Abstract
Purpose of Review
This review presents a framework for constructing a differential diagnosis for chronic anterior knee pain associated with overuse other than patellofemoral pain. Traumatic, systemic, and pediatric injuries will not be covered.
Recent Findings
From superficial to deep, the anterior knee can be conceptually organized into four layers: (1) soft tissue, (2) extensor mechanism, (3) intracapsular/extrasynovial, and (4) intra-articular.
Summary
From superficial to deep, diagnoses to consider include bursitis, patellar and quadriceps tendinosis, fat pad impingement, and plica syndromes.
Keywords: Repetitive stress injuries, Anterior knee pain
Introduction
This review presents a framework for constructing a differential diagnosis for chronic anterior knee pain associated with overuse other than patellofemoral pain. Patellofemoral pain is one of the most common causes of anterior knee pain in the outpatient setting [1]. However, excluding other conditions remains an important part of its diagnosis [2]. Traumatic, systemic, and pediatric injuries will not be covered. From superficial to deep, the anterior knee can be organized into four layers: (1) soft tissue, (2) extensor mechanism, (3) intracapsular/extrasynovial, and (4) intra-articular.
Layer 1: Soft Tissue
This layer includes the skin, subcutaneous fat, bursae, and fascia. Bursitis is a common pathology that can affect this layer.
Bursitis
Definition
Bursae are synovial-lined sacs that facilitate movement between soft tissues [3]. Bursitis describes inflammation of the bursa demonstrated by swelling or thickening of the bursal wall. It can be caused by acute trauma, infection, inflammatory arthritides, or chronic microtrauma. Chronic microtrauma is the most common cause [4]. There are four bursae in the anterior knee: the prepatellar, superficial infrapatellar, deep infrapatellar, and pes anserine bursae. The prepatellar bursa is the most commonly affected area and second most common superficial bursitis after olecranon bursitis [4]. Infrapatellar bursitis must be distinguished from fat pad impingement syndrome as described later in this review. Pes anserine bursitis should be distinguished from tibial stress fracture, chondral fracture, meniscal tear, or osteonecrosis.
Clinical Features
History
Bursitis caused by chronic microtrauma is seen in patients with jobs that require kneeling (miners, carpet layers, clergymen, wrestlers, or surfers) or in patients who play sports with repetitive knee use (elite bicyclists). Other risk factors include thin skin associated with chronic glucocorticoid therapy or old age.
Physical
In chronic bursitis, the bursal fluid accumulates over time leading to more prominent features of swelling and bursal wall thickening compared to pain. Swelling and pain of the bursa may decrease knee range of motion. Warmth over the bursal site is a predictor of infection. Smith found that a temperature differential of greater than 2.2 °C compared to the contralateral side was predictive of septic bursitis with a sensitivity of 100% and specificity of 94% [5].
Diagnosis
The diagnosis of bursitis is based on history and physical exam. Differential diagnoses to consider include joint effusions, cellulitis, and Morel-Lavallee lesions.
Radiography is indicated if there is a history of trauma with concern for fracture or other bony abnormality. Bursae are not radio-opaque and are not readily visible. Ultrasound (US) can be helpful if the bursal swelling is obscured by swelling due to joint effusion or cellulitis. Color doppler can demonstrate hyperemia associated with inflammation.
To rule out infection, labs including blood cell count with differential, blood cultures, C-reactive protein, and erythrocyte sedimentation rate should be collected. Eighty percent of septic prepatellar bursitis cases are due to Staphylococcus aureus [6].
Bursal fluid aspiration is indicated if there is concern for infection or crystal-induced arthropathy. Aspiration should be performed under sterile conditions with a large-bore (18- to 22-gauge) needle with ultrasound guidance as needed. Aspirate should be sent for blood cell count, gram stain, culture, glucose measurement, and crystal analysis. If the bursitis is aseptic and non-inflammatory, aspiration is avoided due to risk of iatrogenic septic bursitis.
