Orthopaedic knowledge update 11 pdf


 

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 .

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Orthopaedic Knowledge Update 11 Pdf

Orthopaedic Knowledge Update 11 (Orthopedic Knowledge Update): Medicine & Health Science Books @ ruthenpress.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.

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, OKU 12 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: Ovid Publisher: Grauer, Jonathan N. Orthopedics Language: English Edition: Doody's Featured Books Instructional Course Lectures, Volume 68 Offers new techniques for solving the tough challenges you encounter in your practice every day with a focus on pediatric orthopaedics, upper extremity and orthopaedic oncology. ASAM Principles of Addiction Medicine Provides health care providers with information to diagnose and treat their patients, and also to positively impact clinical service design and delivery, and global health care policy. Description Details Also Recommended Brings you a comprehensive synthesis of the latest clinical thinking and best practices across all orthopaedic specialty areas.

Joint loading and motion are required to maintain normal adult articular cartilage. Immobilization of a joint will cause a rapid loss of proteoglycans from the cartilage matrix. Proteoglycan content is affected to a greater extent than collagen composition. Because proteoglycan is lost, fluid flux and deformation in response to compression will increase.

Tensile properties, which depend primarily on collagen, are maintained. These biochemical and biomechanical changes are, at least in part, reversible with the restoration of motion. The extent of recovery decreases with increasing periods of immobilization. Increased joint loading, either through excessive use or increased magnitudes of loading, will also affect articular cartilage. Disruption of the intra-articular structures, such as menisci or ligaments, will alter forces acting on the articular surface.

In experimental animal models, responses to transection of the anterior cruciate ligament ACL or meniscectomy have included fibrillation of the cartilage surface, increased hydration, and changes in proteoglycan content.

Significant and progressive decreases in the tensile and shear modulus have been observed in response to transection of the ACL.

While the overall metabolic activity of articular cartilage is low, the activity surrounding each individual chondrocyte and surrounding ECM is quite dynamic.

This activity is determined by a cellular response to soluble mediators nutrients, growth factors, cytokines , mechanical loads, matrix composition, hydrostatic pressure changes, and electric fields. Growth factors, such as insulin-like growth factorI and transforming growth factor-b TFG-b , may stimulate matrix synthesis and cell proliferation.

Chondrocytes synthesize and release these growth factors, which further enhance the metabolic activity of chondrocytes and matrix production. Matrix catabolism is mediated by enzymes, including stromelysin, aggrecanase, and collagenase, which are regulated in a complex manner by local factors such as interleukin1 IL-1 , prostaglandins, TFG-b, tumor necrosis factor, and other molecules.

The ECM is known to act as a signal transducer for the. Biomechanics and Physiology Articular cartilage exhibits a time-dependent behavior viscoelastic when subjected to a constant load or constant deformation. Similarly, when the tissue is deformed and held at a constant strain, the stress will rise to a peak, followed by a slow stress-relaxation process until an equilibrium value is reached. Two mechanisms are responsible for viscoelasticity: During walking or running, articular cartilage is subjected to compressive forces that rise to several times body weight within a very short period of time.

Under this dynamic loading environment, interstitial fluid trapped within the cartilage matrix enables the tissue to resist these high compressive forces without mechanical damage. The instantaneous increased hydrostatic pressure will be sustained within the tissue matrix for an extended period of time. When the interstitial fluid flows through the dense matrix, a frictional interaction between the fluid and the matrix is created, providing a mechanism for energy dissipation.

This phenomenon, the. Orthopaedic Knowledge Update Soft-Tissue Physiology and Repair chondrocytes and may transmit signals that result from mechanical loading of the articular surface to the chondrocytes. The chondrocytes respond to these signals by altering the matrix, possibly through the expression of cytokines that act through local factors.

It has been shown that a persistent abnormal change in joint loading or immobilization of a joint may change the concentration of proteoglycans in articular cartilage and the degree of proteoglycan aggregation that alters the mechanical properties of cartilage. The exact details of how the mechanical loading of joints influences the functions of chondrocytes remains investigational, but deformation of the matrix produces mechanical, electrical, and physiochemical signals that may have major roles in stimulating chondrocytes.

The reversiblity of these chondral injuries is still being debated. It is hoped that ongoing clinical and basic science studies will provide the clinician with new scientific information on the natural history and optimal treatment of these injuries. Isolated partial and full-thickness articular cartilage injuries chondral fractures are often problematic because of the limited blood supply. This relatively poor blood supply in comparison to bony injuries where a vascular response is robust combined with the isolated environment of the chondrocyte makes the potential healing of articular cartilage poor.

Over time, the remaining healthy articular cartilage may be affected, eventually leading to more incongruity and damage. With increasing force, the depth of the injury may extend beyond the articular cartilage into the subchondral bone, resulting in an osteochondral injury.

