Patellar and Quadriceps Tendinopathies and Ruptures
The patellofemoral articulation encounters one of the highest joint reaction forces in the body. Competent patellar and quadriceps tendons are essential for proper function, and these structures contribute to the extensor mechanism. It is important to have a firm understanding of the anatomy and biomechanics of this complex to provide a rationale for sound treatment.
Disease of the extensor mechanism tendons may manifest as tendinosis, tendinitis, or rupture. An orthopaedist must have a thorough understanding of the pathophysiology of these structures because a correct and prompt diagnosis influences treatment options and resultant rates of success. Tendinopathies can occur in the presence of systemic diseases and endocrinopathy and in conjunction with certain medications and hormonal supplementation. As a result, it is important to not only understand the classic presentation of problems affecting these structures but also to maintain a wide diagnostic differential when evaluating these problems.
Advances in imaging continue to assist in the evaluation and treatment of disease. An understanding of the techniques and anticipated radiographic features of these methods is essential. In combination with clinical findings, these studies may not only confirm pathology but can offer options for therapeutic measures and surgical planning.
Extensor mechanism problems affect both adults and children. Certain injuries are more likely to be found in particular age groups and populations. Treatment options in each of these groups depend on age, activity, and diagnosis. Operative and nonoperative treatment plans can be tailored based on these characteristics, and an effective physician must understand the options and indications for both.
Athletes with extensor mechanism injuries often ask, “When can I return to play?” Thus it is important for each sports medicine physician to have an activity-specific understanding of the stresses and effects on healing related to exercise.
Relevant Anatomy and Biomechanics
Anterior knee pain is one of the most common clinical complaints in all age groups and can affect as many as 25% of athletes. The extensor mechanism is composed of the quadriceps, patella, and patellar tendon (or patellar ligament) because of its function of connecting bone to bone. To minimize confusion, the structure are uniformly referred to as the patellar tendon throughout this chapter. Pathology and disability can be derived from any of these structures, as well as the corresponding articular surfaces on the underlying patella and the complementary trochlear groove.
The patella has static stabilizers, including the quadriceps and patellar tendon; osseous anatomy created by the congruence of the patella within the trochlear groove; medial and lateral retinacular structures; and associated ligaments, including the medial patellofemoral (MPFL) and patellomeniscal ligaments. Desio et al. have elaborately described the MPFL and its influence on restraint from lateral subluxation at 20 degrees of knee flexion.
The patella is also surrounded by dynamic stabilizers, which work together to yield balance and function. These structures include the rectus femoris, vastus lateralis, vastus intermedius, and vastus medialis, including the vastus medialis obliquus. Each of these muscles is innervated by the femoral nerve, which is composed of the posterior divisions of the second, third, and fourth lumbar spinal nerves. The direct head of the rectus femoris originates at the anterior inferior iliac spine, whereas the reflected head begins superior to the acetabulum. It therefore crosses both the hip and knee and can serve to flex the thigh and extend the lower leg. The remaining three muscles of the quadriceps femoris include the vastus lateralis, which originates from the lateral lip of the linea aspera and lateral surface of the greater trochanter; the vastus intermedius, which originates from the anterior aspect of the femoral shaft; and the vastus medialis, which originates from the medial lip of the linea aspera and the distal aspect of the intertrochanteric line.
The quadriceps tendon is a confluence of these individual insertions and attaches to the proximal pole of the patella, enveloping it on three sides as it advances from proximal to distal. The tendon has an ample vascular supply but contains an avascular portion in the deep aspect of the tendon that measures approximately 1.5 × 3 cm. Arteries from the descending branches of the lateral femoral circumflex, the descending geniculate, and the medial and lateral superior geniculate arteries provide the tendon with nourishment.
The patellar tendon is a continuation of the quadriceps tendon beyond the distal pole of the patella and inserts on the tibial tuberosity. The blood supply of the patellar tendon is not as rich as that of the quadriceps. Nonetheless, it is supplied by vessels from the infrapatellar fat pad, as well as the inferior medial and lateral geniculate arteries ( Fig. 106-1 ).