Treatment
Bursitis due to chronic microtrauma usually resolves slowly within three weeks to three months [7]. Treatment consists of supportive care including relief of acute symptoms with anti-inflammatory medications, maintenance of knee range of motion, avoidance of exacerbating activities, activity modification with appropriate padding, and treatment of adjacent or ongoing pathology (infections, crystal-induced arthropathy).
Intrabursal corticosteroid injections can provide pain relief and diagnostic clarity. However, in superficial locations, there are theoretical risks of skin atrophy, depigmentation, and iatrogenic infection.
If symptoms remain persistent despite conservative care, bursectomy can be pursued. Compared to open procedures, endoscopic bursectomy is associated with lower complication rates in septic bursitis [8].
Layer 2: Extensor Mechanism
The knee extensor mechanism is comprised of the quadriceps tendon, patella, patellar tendon, and tibial tuberosity. Repetitive stress injuries to these structures are commonly referred to as “jumper’s knee” due to their prevalence in jumping sports.
Patellar Tendinosis
Definition
Tendinopathy develops due to excessive mechanical loading that causes injury and disrepair of the tendon [9]. Patellar tendinosis is typically seen in high-impact jumping sports. Its prevalence is 45% in professional volleyball players and 32% in professional basketball players compared to 2.4% of professional soccer players [10]. Risk factors include weight, body mass index (BMI), waist-to-hip ratio leg length difference, arch height of the foot, quadriceps and hamstring flexibility, and vertical jump performance [11].
Clinical Features
History
Patients present with activity-related pain localized to the distal pole of the patella. Pain initially starts after physical activity but can progress as described by the Blazina classification [12]:
Stage I: Pain during sports
Stage II: Pain during the beginning of sports that disappears after warming up and reappears with fatigue
Stage III: Constant pain during activity and at rest
Stage IV: Patellar tendon rupture
The Victorian Institute of Sport Assessment-Patella questionnaire has also been used to track rehabilitation progress [13].
Physical
Patients have tenderness to palpation at the distal pole of the patella during knee extension that decreases with knee flexion. Special tests include the decline squat test in which the patients perform a single leg squat to 30 degrees of knee flexion with the other knee extended. A positive test is the reproduction of the patient’s symptoms. Other tests include assessment of weak or tight quadriceps (Ely’s test) or hamstrings (passive straight leg raise) [10].
Diagnosis
Patellar tendinopathy is primarily diagnosed by history and physical exam due to discrepancy in imaging abnormalities and clinical presentation [14]. However, Cook demonstrated that the relative risk of future development of symptoms was 4.2 times greater in subjects with abnormal findings on ultrasonography than in control subjects with normal findings [15]. US has been shown to have higher accuracy than magnetic resonance imaging (MRI) (83% versus 70%) [16]. Golman demonstrated that patellar tendon thickness of > 8.8 mm was strongly correlated with a tear of the tendon and patellar tendon thickness > 11.5 mm was less likely to improve with non-operative management.
At US, the patellar tendon has been shown to display sonographic changes including neovascularization, focal areas of hypoechogenicity, and tendon thickening. All of these findings have been associated with pain. Athletes without structural changes or neovascularization appear unlikely to develop tendon pain over the course of several years of ongoing play. Focal hypoechogenicity appears to be one of the stronger risk factors for the development of patellar tendon pain and merits consideration when found in an asymptomatic athlete. In contrast, tendon thickening may represent a compensatory state in the setting of repetitive tendon loading and stress.
Treatment
Initial management consists of conservative treatments for six months [17•].
Conservative treatment includes activity modification and the non-surgical treatments discussed below.
There is strong evidence that eccentric squat therapy can provide symptom improvement for up to 12 weeks with a decrease in the rate of improvement at 6 months [17•]. A recent review demonstrated that isometric exercises may be more effective during competitive seasons for short-term pain relief, while heavy slow resistance training or eccentric exercises may be more suitable for long-term pain reduction and improvement in knee function [18].
Extracorporeal Shock Wave Therapy (ESWT) has been proposed to stimulate healing and neovascularization, suppress nociceptors, and hyperstimulate sensory receptors blocking pain via the gate-control mechanism. The evidence remains unclear as there are no guidelines pertaining to energy levels, numbers of treatment sessions, and numbers of impulses. Recent evidence showed that there exists associations between tendon repair and increases in growth factors in patients receiving ESWT, and these growth factors are assumed to be responsible for the success of treatment [19].