These injuries, which cross the tidemark, cause hemorrhage and clot formation, thereby activating the inflammatory cascade. This type of injury has many biologic differences from a pure chondral injury. Blood products within the fibrin clot release vasoactive mediators and growth factors or cytokines. These factors may stimulate vascular invasion and migration of undifferentiated cells, which may play an important role in stimulating repair of this injury. 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.

The cells in the osseous portion of the defect eventually produce immature bone that is gradually replaced by mature bone. The composition of this repair tissue rarely replicates the structure of the normal articular cartilage and subchondral bone. The subchondral portion of the defect is filled with regions of fibrous tissue and hyaline cartilage.

The composition and structure of the chondral repair tissue are intermediate between those of hyaline cartilage and fibrocartilage. The inferior material properties of this repair tissue within the defect make it more susceptible to injury under physiologic loading conditions.

Articular Cartilage Injury Mechanical injuries to articular cartilage can be separated into 3 distinct types: Microscopic injury may result from a single traumatic event or multiple repetitive loads. A reliable method of detecting damage to articular cartilage in the absence of surface disruption ie, chondral fracture has yet to be developed.

This microscopic mechanism most likely results in damage to the chondrocytes and affects their ability to produce collagen and proteoglycans. The point at which the accumulated microdamage becomes irreversible is unknown. Chondrocytes have the ability to restore lost proteoglycans if the rate of loss does not exceed the rate of production. If there is concomitant damage to the collagen ultrastructural architecture or if a sufficient number of chondrocytes have been damaged, an irreversible degeneration process may ensue.

Although the exact natural history of this type of damage is still being defined, the decrease in proteoglycan concentration, the increase in tissue hydration, and disorganization of the articular cartilage is worrisome.

Clinically, this scenario has been observed in conjunction with knee ligament injuries. The most common location of these lesions is within the lateral compartment of the knee, on the lateral femoral condyle at the sulcus terminalis, and the posterolateral tibial plateau. Although the area may appear normal during arthroscopic examination, recent in vivo histologic studies have shown a significant disruption of the articular.

The efficacy of all current techniques is still being evaluated by basic science research and clinical trials. Depending on the location and depth of the lesion Fig. Pure chondral injuries can. Orthopaedic Knowledge Update 6 General Knowledge be beneficial in the treatment of osteoarthritic joints.

Pure chondral defects also can be surgically treated by autograft or allograft osteochondral techniques. The use of osteochondral grafts for articular cartilage defects of the knee is not new. The use of autogenous osteochondral plugs 2. Much debate continues as to the size of the defect that can be safely treated with this technique.

Donor site morbidity has not been defined.

A cadaveric study showed Figure 2 Meniscus showing complex orientation of collagen fibers of the meniscus. The strength of the menisci of the knee as it relates to their fine structure. J Bone Joint contact pressures, but whether or not articular contact at these sites will lead to Surg ;52B: Osteochondral injuries traumatic or congenital For symptomatic lesions of this size allografts should be conrequire the replacement of both bone and cartilage.

A clot forms, and unclear if autologous osteochondral plugs are superior to these cells have the ability to form fibrocartilage with pre- procedures that penetrate subchondral bone eg, abrasion dominantly type I cartilage. This, however, is different from and microfracture. There is no question, however, that the hyaline cartilage type II , and the resulting mechanical prop- harvesting and transplantation of autologous plugs is more complex and invasive.

Articular cartilage allografts fresh and fresh frozen have The limited ability of host cells to restore articular surfaces has led investigators to seek methods of transplanting cells been used for traumatic and pathologic tumor, degenerative that form cartilage into chondral and osteochondral defects. To date Studies have shown that both chondrocytes and undifferen- long-term success of these grafts has not been determined. The use of trans- with large traumatic femoral osteochondral defects.

Ninety-two fresh osteochondral allografts were used in plants of autogenous chondrocytes to treat localized cartilage defects of the femoral condyle or the patella has been report- transplantation procedures in a group of patients with posted. These early reports suggest that the transplantation of traumatic osteochondral defects of the knee joint. More work is In another series, 37 patients with large femoral condylar needed to assess the function and durability of the new tissue, defects were treated with fresh osteochondral shell alloto determine if it improves joint function and delays or pre- grafts.

Excellent or good results were seen in 8 of the 9 vents joint degeneration, and to ascertain if this approach will patients followed up at 5 years after surgery. Orthopaedic Knowledge Update Soft-Tissue Physiology and Repair Many factors affect the fate of allograft and autograft articular cartilage transplants, including depth, size, and location of the lesion; limb alignment; status of meniscal cartilage; and ligament stability.

All of these factors must be taken into account in the evaluation and management of articular cartilage defects. Growth factors influence a variety of cell activities, including proliferation, migration, matrix synthesis, and differentiation. Many have been shown to affect chondrocyte metabolism and chondrogenesis.