Biomechanics
The knee consists of three compartments: the medial and lateral femorotibial and the patellofemoral articulations or joints. The patella increases the extensor moment arm by transmitting the longitudinal contractile force at a greater distance from the knee axis of rotation ( Fig. 106-2 ). The efficiency of the extensor mechanism increases 1.5 times through this advantage. Patellofemoral contact initiates at 10 degrees of flexion and shifts distally to proximally with increasing degrees of flexion ( Fig. 106-3 ). Weakness of the quadriceps musculature can lead to increased stress and strain throughout the tendons. Ascending stairs can increase forces within the patellar tendon by 3.2 times body weight, and the greatest forces on the structure occur at about 60 degrees of knee flexion.
Huberti and colleagues described a concept referred to as the extensor mechanism force ratio . This ratio is the fraction of the force found in the patellar tendon (distal) divided by the quadriceps tendon (proximal) and is greater than 1.0 when the knee is in less than 45 degrees of flexion. With smaller degrees of flexion, the distal pole of the patella is articulating with the trochlear groove. At this point, the quadriceps tendon has a mechanical advantage. Conversely, with knee flexion angles greater than 45 degrees, the patellar articulation with the trochlea is more proximal and allows for the patellar tendon to have the primary mechanical advantage. This concept explains the position of knee flexion related to the likelihood of tendon failure. At a position of knee flexion less than 45 degrees, the quadriceps tendon is more likely to be injured. On the other hand, with the extremity in greater than 45 degrees of flexion, the patellar tendon is at higher risk for tensile failure.
Tendon Structure
Tendon is a complex material consisting of collagen fibrils embedded in a matrix of proteoglycans. Both quadriceps and patellar tendons are mainly composed of water in the extracellular matrix. However, the predominant cell type found within tendons is the fibroblast. This cell is present in the spaces between the parallel collagen bundles ( Fig. 106-4 ).
Tendon is composed primarily of type I collagen and contains a high concentration of glycine, proline, and hydroxyproline. The secondary structure of collagen is related to the arrangement of each chain in a left-handed configuration. The tertiary structure refers to three collagen chains combined into a collagen molecule. Likewise, the quaternary structure is related to the organization of collagen molecules into a stable, low-energy biologic unit based on the association of its amino acids with adjacent molecules. This quarter-stagger arrangement of adjacent collagen molecules results in oppositely charged amino acids being aligned. A great deal of energy is required to separate these molecules, accounting for the overall strength of this structure ( Fig. 106-5 ).
Tendon possesses one of the highest tensile strengths of any soft tissue in the human body for two reasons. First, it is composed of collagen, which is one of the strongest fibrous proteins in the body. Second, tendon collagen fibers are arranged parallel to the direction of the tensile force. The elastic modulus of human tendon ranges from 1200 to 1800 megapascals (MPa), the ultimate tensile strength ranges from 50 to 105 MPa, and the ultimate strain ranges from 9% to 35%.
Pathophysiology of Tendon Injury
The specific details of tendon injury continue to be investigated. Tendons can become injured as a result of direct trauma with laceration or contusion or indirect trauma through tensile overload. However, it is generally accepted that healthy tendons do not rupture. In a situation in which there is tensile overload of the extensor mechanism, the forces most often result in a transverse fracture of the patella.
Research into the understanding of tendinopathy continues to advance, but it remains one of the most difficult challenges in sports medicine to manage. Its pathogenesis consists of repetitive chronic overloading, ischemia with reperfusion injury, microtrauma, hypoxia, aging, and hyperthermia. These factors can be correlated with skeletal maturity, anatomic location, vascularity, and magnitude of applied forces.
Most tendons are able to withstand tensile forces larger than those exerted by muscles or sustained by bones. Therefore these types of injuries often result in avulsion fractures or tendon disruption at the musculotendinous junction. Midsubstance tendon ruptures are less commonly seen and often occur within the context of preexisting pathology. Kannus and Jozsa studied specimens obtained from the biopsy of spontaneously ruptured Achilles or biceps tendons in 891 patients. Age- and sex-matched control specimens were obtained for comparison, and no normal structures were seen in spontaneously ruptured tendons. Characteristic histopathologic patterns in the ruptured tendons included hypoxic degenerative tendinopathy, mucoid degeneration, tendolipomatosis, and calcifying tendinopathy, either in isolation or combination. These changes were also found in 34% of the control tendons, which is less often than in pathologic specimens.
