Anterior knee pain

Introduction 

Anterior knee pain is a well recognized and common problem in orthopaedic practice, affecting young patients, (mostly adolescent) and old. Besides pain arising from the patellofemoral joint, numerous other disorders can cause anterior knee pain (Figure 1). A reasonable classification relates to the pathoanatomy, (Table 1). Thus, the origin of the pain can be attributed to the patellar cartilage, the tendons, the bone, inflamed bursae, the synovium or internal derangements.

View Large Image Download to PowerPoint

Figure 1 Schematic presentation of the causes of anterior knee pain: Osgood Schlater (1), Sindig-Larsen (2), Lateral patellar compressive syndrome (3), Patellar tendinitis-jumpers knee (4), quadriceps tendinitis (5), Chondromalacia patelae and Reflex sympathetic dystrophy (6), Medial synovial plica (7), Fat pad syndrome (8), Meniscal injury (9).

Table 1. The aetiology of anterior knee pain

	Structure	Possible responsible lesions
	Patellar cartilage	Chondromalacia, chondral and osteochondral lesions, patellofemoral arthrosis
	Tendons	Vastus lateralis strain, patellar tendinitis-jumper's knee, quadriceps tendinitis
	Bone	Patellar algodystrophy/RSD, apophysitis-Osgood-Schlatter, Sindig-Larsen
	Synovia and plicae	Local or diffuse synovitis, plicae syndrome
	Bursae	Prepatellar, deep patellar bursitis
	Internal derangements	Meniscus or LCA lesions, Hoffa/fat pad

Patellofemoral pain can also be caused by patella malalignment - patellar tilt-lateral patellar compressive syndrome (LPCS) and patellar subluxation and dislocation, which should strictly be included in patellofemoral disorders, but actually these conditions overlap each other. The most common and important conditions held responsible for anterior knee pain will be described.

Chondromalacia patellae and patellofemoral arthritis 

Chondromalacia patellae is a condition most commonly found in young people, although pathological chondromalacic changes occur both in both the young (in 50% of cases before 30 years of age) and in the old (10% of cases over 60 years of age). While some1 have reported the initial changes on the medial patellar facet, Insall2, 3 found both facets to be involved. Usually the changes are detected first on the lateral facet, beginning as softening of the cartilage, followed by eburnation of bone.

The load borne by the patellar cartilage is great and consequent damage and lesions can be expected. Goodfellow4 described several different lesions held to be responsible for patellofemoral pain. Deeply localized changes, labelled “basal degeneration”, were described as softening of the cartilage and inability of the cartilage fibers to bind together. In this condition the surface of the cartilage is smooth and looks undamaged. Lesions occur later, in the form of cartilage erosion. Patellar pain is the result of the inability of the deeper cartilage layer to cushion transmission of load to the subchondral bone. Pain occurs when the pressure is greatest, i.e. when the knee is flexed between 90–130 degrees, so that the resultant ridge glides over the femoral surface.

Microscopic findings depend on the stage of chondromalacia, which can be described as closed or open. In the first phase of the closed form of chondromalacia patellae the only finding is cartilage softening, which can be demonstrated at arthroscopy (Figure 2). More precisely, hardening or softening can be measured by a micrometer pressure transducer, which is applied during arthroscopy.5 It is important to note that in 50% of cases with patellar pain and cartilage softening is was no visible macroscopic alteration to the appearance of the cartilage. However, once the superficial layer of the patellofemoral cartilage is disrupted, the diagnosis of open chondromalacia is established (Grade 2; Figure 3). In the second stage there is articular fissuring, (up to 1.3 cm), whilst fibrillation and lesions larger than 1.3 cm are diagnostic of grade III. Stage IV is reached when the subchondral bone is exposed. In all stages of chondromalacia patellae the changes are localized to the cartilage. If they spread over the synovial membrane onto bone, osteoarthritis is present.

View Large Image Download to PowerPoint

Figure 2 Arthroscopic view of chonromalacia patellae: soft cartilage under the probe.

