A look at the pathophysiology and rehabilitation of Osgood-Schlatter Syndrome

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Gym Coach, Vol.2 (2008) 39-45 Commentary Article ©2008 The Gym Press. All rights reserved Gym Coach Vol.2, August, 2008 - 39- A look at the pathophysiology and rehabilitation of Osgood-Schlatter Syndrome Valentin Uzunov Hataitai Gymnastics, Wellington, New Zealand ABSTRACT Osgood-Schlatter Syndrome is childhood prone condition known as an Osteochondrosis. This condition tends effect young athletes participating in sports that involve a lot of running and jumping, such as dance and gymnastics. It tends to manifests itself in boys between 10-15yrs and 8-13yr girls, usually a time of peak height velocity. The common signs and symptoms are local pain, swelling and tenderness over the tibial tuberosity on the dominant leg, which makes participation in sport painful. The condition is self-limiting without complication if sporting activity is stopped and conservative treatment sought. However this presents serious limitations for serious athletes who must continue to training. This article aims to educate coaches on the aetiology, diagnosis, and treatment options of the condition, as well as well discuss the injury prevention and rehabilitation recommendations. It is believed that an appropriate understanding of this condition by coaches is important in order to be able to effectively implement preventative measures in their training programs, make appropriate recommendations to athletes, and work closely with health allies (like physiotherapists, GP, pediatricians) to be able to reduce losses in training time due to OSS. Key Words: Osgood-Schlatter Disease, injury prevention, overuse injury, knee injury INTRODUCTION In 1903, Robert Osgood, a US orthopaedic surgeon, and Carl Schlatter a Swiss surgeon, concurrently described the possible pathophysiology of the disease that now bears their names, Osgood-Schlatter Disease (1). They described it as an avulsion of a small portion of the tibial tuberosity caused by a violent contraction of the quadriceps extensor mechanism (2) Since then its has been more accurately labelled as a syndrome rather then a disease with many proposed theories to further explain its aetiology (OSD aka OSS), such as, degeneration of the patellar tendon, aseptic necrosis, infection, (2), trauma, local alternations of the chondral tissue, overpull by the extensor muscles of the knee, which can result in patella alta, and traction apophysitis, eccentric muscle pull and muscle tightness, and reduced width of the patella angle (3). It is now generally accepted that OSS is an avulsion fracture of the growing tibial tubercle (4), characterized by pain at the tibial tubercle resulting from repeated stress at the insertion of the patellar tendon due to extensor mechanism abnormalities (12). OSS is part of a group of conditions called osteochondrosis. These are a family of orthopaedic disease that occur in children, and involve areas of significant tensile or compressing stress (5) effecting the growing epiphysis (growth plate) (13). These conditions often arise in the knee/s, ankle/s, and elbow/s joints. OSS is categorized as a chronic overuse injury (7), which is most often diagnosed in young athletes (but not entirely exclusive), involved in sports that involve a lot of running and jumping, such as soccer, dance, gymnastics (10). It usually manifest itself in boys around 10-15yrs of age, and in girls around 8-13yrs of age, often coinciding with growth spurts and peak height velocity (1) The condition is usually unilateral (9), with 25% to 50% of patients developing a bilateral condition (11). There is a close relationship between the leg preferentially involved in jumping, and sprinting and it developing OSS (3). Traditional literature suggest that boys are more prevalent to OSS than girls, but more recent evidence indicates that with more and more girls being involved in sport, there is no longer any significant difference (14). The aim of this article is to examine the available literature and the current body of knowledge of the pathophysiology of OSS, in order to give coaches a better understanding and prevention methods. By educating coaches to recognise the possible signs and symptoms of this condition, coaches may be able to identify athletes at high/er risk of developing the condition, and thus be able to plan preventative measures ahead of time. It will also allow for

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A detailed study of the pathophisiology of Osgood-Schlatter Syndrome and a prescrived rehabilitation program suitable for gymnasts.