Mechanical testing performed on the patellar tendon has shown tensile strains to be less midsubstance than at the origin and insertion sites on the patella and tibial tuberosity. Woo et al. demonstrated that at peak load just prior to tendon failure, the end-region strain at the insertion site is three to four times than that seen in the mid body. Thus healthy tendon rarely fails within its substance, and if this occurs, the physician must consider external factors such as metabolic derangements ( Box 106-1 ).
Hyperparathyroidism
Calcium pyrophosphate deposition
Diabetes mellitus
Steroid-induced tendinopathy
Fluoroquinolone-induced tendinopathy
Osteomalacia
Chronic renal insufficiency
Gout
Uremia
Systemic lupus erythematosus
Rheumatoid arthritis
Metabolic abnormalities have been shown to influence the physiologic status and biomechanical function of tendons. These conditions can be innate, induced, or iatrogenic. Conditions such as diabetes mellitus can compromise the blood supply and limit the reparative ability of a structure after injury. Metabolic conditions such as gout, renal failure, hypothyroidism, and chondrocalcinosis can lead to tendinopathy and ruptures. Also, local and systemic corticosteroid injections have been shown to limit the inflammatory phase of healing. Tendon ruptures have been documented after the administration of these agents.
Other drugs have been associated with tendon disease. Fluoroquinolone antibiotics, such as levofloxacin and ciprofloxacin, have been shown to alter the extracellular matrix in tendons and can influence healing after injury. Ciprofloxacin also induces interleukin-1β–mediated matrix metalloproteinase-3 release. Matrix metalloproteinases are a family of proteolytic enzymes that have the ability to degrade the extracellular matrix network and facilitate tissue remodeling. Fluoroquinolones can also inhibit tenocyte metabolism, reducing cell proliferation and collagen and matrix synthesis. Additionally, investigations have noted decreased biomechanical properties of healing patellar tendon with administration of antiinflammatory drugs compared with acetaminophen and controls.
Cyclic tensile loading of tendons is required to maintain normal tendon health. This repetitive mechanical loading of a tendon leads to a cellular response that can either be adequate, leading to adaptation, or inadequate, leading to transient weakness. This process is referred to as mechanobiology or mechanotransduction and couples tendon stretch with a cellular biologic response. Excessive mechanical stretch stimulates an anabolic response, whereas normal stimuli promote a catabolic response. Continued loading in the face of a weakened tendon can lead to an accumulation of injury, thus inhibiting the healing capacity and resulting in an overuse injury. The adaptive and reparative ability of tendon can be overcome when it is repeatedly strained at 4% to 8% of its original length. This stress may result in microscopic or macroscopic injuries to the collagen fibrils, noncollagenous matrix, and microvasculature, resulting in inflammation, edema, and pain.
Tendon pathology has been defined in terms of tendinitis and tendinosis . Tendinitis refers to the presence of inflammatory cells, which can be noted on histologic evaluation. Early pathologic alterations that occur in the presence of repetitive microtrauma to the patellar tendon include inflammatory cell invasion, resultant tissue edema, and fibrin exudation in the paratenon, which is referred to as paratenonitis . Maffulli and colleagues recommended use of the term tendinopathy as a generic descriptor of these clinical conditions described in Table 106-1 . They believe that the terms tendinosis and tendinitis should be reserved for use after histopathologic examination. Continued microtrauma can overwhelm reparative capabilities, leading to chronic inflammation. This process results in fibrosis and thickening of the paratenon and chronic peritendinitis. The development of tendinosis is thought to result from chronic peritendinitis and is characterized by histopathologic findings of mucoid degeneration, tendolipomatosis, and calcifying tendinopathy, either alone or in combination.