View Large Image Download to PowerPoint

Figure 3 Arthroscopic view of open cartilage lesion.

Hungerford discusses closed vs. open chondromalacia,6 while Bentley classifies chondromalacia according to the extent of actual cartilage damage.7 Bauer, Jackson and Dandy classified it according to the architecture of the chondral lesion (Figure 4) - linear, stellate, flap, crater, fibrillation, degrading. Forms 4–6 are described as osteochondral,8 though in reality, the distinction between chondromalacia and osteoarthrosis is very subtle.

View Large Image Download to PowerPoint

Figure 4 a Linear cartilage lesion b Stelate cartilage lesion c Flap cartilage lesion d Crater-Osteochondeal lesion.

Microscopically, there is a continuous surface in closed chondromalacia (Figure 5), with fibrous metaplasia and ground substance swelling characterised by a lower percentage of glycoaminoglycans and an increased water content (over 9%). On the contrary, in the open form of chondromalacia, there is obvious fibrillation on the cartilage surface. As the demands on such cartilage increase, chondrocyte activity increases, but when the demands exceed the chondrocyte potential, failure occurs. The superficial layer loses its support, the cartilage breaks, and a reparative fibroblastic metaplasic response occurs.9

View Large Image Download to PowerPoint

Figure 5 Pathohistology specimen of cartilage in chondromalacia patellae, with intact surface-left (Hematoxyin-Eosin staining, Magnification 10×10).

Briefly, the underlying process is oedema of the cartilage, which is fragile and prone to damage. Microscopic fissures are visible, but the chondrocytes appear to be normal (Figure 6). Later, in stages II and III, the fissures are deeper and extend to the subchondral bone, while the matrix is fragmented. Necrosis is seen in stage IV, with a picture of cartilage damage recognisable as osteoarthrosis.9

View Large Image Download to PowerPoint

Figure 6 Pathohistology specimen of damaged patellar catilage, with fissures which extend to the subchondral bone (Hematoxyin-Eosin staining, Magnification 10×10).

The shape of the patella, expressed as a Wiberg patellar type, does not correspond with chondromalacic changes. Although the changes occur first, and are most profound on the lateral facet, this is explained by vector analysis.9

Chondromalacia of the patella is often seen after prolonged immobilisation, because decreased blood flow results, reducing nutrient be supply to the cartilage. Although patellar cartilage is thicker than the corresponding femoral cartilage, it is more vulnerable. Furthermore, fibrous tissue proliferation covers the cartilage, decreasing protection by the synovial fluid. Over a prolonged period this leads to cartilage damage.9 Furthermore, after some types of knee surgery, such as when fascia lata is used as a graft with tightening of lateral structures, there is increased pressure on the lateral patellar facet. A similar issue occurs when medial harvesting is performed. The patellar cartilage can also be damaged by sharp instruments during meniscetomy and wide nochplasty, when the contact area to the patella is also decreased. Moreover, postoperative haemarthosis may lead to further cartilage damage.

After any kind of knee injury or knee surgery there is a synovial reaction and this has deleterious consequences for the cartilage. Thus, every rehabilitation induced effusion must alert the physician to reduce aggressive physical therapy.

A direct injury to the flexed knee, such as a dashboard injury is likely to result in damage to the patellar cartilage or in osteochondral fractures. Osteochondral fractures of the patella are also seen in recurrent patellar dislocations. On the other hand, repetitive microtrauma is more relevant to chondromalacia originating through enzyme reactions and reactive synovitis thus: trauma → arachnoidic acid appearance → prostaglandin synthesis → sAMP → protease → protein degradation → cartilage softening → degradation of polysaccharides → chemical synovitis → pain.10 In this way, when synovial enzymes attack the cartilage, a vicious circle is established. Some medications (nonsteroidal), can decrease the synthesis of proteoglycans and thus interrupt the circular process.11, 12, 13 The diagnosis of patellar chondromalacia is based on clinical evidence and arthroscopic findings.