Transcript of A look at the pathophysiology and rehabilitation of Osgood-Schlatter Syndrome

Page 1: A look at the pathophysiology and rehabilitation of Osgood-Schlatter Syndrome

Gym Coach, Vol.2 (2008) 39-45 Commentary Article

©2008 The Gym Press. All rights reserved Gym Coach Vol.2, August, 2008 - 39-

A look at the pathophysiology and rehabilitation of

Osgood-Schlatter Syndrome

Valentin Uzunov Hataitai Gymnastics, Wellington, New Zealand

ABSTRACT Osgood-Schlatter Syndrome is childhood prone condition known as an Osteochondrosis. This condition tends effect young athletes participating in sports that involve a lot of running and jumping, such as dance and gymnastics. It tends to manifests itself in boys between 10-15yrs and 8-13yr girls, usually a time of peak height velocity. The common signs and symptoms are local pain, swelling and tenderness over the tibial tuberosity on the dominant leg, which makes participation in sport painful. The condition is self-limiting without complication if sporting activity is stopped and conservative treatment sought. However this presents serious limitations for serious athletes who must continue to training. This article aims to educate coaches on the aetiology, diagnosis, and treatment options of the condition, as well as well discuss the injury prevention and rehabilitation recommendations. It is believed that an appropriate understanding of this condition by coaches is important in order to be able to effectively implement preventative measures in their training programs, make appropriate recommendations to athletes, and work closely with health allies (like physiotherapists, GP, pediatricians) to be able to reduce losses in training time due to OSS.

Key Words: Osgood-Schlatter Disease, injury prevention, overuse injury, knee injury

INTRODUCTION In 1903, Robert Osgood, a US orthopaedic surgeon, and Carl Schlatter a Swiss surgeon, concurrently described the possible pathophysiology of the disease that now bears their names, Osgood-Schlatter Disease (1). They described it as an avulsion of a small portion of the tibial tuberosity caused by a violent contraction of the quadriceps extensor mechanism (2) Since then its has been more accurately labelled as a syndrome rather then a disease with many proposed theories to further explain its aetiology (OSD aka OSS), such as, degeneration of the patellar tendon, aseptic necrosis, infection, (2), trauma, local alternations of the chondral tissue, overpull by the extensor muscles of the knee, which can result in patella alta, and traction apophysitis, eccentric muscle pull and muscle tightness, and reduced width of the patella angle (3). It is now generally accepted that OSS is an avulsion fracture of the growing tibial tubercle (4), characterized by pain at the tibial tubercle resulting from repeated stress at the insertion of the patellar tendon due to extensor mechanism abnormalities (12). OSS is part of a group of conditions called osteochondrosis. These are a family of orthopaedic disease that occur in children, and involve areas of significant tensile or compressing stress (5) effecting the growing

epiphysis (growth plate) (13). These conditions often arise in the knee/s, ankle/s, and elbow/s joints. OSS is categorized as a chronic overuse injury (7), which is most often diagnosed in young athletes (but not entirely exclusive), involved in sports that involve a lot of running and jumping, such as soccer, dance, gymnastics (10). It usually manifest itself in boys around 10-15yrs of age, and in girls around 8-13yrs of age, often coinciding with growth spurts and peak height velocity (1) The condition is usually unilateral (9), with 25% to 50% of patients developing a bilateral condition (11). There is a close relationship between the leg preferentially involved in jumping, and sprinting and it developing OSS (3). Traditional literature suggest that boys are more prevalent to OSS than girls, but more recent evidence indicates that with more and more girls being involved in sport, there is no longer any significant difference (14). The aim of this article is to examine the available literature and the current body of knowledge of the pathophysiology of OSS, in order to give coaches a better understanding and prevention methods. By educating coaches to recognise the possible signs and symptoms of this condition, coaches may be able to identify athletes at high/er risk of developing the condition, and thus be able to plan preventative measures ahead of time. It will also allow for

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coaches to take appropriate treatment steps when symptoms arise during training as well as being able to effectively work with medical allies like physiotherapists in implementing a rehabilitation program for gymnasts who suffer from this condition.

DISCUSSION and REVIEW

Aetiology The exact cause and aetiology of OSS is still debated (2), but there is general consensus in literature that it is probably caused by one or more biological, biomechanical, and physiological factors. These are considered to be: Overpull of the extensor mechanism in the knee, linked with abnormalities in patella position (figure 1) (20), increase external tibial torsion (3), and possibly an increased Q-angle, observed especially in flat footed and knock-kneed children (46).

