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ORTHOPAEDIC KNOWLEDGE UPDATE 11 PDF

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PDF | On Jul 1, , S. Lambert and others published AAOS AAOS Orthopaedic Knowledge Update Shoulder and Elbow: 3: Edited by L. Galatz. Pp. . instability is dealt with in detail in chapters 2, 4 and 11, but there is. American Academy of Orthopaedic Surgeons. Orthopaedic Knowledge Update SECTION EDITORS: THEODORE MICLAU, MD. SAAM MORSHED, MD. OKU 11 condenses three years of critical issues and developments shaping orthopaedic medicine: the advances in clinical thinking, controversial topics and .


Orthopaedic Knowledge Update 11 Pdf

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Orthopaedic Knowledge Update 11 (Orthopedic Knowledge Update): Medicine & Health Science Books @ resourceone.info AAOS OKU - Free ebook download as PDF File .pdf), Text File .txt) or read book online for Orthopaedic Knowledge Update Arthroscopy ; Keep pace with the rapidly changing body of orthopaedic knowledge and clinical practice with OKU's objective, balanced coverage in easily.

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Grauer M. String "". Buy from another retailer. Promocode will not apply for this product. OKU 12 brings you a comprehensive synthesis of the latest clinical thinking and best practices across all orthopaedic specialty areas. Backed by clinical research, informed by practical experience and rigorously edited by specialty thought leaders, OKU12 is the most up-to-date resource available anywhere for delivering high-quality orthopaedic patient care today.

An essential resource at every level of orthopaedic specialization: Table of contents. Section 1 - Principles of Orthopaedics Editor: Joseph M. Lane, MD Chapter 1. Orthopaedic Research Alexander S. Leopold, MD Chapter 3. Waddell, MD; William J. Anderson, MD; S. Patient-Centered Care: Polytrauma Care Raymond Y.

Coagulation and Blood Management Todd P. Pierce, MD; Vincent K. Scillia, MD; Michael A. Mont, MD Chapter Fracture Repair: Update on Mechanism and Antagonists J.

Tracy Watson, MD Chapter Musculoskeletal Biomechanics Marjolein C. Wright, PhD; Julia T. Chen, MS Chapter Musculoskeletal Imaging Principles John A. Mintz, MD; O. Matthew R. DiCaprio, MD Chapter Bone and Calcium Metabolism Brian J. Lane, MD Chapter Naseer, BS Chapter Rodeo, MD Chapter Nerve Disorders Hamish A. Light, MD Chapter Musculoskeletal Oncology: Miller, MD; Lukas M. Nystrom, MD Chapter Upper Extremity Editor: Humerus and Shoulder: Warner, MD Chapter Shoulder Instability Matthew T.

Shoulder and Elbow Tendinopathy Kathleen E. The menisci play an important role in knee stability and proprioception. Individuals who underwent complete meniscectomy before anterior cruciate ligament ACL reconstruction reported subjective complaints and activity limitations more commonly than those whose menisci were intact at the time of ACL reconstruction. Significant correlations were found with pain, swelling, partial giving way, full giving way, and reduced activity status after surgery.

Meniscal Replacement Meniscal regeneration or replacement has been developed in an attempt to interrupt or retard the progressive joint deterioration in patients in whom the meniscus has been removed or completely destroyed. Approaches to meniscal replacement currently include autograft, bovine collagen implants, and allograft. Autograft material used has included fascia lata, fat pad, and ligaments that have been rolled into tubes and sewn into the knee joint.

All of these tissues have failed to restore the normal properties of the meniscus. Meniscal regeneration using an implanted absorbable copolymeric collagen-based meniscal scaffold is currently being investigated in clinical trials. Scaffolds are created by reconstituting enzymatically purified collagen from bovine Achilles tendons.

Human studies of the collagen meniscal implant have shown that at 2 years after implantation, the defects filled generally represented segmental defects in the middle and posterior aspects of the meniscus cartilage. These data seem to demonstrate the successful replacement of at least a portion of each meniscus cartilage. Histologically, progressive resorption of the implant material and replacement by collagen fibers in healthy meniscal fibrochondrocytes appears to occur. Clinically, the patients improved their activity levels and had near-complete relief of pain.

How well these regenerated menisci will protect the joint surfaces will be determined with further study. The definitive success of collagen meniscus implants awaits the results of prospective clinical trials that are now being done. Meniscal Repair The importance of blood supply for meniscal healing has been demonstrated.

An injury in the vascular zone of the meniscus outer third results in the formation of a fibrin clot at the site of injury.

This fibrin clot acts as a scaffold for vessel ingrowth from the perimeniscal capillary plexus and vascular synovial fringe. The lesion may heal by fibrovascular scar tissue in 10 to 12 weeks. The inability of lesions in the avascular portion of the meniscus inner two thirds to heal has led to investigation of methods to provide a blood supply to the injured region.

These methods include creation of vascular access channels, pedicle grafts of synovium placed over the injured meniscus, and abrasion of the synovial fringe to produce a vascular pannus. Study results support the use of an exogenous fibrin clot in meniscal tears in the avascular zone to enhance healing. The clot provides chemotactic and mitogenic factors, such as platelet-derived growth factor and fibronectin, which stimulate the cells involved in wound repair.

The clot also provides a scaffold for the support of the reparative response. In the intra-articular environment, a naturally-occurring fibrin clot from surgical bleeding may be rendered ineffective by synovial fluid dilution. An exogenous clot theoretically concentrates the chemotactic and mitogenic factors to overcome this dilution.

Meniscal Allografts The use of meniscal allograft tissue continues to receive a great deal of attention in orthopaedics. Allograft menisci, if sized correctly, remain the only way available to replace an entire meniscus. Unfortunately, most meniscal reconstructions have been performed on patients who have either complex problems of joint deterioration with meniscal deficiency, ligamentous instability, or combinations requiring both ligamentous, osteochondral, and meniscal reconstruction.