Treatment of patellar chondromalacia 

After the failure of conservative treatment, there are numerous available surgical procedures both for chondromalacic patellae and patellofemoral arthritis, with more or less success. These procedures are: patellar shaving, subchondral bone drilling, cortical abrasions, spongiolisation, lateral retinacular release and elevation of the tibial tubercle. These operations for chondromalacia patellae can be divided into five main groups:

When cartilage operations of the first group are considered, previous biomechanical abnormalities, eg. patellofemoral malalignment, must be excluded.

1.Patellar shaving became popular with the development of arthroscopy and the technological expansion in knee surgery. Motorised shavers are effective in removing cartilage, especially when altered by fibrillation, by removing mobile flaps to make the cartilage surface smooth. Patellar shaving is the most convenient for cartilage fibrillation (grade.II) and it is recommended not to be too aggressive in this procedure. It is not good to convert a partial thickness defect into a full thickness defect, and it is better to use less aggressive shaver tips.

However, patellar shaving gives a satisfactory result in only 25% of cases. The final outcome is reported to be better for grade II than for grade III chondromalacia.9 The results of shaving in postraumatic chondromalacia and especially in osteoarthritis correlate with the severity of cartilage damage, and it seems that success cannot be expected in osteoarthritis of the patella. Only traumatic chondromalacia can be treated by shaving, when there is no patellar maltracking or biomechanical abnormalitiy. Patellar shaving and irrigation removes the flaps and enzyme reactions of the synovial membrane are decreased.8, 9

2.Subchondral bone drilling, cortical abrasion and spongioplasty are suggested as procedures for the treatment of advanced chondromalacia with exposure of the subchondral bone (Stage IV). The aim of the drilling, according to Pridie9 is to encourage fibrous ingrowth from the underlying cancellous bone. This can be done by arthroscopic abrasion (Figure 7) or by complete removal to expose the subchondral bone - “spongiolisation of the patella”, as popularized in 1979 by Ficat,14 who reported satisfactory results in 79% of cases. The ingrowth tissue he found was not cellular, but was of a fibrous nature. Although the biomechanical properties of this tissue are inferior to those of normal cartilage, this method was popular for a time. The results obtained differ between studies, and it has been concluded that this procedure is unpredictable. Sometimes it is carried out with other procedures, which unload the cartilage, when the final outcome has been reported to be better, but the merits of each procedure are unknown.9

View Large Image Download to PowerPoint

Figure 7 Arthroscopic shawing and abrasion procedure of the patellar cartilage.

3.Modern concepts in cartilage treatment include mosaic plasty (chondral blocks obtained from the non weight bearing surface placed on to the damaged areas) and chondral transplantation of tissue produced in laboratories (cell culture) replaced in the knee after 4 weeks (Figure 8a,b,c).

View Large Image Download to PowerPoint

Figure 8 Schematic presentation of transplalation of the prepared cartillage cell culture (a arthroscopic obtained cells, b preparing of hyalograft in laboratory and c insertion the hyalograft into the cartilage defect).

4.Lateral retinacular release is widely performed in the treatment of LPCS and patellar instabilities. This procedure is logically indicated when there is shortening of the lateral retinaculum, whilst it is not recommended for chondromalacia, according to Insall.9 However, when there is no severe cartilage damage, there is a 60% benefit from the lateral release procedure, possibly due to lateral denervation.15

5.Elevation of the tibial tubercle, as a procedure, is supposed to decrease the contact pressure and patellar pain. Maquet16 reported that 2 cm advancement of the tibial tubercle reduced the patellar compression forces by 50% and he proposed medialisation of the patella if there was extensor mechanism malignment (Figure 9). However, at the same time, this procedure also decreased the contact area between the patella and femoral trochlea. Thus, an advancement of 1 cm is the best compromise between the desired reduction of the contact area and decrease of contact pressure.17, 18 On the other hand, Fulkerson,19, 20 contested that the best combination was an average of 14.8 mm ventralisation and 9.2 mm medialisation which markedly decreased pressure on the lateral facet without increasing it on the medial side, and without significant reduction of the contact area. Using these procedures the lateral pressure is switched to the medial facet. This gives the best results in patients with pain only (90–100%), while in arthroses it is not so successful. However, for cases with patellofemoral malignment, depending on the clinical presentation and underlying pathology, different procedures are advocated: lateral release for LPCS, proximal distal realignment for intability. Ventralisation is a treatment option for cases with patellofemoral arthritic changes.