Platelet-rich plasma (PRP) is thought to enhance tissue repair because of its high concentration of growth factors. The evidence for PRP continues to evolve as standardized protocols are developed. A recent systematic review demonstrated that leukocyte-rich PRP had the greatest functional improvement and pain reduction compared to other conservative treatments for chronic tendinopathy [19]. Dragoo demonstrated that a therapeutic regimen of standardized eccentric exercise and ultrasound-guided leukocyte-rich PRP injection with dry needling accelerated the recovery from patellar tendinopathy compared to dry needling alone but the apparent benefit of PRP dissipated after 26 weeks [20]. A randomized controlled trial by Scott demonstrated no difference in pain or function between leukocyte-rich PRP, leukocyte-poor PRP, or saline controls [21].
Dry needling involves inserting needles into the affected tendon and is thought to disrupt degeneration and promote regeneration. A recent review of 3 systematic reviews, 7 randomized controlled trials, and 6 cohort studies supports the efficacy of dry needling for tendinopathy treatment [22]. It is minimally invasive, low risk, and inexpensive.
With the advancement of musculoskeletal ultrasound, novel percutaneous procedures have been developed for the treatment of tendinopathy by using mechanical intervention to stimulant regeneration including percutaneous needle tenotomy, percutaneous ultrasonic tenotomy, high-volume injection, and percutaneous needle scraping [23–25]. Other treatments in use with developing evidence for patellar tendinopathy include sclerosing agents, aprotinin, autologous blood injection (ABI), and hyaluronic acid. A recent systematic review found that isometric and isotonic exercises, patellar strapping, and taping provided significant short-term pain reduction, while eccentric exercise, dry needling, PRP, and ABI provided longer term pain relief and functional improvement [26].
Surgical management consists of tenotomy and debridement. There is unclear evidence supporting the use of surgery for unremitting symptoms. A recent Cochrane review demonstrated that open surgery offered little benefit at 12 months compared with eccentric exercise, while arthroscopic surgery offered reduction in pain and improvement compared to sclerosing injections at 12 months [27]. Comparable results of open and arthroscopic surgery have been described. The mean time to return to sports was 3.9 months for arthroscopic treatment and 8.3 months for open treatment. The average rate of return to sporting activities was 82.3% after arthroscopic surgery and 78.4% after open surgery [28]. Although no current guidelines exist, the arthroscopic approach is preferred due to its comparable results and faster return to sport than open surgery.
Quadriceps Tendinosis
Definition/Etiology
Quadriceps tendinosis is less common than patellar tendinosis (20–25% compared to 65–70% of cases) and is also seen in athletes involved in jumping sports [29•]. Recent studies demonstrate that quadriceps tendinopathy also exists in non-athlete patients and is associated with obesity, overall heavier weights, and increased height [30•]. Compared to the linear patellar tendon, the quadriceps tendon is less stiff and more complex as it connects tissues of different stiffness (bone to muscle) versus the patellar tendon, which connects two structures of similar stiffness (bone to bone). Where materials of different stiffness intersect, stress can be concentrated at their interface [31].
Clinical Features
History
Patients with quadriceps tendinosis present with pain at the superior border of the patella particularly in deep flexion. The Blazina classification system also applies to quadriceps tendinopathy.
Physical
On exam, patients present similarly to patellar tendinosis patients except for localized tenderness at the superior border of the patella.
Diagnosis
The diagnosis of quadriceps tendinopathy is also primarily clinical because imaging findings do not clearly correlate with symptoms. Radiographs findings include patellar pole elongation from osteophyte formation and tendon calcifications. MRI findings include thickened heterogeneous tendon with altered echotexture and increased signal intensity. US findings include increased hypoechoic areas and increased neovascularization.
Treatment
Treatment is similar to patellar tendinopathy with the exception that the quadriceps tendon is preferentially loaded in deep flexion, which should guide physical therapy programs [32].