Determining the outcome of the isolated meniscal reconstruction in these combined cases is difficult. This lack of uniformity between patient selection, surgical technique, and follow-up criteria makes the clinical results between different groups difficult to interpret. Basic science animal studies as well as clinical studies have shown promising results using fresh frozen allograft menisci for transplantation.

However, complete cellular repopulation of the allograft with reconstitution of the normal 3-D collagen ultrastructural architecture has yet to be scientifically proven.

Although it is clear that the meniscal allograft heals. Orthopaedic Knowledge Update Soft-Tissue Physiology and Repair to the peripheral tissue, biopsy specimens have revealed persistent changes within the cellular makeup, cellular content, collagen architecture, and proteoglycan content, raising questions about the long-term viability and the predisposition for further injury.

Growth factors have been shown to stimulate fibroblast cell division in vitro for both the ACL and medial collateral ligament MCL. The response varies by the particular growth factor and differs between the two ligaments. Matrix synthesis also is affected, in particular by transforming growth factor-b TGF-b , as well as epidermal growth factor EGF at the higher doses studied. Furthermore, when the responses of cultured explants from ligament and tendon were compared, the ACL was more sensitive to TGF-b, whereas plateletderived growth factor resulted in a proliferative response in the patellar tendon that was not observed in the ACL.

In addition, combinations of growth factors may have a synergistic effect at the cellular level. An important component to the strength characteristics of the collagen fibers is the formation of cross-links. The ground substance includes proteoglycans, which have the capacity to contain water molecules and to affect the viscoelastic properties of soft tissues. The protein elastin assists with the tissues ability to lengthen under an applied load by storing energy and returning the tissue to its original length when the load is removed.

Other noncollagenous proteins are found in very low concentrations. Structural and mechanical material properties have been demonstrated for a variety of ligaments. Differences in these properties have been reported among various ligaments, but also between different regions of the same ligament, including the inferior glenohumeral ligament and posterior cruciate ligament. The structural properties, expressed by the load-elongation curve Fig. The mechanical properties, expressed by the stress-strain curve Fig.

Stress is defined as force per unit area, and strain describes the change in length relative to the original length. When a ligament is placed under tension, it deforms in a nonlinear fashion. In the initial stages, or toe region, the coiled nature of the collagen and the crimping are recruited to be more aligned along the axis of tension.

Once this is complete, with continued tension, the collagen fibers become taut and then stretch; this is defined as the linear region. The slope of the linear region for the load-elongation curve 9. Ligament Structure and Function Optimal joint function depends on the complex interaction around the joint of ligaments as static restraints and muscletendon units as dynamic restraints, as well as other factors, including articular geometry.

Ligaments are dense connective tissues that link bone to bone. The gross structure varies with the location ie, intra-articular, capsular, and extra-articular and function. Geometric variations within different regions of a ligament, such as the anterior and posterior cruciate and inferior glenohumeral ligaments, are frequently observed.

Under microscopic examination, the collagen fibers are relatively parallel and aligned along the axis of tension, but they have a more interwoven arrangement than that found in tendon.

Characteristic sinusoidal patterns within the bundles, or crimp Fig. Two distinct regions within a ligament may also demonstrate different patterns of collagen alignment or crimping, as well as variations in fiber diameters. Fibroblasts, which are relatively low in number, are responsible for producing and maintaining the extracellular com-. Figure 3 Uniform alignment and crimping of collagen fiber bundles in the anterior axillary pouch of the inferior glenohumeral ligament.

Hematoxylin-eosin, polarized, Inferior glenohumeral ligament: Geometric and strain-rate dependent properties. J Shoulder Elbow Surg ;5: Orthopaedic Knowledge Update 10 General Knowledge of bone-ligament-bone complexes change under a variety of circumstances.

Age has been shown to be the predominant factor in the rabbit MCL. The skeletally-immature specimens failed at the tibial insertion site, whereas in the mature specimens, failure occurred in the midsubstance. Ligament substance appears to mature earlier than the insertion sites. Strain rate, or rate of elongation, has been shown to affect the failure pattern of both the ACL and the inferior glenohumeral ligament.

At higher strain rates, the strength and tensile modulus increased, and failures occurred more in the ligament substance than at the insertion sites, as seen with slower strain rates. The axis of loading has been shown to affect failure patterns. When the ACL was loaded along the axis of the tibia and not the ligament, the femur-ACL-tibia complex demonstrated decreasing load at failure with increasing flexion angle, and failure was more likely to occur in the ligament substance.

Recent investigations with clinical implications have drawn attention to sex differences in the rate of ACL injuries among women and men. It has been theorized that this difference may be a result of the estrogen and progesterone receptors in cells of the ACL.

In an animal model, the ACL failure loads were significantly less in an estrogen-treated group. As ligaments age, the structural and material properties change in response to loading conditions. Reduced properties with aging also have been reported for the anterior portion of the inferior glenohumeral ligament from humans. However, only slight decreases in the structural properties of the MCL bone complexes were noted when skeletally mature specimens were compared with specimens from rabbits at the onset of senescence.

Biochemical changes that occur include a decrease in water and collagen content. In addition, there is a change from a higher concentration of the immature, more labile, cross-links to a higher concentration of the mature, more stable, forms. Fibroblasts are less metabolically active with aging and assume a more elongated shape.

The effect of growth factors on fibroblast proliferation seems to be diminished with age, and fibroblasts in the ACL appear more sensitive than fibroblasts in the MCL. It would appear that whereas maturation influences the insertion sites of ligaments as demonstrated in the failure patterns, aging and senescence have a detrimental effect on the ligament substance.

