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Figure 58-11 Achilles tendon allograft preparation. Line drawings of the allograft with 30 x 10 x 10-mm bone block, before and after fashioning the two tails of the graft. A, Small-fragment fixation of the calcaneal bone block. Graft passage through the patellar drill holes. B, The limbs of the graft are sutured to the quadriceps tendon and medial and lateral retinaculum and then turned down for suture to the patellar tendon graft as well. (From Mills WJ: Reconstruction of chronic patellar tendon rupture with Achilles tendon allograft. Tech Knee Surg 2004;3:154-162.)

The patient who undergoes reconstruction of the patellar tendon with an Achilles tendon allograft follows a similar program but is carefully monitored. Knee motion is not allowed until the wound seals. For 2 weeks, 30 degrees of knee flexion is allowed in a hinged rehabilitative brace. If patellar tendon length is maintained, motion is advanced to 60 degrees of knee flexion for 2 weeks. Again, the position of the patella is con firmed with a plain lateral radiograph. If the position is the same as immediately postoperatively, knee flexion is advanced to 90 degrees. Assuming that patellar tendon length is maintained, unlimited motion is allowed at 6 weeks.29 The quality of tissue, quality of the repair, and knee flexion obtained at the time of surgery determine the progression of activities after repair or reconstruction of the extensor mechanism.


Weakness of the quadriceps muscle may occur in as many as 40% to 50% of patients. Extensor lag is less common in patellar tendon repair compared to those who undergo quadriceps tendon repair. Most patients regain close to full ROM, an argument against the use of augmentation devices and accelerated rehabilitation for repair of the patellar tendon.

Unfortunately, patellofemoral incongruence or osteoarthrosis is seen all too frequently on postoperative radiographs, for example, 12 of 29 patients in one series.30 Of the 12 patients, three had unsatisfactory results. All the patients with unsatisfactory results due to pain in the series of Larsen and Lund31 had patellar incongruence. The Insall-Salvati ratio differed more than 10% from the uninvolved knee in 16 of 29 patients in one series of repairs.30 In a series of 10 patients with athletic patellar tendon ruptures treated with immediate suture repair to bone, two of those patients had significant patella alta (Insall-Salvati ratios of 0.55 and 0.59) that was increased in each patient from preoperatively. Those two had patellar pain post-operatively that limited their sporting activities.5 Even though patients with patellar tendon repair are generally younger than those with quadriceps tendon rupture, return to preoperative activities is not universal for every patient.

Patients with a delayed diagnosis of patellar tendon rupture who undergo reconstruction are less likely to return to full activities. Mills29 reported on five patients with Achilles tendon allo-graft reconstruction of the patellar tendon. Mean average flexion was 123 degrees. Four of five patients achieved full active terminal extension without an extensor lag. No wound complications or graft ruptures were encountered.


A second operation to remove a cerclage wire is usually necessary as painful hardware or wire breakage is common with this method of augmentation. Other complications closely parallel those described previously for quadriceps tendon repair.


Randomized clinical trials are uncommon involving treatment of extensor mechanism disruption. The body of science on extensor mechanism injuries consists of case series, review articles, and a large number of case reports; as such, clinical decision making relies on data with a low level of clinical evidence. Box 58-1 summarizes the general principles involved in diagnosing and treating extensor mechanism injuries.

Due to the strong biomechanical properties of the extensor mechanism, rupture occurs through damaged or degenerative tissue. Particularly in patients with disruption of the quadriceps tendon, systemic disease should be sought and addressed.

Box 58-1 General Principles


Recognize the diagnosis early.


Recognize systemic disease.


Restore appropriate tension to the extensor mechanism.


Repair with grasping suture.


Respect the biology of the injury.


Rehabilitate appropriate to the patient.

Failure to address these factors may jeopardize postoperative success.

A delay in diagnosis and treatment of extensor mechanism disruption is the single most negative impact on outcome from treatment. The clinical findings are straightforward. If the diagnosis is suspected, it is unlikely to be missed.

Extensor mechanism length restoration using the contralateral knee as a control is the first priority. Patients with incon-gruence or malalignment of the patellofemoral articulation after repair or reconstruction are at increased risk of pain.6,30,31 The standard of care is primary repair of the extensor mechanism within 2 weeks of injury with a grasping suture on the tendinous portion of the repair with the suture passed through drill holes. A relatively conservative rehabilitation program focused on restoration of strength, mobility, and functional activities will likely allow the patient to return to daily activities and may allow a return to sporting activities.

Augmentation of the primary patellar tendon repair with wire, Dall-Miles cables, suture, and pull-out wire can be advised for patients undergoing an accelerated rehabilitation program. Factors that affect tissue integrity, healing response, or non-compliant patients may be considered for an augmented repair. In general, augmentation is not necessary in the absence of these factors.

Repair of the chronically ruptured extensor mechanism presents controversy. Up to 6 weeks after injury a repair may be possible; beyond that time, most authors would recommend the Codivilla V-Y plasty as described by Scuderi for the chronic ruptured quadriceps tendon. Use of allograft tissue, prosthetic devices, and soft-tissue grafts should be confined to individual situations rather than general use. Treatment of the chronic patellar tendon rupture is even more controversial. The first principle is to restore length to the extensor mechanism with the use of the normal side as a control if available. Up to 6 weeks from time of the injury, it may be possible to do a primary suture repair. Proponents of allograft tissue report the use of tendon allograft.29 Autogenous semitendinosis and gracilis may substitute for the patellar tendon after appropriate length is restored.


1. Ilan D, Tejwani N, Keschner M, et al: Quadriceps tendon rupture. J Am Acad Orthop Surg 2003;11:192-200.

2. Huberti H, Hayes W, Stone J, et al: Force ratios in the quadriceps tendon and ligamentum patellae. J Orthop Res 1984;2:49-54.

3. Kannus P, Jözsa L: Histopathological changes preceding spontaneous rupture of a tendon: A controlled study of 891 patients. J Bone Joint Surg Am 1991;73:1507-1525.

