,5,23,33 In keeping with the mechanical data and our knowledge of the thermal stability of collagen, the hyalinization and denaturation of collagen do not start until the shrinkage temperature is attained (60 ^ 651C).5,6 With increased energy, more collagen ¢brils in the capsule or ligament undergo conformational change.20 If the heating is continued it may be conducted to deeper layers causing necrosis of muscles and nerves.34 As stated previously, the severity of tissue damage is commensurate with the amount of energy transferred even if the temperature of the probe is kept constant.14 In one of the few studies examining the in vivo response of human capsular tissue to laser, tissues at this stage showed exactly the same histological response as in animal models.35 In surgically transected ligaments a marked in£ammatory response is seen during the ¢rst week.36 However, from the limited data available, it appears that the in£ammation after thermal treatment is not as great as after transection. In an ovine patello-femoral joint capsule treated with laser there was only a mild cellular response with synovial resurfacing at 3^7 days, and in£ammatory cells were not predominant at any time after laser treatment. Within the hyalinized collagen there were no viable cells.22,23,33 Only when power was su⁄cient to cause deep muscle damage (3^5 mm depth of lesion) was a £orid in£ammatory response observed.14 The intermediate phase is characterized by cellular proliferation. From the surrounding untreated zones there is capillary sprouting, further proliferation of synovial cells and ¢broblastic in¢ltration. Hyalinized regions are gradually resorbed and by day 60 are replaced with new, small-diameter collagen ¢brils. These small ¢brils surround the ¢broblasts and replace the normal bimodal distribution of predominantly large and small ¢brils found in normal tissue.22,23,15,33 This pattern suggests that the hyalinized collagen acts as a framework for migration and matrix synthesis.15 Such a homogenous population of small ¢brils is characteristic of scar tissue.37 Controversy exists about the extent of scar formation and ligament regeneration in the remodelling phase. In an ovine model at 6 months following laser shrinkage the ligament appeared ‘normal’ macroscopically and on light microscopy. However, the unimodal distribution of small diameter ‘scar’-type collagen persisted on TEM.22
CAPSULAR SHRINKAGE OF THE SHOULDER
In a sample of laser treated human glenohumeral ligament, at 12 months the normal crimp pattern (the regular wavy undulation of cells and matrix seen in thin histological sections) had returned.35 Levy et al.38 however, examined tissue specimens from radiofrequency-treated patients requiring revision at 5^10 months.They found a population of large diameter ¢brils with normal cross striations. This may represent either insu⁄cient initial treatment or an increase in size of the ¢brils due to load. Several papers have suggested that collagen ¢brils can increase in diameter to counter increasing loads.8,39,40 Interestingly, Lu et al.41 found that the treatment pattern can a¡ect rate and pattern of tissue repair. Monopolar RF energy was applied to sheep knee capsule in a commonly practiced ‘paint brush’ pattern. In a separate group, the energy was applied as a grid pattern where viable tissue was preserved between the treated zones. Tissue shrinkage was similar in both groups but in the grid pattern group, the rate of repair was signi¢cantly faster. This was attributed to greater cellular in¢ltration from the surrounding untreated tissue, and was correlated with a more rapid recovery of mechanical properties. In summary, it appears that as the hyalinized collagen is removed and replaced with new collagen the mechanical properties improve, though may not fully recover.23,15,42 Whether the resultant tissue behaves like ‘normal’ scar or ligament is unclear.
CLINICAL STUDIES The evolution of the arthroscope from its early days as a diagnostic tool, to a therapeutic surgical instrument has occurred rapidly. The advantage of minimally invasive surgery over conventional open procedures has led to the use of arthroscopic thermal shrinkage in a range of conditions ranging from resolving capsular redundancy in unstable shoulders to the tightening of lax cruciate ligament grafts in the knee.This enthusiasm, however, has been tempered by a lack of agreement on the way stability is restored and somewhat variable clinical results. Arthroscopic repair of the detached labrum appears to be a viable option in those patients diagnosed with symptomatic unidirectional instability. Unfortunately despite good short-term results,43 long-term follow-up revealed a failure rate of around 20 ^30%44 ^ 46 with some as high as 50%.47 This has been attributed to a failure to address the plastic deformation of the anterior capsule.45,48 Reducing excess laxity in the capsule has proven to be di⁄cult, but thermal capsular shrinkage may be a useful method to achieve this. Unfortunately there are only few published series49^51 that have observed outcome, mainly in the short term, after surgery and therefore few conclusions can be drawn with certainty.