| New | Old | Definition | Histologic Findings | Clinical Signs and Symptoms |
|---|---|---|---|---|
| Paratenonitis | Tenosynovitis Tenovaginitis Peritendinitis | Inflammation of only the paratenon whether or not it is lined by synovium | Inflammatory cells in paratenon or peritendinous areolar tissue | Cardinal inflammatory signs: warmth, swelling, pain, crepitation, local tenderness, and dysfunction |
| Paratenonitis with tendinosis | Tendinitis | Paratenon inflammation associated with intratendinous degeneration | Same as above, with loss of tendon, collagen fiber disorientation, and scattered vascular ingrowth but no prominent intratendinous inflammation | Same as above, often with a palpable tendon nodule, swelling, and inflammatory signs |
| Tendinosis | Tendinitis | Intratendinous degeneration due to atrophy (e.g., aging, microtrauma, or vascular compromise) | Noninflammatory intratendinous collagen degeneration with fiber disorientation, hypocellularity, scattered vascular ingrowth, occasional local necrosis, or calcification | Often a palpable tendon nodule that may be asymptomatic but may also be point tender; swelling of the tendon sheath is absent |
| Tendon strain or tear | Symptomatic overload of the tendon with vascular disruption and inflammatory repair response | Three recognized subgroups: each displays variable histologic characteristics from purely inflammation with acute hemorrhage and tear to inflammation superimposed on preexisting degeneration, to calcification and tendinosis changes in chronic conditions; in the chronic stage, it may be (1) interstitial microinjury, (2) central tendon necrosis, (3) frank partial rupture, or (4) acute complete rupture | Symptoms are inflammatory and proportional to vascular disruption, hematoma, or atrophy-related cell necrosis; symptom duration defines each subgroup:
|
Yuan et al. and Cook et al. presented evidence that the earliest identifiable morphologic changes in tendinosis occur in tenocytes and not collagen fibers. Microscopic evaluation of degenerative tendons demonstrate a paucity of inflammatory cells, tenocyte morphology and density changes, accumulation of glycosaminoglycans, and collagen fiber thinning and disarray with or without neurovascular proliferation.
Apoptosis may also play a significant role in tendinosis. Yuan et al. demonstrated excessive apoptosis in ruptured human rotator cuff specimens. Likewise, Lian et al. performed a similar study on biopsy specimens in patients with patellar tendinopathy diagnosed clinically and confirmed with magnetic resonance image (MRI). They found that the samples with tendinopathy displayed increased cellularity compared with controls and also contained a higher number of apoptotic cells.
Evaluation of Quadriceps and Patellar Tendinosis
History
Isolated quadriceps tendinopathy has not been well described in the contemporary literature and is often mentioned in the context of bilateral involvement due to underlying medical comorbidity. A few reports have been made of sequelae due to calcific tendinitis leading to chronic enthesopathic changes, and in some cases, bilateral tendon rupture. Likewise, as we further detail in this chapter when discussing the treatment of patellar tendon disease, Doppler ultrasound-guided sclerosing agents have also been explored as investigative options for treating bilateral quadriceps tendinopathy.
Most publications describing extensor mechanism pathology focus on the patellar tendon. Patellar tendinosis, or jumper’s knee, results from microtears of the patellar tendon followed by a chronic inflammatory response. It is an injury that follows excessive use and is commonly seen in athletes who participate in sports that involve jumping, kicking, or leaping, such as volleyball and basketball. Thus it is important to obtain a history of athletic activity from each patient.
Zwerver et al. noted that in nonelite athletes the prevalence of jumper’s knee varied between 14.4% and 2.5% for different sports, and males were twice as likely to be affected. They also identified sport-specific loading characteristics, a higher body weight, a taller stature, and younger age as risk factors for the development of patellar tendinitis. Lian et al. studied the prevalence of jumper’s knee among elite athletes and demonstrated the likelihood of developing tendinopathy while participating in various sports. Cyclists had a zero incidence, whereas male basketball and volleyball players demonstrated a prevalence of 32% and 44%, respectively. Players routinely exhibited symptoms lasting longer than 2 years, and affected athletes had significant pain and functional losses. Hägglund et al. recently studied the epidemiology of patellar tendinopathy in elite male soccer players. Between 2001 and 2009, the investigators followed up on 51 European soccer clubs from the Swedish First and European Football Associations Champions leagues; 1.5% of all injuries consisted of patellar tendinopathies, and each season, 2.4% of players were affected. Additionally, the investigators noted no significant differences with regard to prevalence or incidence between play on artificial or natural turf.
Ferretti et al. demonstrated a linear relationship between training volume and the prevalence of tendinopathy among volleyball players. They also demonstrated a higher prevalence of tendinopathy among players who trained on a harder surface. Backman and Danielson performed a 1-year prospective study investigating the correlation between low ankle dorsiflexion range and an increased risk of patellar tendinitis in junior elite basketball players. They postulated that a decrease in ankle motion may predispose players to the development of tendinitis because of higher level compensatory energy absorbed by the patellar tendon. They concluded that low ankle dorsiflexion is a risk factor for the development of tendinitis in basketball players and that 36.5 degrees was found to be the best cutoff in regard to screening for persons at risk.