View Large Image Download to PowerPoint

Figure 9 Schematic presentation of the Maquet operation- advacement/ventralisation of the patella.

6.Patellar resurfacing. McKeever21, 22 introduced the cobalt-chrome alloy patellar prosthesis in 1955. Since that time, other attempts and improvements in anatomical and biomechanical design of the prothesis have been made. In 1989 Aglietti and Insall designed a new patellar prosthesis in two sizes and they reported a success rate of 67%.23 The operation was performed in strictly selected cases with no damage to the femoral trochlear articulation and in cases with previously failed patellar surgery. Some authors24, 25 resurfaced both femoral and patellar articulations, with success in 72% of cases.

7.Patellectomy is the last option in patellar surgery. It is an amputation, which destroys the ability of the patella to move the extensor mechanism line of action away from the femur. The only rational compensation after patellectomy is anterior displacement of the tibial tubercle. Patellectomy also decreases quadriceps excursion and decreases the quadriceps strength, an effect documented on the Cybex-II machine to be about 50% compared to the opposite knee.9 Clinically, this is most evident during climbing stairs or rising from a chair, and it decreases running ability. Technically, patellectomy can be done through a longitudinal incision (with enucleation of the patella- Figure 10) or through a transverse incision, which is preferable. Other techniques like Z plasty resurfacing with a quadriceps flap or patellar tendon9 have also been described. The success rate after patellectomy in the Insall series was 70.5–76%. Insall recommended patellectomy only for very painful chondromalacia patellae, and for comminuted patellar fractures.

View Large Image Download to PowerPoint

Figure 10 Schematic presentation of the patelletomy.

Tendon pathology 

Lateral patellar strain, patellar and quadriceps tendinitis are overuse syndromes defined by repetitive overloading of the vastus lateralis, patellar or quadriceps tendon, which results in irritation of either the patellar or quadriceps tendon in the midsubstance or its insertion into the patella or tibial tubercle.

Lateral patellar strain or vastus lateralis strain is characterised by pain on the supero-lateral corner of the patella, where. vastus lateralis is inserted. This condition is quite similar to tennis elbow. Therapy consists of the administration of nonsteroidal anti-inflammatory drugs or local steroid injections. Lateral release is the surgical alternative.

The tendon insertion or bone-tendon junction, is the site of painful inflammation, especially when patellofemoral malalignment exists (patella alta, patella baja, patellar subluxation or hypermobile patella). Also, if deformity of the limb axis (genu vara, genu valgam, genu recurvatum) is present, there is a change in patellofemoral physiology, probably leading to both tendon pain and articular cartilage breakdown - patellofemoral arthrosis.9

Patellar tendinitis, common among younger sportsmen (basketball, volleyball) is known as “Jumper's knee”. On the other hand, quadriceps tendinitis is more common in older patients, i.e. in sportsmen in their forties. Patellar tendinitis is more common over all than quadriceps tendinitis.

Insertion tenopathy occurs at the inferior pole of the patella (65%), at the insertion of the quadriceps tendon (25%) and at the insertion of the patellar tendon into the tibial tubercle (1%).

In the aetiology of both kinds of tendinitis lies chronic overload of the tendon, with consequent microtears and focal mucoid degeneration of tendon midsubstance, especially in deep parts and near tendon insertions. The above mentioned mucoid degeneration and fibrinoid necrosis within the tendon is revealed by histological examination.9, 29, 30 An inflammatory component is also present, resulting in weakening of the tendon, especially after longterm tendinitis.