Traction-induced, microtrauma to the

apophysis, due to chronic overuse (12,16), skeletal immaturity, quadriceps muscletendon imbalance, hamstring, and calf flexibility restriction (14, 7) All these factors are reported in literature to either cause or predispose growing children to OSS. In a longitudinal study by Atsushi Hirano et al (2002), MRI was used to track and clarify the nature and course of OSS in 285 boys from high level junior soccer teams. They identified and described 5 stages of the condition, each with its distinct

characteristics and pathological alterations (figure 2). Normal Stage – MRI is normal but symptoms are present. Early Stage – MRI show no avulsion at the secondary ossification centre of the tibial tuberosity, but inflammation around the secondary ossification centre is present. Symptoms are initially not severe, but progresses quickly if no treatment is undertaken Progressive Stage – Presence of partial cartilaginous avulsion from the secondary ossification centre. Patients complain of pain, with obvious swelling of patellar tendon at insertion. Possible thickening of patellar tendon Terminal Stage – Existence of separated ossicles. Symptoms present for period of time (around several months), tenderness, swelling and pain at tibial tuberosity, with possible thickening of patellar tendon at insertion site. Pain triggered at stopping and turning motion. Patellar tendonitis is a possible secondary pathologic complication due to partial tear of the secondary ossification centre. Healing Stage – Osseous healing of the tibial tubercle without separated ossicles. Visible prominence of tibial tuberosity, the patellar tendon could still be thickened at insertion, but not always. Chronic overuse injuries (especially in young athletes) make up 30-50% of all paediatric sport injuries in children (16) Overuse injuries occur when tissue is repeatedly stressed by repeated submaximal (16) and maximal eccentric loading (6). The process starts when repetitive activity fatigues a specific structure such as tendon or

Figure 1 - Diagram of the knee joint

and the extensor machenism made up of the quadriceps muscle group, quadriceps tendon, patella, patellar, retinaculum, patellar ligament and an assortment of other soft tissues in that area. The tibial tuberosity is the associated site of injury in athletes with OSS. Image source: John Hoppkins Sport Medicine

Figure 2 (below) - A typical case study of OSS progression Figure 2 - A typical case study of OSS progression in a active child over a 2.3 years period.(A) At 10.1 years old, development of the tibial tuberosity was in the cartilaginous stage and normal. (B) At 11.3 years old, this image showed that a tear had appeared in the secondary ossification center (arrow) and development of the tibial tuberosity was in the apophyseal stage.(C) After 1 month, the MR image showed an opened shell like separation (arrow) and the disease had advanced to the progressive stage. The growth of the tibial tuberosity had entered the epiphyseal stage. High signal intensity appeared within the patellar tendon. (D) After 2 months the MR image showed that an anterior avulsed portion had been separated (arrow). (E) At 12.4 years old, the ossicle had moved further superiorly (arrow).

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bone. With sufficient recovery the tissue adapts to the demands and is able to undergo further loading without injury. Without adequate recovery, microtrauma develops and stimulates the body‟s inflammatory response, causing therelease of vasoactive substances (histamines, leukotaxin, necrosin), inflammatory cells (macrophages, lymphocytes, and plasma cells), and enzymes that damage local tissue. In chronic or recurrent cases, continued loading produces degenerative changes leading to weakness, loss of flexibility, and chronic pain, all of which as associated with OSS (16, 12). Contributing factors to overused injuries with special consideration to OSS can be classified as intrinsic and extrinsic. With children special consideration needs to be given to the immature musculoskeletal systems (16). Intrinsic factors that need to considered are: Growth-related factors. Cartilaginous tissue in children is more susceptible to repetitive stress, especially in the knees, elbows, and ankles (16). The development of the tibial apophysis begins as a cartilaginous outgrowth. During this stage the tuberosity tissue has a decreased resistance to mechanical stress (16). Secondary ossification centres appear with a subsequent progression to an epiphyseal phase when the proximal tibial apophysis closes and the tibial apophysis fuses to the tibia (22). Calcification of the apophysis begins distally at 9yr of age for girls, and 11yrs for males. Fusion of the apophysis to the tibia can take place via several ossification centres, and occurs on average at 12yr of age for girls and 13yrs of age for boys (also coinciding with the age of OSS development), (23). Prior and during these developmental ages of the tibial apophysis, it is more vulnerable to injury, until the apophysis and epiphyseal are calcified and fused. This is a critical time for all gymnasts who train long hours at young ages. Tumbling and vaulting during this period of time should be carefully monitored and not overdone, especially for gymnasts who are have predispositions. Full floor tumbling should be restricted to once a week, and more time should be spent on predominantly on softer non impacting surfaces, such as rod-floors, tumble tracks, air tracks etc, Vaults should be landed on soft surfaces such a into a pit, soft crash mats. The gymnasts should be restricted to a dozen full vaults a week spread over a week. A second growth that needs consideration is the imbalance between growth and development of long bones, and the adjacent muscle-tendon attachments (16). This imbalance can occur rapidly during a growth spurt (peak height velocity), were bone length can develop faster than muscle-tendon unit (12) Joint tightness, reduced flexibility (of special relevance are the quadriceps, and hamstring muscle groups which are associated with OSS), muscle imbalance, and knee extensor mechanism dysfunction can develop as a result of the imbalanced between growth and development of the bone and muscletendon unit (16).This can lead to increased traction on the apophysis and stress at the joint surface of the knee, which is a well established cause for OSS development (16). Knee extensor mechanism dysfunction is veryoften cited in literature as a