B Figure 4 A, Load-elongation curve demonstrating the structural properties of a bone-ligament-bone specimen and B, stress-strain curve demonstrating the mechanical properties of the ligament substance. Biomechanics of Diarthrodial Joints. Overload occurs at the yield point, where tissue failure is observed. The ultimate load and elongation are defined at this point for the structural properties. The ultimate tensile stress and strain are defined at this point for the mechanical properties.

These sinusoidal curves demonstrate the nonlinear nature of soft connective tissues. In addition, ligament and tendon biomechanical characteristics demonstrate time-dependent viscoelastic behavior. The properties of the insertion sites differ from those of the ligament midsubstance, with greater strain found in these areas when tested under uniaxial tension.

The failure patterns. Response to Exercise and Loading Under conditions in which loading is enhanced for a long period of time, the properties of ligaments demonstrate a. Overall mass increases, and stiffness and load at failure increase. In addition to these changes in structural properties, the material properties are affected with an increase in ultimate stress and strain at failure.

Similar changes have been shown in the experimental setting when the MCL in rabbits was placed under increased tension for a sustained period. Various factors that influence ligament healing include degree of injury, location of the ligament, and modes of treatment. A more severe injury will result in greater damage to the tissue and a larger gap, prolonging and possibly impairing healing. In the case of the rabbit MCL, injuries near the insertions heal more slowly.

Reconstruction of the ACL may counteract this effect. Controlled passive motion leads to a more rapid repair and enhances the collagen alignment and the biomechanical properties of the healing MCL. Immobilization after injury has the opposite effect. The MCL has an intrinsic healing response not observed in the ACL, and this difference may be the result of a number of biologic factors. Intra-articular ligaments, such as the cruciates, have a limited blood supply and are in an environment that does not promote the initial phase of healing, unlike the extra-articular and possibly intracapsular ligaments.

Growth factors have been detected at the site of ligament injury and have been shown to enhance tissue healing.

Recent investigations have studied their effects in the early healing phase. The timing when growth factors are administered and their doses also have been shown to influence healing.

In addition, a plateau effect was noted with the increasing doses used. Others have reported that much higher doses of growth factors studied in vitro may, in fact, be detrimental to the material properties. As the effect of growth factors and other cytokines is further studied, their role in normal development and healing for both intra- and extra-articular ligaments, as well as after ligament reconstruction, will be further defined with possible clinical applications delineated.

Response to Immobilization and Disuse Immobilization and disuse lead to a much more dramatic effect on ligaments and compromise the structural and material properties. In addition, immobilization in two different knee flexion angles did not cause a difference. Thus, changes in both the ligament substance and insertion sites are evident after immobilization.

Subperiosteal bone resorption at the insertion sites from increased osteoclastic activity has been observed to affect failure patterns. With even longer periods of immobilization, degradation of collagen increases as collagen synthesis decreases, resulting in less total collagen. A decrease in water and proteoglycan content contributes to an overall decrease in ligament mass. A smaller cross-sectional area was noted in the ACL, and ultrastructural changes in fibroblasts have been observed after immobilization.

The recovery period after immobilization is more rapid in the ligament substance than at the insertion sites. It may take up to 1 year for the insertion sites to return to a level approaching that of controls.

However, after 9 weeks of immobilization and 9 weeks of remobilization, the material properties were similar to controls, confirming the more rapid recovery of the ligament substance when motion and loading are permitted.

After a rupture in the ligament substance, healing occurs in 3 histologic phases: After healing is complete, collagen fibrils have a greater diameter and are more densely packed, with an increase in total collagen content. The collagen alignment remains at a less organized level compared with controls. An overall increase in cross-sectional area persists and contributes to the return of the structural properties, which approach normal values. However, after remodeling, the material properties that are not affected by tissue geometry.

Grafts for Reconstruction Ligament reconstruction using a graft substitute, particularly of the anterior and posterior cruciate ligaments, is performed to restore joint stability. Choices for autografts include patellar tendon, semitendinosus and gracilis tendons, quadriceps tendon, fascia lata, and iliotibial band. The central third of the patellar tendon is a commonly used graft, and early stud-. Orthopaedic Knowledge Update 12 General Knowledge ies using a mm wide graft demonstrated a higher load at failure than the ACL itself, while other grafts had lower failure loads.

More recent studies have shown that the patellar tendon had greater stiffness, and, therefore, greater structural properties that are affected by size, compared with hamstring tendons. However, the hamstring tendons had higher tensile modulus, or higher material properties, compared with patellar tendon. These findings suggest that a larger size for the hamstring grafts, such as a quadrupled graft that would improve its structural properties, offers a good alternative autograft for ACL reconstruction when compared with the patellar tendon autograft.

However, a hamstring graft with 4 bundles does not necessarily offer a construct that is 4 times as strong as a single tendon. Furthermore, after implantation, no graft substitute has ever demonstrated biomechanical properties near to that of the ACL when studied as long as 3 years after reconstruction. In addition, neither the patellar tendon graft nor the hamstring graft used for reconstruction fully restores the kinematics of the intact knee.

Graft incorporation involves an initial phase of ischemic necrosis, followed by revascularization. Remodeling and maturation include a transition of cellularity, distribution of collagen types, fiber size and alignment, and biochemical characteristics that are more ligament-like. This process appears to be affected by the initial tension placed on the graft. In addition, different levels of growth factors have been detected in early remodeling, suggesting a role in this process.

The insertion sites and incorporation have been studied for patellar tendon and hamstring grafts, both with and without detachment of the tibial insertion. Initial failure after replacement surgery is at the fixation sites.

As these attachments heal, either bone-to-bone or tendon-to-bone failure is more likely to occur within the graft substance. Tibial fixation closer to the anatomic origin of the ACL, investigated using robotic testing, improved initial stability. Allograft tissue, particularly in the settings of multiple ligament injuries and revision ligament surgery of the knee, offers a reliable alternative.