The highest demand and loads on the tendon are generated during deceleration. For example, forces in the patellar tendon reach 500 N during walking, 8000 N when landing after a jump, 9000 N during fast walking and 14.500 N during lifting a weight of 175 Kg.31

During an eccentric contraction acting on acting on the injured patellar tendon, a sharp pain is felt, while during rest the symptoms subside with renewed activity they recur. Both rest and steroids have a negative effect on the mechanical strength of the tendons and ligaments. Although at first sight the exercise programme of Curwin and Stanish for tendinitis seems paradoxal, there is evidence that progressive stresses on the tendon lead to recovery of its tensile strength.32

The diagnosis of patellar or quadriceps tendinosis is based mainly on clinical findings; there is a sudden aching pain, which occurs after repetitive sport activity. In nonathletes the pain may occur after climbing stairs or getting up from a chair, when high patellofemoral loads are created. The pain is well localised, sharp in nature and is associated with thickening of the tendon. Nevertheless, other causes of patellofemoral pain must be excluded and if there has been concomitant disease, one must identify the main problem, i.e. which disease has caused the predominant symptoms.

The classification of tendinopathy according to Blazina et al. 33 is related to the pain characteristics. He described four stages of tendinosis. In the first stage, pain occurs only after the physical activity. In the second stage pain is present both before and after physical activity, but not during the activity, because the pain subsides with warm up, but recurs with fatigue. In the third stage the pain is constant and present both during rest and activity, so it interferes with sporting capability and results in functional impairment. The fourth stage involves a complete rupture of the patellar tendon.

Besides the clinical findings, ultrasound and MRI greatly assist in reaching the final diagnosis. Ultrasonography is inexpensive, widely used and can confirm the clinical diagnosis and indicate the stage of disease. Three main findings can be detected: (Table 2).

Table 2. Tendinitis phase and ultrasound findings

	Phase	Ultrasound findings
	1. Acute phase	The tendon is swollen but homogenous in appearance
	2. Subacute phase	Hypoechogenic zones related to oedema and hyperechogenic zones corresponding to fibrous scar tissue
	3. Chronic tendinopathy	Irregularities of the tendon envelope, tendon is heterogenous but not thickened.

Reflex sywathetic dystrophy 

According to Dandy, pain from the bone may be related to reflex sympathetic dystrophy (RSD) and apophysitis (Osgood Schlater and Sindig-Larsen). RSD is associated with the trauma (even minor) and the consequent vasomotor disturbance is characterised by pain, swelling, stiffness and discoloration. The degree of pain is not correlated to the extent of initial trauma. The four above mentioned symptoms are cardinal for RSD. Secondary findings, such as osteoporosis, skin atrophy, and decreased skin temperature are not usual.34 RSD is also known under other names: causalgia (termed by Mitchell who originally described this entity, 9), Sudeck's atrophy, reflex dystrophy, shoulder-hand syndrome (for the upper limb). Before 1930 this condition was considered to be incurable. Spurling reported successful treatment by cervicothoracic sympathectomy.9 It was evident that irritation of the sympathetic nervous system was integral to RSD. In the older literature causalgia was related only to the hand and foot, but nowadays it is also associated with the knee.34, 35 The symptoms differ between the upper and lower extremities, and also between patients. However, in all the pain is described as burning and deeply aching. It is aggravated by motion, even mere touch, and cold. The pain and tenderness are diffuse, not well localised. Any stiffness is secondary to the pain and can be mild to severe with a semiflexed knee and loss of motion. The extent of stiffness also depends on the duration of illness and, in prolonged cases, there are marked changes in the periarticular soft tissues, such as capsular fibrosis and fibrofatty proliferation inside the joint, which lead to contracture and ankylosis. Swelling around the joint is due to periarticular oedema and occasionally to intraarticular effusion. The skin over the knee is cyanotic, and discoloration increases during exposure to cold. Ficat also stated that there is increased intraosseous pressure and venous stasis. Atrophy of the quadriceps muscle is seen relatively early. The main radiological change in RDS of the knee is osteoporosis of the patella. The osteoporosis is typically patchy in appearance (Figure 11).

View Large Image Download to PowerPoint

Figure 11 Radiography of the osteoporotic patella in the patient with reflex symphatetic dystrophy of the knee (11a- lateral view, 11b-axial patellar view).