main contributing cause for OSS (9, 20). The extensor mechanism in the knee consists of the quadriceps muscle (rectus femoris), patella, patellar tendon, patella retinacula, and the tibial tuberosity (figure 1)(21). The patellar is subjected to great forces from its attachment to the quadriceps rectus femoris muscle (proximally) and the patellar tendon (distally). The hamstrings are also undergoing the same stresses as the quadriceps, because of the difference between the growth rate of the femur, and the hamstring muscle groups. Increased hamstring tightness causes increased patellarfemoral joint reaction forces because of an increased knee flexion moment, which means the quadriceps has to pull harder during athletic activities, consequently placing more traction force on the tibial tubercle (49), Thus it is critical to restore balance between the quadriceps and hamstring strength, and flexibility ratios. There is debate regarding the correct strength H/Q (hamstring/quadriceps) ratio with regard to injury prevention, but a ratio 0.6 at an angular velocity of 1.05 rad.s-1 is frequently quoted as the standard for injury prevention and rehabilitation (50). To a coach this means nothing, as he/she cannot test it. However regularly testing and monitoring the gymnast hamstring and quadriceps ROM and performing 1 hamstring strengthening exercise for every 3 quadriceps dominant exercises will generally help maintain this ratio balanced. In a study by Hiroshi Ikeda et al (1999) published in the journal of orthopedic surgery, they looked at quadriceps strength, between athletic and non-athletic boys, with and without OSS. They determined that repeated traction of the quadriceps muscle on the tibial tuberosity due to abnormal quadriceps tightness, and increased eccentric quadriceps strength, contributed to the development of OSS. Tight quadriceps muscles are not resilient enough to absorb ground reaction forces on impact; as a consequence forces act directly on the bone-tendon junction of the tibial tuberosity (24). In most cases OSS is treated with conservative therapy, as it is normally a self-limiting condition. Once the apophysis and epiphysis close, the symptoms of the condition usually end. This happens at around 18yrs of age for boys and girls, with an excellent prognosis for full recovery (1). Complications can arise during and after skeletal maturity, as a results patients not following physician‟s recommendations, and continue to take full part in sports, without any activity modification or rest (1). The typical complications are tibial tuberosity deformity, which is almost inevitable, nonunion of tendon to tibial tuberosity, patella alta after skeletal maturity, increasing likelihood of lateral patellar dislocation, knee degenerative arthritis, bursal chondromatosis, which has been documented only once, as a result of untreated OSS. Softening of cartilage, displaced avulsion fracture of tibial tubercle, usually occurs in athletes without pre-existing OSS, but the most common reported complication is ossicle formation. (9,1,26,4,10). Most of these complications arise due to extensor mechanism dysfunction, and thus are treated by restoring normal extensor mechanism function (39).

