Patellar Tendinopathy

Description

Patellar tendinopathy is a source of pain in the front of the knee and is characterized by pain localized to the lower pole of the patella. [1] Pain is aggravated by loading and with increased demands on the knee extensor tissue, particularly during activities where the patella stores and releases energy Tendon [2] [3].

Patellar tendinopathy occurs primarily in relatively young (15-30 years) athletes, especially men who participate in sports such as basketball, volleyball, field jumping, tennis, and soccer, where repetitive loading of the patellar tendon is required [4]. the prevalence of this condition Among elite volleyball and basketball players, this percentage has exceeded 40%. [5] While certain intrinsic risk factors for patellar tendinopathy have been identified, such as weight for sex and body mass index, the most important risk factor appears to be training load (i.e., extrinsic risk factor). [6]

Clinically Relevant Anatomy

Cross-section of the tendon. Collagen fibers make up a pale pink background. Fine wire separates fiber bundles. Black dots are tendon cell nuclei. [7]

The quadriceps is attached to the lower pole of the patella via the quadriceps tendon through the femur (i.e., the patella). The patellar tendon then connects the base of the patella to the tibial tuberosity. force generated by the quadriceps The patella acts as a pulley leading to knee extension [8]

A healthy tendon is mainly composed of closely packed parallel collagen fibers (86%) [9]. Collagen is mainly type I. Other components of the tendon matrix are elastin (2%), proteoglycans (1–5%), and inorganic components (0.2%). collagen in tendon Proteoglycan components Decorin and Aggrecan bind to collagen fibers at specific locations[10]

Tenocytes are tendon-specific fibroblasts that produce collagen molecules that aggregate together to form collagen fibers. Fibril bundles are organized into fibers with elongated tenocytes packed tightly between them. Cells communicate with each other through gap junctions This signal enables them to detect and respond to mechanical loads [11].

The blood vessels run parallel to the collagen fibers within the tendon, with some branches anastomosing transversely. The inner tendon is thought to have no innervation, but adjacent to the tendon are nerve endings, and the Golgi tendon organ exists at the junction between tendon and muscle.

Pathological Process

Cook and Purdam described a continuum of tendon pathology with three distinct stages [12]:

1. Reactive tendinopathy
2. Tendon disrepair
3. Degenerative tendinopathy

Load is considered the primary stimulus that drives tendon health forward and backward along the continuum.

Reactive tendinopathy

Non-inflammatory proliferative responses in cells and stroma occur with acute stretch or compression overload. During this phase, tenocytes proliferate and protein production increases. [13] This causes a short-term adaptation to the tendon as it thickens and eventually reduces Relieves stress by increasing cross-sectional area or allowing for accommodation in compression. This differs from the normal tendon’s response to loading, which usually occurs through tendon sclerosis. Clinical reactive tendinopathy occurs during unaccustomed physical activity. less common after a direct hit Like falling directly onto the patellar tendon.

Tendon disrepair

Attempts at tendon healing continued after the reactive phase, but with greater matrix disruption. The number of cells present in the stroma increases, resulting in increased protein production (proteoglycans and collagen). Increased proteoglycans lead to separation and collagen breakdown. Vascularity and neuronal growth may be increased. Clinically, this phase of pathology is seen in chronically overloaded tendons and occurs at all ages and loading settings.

Degenerative tendinopathy

There are areas of cell death due to apoptotic trauma or depletion of tenocytes. There is a large area of matrix disordered and filled with vascular matrix breakdown products and a small amount of collagen. The reversibility of pathological changes at this stage is very small. This stage is Mainly seen in the elderly.

Clinical Presentation

Patellar tendinopathy is one of many potential diagnoses in patients with anterior knee pain. There are two distinct clinical features [2]:

1. Pain limited to the inferior pole of the patella
2. Load-related pain increases with the demands on the knee extensors, especially during activities that store and release energy in the patellar tendon.

Patients may complain of pain when sitting for long periods of time, squatting, and climbing stairs, but these complaints are characteristic of other conditions, such as patellofemoral pain. Pain is rarely felt at rest. Pain that begins immediately upon loading and usually stops almost immediately upon loading delete. Repeated weight bearing may improve pain. An important feature of tendinopathy is that they are dose-dependent pain increases with the magnitude or rate of loading on the tendon [14]. The practical application of this in pain examination should increase When going from shallow squats to deep squats or from small jumps to big jumps.

Weighted activities are primarily weight-bearing activities, such as when walking down stairs or performing incline squats.

Diagnostic Procedures

Jumper’s knee

Knee examination

See previous section for dose-dependent pain. Insufficient energy storage activity can be assessed clinically by observing jumps and jumps. Individuals with a history of patellar tendinopathy may use a straight-knee vertical jump landing strategy [15].

Examination of the entire lower extremity is necessary to identify associated deficiencies in the hip-knee and ankle/foot regions. Atrophy, decreased strength, poor foot posture, quadriceps and hamstring inflexibility, and decreased ankle dorsiflexion are associated with patellar tendinopathy and should has also been evaluated [2].

Imaging of the patellar tendon does not confirm patellar tendon pain because the pathology observed by ultrasound imaging may be present in asymptomatic individuals [16].

Outcome Measures

• Pain provocation (Visual Analog Scale or Victorian Institute for Movement Assessment-patella [17])
• Tendon swelling
• Return to activity

Medical Management

Non-steroidal anti-inflammatory drugs

The use of nonsteroidal anti-inflammatory drugs (NSAID’s) in the acute and chronic phases of tendinopathy remains controversial. NSAIDs have been reported to hinder soft tissue healing. While the pain may be lessened, they have a negative effect on the tendon Repair [18]. In reactive tendinopathy, this may be the preferred effect, as this may inhibit proteins that cause tendon swelling [19].

Corticosteroid injections

Corticosteroids are used to reduce pain, but also reduce cell proliferation and protein production, and are therefore useful in reactive tendinopathy. Repeated administration of peritendonal corticosteroids at 7 and 21 days after tendon injection has been shown to reduce tendon diameter [20].

Surgical treatment

Tendon surgery for chronic pain has produced mixed results, with 50-80% of athletes able to return to their previous level of activity [21]. Surgical outcomes in non-active populations are inferior to those in active populations [22]. For all patients who fail, surgery is considered a reasonable option conservative intervention.