Final allograft incorporation in ACL surgery is similar to that seen in autografts, but occurs at a slower rate, with inferior properties found at 6 months compared with autografts in the animal model. Studies designed to assess the temperature level necessary to cause shortening of collagen using heated fluid baths at controlled levels demonstrated more dramatic effects at 65C and above.

A threshold to shrinkage of 60C after 3 to 5 minutes duration in the fluid bath was noted in one study. As temperatures increased, the shrinkage was greater and occurred more rapidly, along the dominant alignment of the collagen fibers.

Furthermore, with increasing temperatures, greater alteration in the collagen structure was noted histologically. At temperatures above 80C, collagen tissue was grossly observed to fall apart in one study, whereas others reported an amorphous histologic appearance of the collagen, with loss of fibrillar structure, at 80C. In vitro animal studies with increasing laser energy using the holmium: Ultimate failure loads were decreased, with tissue failure occurring in the region of the lased tissue.

A clear change in the collagen fiber structure has been observed histologically, with denaturation of the tissue and increasing size of the area affected as increasing energy was used. Although no difference was found for ultimate stress or elastic modulus between lased and nonlased specimens, the ultimate strain was higher and the energy absorbed during cyclic loading was lower in the laser-treated specimens.

Tissue failure was not observed through the laser-treated region. In vivo studies in rabbit patellar tendon treated with the Ho: YAG laser demonstrated tissue shortening initially, with localized, although severe, changes in the collagen found on histology. However, after 8 weeks of unrestricted activity, the tissue was lengthened Fig. In addition, a more generalized fibroblastic response throughout the entire tissue was noted, with small diameter collagen fibers replacing the normal distribution of both large and small fibers.

Others have noted thickened synovium, with inflammation, tissue necrosis, and decreased cellularity in the glenohumeral capsular tissue in dogs at 6 weeks after a laser procedure.

Because of the amount of tissue alteration reported as well as observations of tissue lengthening and altered biomechanical properties in animal and human studies, these factors must be carefully considered and further studied before general application of procedures using thermal energy to shrink capsular tissue is. Response of Collagenous Tissue to Thermal Energy Whereas laser and other electrosurgical devices usually have been used to incise and ablate soft tissues, these instruments have more recently been used to deliver thermal energy to selectively shrink capsular tissue during arthroscopic procedures, in particular in the glenohumeral joint.

Experimental and clinical evidence has demonstrated that collagenous tis-. Figure 6 Schematic representation of the microarchitecture of a tendon. Adapted with permission from Kastelic J, Baer E: The Mechanical Properties of Biologic Materials.

Cambridge, Cambridge University Press, , pp Tissue shrinkage using a holmium: A postoperative assessment of tissue length, stiffness, and structure. Am J Sports Med ; To date, the difference between the use of laser and other electrosurgical devices to effectively shrink collagenous tissue has not been defined. Tendon Structure and Function Tendons are dense, primarily collagenous tissues that link muscle to bone.

As a highly specialized tissue with paralleloriented bundles of collagen, the tendons primary function is to transmit the load generated by muscle to bone. Synovial sheaths surround some tendons, such as flexor tendons of the hand, to facilitate excursion and gliding. Histology reveals crimping and low cellular density in addition to the highly uniform, parallel alignment of the fibers Fig. Proteoglycans have a very small concentration in tendons, but serve to support the structure and function of collagenous tissues.

Regions of tendons that are subjected to compressive loads are more fibrocartilaginous and have a higher. A lower glycosaminoglycan content is associated with smaller proteoglycans, including decorin, in tendons undergoing primarily tensile loads. Cyclic compressive loading of tendon has been shown to stimulate production of aggrecan and biglycan, and this appears to be further enhanced by TGF-b. Removal of compression in a zone of fibrocartilaginous tendon in an in vivo animal model results in a decrease in glycosaminoglycan content, cellular density, cross-sectional area, and compressive stiffness.

The organization and composition of tendon make it ideally suited to resist high tensile forces. Tendons deform less than ligaments under an applied load and are able to transmit the load from muscle to bone. It has been demonstrated that under tension the fibrocartilaginous zone of tendon, which experiences both tensile and compressive forces, has decreased material properties compared with regions of tendon primarily exposed to tensile forces.

However, the greater cross-sectional area observed in the fibrocartilaginous zone may represent a response by the tissue to enhance its structural properties under tension. Structural and degenerative changes as a result of aging have been reported.

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The overall diameter of the Achilles tendon decreases. The mean collagen fibril diameter decreases with increasing age, as do total cell count and the amount of crimp. A decrease in the endoplasmic reticulum within the fibroblast suggests diminished cellular metabolic activity. The biochemical composition changes with an increase in collagen content and amount of cross-links and a decrease in glycosaminoglycans.

Biomechanically, an increase in stress at failure and in stiffness during maturation and then a decrease with senescence has been. Orthopaedic Knowledge Update 14 General Knowledge noted.

The effects of decreased activity, or relative disuse, play a role in the changes seen with aging tendon. Response to Exercise and Loading Controlled increases in training appear to have differential effects on tendons. The biomechanical properties of swine flexor tendons did not change after exercise, although a beneficial effect was noted at the bony insertion sites. However, swine extensor tendons subjected to a long-term exercise regimen responded by developing increased cross-sectional area and tensile strength.

This suggests that extensor tendons have the capacity to respond to a training regimen, whereas flexor tendons function on a regular basis at their peak. Investigators have reported an increase in the number and density of smaller diameter fibrils in response to exercise.

Although further investigations are warranted, it may be that the muscle and the tendon-bone insertion sites have a greater capability to adapt to an environment of sustained increases in loading than the tendon itself. Figure 7 Drawing of an immobilized tendon illustrating extrinsic and intrinsic repair. Courtesy of Richard H. Response to Immobilization and Disuse Restriction of motion to protect injured tissue or aid in the repair process can affect tendons.