Symptoms may occur in young adults undergoing a rapid phase in growth. In these cases, a relative discrepancy in tendon length may be found compared with adjacent bony structures. This finding occurs when the tendon does not lengthen as quickly as the bones to which it is attached.
Commonly, patients report discomfort in the distribution of the patellar tendon. Traditionally, pain in persons with tendinopathy has been attributed to inflammation. However, Khan et al. reported that chronically painful Achilles and patellar tendons showed no evidence of inflammation, and many tendons with intratendinous lesions detected on MRI or ultrasound were asymptomatic. Different causes have been proposed to explain the origin of pain in degenerative tendons, including elevated concentrations of glutamate, prostaglandin E 2, and substance P in symptomatic persons.
Physical Examination
A patient may have tenderness over the patellar tendon and signs of inflammation, such as redness, swelling, warmth, and crepitation. Pain is often centered on the distal patellar pole and the proximal part of the patellar tendon. Tenderness to palpation may be present with the knee in extension and absent with the knee in flexion. The patient may have a feeling of “bogginess” centered over the tendon itself and may also have pain with resisted extension and with full passive flexion.
Blazina et al. established a classification for patellar tendinopathy. In stage 1, pain is present only after activity. In stage 2, pain is present at the beginning of activity, disappears after a warm-up, but may reappear with fatigue. In stage 3, pain is constant, both at rest and with activity. In stage 4, the patellar tendon is completely ruptured.
Imaging
Imaging is not routinely necessary for the treatment of patellar or quadriceps tendinosis. However, plain radiographs should be obtained in the initial evaluation of all patients with patellar tendinitis. One should be alert for the presence of traction osteophytes at the distal pole of the patella, tendon calcification, and even decreased bone mineral density at the sites of attachment. Other modalities such as ultrasound and MRI are used when nonoperative treatments have failed to produce anticipated improvements or when planning surgical intervention. Ultrasound evaluations can demonstrate a hypoechoic signal within the fibers of the patellar tendon. Warden et al. performed MRI and grayscale and color Doppler ultrasound on 30 patients with clinically diagnosed patellar tendinopathy and 33 activity-matched asymptomatic control subjects. These investigators concluded that ultrasonography was more accurate than MRI in confirming clinically diagnosed patellar tendinopathy. They added that combining grayscale and color Doppler ultrasound best confirms clinically diagnosed patellar tendinopathy because of the high sensitivity of grayscale and the strong likelihood that symptomatic persons would demonstrate a positive color Doppler test ( Fig. 106-6 ).
Sagittal MRI may demonstrate thickening of the patellar tendon, especially on the posterior, central, or medial aspects ( Fig. 106-7 ). MRI may also demonstrate foci of abnormal signal intensity in the posterior portion of the proximal patellar tendon ( Fig. 106-8 ). Furthermore, absence of abnormality on T2-weighted images can suggest that nonoperative treatments may be more effective.
Treatment Options
Nonoperative
Various recommendations have been suggested in the management of acute and chronic tendon disorders. However, few well-constructed studies have been performed to demonstrate the efficacy of these treatments. Initial management includes activity modification, the initiation of active rest, the use of antiinflammatory medications, and the administration of cryotherapy. Stretching and isometric strengthening of the quadriceps should be started immediately. However, isotonic or isokinetic exercises should only begin once symptoms have improved.
Operative
When nonoperative means have failed to produce improvement in symptoms and imaging studies confirm evidence of intratendinous degenerative changes, operative intervention may be considered. One option is to split the tendon longitudinally and excise the gelatinous material between normal fibers. The remainder of the tendon should be closed with absorbable suture. Roels et al. presented a series of 10 subjects with this technique, and all patients were able to return to sports.
Decision-Making Principles
Bahr et al. performed a randomized controlled trial on surgical treatment versus eccentric training for patellar tendinopathy. Thirty-five patients (40 knees) with grade 3 patellar tendinopathy were randomly assigned to surgical or eccentric strength training. No advantage was demonstrated for operative treatment compared with eccentric exercise. The authors concluded that eccentric training should be initiated for 12 weeks before an open tenotomy is considered.