Layer 3: Intracapsular/Extrasynovial
This layer includes the fat pad.
Fat Pad Impingement Syndromes
Definition
The fat pads of the knee are highly innervated and vascularized adipose and fibrous tissue structures that improve articular congruity and provide cushioning for the articular surfaces [33]. There are three fat pads in the anterior knee joint. The intracapsular infrapatellar fat pad, also known as the Hoffa fat pad, is the largest and most commonly injured. The two smaller fat pads located superiorly are the suprapatellar and prepatellar fat pads. Due to its similar location, differentiating Hoffa fat pad disease from patellar tendinopathy is difficult. Brukner found that 78% of college athletes diagnosed with patellar tendinopathy had an increased uptake in the fat pad on T2-weighted MRI [34]. Injury to the fat pad occurs due to bleeding or inflammation due to overuse or impingement related to abnormal patellar tracking. Hoffa’s disease affects middle-aged adults and is more common in females. Possible risk factors include knee laxity, dysplasia of the patellofemoral mechanism, genu recurvatum, participation in jumping sports, and iatrogenic (trauma to fat pad during surgical procedures) [35].
Clinical Features [36•]
History
Patients present with burning or aching anterior knee deep to and on either side of patellar tendon near the inferior pole of the patella. The pain is elicited with full or dynamic extension and may be associated with a grinding sensation. Patients have relief while standing with hyperextended knees.
Physical
To identify fat pad impingement, clinicians can perform the Hoffa test. Firm pressure applied with the thumb inferior to patella with knee in 90 degrees of flexion then fully extended. A positive test demonstrated increased pain during the last 10 degrees of extension. Repeat on both medial and lateral sides of the patella. Often, it is difficult to distinguish between infrapatellar fat pad irritation and patellar tendon pathology due to their location. However, patellar tendinopathy occurs more prominently with loading, particularly eccentric quadriceps contraction.
Diagnosis
Imaging studies can help guide the diagnosis. The most effective modality is MRI that demonstrates edema, fibrosis, calcifications, or bleeding. Radiography and computed tomography are used for detecting osteochondral metaplasia in severe cases.
Treatment
Non-operative treatments include activity modification, topical or oral analgesics and non-steroidal anti-inflammatory drugs (NSAIDs), and physical therapy and taping to offload the fat pad. Fat pads can also be injected with corticosteroid in the acute stage to alleviate pain and limit fibrous remodeling.
Operative treatments include fat pad excision, debridement of hypertrophic fibrosis, and anterior interval release.
There is evolving evidence that the infrapatellar fat pad may play a role in osteoarthritis pathology and pain mechanisms [37].
Layer 4: Intra-articular/Bony
This layer includes the plica and synovium.
Plica Syndromes
Definition
Plicae are folds of synovial tissue due to incomplete resorption of embryonic septa that separate the knee joint into medial, lateral, and suprapatellar compartments [33]. Anatomic studies indicate that 90% of adults have one or more plicae in their knee joints. The vast majority of plicae are incidental and asymptomatic. There are four possible plicae: suprapatellar, infrapatellar, medial, and lateral. Patients commonly have more than one plica [38]. Medial plicae are the most common type of plicae and are most often symptomatic. Plica become pathological when they become inflamed associated with trauma, overuse, adolescent growth spurt, poor quadriceps tone, muscle imbalance around the knee, patellar maltracking, hematoma, diabetes, and inflammatory arthropathy [39•].
Clinical Features
History
Patients with plica syndrome experience anterior knee pain localized to the affected plica associated with snapping, clicking, catching, clunking, grinding, or popping inside the knee during flexion and extension. Pain can be brought on by repetitive knee flexion or extension or prolonged knee flexion. Patients may have a history of a recent increase in activity level or twisting injury with subsequent development of an effusion.
Physical
On physical exam, the plica is typically tender to palpation with the knee extended and relaxed. The knee joint may be mildly swollen and stiff. Plica syndromes are often missed because they are difficult to distinguish from meniscal tears, articular cartilage injuries or osteochondritic lesions.