The natural history of RSD is gradual, with spontaneous recovery over a period of over 2 years in three phases - pain, stiffness, gradual recovery. RDS may be divided into three stages: acute, subacute-dystrophic and chronic-atrophic. The acute stage, characterised by pain, stiffness, sweating and coldness lasts for 3 months. The duration of the second-subacute stage is from 3–12 months, when the pain reaches the maximum and the patchy osteoporosis is seen on radiographs. After one year the disease is considered chronic and is characterised by pronounced periarticular fibrosis, osteoporosis and skin atrophy.

The aetiology of RSD consists of a vicious circle that starts with a painful stimulus, evoking an efferent impulse and consequent vasoconstriction, ischemia and pain.9 Thus, the pain is caused by vasospasm and ischemia. The painful stimulus may be trauma but also surgery, which must be borne in mind prior to operative interventions. The main point is that the trauma is often minor and it is assumed that the patient must have a predisposition for RDS, i.e. the patient has a hyperreactive sympathetic system. The initial trauma is usually related to the patellofemoral joint.9 Katz reported cases with previous surgery of the patellofemoral joint, such as shaving or lateral release. Even injury to a nerve around the knee can trigger RSD. In some cases damage to the infrapatellar branch of the saphenous nerve has resuited in RSD -in 17% CD of Katz's series.35 The pathogenesis of RSD is explained by chronic irritation of the sensory nerve, which causes increased afferent input and activation of the internuclear neurons in the spinal cord. This results in sympathetic hyperreactivity (overactivity). Melzack and Wall 36 described specialised cells in the substantia gelatinosa of the dorsal horn, which could modulate the central-cortical transmission of the afferent-pain impulses to the brain. Sympathetic small C-fibers suppress the inhibitory effect of the cells described by Melzack and allow the pain impulses to reach the brain, whilst large A-fibres stimulate the inhibitory effects of the substantia gelatinosa - this is the so called Gate Theory. Alternatively, the Peripheral Theory suggests the development of artificial synapses, at the place of trauma, between the afferent sensory fibres and the sympathetic efferent fibres.9 According to this theory afferent impulses directly and automatically cause an efferent sympathetic response with vasospasm and pain. This is the most probable theory when peripheral nerve injury exists, whilst in others the “Gate Theory” is more appropriate.

In most cases the diagnosis of RSD can be made from the findings after a proper clinical examination. The main symptom is pain, which is disproportional to the initial injury. The key to RSD is the presence of unduly prolonged pain with vasomotor disturbance and joint stiffness.

Radiography is important, because it can exclude other bone lesions and to confirm the patchy osteoporosis primarily localised to the patella (Figure 11), although it is not a constant finding in RSD.8 Some authors37 reported that bone scans (scintigraphy) have a sensitivity of 66–88% in RSD. Thermography has a similar sensitivity and it is used to document temperature changes in the affected joint-limb; a decrease of 1 degree Celsius is relevant.34 The technique of isolated cold stress testing is also valuable.37

Arthroscopy has been employed in the diagnosis of RSD to confirm the absence of significant intraarticular pathology,38 but one must bear in mind that arthroscopy is potentially a dangerous and exacerbating procedure for a patient with RDS.

Sympathetic blockade may be the most direct and effective procedure to confirm RSD. A local anesthetic can be applied either around the lumbar ganglia (sympathetic chain) or into the epidural space- epidural sympathetic blockade.34 The first method can be easily interpreted (Insall).

The treatment of knee RSD consists of physical therapy, transcutaneous electric nerve stimulation, sympathetic blockade and/or steroids. However, first it must be said that RSD is a self–limiting disease, although in many people it persists for years. In one study, 100% of patients still had pain in the affected limb after 5 years follow-up and that is why treatment must be started early.39

Physical therapy is effective in mild cases of RSD, alone or in combination with sympathetic blockade. Only gentle, active movements are allowed, while passive and aggressive manipulation should be avoided. The extremity should be elevated at rest, but weight bearing is encouraged and tolerated. Transcutaneous electric nerve stimulation is also recommended.39

Sympathetic blockade is the most common form of RSD treatment, since it can break the vicious circle of pain. Additionally oral sympathetolytic drugs and Nifedipine could be considered.