Without stress as a stimulus, both the midsubstance of tendons and the insertion sites appear to be affected, demonstrating diminished biomechanical properties. After immobilization, stiffness decreases within the tendon. Presumably, other biomechanical as well as biochemical and histologic changes occur, but these have yet to be demonstrated specifically for tendon. Whether or not such changes are reversible also is unknown. Response to Injury and Mechanisms of Repair Injury or damage to tendons can result from 1 of 3 mechanisms: Transections or partial lacerations are associated with trauma and are most common in the flexor tendons of the hand.

Bone avulsions can occur after overwhelming tensile loads, as seen in the flexor digitorum profundus insertion into the base of the distal phalanx of the ring finger. Degenerative changes within tendon can arise from repetitive tensile loading during the life of an individual; however, impingement of tendon by a rigid surface, such as with the rotator cuff beneath the acromion, is an important factor leading to tendon failure.

At the point where the tendon is overloaded, individual fibers can fail, with the load transferred to adjacent collagen fibers. Continued loading will lead to further failure until the applied force ceases or the tendon ruptures. If the injury is incomplete and the healing. Repetitive microtrauma to the tissue is seen in overuse injuries.

The bone-tendon junction also may be involved in the injury process.

Tendon healing after an acute injury follows similar phases to other soft-tissue healing. The inflammatory response provides an extrinsic source for cellular invasion to begin the repair process. For injury to avascular tendons within a synovial sheath eg, flexor tendons of the hand , an intrinsic mechanism for tendon healing has been proposed that appears to be modulated by the stress of passive motion, thereby questioning the role of the extrinsic inflammatory response.

Cells from within the tendon proliferate at the wound site along with increased vascularity leading to collagen synthesis and further tissue maturation with time. Although evidence for both intrinsic and extrinsic mechanisms of healing has been supported, other factors may determine which is the primary mechanism for healing, such as the local environment, vascularity, or stress.

In the initial phase of healing after tendon repair, the tensile strength is significantly less than for controls. At 3 weeks, the tensile strength increases more progressively. Controlled passive motion has been shown to decrease adhesions, lead to a stronger repair, and accelerate gains in tensile strength. Collagen reorganization and alignment, as well as maturation, appear to benefit from controlled application of stress.

In vitro experiments using cyclic tension have demonstrated an enhanced intrinsic response, with proliferation and migration of fibroblasts in the line of tension and increased collagen synthesis, resulting in a thickened epitenon. In vivo experiments on partial flexor tendon lacerations support the role of tension, in addition to motion, which leads to.

Orthopaedic Knowledge Update Soft-Tissue Physiology and Repair increased tensile strength as well as increased cellular activity in the epitenon and well-developed collagen fiber formation by 4 weeks.

With improved suture techniques for flexor tendon repairs, such as a 6-strand repair and modified epitendinous suturing, early active motion may now be possible while avoiding gap formation at the suture repair site.

Such advances also may have a positive effect on the biomechanical characteristics and adhesion formation without significantly increasing resistance to gliding. Understanding of the role of growth factors and cytokines in connective tissue healing is evolving. In animal models of tendon transection, PDGF, produced at the site of tendon injury as a result gene therapy, and insulin-like growth factor I, introduced directly into the site of tendon injury, have been shown to enhance the healing process.

The function of these proteoglycans in tendon was thought to be analogous to their function in articular cartilage, to resist compression. Increased glycosaminoglycan content and proteoglycans also have been noted in the rotator cuff tendons, as well as variations in proteoglycan gene expression between different portions of the rotator cuff tendon.

Although the presence of proteoglycans in the rotator cuff may indicate a pathologic response to compression, such as that proposed by the impingement theory, their distribution found within the tendon substance may be a normal adaptive response to its structure and function.

In addition, it would appear that rotator cuff pathology results not only from extrinsic causes, such as impingement beneath the coracoacromial arch, but may result in part from intrinsic causes, including tensile overload and degeneration, or a combination of processes. This has recently been investigated using in vivo animal models. The reported hypovascularity of the supraspinatus tendon also may be involved in the pathologic process; however, its role is now less clear.

More recently, attention has been drawn to the potential for injury to the articular surface of the rotator cuff tendon from repetitive compression on the posterior superior glenoid rim.

The potential for healing in the unrepaired rotator cuff tendon appears to be limited, despite evidence of granulation tissue formation at the tendon edge and a vascular response. Tendon has been shown to heal well to bone, and in the repaired rotator cuff tendon studied in an animal model, there appears to be no advantage in the healing process to repairing the tendon edge to a cancellous trough because similar properties were noted with rotator cuff tendon healing to cortical bone.

Biomechanical testing has demonstrated that the strength of a suture repair through transosseous tunnels is enhanced by using a braided suture material in a locking fashion, such as the modified Mason-Allen technique, and it would seem preferable to use a nonabsorbable material to maintain its properties during the healing process.

In a transosseous repair, having a cortical bone bridge of 1 cm rather than 0. Rotator Cuff Tendons Several aspects of the anatomy and biology of the tendons of the rotator cuff suggest that they have slightly different properties than other tendons, such as the flexor tendons.

The supraspinatus, infraspinatus, teres minor, and subscapularis tendons do not have separate insertions, but rather interdigitate with the adjacent tendon to form a continuous insertion on the greater and lesser tuberosities of the humerus.

Particularly in the supraspinatus and infraspinatus, a complex, 5-layered structure has been observed, composed of tendon fibers, loose connective tissue, and capsule, as well as the coracohumeral ligament in the anterior portion of the supraspinatus.

The varied orientation of the tendinous fibers and the interwoven fiber patterns observed suggest an important role in the mechanical response to an applied load, but also may account for pathologic conditions, such as intratendinous tears. In addition, this normal anatomy of the tendon insertion does not appear to be altered by increasing age, although tendon degeneration may occur. The biomechanics of the rotator cuff tendons has not been as well studied as that of other tendons, in part because of its more complex structure.