4. Siwek CW Rao JP: Ruptures of the extensor mechanism of the knee joint. J Bone Joint Surg Am 1981;63:932-937.

5. Scuderi C: Ruptures of the quadriceps tendon. Study of twenty tendon ruptures. Am J Surg 1958;95:626-634.

6. Kelly DW, Carter VS, Jobe FW et al: Patellar and quadriceps tendon ruptures-jumper's knee. Am J Sports Med 1984;12:375-380.

7. Greenspan A, Norman A, Tchang FK-M: "Tooth" sign in patellar degenerative disease. J Bone Joint Surg Am 1977;59:483-485.

8. Zeiss J, Saddemi S, Ebraheim N: MR imaging of the quadriceps tendon: Normal layered configuration and its importance in cases of tendon rupture. Am J Roentgenol 1992;159:1031-1034.

9. Yu J, Petersilge C, Sartoris D, et al: MR imaging of injuries of the extensor mechanism of the knee. Radiographics 1994;14:541-551.

10. Berlin R, Levinsohn E, Chrisman H: The wrinkled patellar tendon: An indication of abnormality in the extensor mechanism of the knee. Skeletal Radiol 1991;20:181-185.

11. Ong BC, Sherman O: Acute patellar tendon rupture: A new surgical technique. Arthroscopy 2000;16:869-870.

12. Richards DP, Barber FA: Repair of quadriceps tendon ruptures using suture anchors. Arthroscopy 2002;18:556-559.

13. Rougraff BT, Reeck CC, Essenmacher J: Complete quadriceps tendon ruptures. Orthopaedics 1996;19:509-514.

14. Scuderi G: Quadriceps and patellar tendon disruption. In Scott W (ed): The Knee. St. Louis, Mosby, 1994, pp 469-478.

15. Yilmaz C, Binnet MS, Narman S: Tendon lengthening repair and early mobilization in treatment of neglected bilateral simultaneous traumatic rupture of the quadriceps tendon. Knee Surg Sports Traumatol Arthrosc 2001;9:163-166.

16. Wenzl M, Kirchner R, Seide K, et al: Quadriceps tendon ruptures—is there a complete functional restitution? Injury 2004;35:922-926.

17. De Baer T, Geulette B, Manche E, et al: Functional results after surgical repair of the quadriceps tendon rupture. Acta Orthop Belg 2002;68:146-149.

18. Konrath G, Chen D, Lock T, et al: Outcomes following repair of quadriceps tendon ruptures. J Orthop Trauma 1998;12:273-279.

19. Vidil A, Ouaknine M, Anract P, et al: Trauma-induced tears of the quadriceps tendon: 47 cases. Rev Chir Orthop Reparatrice Appar Mot 2004;90:40-48.

20. Shah K: Outcomes in bilateral and simultaneous quadriceps tendon rupture. Orthopaedics 2003;26:797-798.

21. Basso O, Johnson D, Amis A: The anatomy of the patellar tendon. Knee Surg Sports Traumatol Arthrosc 2001;9:2-5.

22. Lairungruang W, Kuptniratsaikul S, Itiravivong P: The remained patellar tendon strength after central on third removal: A biomechanical study. J Med Assoc Thailand 2003;86:1101-1105.

23. Kennedy JC, Willis RB: The effects of local steroid injections on tendons: A biomechanical and microscopic correlative study. Am J Sports Med 1976;4:11-21.

24. Wong M, Tang Y, Lee S, et al: Effect of dexamethasone on cultured human tenocytes and its reversibility by platelet-derived growth factor. J Bone Joint Surg Am 2003;85:1914-1920.

25. Ravelin R, Mazzocca A, Grady-Benson J, et al: Biomechanical comparison of patellar tendon repairs in a cadaver model: An evaluation of gap formation at the repair site with cyclic loading. Am J Sports Med 2002;30:469-473.

26. Larson RV Simonian RT: Semitendinosus augmentation of acute patellar tendon repair with immediate mobilization. Am J Sports Med 1995;23:82-86.

27. Shelbourne K, Darmelio M, Klootwyk T: Patellar tendon rupture using Dall-Miles cable. Am J Knee Surg 2001;14:17-21.

28. Bhargava SP, Hynes MC, Dowell JK: Traumatic patella tendon rupture: Early mobilization following surgical repair. Injury 2004; 35:76-79.

29. Mills WJ: Reconstruction of chronic patellar tendon rupture with Achilles tendon allograft. Tech Knee Surg 2004;3:154-162.

30. Kasten P, Schewe B, Maurer F, et al: Rupture of the patellar tendon: A review of 68 cases and a retrospective study of 29 ruptures comparing two methods of augmentation. Arch Orthop Trauma Surg 2001;121:578-582.

31. Larsen E, Lund PM: Ruptures of the extensor mechanism of the knee joint: Clinical results and patellofemoral articulation. Clin Orthop 1986;213:150-153.


Arthritis in the Athlete

Stephen French and Robert Litchfield

In This Chapter

Physical therapy and conditioning

Glucosamine/chondroitin sulfate

Nonsteroidal anti-inflammatory drugs (NSAIDs)

Corticosteroid injection


Bracing and orthotics


Realignment osteotomy

Surgery—high tibial osteotomy Arthroplasty in the athlete

One of the goals of modern medicine is to extend the quality-of-life years of the population. Advances in this direction have resulted in a population who is living longer and more active lives. Improvements in workplace productivity, personal income, and better working conditions have also created more time for leisure activities for the population. These factors, combined with the aging "baby boomer" population, who will comprise almost 20% of the United States population aged 60 or older by the year 2020, have created a significant population of "aging athletes" (Population Division of the Department of Economic and Social Affairs of the United Nations Secretariat, 1998). Sports medicine physicians are being challenged to create a treatment strategy for arthritis in the athlete.