Bone matrix has been found to contain a variety of these molecules as well. The osteochondral injury and exposure of bone as a result of loss of articular cartilage may release agents that affect the formation of cartilage repair tissue.

These agents probably have an important role in the formation of new articular surfaces after currently used surgical procedures, including resection arthroplasty, penetration of subchondral bone, soft-tissue grafts, and possible osteotomy. The treatment of chondral defects with growth factors or cell transplants requires a method of delivery for the growth factors or cells in the defect.

The success, therefore, depends on the use of an artificial matrix. Investigators have reported that implants formed from a variety of biologic and nonbiologic materials may facilitate the restoration of an articular surface.

It is difficult at this time to make any comparison between the relative merits of different types of artificial matrixes.

The outer aspect of each meniscus obtains its blood supply from a circumferentially arranged perimeniscal capillary plexus from the superior and inferior geniculate arteries. A vascular synovial fringe extends 1 to 3 mm over the femoral and tibial surfaces of the peripheral aspect of each meniscus.

The inner two thirds of the meniscus is essentially avascular and receives its nutrition from the synovial fluid. Menisci have been found to contain both free nerve endings and corpuscular mechanoreceptors concentrated at the meniscal root insertion sites as well as the periphery. The menisci may act as a source of proprioceptive information for muscular coordination about the extremity.

Kinematic analysis of the knee has demonstrated that the menisci are dynamic structures that move anterior with extension and posterior with flexion. The lateral meniscus is more mobile than the medial, and the anterior portion of the lateral meniscus has the greatest mobility.

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The relative immobility of the medial meniscus may help explain why there is a higher prevalence of medial meniscal lesions. Menisci, through their shape and structure, provide several very important functions in the knee joint. The shapes of the medial and lateral menisci improve the congruency of the articulating surfaces and increase the surface area of joint contact, thus adding load transmission across the knee joint.

Their viscoelastic properties allow their stiffness to increase with higher deformation rates. The medial meniscus also provides a very important secondary restraint to anterior translation of the tibia. This function has not been seen with the lateral meniscus. With weightbearing, centrifugal radial forces are resisted by the firm attachments of the anterior and posterior horns of the menisci to the tibia. This situation produces large circumferentially oriented hoop tensile stresses, which are countered by the circumferential arrangement of most collagen fibers in the meniscus.

Proteoglycans contribute to the compressive properties of the menisci through their ionic repulsive forces, which increase matrix stiffness, and by contributing to the osmotic pressure within the meniscus. Compressive forces in the knee generate tensile stresses in the meniscus.

There are significant regional variations in the tensile strength and stiffness of differing anatomic portions of the menisci that appear to be a result of differences in collagen ultrastructure rather than of biochemical variations.

The presence of radial fibers in a particular portion of the meniscus may increase tensile stiffness and strength under radially applied tension. Meniscal Cartilage Structure and Function The meniscus is a specialized fibrocartilaginous structure capable of load transmission, shock absorption, stability, articular cartilage nutrition, and proprioception. It is composed of a complex 3-dimensional 3-D interlacing network of collagen fibers, proteoglycan, glycoproteins, and interspersed cells of fibrochondrocytes that are responsible for synthesis and maintenance of the ECM.

The ECM is composed of primarily type I collagen. Most of these fibers are oriented circumferentially to resist tension. The complex 3-D collagen architectural arrangements explain this unique function Fig. The meniscal cartilage, like articular cartilage, possesses viscoelastic properties.

The ECM is a biphasic structure composed of a solid phase eg, collagen, proteoglycan , which acts as a fiber reinforced porous-permeable composite, and a fluid phase, which may be forced through the solid matrix by a hydraulic pressure gradient. Although these properties are shared with articular cartilage, the meniscus is more elastic and less permeable than articular cartilage. Meniscal Injury The detrimental effects of both complete and partial meniscectomy have been demonstrated in numerous experimental and clinical studies.

Loss of the meniscus alters the pattern of load transmission in the knee and results in accelerated articular cartilage degeneration. Experimental studies have shown that higher peak stresses and greater stress concentration in the articular cartilage, decreased shock-absorbing capability, and alterations in the pattern of strain distribution in the proximal tibia occur with meniscal deficiency.

The degree of degenerative knee joint changes has been shown to be directly proportional to the amount of meniscus removed.

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The removal of any meniscal tissue should not be viewed as a benign procedure. 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.

If you continue browsing the site, you agree to the use of cookies on this website. See our User Agreement and Privacy Policy. See our Privacy Policy and User Agreement for details. Published on May 7, SlideShare Explore Search You. Submit Search. Successfully reported this slideshow. We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads.

You can change your ad preferences anytime. Upcoming SlideShare. Like this presentation? Why not share! 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.

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. 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.

Orthopaedic Knowledge Update 11

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.

Orthopaedic Surgery

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.

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.

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.

Orthopaedic Knowledge Update 11 — caite. 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. 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.

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