When persons present with a history and physical examination consistent with patellar tendinitis, the first step is to obtain plain radiographs of the knee. We examine the images carefully for the presence of osteoarthritis, patellar malpositioning, or spur formation. However, the radiographs typically do not change our first step of treatment. We also consider obtaining an MRI of the knee based on the severity and duration of symptoms. These images help us to determine prognosis and likelihood of recovery. Patients with pain and obvious osteophyte formation at the distal pole of the patella are less likely to recover after nonoperative intervention.
After the initiation of physical therapy, a clinical reevaluation at 6 weeks is routine. This appointment is made for patient reassurance and evaluation of compliance with the treatment regimen. Correspondence with the physical therapist assists in making subsequent recommendations. Improvement at 6 weeks is a good indicator of future clinical success, but failure to improve offers no insight. A full 3 months of therapy should be completed as previously outlined to improve symptoms.
If nonoperative interventions fail to produce clinical improvement, a discussion outlining surgical options and the risks and benefits of each procedure may be appropriate. Our preferred treatment of refractory patellar tendinitis is to perform a midline incision centered over the proximal third of the patellar tendon. We essentially perform a patellar tendon harvest with excision of the diseased portion of the tendon as if we were obtaining a tissue for an anterior cruciate ligament (ACL) reconstruction with an autologous bone–patellar tendon–bone (BTB) graft. Based on the location of the tendinopathy, we may or may not include the opposite bone-tendon interface. If disease is proximal only, we focus the harvest at this location and remove only the isolated area involved.
Return to Play
Although most operatively treated injuries end an athlete’s playing season, return to play the following season is common. Far more commonly, given the subacute nature of the problem, athletes are able to complete their current season with appropriate nonoperative recommendations and treatments and contemplate the necessity of surgical intervention during the off-season.
Results
Panni et al. performed a clinical cohort study of 42 patients with patellar tendinopathy. After 6 months of nonoperative treatment as previously outlined, 33 patients (79%) showed symptomatic improvement and were able to return to sports. Kon et al. published a prospective study of 20 male athletes with a mean history of 20.7 months of pain and noted no adverse reactions and improved outcomes with the administration of platelet-rich plasma (PRP) in patients with chronic patellar tendinitis. Likewise, Gosens et al. showed that patients treated with PRP injections for patellar tendinopathy displayed significant improvement, but patients previously treated with other modalities including cortisone, ethoxysclerol, or surgical management did not display significant improvement. Despite these positive results, overall concerns for lack of standardization among study protocols, delivery mechanisms, and separation techniques have generated mixed reviews regarding the efficacy of this treatment. In regard to ACL reconstruction, de Almeida et al. performed a prospective randomized controlled trial of 27 patients, of whom 12 received PRP in the patellar tendon donor site after graft harvest for ACL reconstruction. MRI was used to assess healing 6 months after surgery, and questionnaires were distributed. The authors concluded that PRP had a positive effect on the harvest site based on MRI and reduced pain in the immediate postoperative period.
Additionally, ultrasound-guided sclerosis has also been explored as a nonoperative adjunct. Hoksrud and Bahr investigated the effects of scleroring treatments for patellar tendinitis at a mean of 44 months after the procedure. They concluded that polidocanol was effective for the majority of patients, but one third of their subjects elected to seek additional treatment through arthroscopic surgery during the study period. After this investigation, Hoksrud et al. also performed an additional prospective trial investigating sclerosing treatment on patellar tendon pain and function in 101 patients. They recruited subjects clinically diagnosed with jumper’s knee and neovascularization evident on power Doppler ultrasound in areas corresponding with pain. The subjects received up to a maximum of five ultrasound-guided injections of polidocanol at 4- to 6-week periods. The authors concluded that the treatment resulted in moderate improvement in knee function and pain. Despite this benefit, they noted that the majority of patients continued to have reduced function and significant pain 2 years after treatment.
Clarke et al. have recently investigated the use of the injection of laboratory-amplified tenocyte-like cells for the treatment of patellar tendinopathy. They studied 60 patellar tendons in 46 patients with refractory symptoms and compared the outcomes of injecting collagen-producing cells derived from dermal fibroblasts suspended in plasma with plasma alone. They concluded that injection of the skin-derived tendonlike cells is a safe option for short-term treatment of patellar tendinopathy and demonstrated greater improvement in pain and function compared with plasma alone.