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Ossicle formation occurs as a result of a partial tear developing in the secondary ossification centre during the progressive stage. If the tear extends to the anterior parts that consist of bone and cartilage, small regions of the preossification or anterior secondary ossification centers may be avulsed superiorly forming an open-shell like separation (Figure 2, C). (2). If the gap formed is small, fibrocartilage can bridge the gap and ossify, with such a situation leading to the healing stage of OSS (2, 4). If the gap is large, fibrocatilage will not be able to bridge the gap and, the avulsed fragment/s mature to form separate ossicles/s within the patellar tendon, with such a situation being characteristic of the terminal stage of OSS (2). Approximately 10% of ossicles fail to unite with the tibial tubercle. These patients will continue to experience anterior knee pain, even after ossification of tibial tuberosity, and will require surgical excision to alleviate the pain (4). Diagnosis Diagnosis of OSD is not clinically challenging once signs and symptoms are clearly present, but it is very difficult to diagnose clinically at its onset (12, 2). In most circumstances patient who have obvious signs and symptoms, can be diagnosed by a family physician, with a physical exam (15). However based on the study by Atsushi Hirano et al. (2002) it is advised that a specialist, sports doctor, or physiotherapist, make the diagnosis using a physical exam and an MRI (ideally) or X-ray as well. This is particularly applicable if check-up is done at onset of symptoms. Prior to making a definite diagnosis, doctors should also rule out other possible anterior knee pain conditions, such as, Sindling-Larson-Johansson syndrome, osteomyelities, tibia, fibula, femur or patellar fracture, tumor, patellar tendonitis (jumpers-knee), slipped capital femoral epiphysis, Perthes disease, petellofemoral syndrome, and osteochondrosritis dissecans, some of which may require a imaging study , and thus further supporting the need to have and MRI or X-ray done for a definitive diagnosis (1,17, 10). The standard clinical diagnostic signs, symptoms, and tests are: 1. Pain, swelling and aching around tibial tubercle, with the possibility that the tibial tubercle is reddened, raised or tender to palpation (12), 2. Visible enlargement or prominence of tibial tubercle (1). 3. Pain generally occurs during activities involving the legs (especially eccentric contractions of quadriceps) and goes away with rests (24). 4. There is no history of the knee giving way, locking out, or catching (10). 5. Pain worsens with activities that require squatting, walking up and down stairs, and forceful contractions of the quadriceps muscle. (17). 6. No signs of effusion, minuscule damage, and normal neurovascular examination (1). 7. No limitations in the hip ROM, and especially no pain with hip internal rotation (symptoms of slipped capital

femoral epiphysis and Perthes disease, which can cause referred pain to knee) (10) Commonly used diagnostic tests for OSD are: 1. Pain elicited with extension of the knee at 900 of flexion, while a resisted straight-leg raise does not. (14) 2. An alternative test is to force the tibia into internal rotation, while slowly extending the knee from 900 of flexion; at about 30deg, flexion produces pain that subsides immediately with external rotation of the tibia. (40) 3. Pain can also be reproduced with passive hyperflexion of the knee. (17). 4. A positive Ely test (19) 5. Point tenderness eliciting pain approximately 2inches under knee cap over tibial tuberosity. (18) 6. Full ROM is available at the knee, but tightness in hamstring muscle group is noticeable (1). OSS Prevention and Rehabilitation As the late Dutch humanist and theologian Desiderius Erasmus Roterodamus said “prevention is better then cure”. This is always the case, and it‟s important that coaches understand and implement preventative measure to identify young gymnasts who are prone or at greater risk of developing this condition. From the discussion of the pathophysiology of the condition, there are several preventative strategies useful to coaches. 1-Regular physical testing of the quadriceps and hamstrings to determine the risk of imbalance in strength and flexibility. 2- Coach awareness. Coaches need to know the signs and symptoms of kids at risk, or who are showing potential onset symptoms. 3- Adding regular quadriceps stretches into every flexibility program, from day 1 of sport involvement, to balance out all the hamstring flexibility done in gymnastics 4- Inclusion of 1 hamstring exercise for every 3 quadriceps exercises, matched in intensity. 5- Regular height measurements of gymnasts in order to be able to track height velocity. Its important to be aware of when the gymnasts is having/starting a growth spurt as gymnasts are most at risk during this developmental stage. Gymnasts undergoing a growth spurt should have their training revised to reduce the volume and frequency of high intensity, high impact, lower body activity, which involves strong eccentric quadriceps contractions such as tumbling on the floor, vaulting, and repetitive high landings. Gymnasts can continue to work their skills, but at a modified and reduced rate while undergoing the growth spurt. It is important to be vigilant for gymnasts, who show signs and symptoms, and to monitor their training programs effectively, to prevent gymnasts from doing too much to soon. This condition is easily preventable with smart training and program design. For gymnasts who have developed this condition treatment without complications can be divided into three phases: acute, recovery, maintenance. Treatment management is

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usually conservative, for 6months to a 1 year (12). During the acute phase treatment management should concentrate on reducing the signs and symptoms of inflammation, and pain (12). The best treatment management depends on the severity of the symptoms, and the initial management of the first signs leading to the initial diagnosis of OSS. This has a significant impact on the course of the rehabilitative process during the recovery phase (12, 10). Recommended options to manage the condition are: RICE (rest, ice, compression, elevate), warming up properly before activity, icing for 20min after activity, short term rest or immobilization (2-3wks),

activity modification like running slower, avoiding deep knee bending footwear, and use of a infrapetellar strap (figure 3) during activity (12,18, 1,14 31,9,28,64). Unfortunately these remedies have shown little evidence of improving outcome, but have been shown to be effective means of pain management (35).

