**Abstract**

"Patellar tendinopathy" is also known as "Jumper's knee" and is a common cause of impaired function in athletes who participate in sports that require jumping and running activities. The exact etiology of disease is still unknown and several theories have been postulated for its pathogenesis. It usually presents as anterior knee pain that is related to the sports activity and might lead to decreased sports participation. USG and MRI are the main modality of investigation that aids in the diagnosis. Non-operative therapy forms the main stay of treatment in form of rest, brace, physical therapy and anti-inflammatory medications. Other adjuncts such as cryotherapy, corticosteroids injection, platelet -rich plasma injections and electrical therapy like TENS or ESWT have been used with some success. Operative intervention in form of open or arthroscopic procedures are reserved for chronic and refractory cases.

**Keywords:** patellar tendinopathy, degenerative, tendinitis, jumper's knee, enthesis, eccentric, cryotherapy

### **1. Introduction**

Tendinopathy is a broad term encompassing painful condition in and around tendon due to overuse. It commonly affects the Extensor mechanism (patellar tendon) around the knee and is termed as "jumper's knee" [1, 2]. It is characterized by an initial reactive or inflammatory response followed by stage of degeneration. The prevalence of patellar tendinosis is seen greatest in young adults who are engaged in high demand sports that involves running, jumping and cutting movements. It has been estimated to range from 40%-50% in elite volleyball players and 35%-40% in high level basketball players [3]. It can also affect sedentary individuals and an estimated prevalence of 14.2% is seen in general population [4].

The disease pass through two stages, acute and chronic and presentation vary according to the stage of disease. It usually present as anterior knee pain, swelling and impaired function in acute stage, while in chronic stage it may presents as long standing anterior knee pain with profound muscle wasting without the sign of inflammation or impaired function. The tendo-osseous junction on the inferior pole of patella is the usual affected site. The exact etiology of disease is still unknown. However, various risk factor have been identified which may contribute in development of patellar tendinopathy such as impaired quadriceps flexibility and strength, high body mass index (BMI), leg length discrepancy, impaired hamstring flexibility and vertical jump performance, as all these factors increases the strain over the patellar tendon [5]. Several theories have been postulated on pathogenesis of patellar tendinopathy including vascular [6], mechanical [7], nervous [8] and impingement related. However the chronic repetitive tendon overload theory is the most accepted theory for patellar tendinosis.

The term "patellar tendinitis" which is often used for patellar tendon pain appears to be misnomer for patellar tendinopathy. Multiple histo-pathological studies have reported that the primary pathology in most of painful tendon is degenerative rather than inflammatory [9–11]. However Fredberg et al. [12] challenged the concept of patellar tendon pain due to degenerative cause and stated that it is rather the presence of inflammatory process that is responsible for pain. While some histopathological studies [13, 14] have shown that pro-inflammatory chemical agent such as cyclooxygenase, growth factors, and prostaglandins are present in acute stages and macrophage and lymphocyte in chronic tendinopathy, we still need further research and more evidences to prove the theory.

The management of patellar tendinopathy has always been challenge to the healthcare professionals. It usually requires a multimodal approach and based upon the current literature and clinical practice an effective conservative intervention in the form of rest, NSAIDS and physiotherapy is indicated in acute phase and surgical procedure are reserved for chronic and long standing cases.

### **2. Anatomy**

Patellar tendon is the continuation of the common tendon of insertion of quadriceps, extending from the inferior pole of patella to the tibial tuberosity. In adult, the patellar tendon is around 25–40 mm wide in the coronal plane and 4–5 mm deep in the sagittal plane and 4–6 cm long. Macroscopically it appears white, glistening and stringy with collagen fiber in tendon are arranged in parallel fashion.

The blood supply of the tendon is through the anastomotic vascular ring lying in the thin layers of loose connective tissue that covers the fibrous expansion of the rectus femoris. The formation of the ring is through the anterior tibial recurrent artery and genicular arteries mainly the lateral superior, lateral inferior and medial inferior artery [15, 16].

The patellar tendon attachment to bone (patella or tibia) has fibrocartilaginous enthesis with four distinct tissue zones–dense fibrous connective tissue, uncalcified fibrocartilage, calcified cartilage and bone [17]. The patellar tendon lack of well-developed proper paratenon, while the posterior surface of tendon which is in direct contact of fat pad, which is highly vascular and innervated. According to Duri et al. [18] the intensity of pain in some patient with patellar tendinopathy is due to involvement of fat pad. Patellar tendon pathology usually involve the enthesis site, it most commonly involve the inferior pole of patella but can also involve tibial tubercle or proximal aspect of patella in quadriceps tendon. Macroscopically the diseased portion of tendon become disorganized and appears yellow-brown in color.