For the purposes of this volume, we examine the occurrence and treatment of primary osteoarthritis in the adult athletic population. Figures for the United States in the year 2000 indicate that arthritis is a public health burden second only to heart disease in disability expenses, with approximately 38 million people requiring treatment at a cost of $72 billion or 2.5% of the gross national product.1,2

The development and progression of osteoarthritic cartilage changes are influenced by genetic, physiologic, and geometric factors. An error in the DNA sequence for type II collagen that represents an amino acid substitution of one base sequence of cysteine for arginine has been shown to be present in osteoarthritic cartilage.3 There are changes in the load-bearing properties of articular cartilage with age, such as increased cellular death, proteoglycan loss, and a loss of the cartilage matrix. While these changes do occur with age, the symptoms of osteoarthritis are, fortunately, present in only half of the population older than 65 years. The development and progression of symptomatic osteoarthritis are potentiated by a change in the joint architecture. Nonanatomic joint geometry will lead to degeneration of the articular cartilage surface at an increased rate. It is common in the athletic population to have sustained an injury to a joint at an earlier time, such as a small meniscus tear or a low-grade ligament strain, changing the joint architecture slightly, which can later lead to a rapid progression of symptomatic arthritic change. Adults who have previously competed at high-level sports and those who remain active are keenly aware that sporting activities can take a toll on their bodies and lead to the "wear and tear arthritis" that is common in the "master athlete." They must also be made aware of the tremendous benefits that can be gained from maintaining an active lifestyle, an appropriate body mass index, and good muscle tone and encouraged to continue to participate in activities that are appropriate for their abilities.


Physical Therapy and Conditioning

The physician treating symptomatic osteoarthritis has a number of interventions at his or her disposal. Patients with symptomatic osteoarthritis in a weight-bearing joint who have an elevated body mass index can expect an improvement in their symptomatology with a 10% reduction in mass. A dedicated physiotherapy regimen that focuses on improving the strength and flexibility of musculature surrounding an arthritic joint will improve objective pain scores in symptomatic arthritis. The athletic population with arthritis tend to be excellent candidates for a focused physical therapy and conditioning program as they often have participated in these type programs during their competition days. The role of preactivity stretching, maintaining muscle conditioning, and the use of rest, ice, compression, and


• An aging population that desires to remain active has resulted in increased demands on medical providers to treat arthritis in athletic individuals.

• Generalized conditioning, reduction in body mass index, and strength and flexibility training have all been shown to be beneficial in improving symptoms.

• Glucosamine, chondroitin sulfate, NSAIDs, viscosupplementa-tion, and intra-articular corticosteroids all have a role in the treatment of arthritis.

• Unloader bracing is used to improve the distribution of forces through the entire joint.

• Realignment osteotomy can provide significant symptomatic relief by redistributing load to more normal articular cartilage while preserving the patient's own joint.

elevation of the affected body part is usually well-known in the adult athlete and should always be encouraged as a first-line therapy and maintenance strategy. The opportunity for group activities such as conditioning classes with goals formed around some manner of competition, weight loss, or strength improvements can be excellent motivational tools.

Nutritional Supplements

The use of nutritional supplements is now quite common in the athletic population. Athletes who are experiencing arthritic symptoms are likely to try to treat their pain with the use of nutritional supplements in addition to other modalities. Chon-droitin sulfate and glucosamine sulfate are the most commonly used supplements in this role. As substances that are classified as nutritional supplements that have an intended effect of treatment of a medical condition, they have commonly become referred to as "nutriceuticals."

In both osteoarthritis and rheumatoid arthritis, patients have an increased excretion of glucosamine in the urine. As a naturally occurring substance, it stimulates glycosaminoglycan and proteoglycan synthesis, which are involved in the formation and repair of articular cartilage. Chondroitin sulfate is a gly-cosaminoglycan composed of units of glucosamine with attached sugar molecules. Both chondroitin sulfate and glucosamine are derived from animal sources.4

As dietary supplements, nutriceuticals such as glucosamine and chondroitin sulfate are not subjected to analysis by the U.S. Food and Drug Administration prior to sale. There exists no standardization of testing, and producers regulate the content of their product according to their own guidelines. This has created a concern that substances in this category may not be exactly represented by the labeled amounts of ingredients of the package. A recent consumer monitoring group completed a study that concluded that almost half of the glucosamine/chon-droitin supplements tested did not contain the labeled amounts of ingredients.5

To date there has been only one scientific study that has shown an improvement in symptoms with glucosamine compared to placebos. In this study, 212 patients with symptomatic knee arthrosis received either 1500mg glucosamine daily for 3 years or placebo. A digital knee radiograph study before and after treatment showed progressive joint space narrowing in the placebo group versus no significant narrowing in the glucosamine group. WOMAC (Western Ontario and McMaster University Osteoarthritis Index) knee scores were improved in the glucosamine group and worse in the placebo group.4 With the results of this single study, there is at present no compelling evidence from randomized, double-blind, controlled trials that shows a clear benefit of glucosamine or chondroitin sulfate as a medication for the treatment of painful osteoarthritis.

The National Institutes of Health are currently completing what is hoped to be the definitive trial (the Glucosamine/Chon-droitin Arthritis Intervention Trial [GAIT]) of these nutritional supplements. The study is designed to determine whether glucosamine, chondroitin sulfate, and/or the combination of glucosamine and chondroitin sulfate are more effective than placebo and whether the combination is more effective than glu-cosamine or chondroitin sulfate alone in the treatment of knee pain associated with osteoarthritis of the knee.

Nonsteroidal Anti-inflammatory Drugs

Athletes may to be used to the concept of minor aches and pains associated with their sporting activity, and "playing with pain"

is often a common scenario in the athlete with arthritic symptoms. It is also very common for athletes to have taken various analgesic remedies during their competition days and the history of analgesic use should be determined for each patient. As a treating physician of an athlete with arthritic symptoms, it is important to establish the medications that an athlete has used previously for his or her condition and to determine whether the medications have been used on an appropriate dosing schedule. Often medications are taken as an occasional pain reliever on an irregular and inappropriate dosing schedule that may not be of help to the patient and may even be harmful. Our role should be to assess the patient's symptoms and to create an appropriate treatment plan that can realistically be followed.