Two physical exam maneuvers can suggest plica syndrome: the Stutter test and the Hughston test. Both tests must be positive to support the diagnosis of plica. The Stutter test is performed with the patient sitting upright with knees at 90 degrees of flexion with feet dangling. The examiner places his or her index and middle fingers on the center of the patella of the affected leg, while the patient then extends their affected knee. Feeling a stutter of the patella is a positive test. In the Hughston test, the patient lies supine with the knees extended. The examiner stands on the side of the affected knee with one hand around the plantar aspect of the patient’s heel and the other palm covering the patient’s patella. The examiner then pushes the patella medially and internally rotates the tibia while taking the patient’s knee through flexion and extension. The test is positive if the patient’s pain is reproduced or the practitioner appreciates popping during the range of motion.
Diagnosis
Plica syndrome is diagnosed clinically, but imaging can help identify predisposing causes, rule out other etiologies, and assist in surgical planning. Weight-bearing anteroposterior, lateral, and skyline radiographs should be obtained to rule out bony intra-articular pathology.
Arthrography, US, and MRI can demonstrate the presence of a plica but are unreliable in predicting pathology. MR arthrography can improve plica syndrome diagnosis [40]. A literature review revealed multiple studies which looked at 492 knees and compared the sensitivity and specificity of physical exam compared to US and MRI [41]. The results were that physical exam had a 90% sensitivity and 89% specificity, US had 90% sensitivity and 83% specificity, and MRI had 77% sensitivity and 58% specificity. The gold standard for diagnosis is arthroscopy.
Treatment
Medial plicae can be classified by the Sakakibara arthroscopic classification:
Type A: Elevation in the synovial wall
Type B: Appear shelf-like, but not covering the anterior surface of the medial femoral condyle
Type C: Large, shelf-like appearance and covering the anterior surface of the medial femoral condyle
Type D: Fenestrated plica with a central defect
The Sakakibara classification system helps guide treatment. Types A and B have a low likelihood to cause pain and respond better to conservative therapies. Types C and D may impinge on the medial condyle due to their larger size.
Physical therapy programs involve strengthening the joint capsule musculature, hamstrings, and quadriceps and correct patellar maltracking. Taping around the patella has been shown on MRI to have statistically improved tracking [42]. Topical and oral NSAIDs and ice can reduce inflammation. Patients should also avoid activities that exacerbate pain. At least 3 months of conservative treatment is recommended before advancing to more aggressive therapies. One study demonstrated that 49 of 55 patients treated conservatively returned to their prior baseline without a return of symptoms. The remaining 6 patients were also able to return to their prior baseline, but they reported an occasional return of symptoms, which were tolerable [43].
Intraplical corticosteroid injection is beneficial for pain relief early in the disease process. Research of 31 patients with medial plica syndrome treated with intraplical steroid injection found that 73% had a full return to activity with complete pain relief [44].
Resection via arthroscopy is a favorable option for medial plicae that do not respond to conservative treatment or if cartilage damage is suspected, such as in type C and D lesions, even if conservative measures have not been completed for 3 months. Complete resection is paramount since synovial tissue is highly sensitive and has a propensity to fibrose causing persistent symptoms.
Once appropriately treated, there is a favorable prognosis for plica syndrome. One study of 969 patients found that at a median follow-up of 27.5 months, 10% had not responded to treatment, whereas 26% improved, and 64% were symptom-free [45].
Summary
In summary, this article has reviewed a four-layer framework for constructing a differential diagnosis for chronic anterior knee pain associated with overuse other than patellofemoral pain. From superficial to deep, diagnoses to consider include bursitis, patellar and quadriceps tendinosis, fat pad impingement, and plica syndromes.
Declarations
Human and Animal Rights and Informed Consent
This article does not contain any studies with human or animal subjects performed by any of the authors.
Conflict of Interest
Anne Kuwabara and Michael Fredericson declare that they have no conflict of interest.
Footnotes
This article is part of the Topical Collection on Non-Operative Management of Anterior Knee Pain
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Contributor Information
Anne Kuwabara, Email: amk1@stanford.edu.
Michael Fredericson, Email: mfred2@stanford.edu.
References
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