For acute flare-ups, and relief of inflammation, the use of anti-inflammatory medication, an algesics, and cryotherapy is

recommended. If pain is mild, and there is no inflammation, using a heating pad or warm, moist compresses for 15min be fore activity can help reduce symptoms and pain, as well as 15-20min of icing after activity (6,32). During the acute phase it is very important that symptoms of inflammation are first controlled. Physical therapy is not commenced immediately as it can exacerbate acute symptoms. For the ambitious athlete suspending physical activity altogether is not an option, so coaches must effectively modify their training program till pain is relieved. The only form of physical therapy allowed is hamstring, calf, and hip stretching which can begin immediately as recommended by a qualified physiotherapist not a GP (6, 14). Long term immobilization (6wks+) is only recommended for extremely severe cases, (especially in children) (12), usually enforced by using a cast where compliance to conservative treatment is not adhered too (27,10). The recovery phase can start once pain is controlled and the inflammation disappears. The main focus of the rehabilitation program is to return the patient to his or her sport or activity as safely as possible (7). Hamstring and quadriceps stretching and hamstring strength are the main objectives. (12) Quadriceps strength in usually not a problem in young athletes, but it can become a problem in chronic cases, resulting in muscle atrophy, requiring strengthening exercises as well (12). Initially in the strengthen program for chronic cases with muscle atrophy, exercises should be done with minimal knee flexion in order to reduce the load on the tibial tubercle (19).

Exercises should be pain-free, involving isometrics or low load high repetition knee extension exercises (12). Stretches must target the quadriceps muscle belly with minimal stress to the tibial tubercle, two joint stretching exercises should be incorporated only when adequate flexibility is achieved. (12) Overzealous stretching can lead to complication rather than benefits and should be discouraged. (12). Studies show that physical load restriction during the acute and recovery phases has great benefits in prevention of complications, and during the course of OSD. (33). Conservative therapy is initiated during the normal, early and progressive stages of the course of OSS, there is a 90% chance of an early recovery and progression to the maintenance stage and eventually the healing stage if treatment begins with the first signs of OSS. (2). From the study by Atsushi Hirano et al (2002), it takes on average 3.8weeks to return to modified training if treatment starts from the normal or early stage, 6.3 weeks from progressive stage, and 13.2 weeks from the terminal stage, but usually not symptom free. In the terminal stage, symptoms alleviation is a result of reduced patellar tendonitis which is a secondary complication. (2). In other literature the most often reported prognosis is 6-24months till return to sport (1). However it must be remembered that “everyone recovers from injury at a different rate” (7), and these recovery times are averages, and should only be used a guidelines. Gymnasts can also continue working on elements that do not aggravate their condition. The progression to the maintenance phase is usually through the recommendation by a general physician or physiotherapist after an examination, showing clear signs of recovery. Care must be taken to ensure that the athlete is not returning to sport too soon, as complication can arise. (1). A number of functional tests can be performed to test the patient‟s ability to safely return to sport. Functional progressions that can be used to determine if patient is ready to return to sport are (7): 1. The patient tibial tuberosity is no longer tender to touch. 2. The injured knee can be fully straightened and bent without pain. 3. The knee and leg have regained normal strength compared to the uninjured knee and leg. 4. Individual is able to jog straight ahead without limping. 5. Individual is able to sprint straight ahead without limping. 6. Individual is able to do 45-degree cuts. 7. Individual is able to do 90-degree cuts. 8. Individual is able to do 20-yard figure-of-eight runs. 9. Individual is able to do 10-yard figure-of-eight runs. 10. Individual is able to jump on both legs without pain and jump on the injured leg without pain If pain returns it is recommended that patient take a further 6months, continuing conservative therapy, and rehabilitation program (26).

Figure 3 – A standard infrapetella strap, has been shown to decrease pain in 19 of 24 (79%) knees after 6 to 8 weeks of use in one study (64).