However, variations in geometry and mechanical properties have been observed within the supraspinatus tendon, with its posterior third noted to be thinner and the anterior third found to be mechanically stronger than the middle or posterior portions. In addition, mechanical testing of the articular and bursal sides of the supraspinatus tendon suggests that the articular side may be at greater risk for failure under tension.

Other characteristics unique to rotator cuff tendons include the presence of the coracoacromial arch and the variation of acromial morphology.

The observation of greater amounts of glycosaminoglycans and the proteoglycans, aggrecan and biglycan, are associated with the more fibrocartilaginous tis-. Muscle Structure and Function Skeletal muscle originates from bone and adjacent connective tissue surfaces and inserts into bone via tendon. The myotendinous junction is a highly specialized region for load. Orthopaedic Knowledge Update 16 General Knowledge transmission, with an increased surface area from membrane infolding.

When the muscle fiber shortens, it is referred to as a concentric contraction. In an eccentric contraction, the muscle generates a force greater in magnitude than a concentric contraction, while the muscle fiber lengthens. An important effect of an eccentric contraction is deceleration of the portion of the limb the muscle acts upon, while acceleration occurs from a concentric contraction.

The characteristics of the muscle contraction depend on the muscle fiber types. Most muscles in the body comprise equal amounts of 2 types of fibers, type I and type II Table 1. Type I, or slow-twitch oxidative fibers, predominate in postural muscles and are well suited for endurance by an aerobic metabolism, an ability to sustain tension, and relative fatigue resistance, with higher amounts of mitochondria and myoglobin. In addition to the slow rate of contraction, slow oxidative muscle fibers also have a relatively low strength of contraction.

On the other hand, type II fibers, or fast-twitch fibers, have a fast rate of contraction with a relatively high strength of contraction. The type IIB, or fast-twitch glycolytic fibers, are more common in muscles that rapidly generate power but have a greater dependence on anaerobic metabolism and are less capable of sustaining activity for prolonged periods due to buildup of lactic acid.

The characteristics and composition of the type IIA, or fast-twitch oxidative glycolytic fibers, which have aerobic capacity, are intermediate between type I and type IIB.

Like other tissues in the body, skeletal muscle undergoes changes with aging. Muscle mass decreases slowly between 25 and 50 years of age. From this point, the rate of muscle atrophy increases, but the loss of muscle size and strength can be diminished with strength training. With aging, the total number of muscle fibers decreases and muscle stiffness increases, which may be related to the increase in collagen content seen with aging.

Furthermore, muscle fiber diameter decreases with aging, primarily in type II fibers. These effects also may be the result, in part, of decreased activity and mobility with increasing age. Response to Exercise and Loading Training and exercise can stimulate alterations in skeletal muscle if the activity is sustained and there is sufficient load. Under an appropriate program of exercise and loading, muscle can increase its functional capacity to respond.

For example, low tension, high repetition training of a relatively long duration results in greater endurance, which is to the advantage of the long-distance runner. An increase in capillary density and mitochondria concentration is associated with. Speed of contraction Strength of contraction Fatigability Aerobic capacity Anaerobic capacity Motor unit size Capillary density. Anatomy, physiology, and mechanics of skeletal muscle, in Simon SR ed: Orthopaedic Basic Science.

Orthopaedic Knowledge Update Soft-Tissue Physiology and Repair greater capability for oxidative metabolism, primarily affecting type I, slow-oxidative fibers.

Furthermore, resistance to fatigue is increased by these adaptations Fig. Muscle flexibility can be enhanced by warming or stretching of muscles. Conversely, application of cold to a muscle group will decrease its flexibility. Together, heat and stretching have a combined beneficial effect on muscle flexibility. In addition, the risk for muscle strain injury appears to be diminished by these factors. High tension, low repetition training emphasizes development of greater muscle strength and power.

When loads are progressively increased, muscle size increases, mostly from muscle hypertrophy of primarily type II fibers. This mode of training benefits the sprinter, who requires short and powerful bursts of speed to achieve higher performance. Unlike endurance training, which can be performed more frequently, strength training requires a period of rest or recovery for the muscle tissue and should not be performed daily.

Under this regimen, anaerobic metabolism is maximized and tissue injury avoided. Figure 8 Representative isometric tension-length curve of skeletal muscle. Response to Immobilization and Disuse When stimulation to the muscle fibers is withdrawn, the adaptations in skeletal muscle can be reversed. If muscles are further unloaded, either by disuse or immobilization, the effect on skeletal muscle is magnified. Loss of endurance and strength is observed in the muscle groups affected.

As muscle atrophies, changes are observed at both the macro- and microstructural levels, with decreasing fiber size and number, as well as changes in the sarcomere length-tension relationship. Changes at the cellular and biochemical level occur, and these may affect the aerobic and anaerobic pathways of energy production. Immobilization of muscle in a lengthened position has a less deleterious affect. This is a result of the relatively greater tension that is placed on these muscle fibers and their physiologic response to the load, compared with muscles immobilized in a shortened position.

In addition to the effects on muscle, immobilization has an effect on the bone and motor end plates. With remobilization after a similar period of immobilization 4 weeks , the detrimental changes in muscle cross-sectional area and receptors in the motor end plate can be reversed, but the bone density is not completely restored.

In an animal model of remobilization after immobilization, growth hormone stimulation as measured by levels of insulin-like growth factor IGF-1 resulted in greater return of muscle size and strength during the period of remobilization compared with controls. Response to Injury and Mechanisms of Repair Muscle injury can result from an indirect overload that overwhelms the muscles ability to respond normally or a direct injury, such as a contusion or laceration.

The indirect mechanism of injury includes muscle strains and delayed-onset muscle soreness. Injury from muscle strains in which muscles are unable to accommodate the stretch during eccentric contractions is commonly reported in sports activity.