Panni et al. treated nine patients with Blazina stage 3 tendinopathy who had not responded to nonoperative management with surgical removal of degenerative tendon, placement of multiple longitudinal tenotomies, and drilling of the distal pole of the patella. At a mean of 4.8 years, clinical results were good to excellent in all patients.
Shelbourne et al. performed a similar study investigating 16 elite athletes with 22 symptomatic and MRI-documented cases of patellar tendinitis who did not respond to nonoperative management. These patients underwent excision of the necrosis with placement of longitudinal cuts in the tendon to stimulate healing. Subjective improvement was noted in all 16 athletes when they were examined at a mean of 8.1 months. Fourteen of 16 patients (87.5%) were able to return to sport at the same level of intensity.
Arthroscopic patellar tenotomy has been advocated based on a retrospective outcome study (see Fig. 106-9 for a treatment algorithm). Likewise, arthroscopic debridement has also recently been investigated. Pascarella et al. noted that although open surgery is typically recommended for persons who have not responded to nonsurgical management, arthroscopy may be considered a safe and effective option. They studied 73 knees in 64 patients (of whom 27 were professional athletes) who underwent debridement of Hoffa’s body posterior to the patellar tendon, debridement of the abnormal tendon, and excision of the distal pole of the patella. The investigators concluded that arthroscopic surgery provided significant improvement with regard to symptoms and function with maintained benefits for at least 3 years. However, they also noted that some patients were unable to return to sport at their preinjury level, and even if they did, they participated with symptoms.
Complications
Complications can occur, and as with most surgical procedures, include considerations such as infection, stiffness, pain refractory to treatment, and the need for further surgery. Most of these complications can be minimized with meticulous surgical technique and appropriate rehabilitation principles.
Future Considerations
Other investigative modalities include extracorporeal shock-wave therapy, pulsed magnetic fields, direct current applied to tendons, laser therapy, radiofrequency ablation, administration of cytokines and growth factors, gene therapy, bone morphogenic protein–12, gene transfers, and tissue engineering with mesenchymal stem cells.
Recently, PRP therapies have attracted great attention and offer an additional nonsurgical option for treatment of tendinitis. Emerging research focusing on patellar tendinitis has yielded promising outcomes.
Classification of Quadriceps and Patellar Tendon Ruptures
Although ruptures of the patellar and quadriceps tendons occur with relative infrequency, they are serious injuries that require surgical intervention in an effort to restore essential function. Ruptures in patellar tendons are thought to occur less frequently than in quadriceps tendons. They are usually seen in patients younger than 40 years, whereas quadriceps ruptures are more common in patients older than 40 years and are often associated with underlying medical conditions. Galen is credited with first describing a patient with a ruptured extensor mechanism. This injury was sustained as a result of a “wrestling match.” McBurney was the first to publish a single case in 1887. He described a 50-year-old man who was struck by the edge of a heavy box just above the patella. The patient’s ruptured quadriceps tendon was sutured successfully with catgut and silver wire.
Spontaneous ruptures tend to occur in elderly patients with minimal trauma as a result of degenerative changes related to aging. Additionally, preexisting medical problems such as chronic steroid use, rheumatoid arthritis, and diabetes mellitus may act as predisposing factors. Anabolic steroid use is also associated with an increased risk for tendon ruptures. Recently, an association between androstenediol supplements and tendon rupture was presented.
In addition, polymorphisms in genes coding for collagen may be implicated in tendon rupture. Galasso et al. described a case report of a patient with collagen type V alpha 1 polymorphism who incurred spontaneous, simultaneous quadriceps tendon ruptures. Compared with three sex- and age-matched control subjects, histologic analysis of his tissue revealed a significant reduction in type V collagen and an alteration in collagen structure.
Patellar tendon rupture is the third most common cause of disruption of the extensor mechanism of the knee, following patellar fracture and quadriceps tendon rupture. Zernicke et al. estimated that a force of 17.5 times body weight is required to cause rupture in healthy patients, supporting the notion that normal tendons do not tear.
It is important to establish prompt diagnoses for patellar and quadriceps tendon disruptions because of the consequences of neglected injuries. Accentuated scar tissue formation, tendon shortening and retraction, and muscular atrophy are all problems encountered with chronic tears.
No widely accepted classification system exists for patellar tendon or quadriceps tendon ruptures. Clinically, it is helpful to group them based on the location, configuration, and chronicity of rupture ( Table 106-2 ).
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