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CONCLUSIONS OSS is a common overuse injury that occurs equally in active boys and girl who participate in sports involving regular running and jumping, particularly if done on hard surfaces. There are 5 stages to the condition, with symptoms presenting themselves in the Early stage. The condition is self-limiting, and can be treated effective if diagnosed in the early stage with conservative treatment, and rehabilitative exercises, with minimal restrictions. If the condition is untreated and it progresses to the terminal stage, the condition can greatly restrict sport participation,

and may eventually lead to the need for surgery if ossicles calcify. Coaches should understand the aetiology of this condition in order to indentify athletes at risk and implement the necessary injury preventative measures. Rehabilitation is effective only when the acute symptoms are under control Every care is taken to assure the accuracy of the information published within this article. The views and opinions expressed within this article, are those of the author/s, and no responsibility can be accepted by The Gym Press, Gym Coach or the author for the consequences of actions based on the advice

ACKNOWLEDGEMENTS

This article is an abbreviated version of original manuscript by Valentin Uzunov (2007). An in-depth look at the pathophysiology and treatment of Osgood-Schlatter

Disease. Research project submission for Massey University. If you would like a copy of the full unmodified version, contact Valentin Uzunov a

[email protected]

Address for correspondence: Valentin Uzunov, Hataitai Gymnastics, Wellington, New Zealand. [email protected]

REFERENCES and RECOMMENDED READINGS 1 .Munisha Mehra Bhatia (2004). Osgood-Schlatter Disease, Emedicine [e-journal] http://www.emedicine.com/sports/topic89.htm, date accessed: Jul 13 2004 2. Atsushi Hirano, Toru Fukubayashi, Tomoo Ishii, Naoyuki Ochiai. (2002) „Magnetic resonance imaging of Osgood-Schlatter disease: the course of the disease‟. Skeletal Radiology, Vol 31; 334-342 3. Antonio Gigante, Claudia Bevilacqua, Massimo G Bonetti & Francesco Greco (2003) „Increased external tibial torsion in Osgood-Schlatter disease‟. Acta Orthopaedica Scandinavica, Vol. 74 No.4;431-436 4. Kazunari Ishida, Ryosuke Kuroda, Keizo Sato, Tetsuhiro Iguchi, Minoru Doita, Masahiro Kurosaka, & Tetsuji Yamamoto (2005) „Infrapatellar Bursal Osteochondromatosis Associated with Unresolved Osgood-Schlatter Disease‟. Journal of Bone and Join Surgery, Vol. 87 No.12; 2780-2783 5. Sue E. Huether & Kathryn L. McCance (2004) Understanding Pathophysiology; Missouri St Louise; Mosby. 6. L. Pearce McCarty III (2005). „Treating patients with patellofemoral conditions--Most can be managed nonoperatively‟. The Journal of Musculoskeletal Medicine, Vol. 22; 667-673 7. McKesson Health Solutions (2004).‟Osgood-Schlatter Disease‟. Pediatric Advisor. Jan 1. 2270. 9. James F. Dunn Jr. (1990) „Osgood-Schlatter disease‟. American Family Physician, Vol.41, No.1; 173(4). 10. Eric J. Wall (1998).‟ Osgood- Schlatter Disease; Practical Treatment for a Self-Limiting Condition‟. The Physician and Sportsmedicine. Vol.26, Iss. 3; 29 11. Cliggot Publishing Co. (2001). Consultant, Vol 41,Iss 10; 1479 12. William E. Prentice & Michael I. Voight, (2001). Techniques in Musculoskeletal Rehabilitation. New York: McGraw Hill 13. Leslie Klenerman (1994). „Musculoskeletal injuries in child athletes (ABC of sport medicine)‟. British Medical Journal. Vol 308, No. 6943 ; 1556(4) 14. David M. Peck (1995).‟ Apophyseal injuries in young athletes‟. American Family Physician. Vol. 51,No. 8; 1891(7) 15. OJ Bloom, & Leslie Mackler, Barbee J. (2004)‟What is the best treatment for Osgood-Schlatter Disease?‟. The journal of family practice. Vol. 53, No. 2. 16. John. P. DiDiori. (1999)‟Overuse injuries in children and adolescents‟. The Physician and Sportsmedicine. Vol 27, Iss. 1; pg75 17. Walter L. Calmbach & Mark Hutchens (2003).‟Evaluation of Patients Presenting with Knee Pain: Part II. Differential Diagnosis. American Family Physician. Vol.23, No.9:917-922 18. Sheila Globus (2002).‟Osgood-Schlatter: More than growing pains. Current Health. Stamford. Vol. 28, Iss. 5; 20 19. Gregory S. Kolt & Lynn Snyder-Mackler (2003). Physical Therapies in Sport and Exercise. London; Churchill Livingstone 20. R.P. Jakob, S. Von Gumppenberg, and P Engelhardt (1989).‟Does Osgood-Schlatter Disease Influence the Position of the Patella‟. The Journal of Bone and Joint Surgery.Vol.63-B, No. 4, 579-582 21. H. Ware (1996).‟Injury to the extensor mechanism in the knee‟. The Knee. Vol. 3 Iss. 1; 94(2) 22. Graf BK. Fujisaki CK, Reider B,(1991), Disorders of the patellar tendon‟ in: Reider B, ed.. Sport Medicine: The school aged Athlete. Philladelphia, Saunders, 1991. p355