### **3. Epidemiology**

Jumper's knee is commonly seen in people involved in contact sports such as basketball, volleyball, high jump, long jump, tennis and running [1]. The factor contributing factor in development of patellar tendinopathy can be classified as extrinsic factor or intrinsic factor [19]. The intrinsic factor can be sex, race, bone structure, bone density, muscle length, muscle strength, joint range of motion. While extrinsic factors are training volume (duration, frequency and intensity), specific sports activity, specific movements like quick acceleration, deceleration, cutting action and

**59**

*Patellar Tendinopathy: "Jumper's Knee" DOI: http://dx.doi.org/10.5772/intechopen.84642*

disruption of collagen cross links.

**5. History and physical examination**

while ascending or descending stairs.

malalignment of the leg.

**4. Pathogenesis**

training surfaces. Ferreti [20] observed direct relation between the patellar tendinopathy with number of weekly training session and training over the hard surface. The condition is more commonly seen in males than females [21]. This condition

Tendons display a classical stress-strain curve, during the increased flexion the maximum load is located in deep posterior portion of patella, close to center of rotation knee and inferior pole of patella. The crimp pattern of the tendon disappears when the length of the tendon is stretched greater than 2%. With further stretch greater than 5%, the tendon fibers become more parallel and the tendon follows a linear response to stress [22, 23]. Beyond this, tendon failure starts to begin with

The force experienced by patellar tendon on a level ground while walking is 0.5 kN, which increases to 8 kN during landing from a jump, 9 kN during fast running and further to 14.5 kN during competitive weight lifting. A basketball player, on an average, jumps 70 times per game where the vertical component of the ground reaction force reaches to about six to eight times the body weight. Thus, sport activities can impose high levels of stress on the tendon, enough to cause its failure. This increased strain result in alteration of cellular activity level by affecting the tenocytes and altering the protein and enzyme production with deforming of nucleus [7, 24]. The tendon fibroblast are loaded with increased prostaglandins E2, leukotrienes B4, VEGF and matrix metalloproteinase which contribute to tendinopathy. This increased strain result in alteration of cellular activity level by affecting the tenocytes and altering the protein and enzyme production with deforming of nucleus [7, 24]. The tendon fibroblast are loaded with increased prostaglandins E2, leukotrienes B4,

VEGF and matrix metalloproteinase which contribute to tendinopathy.

In chronic patellar tendinopathy, there will be absent or minimal inflammation [10, 13, 21]. The diseased tendon shows hypercellularity with atypical fibroblast and endothelial cell proliferation with neovascularization [13, 21, 25, 26]. There will be loss of longitudinal collagen fibers and demarcation between collagen bundles with relative expansion of tendon. There will be abundant number of cell undergoing apoptosis with abundance of pre-apoptotic proteins and gene [27, 28]. Macroscopically tendinopathy will have disorganized appearance described as mucoid degeneration [20, 29].

The clinical diagnosis of jumper's knee is based on the subjective sensation of the pain and restriction of activities. The symptoms are insidious in onset but usually relates to an increase in frequency or intensity of activity involving rapid repetitive ballistic movements of the knee joint. It starts with a dull aching pain in the anterior aspect of the knee after a strenuous activity and further progresses to a state where it interferes with the performance of the individual. Patients also complain of pain

The key physical finding of the patellar tendinopathy is tenderness at the inferior pole of patella when the knee is at full extension with gradual decrease in the pain when the knee is flexed gradually. It is generally accompanied by few signs of soft tissue inflammation [1]. The condition often associated with abnormalities of patellar tracking, chondromalacia patellae, Osgood-schlatter disease or mechanical

is not a self-limiting one and symptoms may prevail after treatment.

### *Patellar Tendinopathy: "Jumper's Knee" DOI: http://dx.doi.org/10.5772/intechopen.84642*

training surfaces. Ferreti [20] observed direct relation between the patellar tendinopathy with number of weekly training session and training over the hard surface.

The condition is more commonly seen in males than females [21]. This condition is not a self-limiting one and symptoms may prevail after treatment.

### **4. Pathogenesis**

*Tendons*

**2. Anatomy**

inferior artery [15, 16].

**3. Epidemiology**

theory for patellar tendinosis.

tendinopathy including vascular [6], mechanical [7], nervous [8] and impingement related. However the chronic repetitive tendon overload theory is the most accepted

The term "patellar tendinitis" which is often used for patellar tendon pain appears to be misnomer for patellar tendinopathy. Multiple histo-pathological studies have reported that the primary pathology in most of painful tendon is degenerative rather than inflammatory [9–11]. However Fredberg et al. [12] challenged the concept of patellar tendon pain due to degenerative cause and stated that it is rather the presence of inflammatory process that is responsible for pain. While some histopathological studies [13, 14] have shown that pro-inflammatory chemical agent such as cyclooxygenase, growth factors, and prostaglandins are present in acute stages and macrophage and lymphocyte in chronic tendinopathy, we still need