45 Savoie and Field49 used a radiofrequency device in 30 patients with signs of multidirectional instability. Postoperatively an initial period of immobilization for 1^3 weeks was followed by an active rehabilitation protocol protocol until week 8. There was a gradual introduction of resistance strengthening until, at around 4 months, normal activity was allowed. No passive stretching of the capsule was allowed. At a mean follow-up of 26 months, 94% of patients had a satisfactory result on all outcome scales, which included return to sporting activity. Fanton50 similarly treated 54 patients, with a mean follow-up of 2 years. He documented a 90% success rate. Tyler et al.51 reviewed 75 patients 3 years after surgery. Almost all had a strict period of immobilization followed by muscle strengthening exercises that were designed to protect the anterior capsule. There were ¢ve failures (6%), three of which were in patients who had not received this capsular protective physiotherapy. The authors did not describe the return to sporting activity. Conversely, Miniaci52 conducted a 2-year prospective review of 19 multidirectional instability patients treated with monopolar radiofrequency. Patients were immobilised for 3 weeks after treatment. Nine patients had recurrence of their instability occurring on average 9 months after treatment. Interestingly, all those with predominantly posterior instability failed. Levy et al.53 had failure rates of 24% and 36% for RF and laser capsulorrhaphy, respectively. However, this cohort of MDI patients included some who had had previous failed open procedures and all had relatively unrestrained postoperative mobilization. Other studies with much shorter followup periods have emphasized the importance of this controlled return to activity.54,55 Experience of thermal shrinkage in other joints is even more limited.Ola¡ et al.56 applied radiofrequency shrinkage to the stabilization of chronic anterolateral ankle instability. In their retrospective review of10 patients, with a relatively short mean follow-up of 9.675.44 months, they found that all ankles were stable. This was supported by a statistically signi¢cant reduction in talar translation (as seen in the anterior draw test) and improvement in stability score (subjective, retrospective review). Postoperative management focused on the immobilization and protection of the treated ligament for 6 weeks.Thabit57 treated lax anterior cruciate ligaments (ACL), and ACL grafts with monopolar radiofrequency energy. Short-term results (18 months) were excellent in 23 out of 25 patients, although one sustained spontaneous rupture 2 months following surgery (attributed to a lack of patient compliance), and another had increased laxity. Long-term results are not known. Bailie et al.58 recount 17 patients who had radiofrequency treatment to lax ACL grafts (7) and ligaments (10). Ten ACL cases failed after an average of 4 months. Of the seven successful patients (at short time follow-up), six were native ligaments.
46
Few complications of capsular shrinkage have been reported to date. Of concern, however, are the recent reports of autolysis of treated tissue. Perry and Higgins59 recount a case of radiofrequency treatment of a slightly lax cruciate ligament graft following cruciate reconstruction. At arthroscopy, 5 months after thermal shrinkage, they found an empty notch with friable stumps. Sekiya et al.60 describe a similar case where a lax cruciate graft had been treated as above. Three weeks later after a trivial injury they found ‘no remnant of the previous hamstring autograft.’ It is possible that using too much power, too long a contact period, and failure to protect the treated tissue, may have caused these ¢ndings, although Sekiya et al. proposed a possible autoimmune reaction. Axillary neuropraxia is clearly a risk in the shoulder, in view of the nerves proximity to the inferior recess of the joint. Fanton50 described one case of axillary neuropraxia and one case of adhesive capsulitis after thermal shrinkage of 54 shoulders. Miniaci52 described a transient neuropraxia in 21% of his patients. Greis et al.61 recommended reducing the power and moving the probe continually whilst in the axillary recess. The exact mechanism of restoring joint stability by thermal shrinkage remains unclear. It seems unlikely to be a purely mechanical e¡ect, since as isolated structures shoulder ligaments are not strong enough to prevent dislocation.Ligaments are also sites of proprioceptive nerve endings.62,63 Savoie has postulated that in the unstable patient the lax capsule provides inappropriate proprioception for the rotator cu¡. By tightening this redundant capsule, we allow the cu¡ to regain a more normal ¢ring pattern, thereby restoring normal function.38,49,64 Exactly how this may occur is unclear, since the temperature required to shrink collagen is also likely to destroy proprioceptive nerve endings.
CONCLUSION From the information available thermal shrinkage of lax ligamentous tissue appears to be an e¡ective method of reducing the volume of redundant capsule. The reduction of intracapsular volume is probably limited by the linear extent of shrinkage achieved (15^20%). A grid-type pattern of application seems to confer a more rapid histological and mechanical recovery. During the early postoperative period the treated tissue is less sti¡, not as strong and more prone to ‘stretch out’, under physiological loads. The treated tissue appears to be replaced by a form of scar tissue, the mechanical properties of which approach those of the non-treated capsule at around 3 months after surgery.The exact mechanism of restoring joint stability is still unknown, but may partly be due to proprioceptive changes in the cu¡ and capsule.
CURRENT ORTHOPAEDICS
The clinical data so far are limited in number and in the extent of follow-up. However, early results of glenohumeral ligament shrinkage are promising and in some cases comparable to conventional surgery. In view of the basic scienti¢c evidence a conservative rehabilitation protocol seems prudent following either laser or radiofrequency shrinkage. The application of thermal shrinkage outside the shoulder is still controversial, particularly in view of the reported cases of autolysis of wholly intraarticular ligaments or grafts. Further work is required to overcome several technical di⁄culties, such as controlling lesion size, depth and the e¡ects of various treatment patterns.
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