Pharmaceutical interventions target the painful inflammation from the joint capsule, ligaments, synovium, and subchondral bone, which are responsible for the noxious nerve stimuli and pain of arthritis. Interestingly, articular cartilage does not contain nerve tissue. The transmission of painful stimuli is mediated by prostaglandin synthesis. NSAIDs decrease the production of prostaglandins by inhibiting cyclooxygenase (COX), an enzyme that catalyses the first two steps in the production of prostaglandins from arachidonic acid. Prostaglandins are also involved in the maintenance and protection of gastric mucosa, and it is the disruption of this role that can potentiate NSAID-associated gastrointestinal bleeding.

While NSAIDs remain a mainstay of treatment for management of arthritis related pain, the incidence of NSAID-associated gastrointestinal bleed complications has created a significant public health burden, where an estimated 33% of the money spent to treat arthritis each year is spent on treatment of NSAID-related gastrointestinal disorders.1 This recognized complication rate has created a tremendous need for the development of NSAIDs that are less harmful to the gastrointestinal tract. COX has more than one form; COX-I has a role in the physiologic maintenance of all tissues, including gastric mucosa, while COX-II is the inducible form of the enzyme involved in the conversion of arachidonic acid to prostaglandins. COX-II-specific NSAIDs or COX-II inhibitors were developed to decrease prostaglandin production with less effect on the COX-

I homeostasis role. COX-II inhibitors have been shown to have a lower rate of gastrointestinal complications at a rate of 0.2% of patients per year of use versus 1.7% of patients per year of use of traditional NSAIDs.

COX-II inhibitors as a class of drug include several different proprietary formulae, one of which is sulfonamides or celecoxib (Celebrex). As sulfur-containing compounds, there had been concerns that people with "sulfa allergies" would also have a hypersensitivity reaction to these sulfonamides. However, sulfonamide antimicrobials as a derivative of sulfanilamides are arylamines, while celecoxib is a nonarylamine as is hydro-chlorothiazide and DiaBeta (glyburide). A meta-analysis of the North American trials of nonarylamine sulfanilamide COX-

II inhibitors showed no statistical increase in hypersensitivity reactions in sulfa-allergic patients treated with celecoxib compared to placebo. There may be, however, a cross-reactivity in patients with a confirmed allergy to nonarylamine sulfanilamide compounds such as hydrochlorothiazide and celecoxib, and thus prescribing physicians need to proceed with appropriate caution.1

Recently, concerns regarding the possibility of increased cardiovascular events such as myocardial infarction and stroke in patients taking COX-II inhibitors prompted a voluntary removal of rofecoxib (Vioxx) from the market (Merck and Co. news release, "Merck Announces Voluntary Worldwide Withdrawal of Vioxx," September 30, 2004; available at:, and the U.S. Food and Drug Administration requested a withdrawal of valdecoxib (Bextra) from the market ("FDA Announces Series of Changes to the Class of Marketed Nonsteroidal Anti-inflammatory Drugs [NSAIDs]," April 7, 2005) and a change in the labeling of all NSAIDs (other than aspirin) to reflect the possibility of cardiovascular and gastrointestinal risks. In 1999, researchers had reported that COX-II inhibitors had an inhibitory effect on prostacyclin, which, through its action on the endothelial cells lining blood vessels, maintains thrombosis homeostasis and vascular resistance. With the progression of clinical trials using COX-II inhibitor medications, the possibility of increased occurrence of myocardial and cere-brovascular thrombotic events has been postulated, yet not all COX-II inhibitors appear to have this association, and investigations of the safety of these medications are ongoing. While complete understanding of the clinical safety of all COX-II inhibitor-specific and non-COX-II inhibitor-specific NSAIDs remains to be determined, at present they remain a useful treatment for the inflammation-associated pain of arthritis in the appropriate patient.

Corticosteroid Injections

Corticosteroids inhibit the production of the pain mediator prostaglandin from arachidonic acid. Intra-articular steroid injections aim to deliver a higher dose of corticosteroid directly to the site of inflammation and pain in arthritis than would be achievable with oral or intravenous delivery. In addition, highdose local delivery of corticosteroid decreases the vasodilation and permeability of inflammation and may improve the edema and pain of arthritis. Intra-articular steroid delivery has a lengthy clinical history. Recent meta-analyses reported, from the six studies reviewed, an improvement in the various outcome measures at 2 weeks in 74% of patients treated with steroid injection versus 45% of patients treated with placebo. In the three studies that included results at 16 to 24 weeks after injection, the reported improvement decreased to 33% of patients treated with steroid injection versus 16% of patients who received placebo.6,7

Injectable steroid preparations vary in their solubility, and insoluble steroid esters may have a longer duration. More insoluble steroids are appropriate for intra-articular delivery, while soft-tissue injections should use more soluble steroid preparations (such as Celestone [betamethasone]) to limit soft-tissue atrophy.4 While there is no established dose or delivery frequency for the administration of intra-articular steroid in the arthritis literature, the frequency of steroid injections should not exceed one every 3 months.8


Arthritis involves changes in the joint surface as well as the synovial fluid within the joint. Osteoarthritic joints have a lower than normal concentration of hyaluronic acid, and viscosupple-mentation delivers a preparation of hyaluronic acid within the joint with the goal of restoring a more normal joint fluid viscosity and improving the viscoelastic properties for proper joint mechanics. Viscosupplementation has been used in Europe for several years and received U.S. Food and Drug Administration approval in 1997. Hyaluronic acid preparations derived from rooster combs or those manufactured from bacterial cultures are available. Patients with severe hypersensitivity to poultry products are advised to consider the manufactured preparation. The schedule of injections for viscosupplementation delivery varies by proprietary preparation.

While the effect appears to be transient, viscosupplementa-tion has been shown to restore rheologic homeostasis in the osteoarthritic joint with improved WOMAC pain and function scores by 10% to 15% at 12 months following delivery in 62% of patients.9 Many athletes may have previously received intra-articular steroid injections and thus may be quite open to the concept of a trial of viscosupplementation. It is important, however, that patients understand that viscosupplementation will work gradually, does not contain analgesic agents, and requires a full course of injections to determine its effect.