Steroids are given in high doses (60–80 mg per day) with favorable results, possibly due to their stabilising effect on the basal membrane and consequent reduction of permeability. Also, Solu Medrol provides a local effect in 75% of cases.9

RSD is an underdiagnosed condition in knee pathology, and it is most probable in a patient with diffuse, prolonged nonspecific pain, when there is no adequate response to analgesics.

Local synovitis and synovial plicae 

Local synovitis and synovial plicae can be the cause of anterior knee pain. Synovitis may be associated with anterior knee pain, because inflamed synovia are tender and painful. Synovitis can be localized or diffuse. The treatment of synovitis consists of arthroscopic shaving or synoviectomy if conservative measures have failed.

Plicae are normal anatomic findings (Figure 12), and they are occasionally thought to be symptomatic. Half of patients with a plica and symptoms have a recent history of blunt trauma to the anterior knee.8, 9 Pain is localised to the anterior aspect of the knee, with tightness in the suprapatellar region during knee flexion. Impingement of medial knee plicae occurs, with thickening and inflammation over the articular cartilage (Figure 13). In these cases, resection of the plicae result in a pain free knee in 85% of cases. However, plica syndrome forms only 5% or less of knee pathology and Dandy discusses overtreatment of the plica syndrome. Plicae, in fact, rarely cause problems and many of the so called inflamed and resected plicae are likely unrelated to the symptoms.40

View Large Image Download to PowerPoint

Figure 12 Schematic presentation of the knee's plicae: suprapatelar a, medial patellar plica b and infrapatellar plicae c.

View Large Image Download to PowerPoint

Figure 13 Arthroscopic picture of inflamed medial patellar plicae.

Peripatellar bursitis 

Peripatellar bursitis should be differentiated from the tendinopathies. It is an occupationaly related condition. Besides prepatellar and superficial and deep infrapatellar bursae, there can be many other bursae around the knee, among which pes anserinus bursis is well recognised (Figure 14).

View Large Image Download to PowerPoint

Figure 14 Schematic presentation of knee bursae: suprapatellar a, superficial prepatellar b, superficial infrapetallar c and deep infrapatellar bursae d.

Pathophysiologically there is inflammation in “housemaids knee” and irritation of the prepatellar bursa. The patellar tendon bursa can also be inflamed (the bursa between the patellar tendon and the upper part of the tibia) In which case pain is elicited by pressure of the patellar tendon on the upper tibia. Inflammation of both bursae is easily recognised, but pes anserinus bursitis is commonly misdiagnosed as meniscal pathology, osteonecrosis or osteoarthritis. X-ray examination, and especially MRI and ultrasound scans, are helpful. The treatment cf prepatellar bursitis is conservative and it consists of avoiding kneeling combined with -analgesics, rest and ice, leading to pain relief. Occasionally, when infection complicates the condition, incision and drainage, irrigation and adequate antibiotic therapy are required.

Internal derangement, meniscal and LCA lesion 

These must be diagnosed and treated in order to solve the anterior knee pain problem. Inflammation of the fat pad and synovial folds has been described in 1904 as a cause of anterior knee pain (Hoffa). The fat pad syndrome is a consequence of isolated trauma to the infrapatellar fat pad, especially during knee hyperextension, and it is characterized by tenderness and local swelling. In most cases the pain subsides with conservative therapy. In some cases surgery is indicated.8, 9

Conclusion 

Anterior knee pain is common and one should be aware of numerous conditions which can present in this way. Nowadays, modern imaging techniques enable more precise diagnosis and more satisfactory treatments are evolving. Furthermore advancing technologies and surgical procedures are proposed for the treatment of cartilage breakdown, tendons and synovial pathology, meniscus and ACL injuries that hold promise for the near future. At present however, algodystrophy or complex regional pain syndrome still responds best to nonoperative means.