Muscles that function across 2 or more joints, such as the hamstrings, are at greater risk for strain injury. In addition, fatigue has been associated with increased rates of strain injury when muscle has a diminished ability to perform and act as an energy or shock absorber.

Fatigued muscles have been shown to absorb less energy than muscles that are not fatigued.

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The spectrum of muscle strain injury can range from microscopic damage or partial tears to complete tears and disruption with a palpable defect within the muscle. The degree of injury from a tensile overload will dictate the potential of the host response and the time course for repair. The status of muscle contraction at the time of overload usually is eccentric, and failure most often occurs at or near the myotendinous junction unless there is previous injury to the.

Orthopaedic Knowledge Update 18 General Knowledge muscle. Although muscle strain injury may predominantly affect fast glycolytic fibers, this does not appear to be the result of the low oxidative capacity of these fibers. After muscle injury, healing is initiated in the inflammatory phase. The repair process includes fibroblast proliferation and collagen production leading to scar formation, with muscle regeneration resulting from myoblasts stemming from satellite cells.

Both of these processes occur at the same time; however, motion during healing has been shown to limit scar size. It also has been demonstrated that muscles in the process of healing are at an increased risk for reinjury, suggesting that return to strenuous activity should be delayed until satisfactory healing has taken place. The role of growth hormones in the healing process is evolving.

Nonsteroidal anti-inflammatory medications may enhance recovery initially, as shown in an animal model, up to 7 days after muscle injury. However, these medications have a deleterious effect on the functional recovery of muscle when studied at 28 days, possibly because the inflammatory response is suppressed.

Delayed-onset muscle soreness within 24 to 72 hours is another form of indirect injury to the muscle. However, this occurs within the muscle fibers as a result of intense training or exercise to which the muscle is unaccustomed. The cellular and microstructural changes that occur and the weakness that is present are reversible.

Muscle contusions result from a direct blow, usually to the muscle belly. The degree of hematoma formation, subsequent inflammation, and delay in healing is directly proportional to the compressive force absorbed, and it will also affect the amount of scar formation and muscle regeneration. However, when muscle is contracted, it is less vulnerable to this type of injury. A more rapid recovery is observed under conditions that promote increased vascularity, as seen in limbs that undergo early motion, and, possibly, in a younger age group.

Heterotopic bone, or myositis ossificans, is not an infrequent finding after a more severe contusion injury, but this finding should not be treated surgically until healing is complete and the resulting bone is fully matured.

Repair and recovery after muscle laceration depends on regeneration across the site and reinnervation.

Muscle distal to the site of injury that regenerates but is incompletely reinnervated has diminished function. The use of a tourniquet during arthroscopic knee procedures and its effect on thigh musculature have been investigated.

When applied for an average duration of less than 50 minutes, it did not affect quadriceps or hamstring recovery at 4 weeks when compared with procedures performed without a tourniquet. Tourniquet pressure in this study was determined from thigh circumference and systolic blood pressure. The effect of tourniquet use was also studied after arthroscopic ACL reconstructions averaging 87 minutes, with the tourniquet set to mm Hg over systolic blood pressure.

At 1 month, diminished thigh girth and a greater incidence of abnormal electromyographic studies were suggested but not shown statistically. At 6 and 12 months postoperatively, all muscle parameters studied were similar in the groups treated with and without a tourniquet. In another study, an animal model had a greater loss from direct compression on the underlying tissue than from muscle ischemia distal to the tourniquet when studied 2 days later.

It would appear that tourniquet use, as studied thus far, does not have any harmful effects on muscle functional recovery in the clinical setting. Nerve Structure and Function The nerve cell body gives rise to a single axon, the extension that conveys the signal of information as a graded or action potential within the peripheral nervous system. A sensory axon carries this signal as an electrical impulse from the periphery to its cell body in the dorsal root ganglion afferent , whereas a motor axon carries information from the cell body in the anterior horn in the spinal cord efferent to the end organ.

Cell bodies in the autonomic nervous system are in paravertebral ganglia. Although all axons have a surrounding Schwann cell, an axon that is insulated with a myelin sheath from many Schwann cells aligned longitudinally has a higher conduction velocity than an unmyelinated axon.

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This rate is further enhanced by a small interruption in the myelin sheath called the node of Ranvier Fig. Figure 9 The Schwann cell tube and its contents.

Reproduced with permission from Brushart TM: Peripheral nerve biology, in Manske PR ed: Hand Surgery Update. Orthopaedic Knowledge Update Soft-Tissue Physiology and Repair Materials, such as proteins, that support the structure and function of the axon are produced within the cell body and travel along the axon via slow and fast antegrade transport systems.

Materials, including waste products, return to the cell body via a fast retrograde transport system. The rate of transport is diminished with decreasing temperature; transport stops at 11C as well as after a period of anoxia.

The ultrastructure of a peripheral nerve begins with the axon and myelin sheath, which make up the nerve fiber, and is enclosed within a basement membrane and connective tissue layer, the endoneurium Fig. These fibers are grouped into a bundle called a fascicle, which is surrounded by the perineurium. The perineurium serves as a barrier to diffusion of fluid. A variable number of fascicles together form the peripheral nerve.

The peripheral nerve is enclosed by the outer epineurium, which has an interstitial or inner component between the fascicles to protect and support the nerve. Intra- and interfascicular connections are typical.

Blood vessels travel within the epineurium and have a system of branches around and within the fascicles, extending to capillaries at the endoneurium. Peripheral nerves demonstrate viscoelastic properties typical of other connective tissues; however, low levels of strain can lead to alterations in peripheral nerve conduction. Injury, Degeneration, and Regeneration Different types of injury patterns occur after traumatic insult to a peripheral nerve. First-degree injury, or neurapraxia, involves loss of conduction across the injured segment of nerve without wallerian degeneration or degradation.