The U.S. Food and Drug Administration classifies viscosup-plements as a device and not a drug. Medical insurance coverage may reimburse the cost of devices and procedures that are deemed "medically necessary" as treatment for arthritis, according to the labeled uses of the "medical device" as approved by the U.S. Food and Drug Administration. At present, Medicare will provide coverage of hyaluronic acid-based products that are used to treat osteoarthritis of the knee only. Current Medicare policy requires radiographic evidence of the established diagnosis of osteoarthritis and the current approved treatment course will be paid for only if given not more than once every 6 months.

Bracing and Orthotics

Symptomatic knee arthrosis is often associated with nonanatomic joint malalignment, which results in uneven load distribution of the weight-bearing axis through the knee. The malalignment may be a result of a previous cartilage injury with cartilage volume loss (such as a meniscal injury that may have been surgically repaired) or a ligament insufficiency leading to attenuation of the remaining structures and nonanatomic joint loading, or it may be due to progressive bone deformation as part of an arthritic process in addition to a primary joint malalignment such as tibia vara. Whatever the cause of nonanatomic joint loading, the concentration of load-bearing forces through one point rather than anatomic distribution of the forces will lead to degenerative joint disease progression at an increased rate.

The role of orthotics and bracing in the treatment of osteoarthritis is to attempt to alter the joint architecture to better distribute the effective forces of the weight-bearing axis through the entire joint. Orthotics are intended to realign the foot and ankle to create a solid, stable platform for the rest of the body during the stance phase of weight bearing. Functional knee bracing may be helpful in patients with unicompartmental arthrosis and a malalignment that is correctable with a force that is attainable by the brace.10 Typically this may be a custom-molded medial unloader brace for a correctable varus mal-alignment, with isolated medial compartment symptoms. Custom-molded unloader braces can also be made for valgus malalignment and used with success. Important considerations for the use of unloader bracing and orthotics are whether the implement can achieve the desired correction to relieve the symptoms and whether the patient tolerates the application of this corrective force through the contact points with the implement for the desired period of symptomatic benefit. The well-fitted functional brace will not benefit the patient if use of the brace cannot be tolerated.

Discussion of the use of bracing in a protective role for ligaments and menisci is beyond the scope of this chapter, and the reader is directed to the position statement of the American Association of Orthopaedic Surgeons on the use of knee braces for a more complete discussion. This resource also contains recommendations for some common clinical scenarios where knee bracing has been considered.


Arthroscopy and Arthroscopic Débridement

Arthroscopic débridement is commonly considered as an intervention for treatment of symptomatic knee arthrosis in the athletic population. There are several theories as to the possible mechanism of benefit of an arthroscopy to relieve arthritic symptoms. With arthroscopy, the irrigation of the joint may remove particulate debris and dilute and remove inflammatory mediators and degenerative enzymes, and it has been postulated that pain impulses may be interrupted by chloride ions from the irrigation solution. Arthroscopic instruments can also be used for mechanical débridement to create a smoother remaining articular surface with stable borders. With intra-articular instrumentation, it is also possible to remove painful impinging osteophytes, débride degenerative meniscal tears, and remove loose bodies. It may also be that the benefit of arthroscopy is in some way a placebo effect.11

The published results of the benefit of arthroscopy have varied, with no standardization of inclusion and exclusion criteria, and no standardization of the outcome measures or the surgical technique of the intervention. This lack of standardization makes prediction of the success rate of arthroscopic débride-ment for symptomatic knee arthrosis difficult12; however, a nonrigorous meta-analysis indicates that approximately 60% of appropriately selected patients reported improved symptomatology at 3 years postoperatively.4 While many patients report an improvement in their symptoms, arthroscopic débridement does not stop the progression of arthrosis and the benefits predictably decrease with time.

Knee arthroscopy primarily involves the use of an arthro-scopic shaver to mechanically débride tissue and can be used to attempt to create a smooth cartilage surface. Attempts to use radiofrequency probes to débride irregular osteoarthritic cartilage have been successful in creating débrided surfaces that may be smoother than what is achievable with standard arthroscopic shavers. Radiofrequency energy imparts high temperature on the chondrocytes, which are very temperature sensitive, and may lead to chondrocyte cell death.

For treatment of full-thickness lesions, microfracture to promote fibrocartilaginous ingrowth in the area of the lesion has been shown to have good to excellent results for focal lesions.13 Instrumentation such as a microawl is used to penetrate down through the base of the focal lesion, through the subchondral bone, into the vascularized metaphyseal bone. It is postulated that the pluripotent stem cells in the marrow are then released into the area of the focal defect where they form a fibrin clot that can reform into fibrocartilage. Continuous passive range of motion and limited weight bearing for 6 weeks postoperatively may be beneficial to the stability of the fibrocartilage "repair." As primarily type I cartilage, fibrocartilage expectedly has less rigorous wear characteristics than type II hyaline cartilage, and attempts to encourage more extensive fibrocartilaginous ingrowth for advanced degenerative arthrosis have not been shown to be any more successful than arthroscopic débridement alone.14

Cartilage Transplantation

Focal articular cartilage defects are difficult to treat, and the surgical options for this entity have previously been relatively limited. In addition to the previously discussed microfracture technique that attempts to patch an articular defect with type I fibrocartilage, there are emerging technologies focusing on transplanting viable type II articular cartilage into these defects.

"Mosaicplasty" refers to the transfer of full-thickness articular cartilage with its corresponding subchondral bone plug from a non-weight-bearing area of the knee to a corresponding bone plug hole drilled into the base of the full-thickness cartilage lesion. This procedure is technically challenging but its use is increasing. While still considered an advanced surgical principle that is not universally offered, it has shown favorable bone growth and favorable cartilaginous incorporation for focal defects.15

Realignment Osteotomy

Knee arthrosis is frequently associated with malalignment. The load across the knee joint is a function of alignment; changes in the axial alignment of the femur or tibia in either the coronal or sagittal plane will influence the distribution of this load resulting in abnormal stresses on articular cartilage. The goal of realignment osteotomy for treatment of knee pain related to arthrosis is to transfer the effective weight-bearing axis from the arthritic cartilage to the more normal cartilage.