The management of patellar tendinopathy has always been challenge to the healthcare professionals. It usually requires a multimodal approach and based upon the current literature and clinical practice an effective conservative intervention in the form of rest, NSAIDS and physiotherapy is indicated in acute phase and surgical

Patellar tendon is the continuation of the common tendon of insertion of quadriceps, extending from the inferior pole of patella to the tibial tuberosity. In adult, the patellar tendon is around 25–40 mm wide in the coronal plane and 4–5 mm deep in the sagittal plane and 4–6 cm long. Macroscopically it appears white, glistening and

The blood supply of the tendon is through the anastomotic vascular ring lying in the thin layers of loose connective tissue that covers the fibrous expansion of the rectus femoris. The formation of the ring is through the anterior tibial recurrent artery and genicular arteries mainly the lateral superior, lateral inferior and medial

The patellar tendon attachment to bone (patella or tibia) has fibrocartilaginous enthesis with four distinct tissue zones–dense fibrous connective tissue, uncalcified fibrocartilage, calcified cartilage and bone [17]. The patellar tendon lack of well-developed proper paratenon, while the posterior surface of tendon which is in direct contact of fat pad, which is highly vascular and innervated. According to Duri et al. [18] the intensity of pain in some patient with patellar tendinopathy is due to involvement of fat pad. Patellar tendon pathology usually involve the enthesis site, it most commonly involve the inferior pole of patella but can also involve tibial tubercle or proximal aspect of patella in quadriceps tendon. Macroscopically the diseased portion of tendon become disorganized and appears yellow-brown in color.

Jumper's knee is commonly seen in people involved in contact sports such as basketball, volleyball, high jump, long jump, tennis and running [1]. The factor contributing factor in development of patellar tendinopathy can be classified as extrinsic factor or intrinsic factor [19]. The intrinsic factor can be sex, race, bone structure, bone density, muscle length, muscle strength, joint range of motion. While extrinsic factors are training volume (duration, frequency and intensity), specific sports activity, specific movements like quick acceleration, deceleration, cutting action and

further research and more evidences to prove the theory.

procedure are reserved for chronic and long standing cases.

stringy with collagen fiber in tendon are arranged in parallel fashion.

**58**

Tendons display a classical stress-strain curve, during the increased flexion the maximum load is located in deep posterior portion of patella, close to center of rotation knee and inferior pole of patella. The crimp pattern of the tendon disappears when the length of the tendon is stretched greater than 2%. With further stretch greater than 5%, the tendon fibers become more parallel and the tendon follows a linear response to stress [22, 23]. Beyond this, tendon failure starts to begin with disruption of collagen cross links.

The force experienced by patellar tendon on a level ground while walking is 0.5 kN, which increases to 8 kN during landing from a jump, 9 kN during fast running and further to 14.5 kN during competitive weight lifting. A basketball player, on an average, jumps 70 times per game where the vertical component of the ground reaction force reaches to about six to eight times the body weight. Thus, sport activities can impose high levels of stress on the tendon, enough to cause its failure. This increased strain result in alteration of cellular activity level by affecting the tenocytes and altering the protein and enzyme production with deforming of nucleus [7, 24]. The tendon fibroblast are loaded with increased prostaglandins E2, leukotrienes B4, VEGF and matrix metalloproteinase which contribute to tendinopathy. This increased strain result in alteration of cellular activity level by affecting the tenocytes and altering the protein and enzyme production with deforming of nucleus [7, 24]. The tendon fibroblast are loaded with increased prostaglandins E2, leukotrienes B4, VEGF and matrix metalloproteinase which contribute to tendinopathy.

In chronic patellar tendinopathy, there will be absent or minimal inflammation [10, 13, 21]. The diseased tendon shows hypercellularity with atypical fibroblast and endothelial cell proliferation with neovascularization [13, 21, 25, 26]. There will be loss of longitudinal collagen fibers and demarcation between collagen bundles with relative expansion of tendon. There will be abundant number of cell undergoing apoptosis with abundance of pre-apoptotic proteins and gene [27, 28]. Macroscopically tendinopathy will have disorganized appearance described as mucoid degeneration [20, 29].

### **5. History and physical examination**

The clinical diagnosis of jumper's knee is based on the subjective sensation of the pain and restriction of activities. The symptoms are insidious in onset but usually relates to an increase in frequency or intensity of activity involving rapid repetitive ballistic movements of the knee joint. It starts with a dull aching pain in the anterior aspect of the knee after a strenuous activity and further progresses to a state where it interferes with the performance of the individual. Patients also complain of pain while ascending or descending stairs.

The key physical finding of the patellar tendinopathy is tenderness at the inferior pole of patella when the knee is at full extension with gradual decrease in the pain when the knee is flexed gradually. It is generally accompanied by few signs of soft tissue inflammation [1]. The condition often associated with abnormalities of patellar tracking, chondromalacia patellae, Osgood-schlatter disease or mechanical malalignment of the leg.