Because the axon is not disrupted, recovery is complete. A second-degree injury, or axonotmesis, is damaging because the axon is disrupted. The remaining axon distal to the site of injury and a small portion of the proximal axon degenerate. The Schwann cell layer, termed the endoneurial sheath, remains intact and serves to guide the regenerating axon during recovery. Neurotmesis is more severe because the nerve itself is disrupted. In a third-degree injury, the structures within the perineurium, the nerve fibers of the fascicle, are damaged.

Because the endoneurial tubes are disrupted, regeneration occurs in a disorderly fashion. A nerve with fibers that serve a similar function and a distally located nerve injury have a more favorable prognosis. The interfascicular structure is lost, but the outer epineurium remains intact in a fourthdegree injury. The chances for an effective regeneration process are minimal; surgery usually is indicated.

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The most severe damage occurs in a fifth-degree injury. The nerve is completely disrupted and scar is likely to form between the severed ends; surgical repair is necessary for recovery. The process of wallerian degeneration begins immediately after transection of a nerve fiber. A neuron is more likely to survive when the injury is further distal, away from the cell body.

The neuron appears to change from its usual functions to removal of cellular debris and production of the proteins necessary for regeneration. Within hours, changes are noted in the cell body, and the process of regeneration begins as growth cones project from the proximal stump of the axon and the nearest intact node of Ranvier.

Schwann cells that accompany axonal growth bands of Bungner guide the process of regeneration and synthesize nerve growth factor, but also are the limiting factor to the rate of growth.

The zone of injury must be crossed and contact made with the endoneurial tubes of the distal stump for regeneration to proceed. Greater damage, further distance, and increased scar in this zone have an adverse effect. Surgical repair counteracts these problems. Reinnervation to a muscle is more timedependent than reinnervation to a sensory end organ. Several factors applied locally or systemically enhance regeneration; these factors include hormones, proteins, and growth factors.

Insulin-like growth factor IGF , which is present in regenerating nerves and nerve targets, has neurotropic activity. Anti-IGF serum causes a sustained decrease. Figure 10 Schema of peripheral nerve trunk shows epineurium ep , perineurium p , and endoneurium end.

Peripheral nerve: Injury and Repair of the Musculoskeletal Soft Tissues.

Orthopaedic Knowledge Update 20 General Knowledge in the rate of axon regeneration. Systemic administration of IGF has shown a small but significant improvement in regeneration after a nerve crush injury. Acidic fibroblast growth factor enhances regeneration distances when administered locally or systemically. Direct current electrical fields and hyperbaric oxygen also promote regeneration. In an animal study, collection of axoplasmic fluid and its reinjection proximal and distal to the repair site resulted in increased axon count and better return of limb function compared with controls.

Local environmental factors also can influence axonal growth and direction. Alternatives include conduits, such as a vein or synthetic tube, and allografts, which avoid donor-site nerve loss and morbidity.

The best results occur in younger individuals. Shorter grafts in more distal locations have greater recovery. Tension at the graft repair site must be avoided. This text offers the most comprehensive review for basic science of soft tissues, as well as the entire neuromusculoskeletal system. Nerve Repair Peripheral nerve repair is used to reestablish continuity of the nerve; results are best when repair is done tension-free soon after nerve transection.

A primary repair is preferable to the alternative techniques of nerve grafting but repair under tension requires the latter. Mobilization of the nerve stump and tension should be limited because diminished perfusion and ischemia can result. Primary repair is less likely in more severe trauma, such as crush injuries in which a larger amount of damaged tissue at the ends of the 2 stumps requires resection before nerve repair.

Younger patients and more distal locations of injury have better prognoses. Of the 2 types of nerve repair, a fascicular suture repair, theoretically, has a better chance to correctly restore nerve function than does an epineurial suture.

However, the only prospective comparison of fascicular and epineurial digital nerve repairs in humans showed no difference between the 2 groups. Regardless of the technique used for nerve repair, an atraumatic technique under magnification and without tension is beneficial.

Fascicular repair necessitates identification of matching fascicles of the proximal and distal stumps, which provides improved alignment, although greater scarring can result from the intraneural dissection.

In addition to direct observations, intraoperative awake stimulation and staining techniques aid with alignment of the fascicles. When fascicular matching is not possible, based on the internal topography of the peripheral nerve at the level of transection, epineurial suture repair is preferable.

Effect of cultured autologous chondrocytes on repair of chondral defects in a canine model. J Bone Joint Surg ;79A: Using a canine model, the authors studied 3 treatment groups of cartilage repair 12 to 18 months follow-up: They could detect no significant difference among the 3 groups. Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation. N Engl J Med ; Two-year clinical results of patients undergoing chondrocyte transplantation combined with a periosteal flap are presented.

Fourteen of 16 patients with femoral condyle defects had good to excellent results, but patients with patellar lesions did poorly. Tissue design and chondrocyte-matrix interactions, in Cannon WD Jr ed:Structural and degenerative changes as a result of aging have been reported.

It would appear that whereas maturation influences the insertion sites of ligaments as demonstrated in the failure patterns, aging and senescence have a detrimental effect on the ligament substance. They could detect no significant difference among the 3 groups.

Gross motion or pain at the fracture site and radiographic evidence of persistent radiolucency are factors suggesting failure of healing.

A primary repair is preferable to the alternative techniques of nerve grafting but repair under tension requires the latter. Views Total views. Alternatives include conduits, such as a vein or synthetic tube, and allografts, which avoid donor-site nerve loss and morbidity. Ligament Structure and Function Optimal joint function depends on the complex interaction around the joint of ligaments as static restraints and muscletendon units as dynamic restraints, as well as other factors, including articular geometry.

Show related SlideShares at end. The undifferentiated mesenchymal cells that migrate into the chondral portion of the defect produce a repair cartilage that has a combination of types II and I collagen.