While the definition of "appropriate" postoperative alignment has been studied extensively, there is no clear consensus on the desired correction angle when performing an osteotomy in the younger patient with a cartilage defect.16 In the patient with varus gonarthrosis, we prefer a weight-bearing line that intersects at a point 62% of the tibial width from the edge of the medial plateau to produce a mechanical axis of 3 to 5 degrees.17 Traditionally, varus gonarthrosis was considered the indication for a valgus-producing osteotomy. The indications for realignment osteotomy have grown to include a correction of valgus malalignment, as an adjunct to ligament reconstruction to help protect the repair and restore joint mechanics, or as an unloading procedure in the event of a significant cartilage defect18 (Table 59-1).

The treatment options for an active patient with isolated cartilage lesions are relatively limited, and an osteotomy can be considered as a treatment option to help unload the involved compartment, but there are limitations to the application of this procedure. While a realignment osteotomy through the knee to transfer the load-bearing axis away from the lesion may be a viable treatment, severe degeneration in the opposite tibiofemoral compartment and a gross loss of range of motion will certainly affect the outcome of an osteotomy and may be considered a relative contraindication. A valgus osteotomy should be avoided in those who have previously undergone a

Table 59-1 Indications for Knee Osteotomy

Malalignment Malalignment



and and



arthrosis instability


articular cartilage






Table 59-2 Specific Indications for Individual Osteotomy Techniques

Varus <25deg Varus >25deg Valgus <15deg Valgus >15deg

Increased Tibial Slope

Decreased Tibial Slope

Medial opening HTO


Lateral closing HTO


Medial closing HTO


Lateral opening HTO


External fixation HTO




Anterior closing HTO


Anterior opening HTO


HTO, High tibial osteotomy.

HTO, High tibial osteotomy.

lateral meniscectomy. However, in the very young athlete with early signs of degenerative joint disease, a lateral meniscectomy should be considered only a relative contraindication, and in the case of severe varus alignment, a high tibial osteotomy to correct to a neutral alignment will preserve favorable joint mechanics (Table 59-2). Higher correction angles may require a change in the traditional fixation implants, but the principles remain the same.

Limb alignment is determined by the line extending from the center of the hip to the center of the ankle, that is, the mechanical axis of the limb. This line typically passes immediately medial to the center of the knee, and, by definition, malalign-ment occurs when this line does not lie close to the center of the knee.19 Sagittal plane alignment should also be considered. This involves evaluation of the posterior tibial slope angle on a lateral radiograph. Tibial slope has been defined as the angle between a line perpendicular to the mid-diaphysis of the tibia and the posterior inclination of the tibial plateau. Measurements based on lateral radiographs have shown the tibial slope of the knee to average 10 ± 3 degrees.

Surgical Technique for High Tibial Osteotomy

For the treatment of varus arthrosis, common in athletes, a medial opening, high tibial osteotomy is a very useful tool for correction of alignment in the coronal and sagittal planes. The procedure is carried out through a vertical skin incision, which extends 5 cm distally from the medial joint line and is centered between the anterior tubercle and the posteromedial border of the tibia (Fig. 59-1A). The gracilis and semitendinosus tendons and the superficial medial collateral ligament are preserved and retracted medially to expose the posteromedial border of the proximal tibia (Fig. 59-1B). A guide pin is inserted obliquely along a line proximal to the tibial tubercle starting approximately 4 cm below the medial joint line in the region of the transition between metaphyseal and diaphyseal cortical bone on radiographs and extending to a point 1 cm distal to the lateral joint line.

Figure 59-2 illustrates the opening wedge technique, which is monitored throughout with a mobile, low-dose ionizing radiation fluoroscopy unit. The osteotomy is made below the guide pin using a small oscillating saw to breech the medial, antero-medial, and posteromedial cortices. This is followed by narrow, sharp, thin, flexible osteotomes to a point just 1 cm short of the lateral cortex. Frequent imaging helps prevent violation of the lateral cortex and/or misdirection of the osteotome. The osteotomy is opened gradually to the desired correction angle first with distracting osteotomes to confirm the mobility of the osteotomy and then a calibrated wedge to maintain the appropriate measured distraction. The distracted osteotomy is then fixed with a four-hole Puddu plate secured with two 6.5-mm cancellous screws proximally and two 4.5-mm cortical screws distally. Bone grafting is recommended in all opening wedge osteotomies greater than 7.5mm. Allograft cancellous bone chips and/or tricortical blocks may be used unless there is an expressed desire by the patient for autograft bone. In our practice, osteotomies less than 7.5 mm are rarely grafted.

The pearls and pitfalls of a medial opening wedge osteotomy are presented in Table 59-3. Dissection of the most superior fibers of the patellar tendon insertion on the tibial tubercle improves exposure and protects the patellar tendon when completing the anterior extent of the corticotomy, which must be distal to the patellar tendon insertion. The use of a low-dose ionizing radiation fluoroscope throughout the procedure is critical to ensure all the following: proper guide-pin placement, prevention of lateral cortex violation, avoidance of misdirection of the osteotome, avoidance of intra-articular screw placement, and adequate setting of the bone graft and filling of the defect.

The tip of the fibular head is a helpful reference when aiming the guide pin. The correct obliquity of the osteotomy relies on proper placement of the guide pin. For larger corrections, placement should be more horizontal. Greater obliquity increases the risk of fixation failure but, on the other hand, provides increased depth, which may be appropriate for smaller corrections. The osteotomy should always be carried out parallel to the joint line in the sagittal plane and below the guide pin to help prevent intra-articular fracture. The use of thick, traditional-type osteotomes can apply a greater distraction moment when completing the osteotomy and carries an inherent risk of creating an extra- and/or intra-articular fracture. This is considerably minimized with thin, flexible osteotomes (Fig. 59-3). However, these should be advanced with frequent fluoroscopy checks to avoid misdirection.

To avoid altering the posterior tibial slope, the distraction of the osteotomy anteriorly (at the tibial tubercle) should be approximately one half its distraction posteromedially. This is facilitated by using trapezoidal distraction block Puddu plates rather than the traditional rectangular version. The plate should be positioned as far posterior as possible along the medial cortex

Tibial Tubercle Osteotomy Scar

Figure 59-1 The surgical approach to medial opening wedge high tibial osteotomy. A, The skin incision is centered between the posteromedial border of the tibia and the tibial tubercle and extends distally from the medial joint line. B, The posteromedial border of the tibia is exposed with a blunt retractor placed deep to the superficial medial collateral ligament. The pes anserinus is left intact.

Figure 59-1 The surgical approach to medial opening wedge high tibial osteotomy. A, The skin incision is centered between the posteromedial border of the tibia and the tibial tubercle and extends distally from the medial joint line. B, The posteromedial border of the tibia is exposed with a blunt retractor placed deep to the superficial medial collateral ligament. The pes anserinus is left intact.

Pudu Plate Tibial Osteotomy

Figure 59-2 The use of intraoperative fluoroscopy during medial opening wedge high tibial osteotomy. A, The guide pin is directed toward the tip of the fibular head and from a point 4cm distal to the medial joint line. Placement should be optimal before proceeding. B, The osteotomy is made below the guide pin. C, The osteotomy is gradually opened to the desired width using a calibrated wedge. D, Fixation is achieved with a four-hole Puddu plate. Care is taken to avoid intra-articular or intraosteotomy screw placement. E, Here the defect has been filled with tricortical bone graft.

Figure 59-2 The use of intraoperative fluoroscopy during medial opening wedge high tibial osteotomy. A, The guide pin is directed toward the tip of the fibular head and from a point 4cm distal to the medial joint line. Placement should be optimal before proceeding. B, The osteotomy is made below the guide pin. C, The osteotomy is gradually opened to the desired width using a calibrated wedge. D, Fixation is achieved with a four-hole Puddu plate. Care is taken to avoid intra-articular or intraosteotomy screw placement. E, Here the defect has been filled with tricortical bone graft.

Table 59-3 Pearls and Pitfalls of Corrective Osteotomy



All osteotomies

Adequate exposure

Use of intraoperative fluoroscopy and guide pins Accurate preoperative planning and radiographic evaluation

Violation of opposite cortex Making asymmetrical bone cuts in sagittal plane Opening the osteotomy before the anterior and posterior cortices are osteotomized

High tibial lateral closing

Make osteotomy 2 cm distal to lateral joint line Complete posterior cortical resection in piecemeal fashion with Kerrison rongeurs

Decreasing tibial slope inadvertently

High tibial medial opening

Use oscillating saw to breach cortex only

Make osteotomy below the guidepin

Pay particular attention when securing osteotomy plate

Suboptimal guidepin positioning Neglecting the posterior tibial slope when making the osteotomy

to ensure that the distraction is maximized posteromedially and minimized anteriorly. Careful attention to this detail will help decrease the risk of increasing tibial slope on distraction of the osteotomy. Tension of the medial collateral ligament should be assessed during distraction and lengthening by fenestration of the medial collateral ligament may assist in achieving larger corrections.

Finally, strict attention to detail is necessary to avoid intra-articular or intraosteotomy screw penetration during fixation of the plate and to ensure that the defect is completely obliterated with bone graft or a substitute; frequent rechecks with fluo-roscopy are beneficial.

Figure 59-3 Thin flexible osteotomes used to complete the osteotomy. The osteotomy can then subsequently be opened with distracting osteotomes to the desired correction. This applies less distraction moment on the initial bone cut and thus decreases the chance of intra-articular fracture.

Rehabilitation Following an Osteotomy

The rehabilitation schedule is presented in Table 59-4. Early postoperative knee range-of-motion exercises benefit joint healing and articular cartilage nourishment as well as lower limb neuromuscular function. In addition, the return to normal weight bearing is essential for healthy bone turnover and healing. Postoperative physical therapy programs should focus on these components while respecting the desired outcomes of the realignment procedure, which include union and restoring and maintaining alignment.

Restoring full range of motion is an important factor in the long-term success of the surgical procedure, and we encourage range-of-motion exercises to begin as soon as possible. Full extension should be achieved by postoperative week 6. If progress is behind schedule, active exercises with slight volitional overpressure are recommended.

The weight-bearing progression will depend on the nature of the osteotomy and any other cartilage restoration procedure performed. After an opening wedge osteotomy, patients are restricted to touch weight bearing, equivalent to 25 to 40 pounds, for the first 6 weeks. If any osteocartilaginous procedure has been performed in combination, the opening wedge protocol takes preference. Following closing wedge osteotomy, we allow protected weight bearing for the first 6 weeks. If a cartilage restoration procedure has been performed also, a partial weight-bearing protocol should take preference.

From the 6-week mark, the progression of weight bearing is dependent on the appearance of the radiograph at this stage. It would be anticipated that any closing wedge osteotomy could progress to weight bearing as tolerated at this point, with the use of a cane or a single crutch, if consolidation and progression to union are occurring. An opening wedge osteotomy should progress to partial weight bearing for 3 weeks and then to protected weight bearing for 3 weeks if consolidation is evident on the radiograph, and there is no evidence of hardware loosening or change in position.

Neuromuscular programs aimed at the maintenance of surrounding joint strength and muscle function, as well as pain management modalities, should be employed during the initial postoperative 6 weeks. During weeks 6 to 12, a more functional program can be instituted, while methods to improve muscular endurance can be instituted after postoperative week 12. Gait retraining and returning to a fully functional state should be additional goals throughout the rehabilitation process. More directed therapy to correct additional functional impairments should also take place after week 12.

Figure 59-3 Thin flexible osteotomes used to complete the osteotomy. The osteotomy can then subsequently be opened with distracting osteotomes to the desired correction. This applies less distraction moment on the initial bone cut and thus decreases the chance of intra-articular fracture.

Table 59-4 Postoperative Rehabilitation Guidelines




Passive range of motion using slider board Pedal rocking on bicycle Isometric quadriceps setting


Full-circle pedaling on bicycle, very light resistance

Active range of motion

Side-lying gluteus medius strengthening

Hip abduction/adduction, flexion, and extension with resistance fixed above knee, e.g., pulley or resistance tubing Pool exercises, hip abduction/adduction, flexion, and extension; knee flexion and extension Gait pattern training with crutches focusing on proper heel strike/toe off Pool, deep water running or cycling

Leg press or squat with weight off-loaded to 24-40 pounds (watch range-of-motion restriction associated with any cartilage/meniscus restoration/repair)


Pool, shallow water walking as weight-bearing restrictions allow

As a general guideline, when 60% of body is submerged, 60% of body weight is off-loaded Standing/seated calf raise

Bilateral wobble board balancing as weight-bearing status allows Knee flexion/extension with very light resistance

Upon full weight bearing

Gait training to restore normal gait

Step up and step down to work on alignment and eccentric control Elliptical trainer and bicycle for cardiovascular conditioning

Complications of an Osteotomy

The list of possible intraoperative, early postoperative, and late postoperative complications following any realignment procedure around the knee is exhaustive. The early complications of upper tibial osteotomy are those of any surgical operation on the lower extremity including compartment syndrome, infection, neurovascular injury, deep vein thrombosis, and pulmonary embolus. These, as well as some that require specific mention, should be included in any list of complications of osteotomy around the knee, namely, delayed or nonunion.

The frequency of thromboembolic disease is lower following osteotomy than total knee arthroplasty, and the proper method of prophylaxis is controversial. We currently do not use chemical prophylaxis in patients undergoing knee osteotomy. Mobilization is encouraged on postoperative day 1. Patients with specific risk factors for deep venous thromboembolism or pulmonary embolism are anticoagulated with low molecular weight heparin given subcutaneously for the perioperative period and undergo lower limb venous studies prior to discharge from the hospital. Patients with a history of deep vein thromboembolism or pulmonary embolism are anticoagulated for 6 weeks with Coumadin.

The avoidance of intraoperative complications of any osteotomy is especially important with osteotomy around the knee. Intra-articular fracture, intra-articular screw placement, and violation of the opposite cortex with resultant instability of the osteotomy are all avoidable and will all have a significant outcome on the osteotomy. Prevention of these complications by continuous fluoroscopy use is the best form of management; otherwise, early recognition and immediate management are suggested.

Intra-articular fracture should be assessed intraoperatively with fluoroscopy and a decision made whether interfragmentary screw stabilization is required. A fracture detected postopera-tively may require internal fixation with or without revision of the osteotomy or a simple modification of the postoperative rehabilitation protocol with immobilization and non-weight bearing for a period and radiographic monitoring of the fracture. Violation of the opposite cortex in an opening wedge osteotomy of the tibia usually does not require any additional treatment.

Under- and overcorrection is a significant concern in tibial realignment osteotomies. Numerous authors have discussed overcorrection into valgus.20,21 Because, cosmetically, producing a valgus deformity is less well tolerated than producing varus alignment, it is best to err on the side of "avoiding excessive valgus." Critical assessment of the alignment both intraopera-tively and in the early postoperative period should take place, and if "overcorrection" or "excessive" varus or valgus correction has occurred, the osteotomy should be revised, as the primary surgical goals have not been attained.

Realignment osteotomy about the knee is a very useful tool for the treatment of arthrosis with the benefits of a capacity for correction in multiple planes, the capacity to restore anatomy to a more favorable alignment, and the benefit of maintaining the integrity of the patient's own joint with the goal of a high level of function (Fig. 59-4).

Arthroplasty in the Athlete

Joint arthroplasty has provided a tremendous tool for the relief of arthritis sufferers and is one of the most cost-effective medical interventions available to restore functional lives.22 The goal of arthroplasty is to alleviate pain first and to maintain function. Improvement in function is not the specific intended goal. This is especially true of total knee arthroplasty. With respect to active athletes who are severely affected by arthritis pain, it is most important that this type of patient understand that a unicondylar or a total knee arthroplasty is intended for pain relief, and a modification of activities to avoid high-impact and loading activities would be advised to prolong the life span of the implant.

Because the technical challenges of early revision surgery and the morbidity associated with early implant failure are so sig

Figure 59-4 A 31-year-old man with isolated medial compartment articular cartilage disease, varus malalignment, and intact anterior and posterior cruciate ligaments. A, The anteroposterior view shows the weight-bearing line (WBL) through the center of the medial compartment and the predicted correction angle. B, Postoperatively, the mechanical axis of the limb is normalized.

Figure 59-4 A 31-year-old man with isolated medial compartment articular cartilage disease, varus malalignment, and intact anterior and posterior cruciate ligaments. A, The anteroposterior view shows the weight-bearing line (WBL) through the center of the medial compartment and the predicted correction angle. B, Postoperatively, the mechanical axis of the limb is normalized.

nificant (autolysis, bone loss, nerve and blood vessel compromise), active and athletic patients who are considering knee arthroplasty are best served by a full understanding of the lim itations of the procedure. In some cases, the procedure must be delayed until the patient reaches the point at which his or her activity level is appropriate for the limitations of the implant.


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Overuse Injuries

Stephen FF Brockmeier and John J. Klimkiewicz

In This Chapter

Patellar tendinosis Quadriceps tendinosis Iliotibial band friction syndrome Popliteus tendonitis Semimembranosus tendonitis Prepatellar bursitis Pes anserine bursitis Infrapatellar fat pad syndrome

The etiology of overuse injuries can often be attributed to both intrinsic and extrinsic factors. Intrinsic causes can include limb malalignment, leg length discrepancy, muscle/tendon tightness or imbalance, foot abnormalities, and concomitant pathology or injuries about the knee such as meniscal or ligamentous injuries. Extrinsic factors are thought to play a large role in the development of many overuse injuries. The concept of Leadbetter's "Rule of Toos" in which athletes train too hard, too often, and return to sport too soon and too much after an injury often applies.1 A recent change in the rate, duration, or intensity of activity frequently precedes the development of one of these disorders. Specific activities and training errors are often associated with specific conditions.

Overuse injuries are chronic syndromes

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