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23. Kujala UM, Kvist M, Heinonen O (1985) Osgood- Schlatter Disease in Adolescent Athletes: ‟Retrospective study of incidence and duration. American journal of Sport Medicine. Vol.13 :239 24. Hiroshi Ikeda, Hisashi Kurosawa, Keishoku Sakuraba, Hauyasu Ohta and SunGon Kim (1999).‟Analysis of quadriceps muscle strength and tension in adolescent athletes with Osgood-Schlatter disease. Journal of Orthopedic Surgery. Vol 7, Iss.1; 27-31 26. Debera Brodwell Jackson, Rebecca B. Saunders (1993).‟Child Health Nursing: A comprehensive approach to care of children and their families; Philadelphia: Lippincott Company 27. Kathryn L. McCance & Sue Heather, (2002) Antrophysiology: The Biologic Basis for Disease in Adults & Children; St. Louis: Mosby 28. Dr Emma Lackey and Dr Ron Sutton(2006).‟Clinical: Rest is the best treatment for common knee swelling. GP. Feb 17, 2006, p30 31. Steven I. Subotnick (1977). The running foot doctor; California: World Publications 32. Robert C. Meisterling, MD, Eric J. Wall, MD, Michael R. Meisterling, (1998).‟Coping with Osgood-Schlatter Disease. The Physician and Sportsmedicine. Vol.26, Iss.3; pg39 33. Viktoras Gerulis, Romas Kalesinskas, Sigitas Pranckevicius, Paulius Bergeris, (2004)‟ Importance of conservative treatment and physical load restriction to the course of Osgood-Schlatter‟s disease‟.Medicina. Vol 40, No. 4:pg363-369 35. K. Dean Reeves, Brad Fullerton, Gaston Topol, and Greg Bancroft (2006) „Study seeks treatment to keep athletes in the game: The effects of Osgood-Schlatter disease can extend beyond resolution of pain to a patient‟s sports career‟. BioMechanics Magazine Online [e-magazine] http://www.biomech.com/showArticle.jhtml?articleID=185302966. April 2006 issue. Date accessed: 7.5.06 39. Freddie H. Fu & David A. Stone (1994). Sport Injuries: Mechanisms, Prevention, Treatment. Baltimore, Maryland; William & Wilkins 40. Springhouse publishing company (2005) Professional guide to diseases. Pennsylvania; Lippincott Williams and Wilkings 46. Medical multimedia group (2005).‟A patient‟s Guide to Osgood-Schlatter Lesion of the Knee”. eOrthopod [http://www.eorthopod.com/eorthopodV2/index.php/fuseaction/topics.detail/ID/1e69153b4390c6eff3095daeefe6031a/TopicID/9c2c5ae2333ff1b24f5fb4a3abba8184/area/46 ]. Date accessed 23.05.2006. 49. Naoko Aminaka; Phillip A. Gribble (2005).‟A systematic review of the Effects of Therapeutic Taping on Patellofemoral pain syndrome‟. Journal of Athletic Training. Vol. 40(4): pg 341-351 50. Rosalind Coombs and Gerard Garbutt, (2002).‟ Developments in the use of the hamstraing/quadriceps ratio for the assessment of muscle balance‟. Journal of sport science and medicine. Vol.1: Pg 56-62\ 51. M.G.E. Peterson, M. Murray-Weir, L Root, M. Lenhoff, L. Daly, C. Wagner, (2000.)”Bootstrapping Gait Data from People with Cerebral Palsy,” cbms, p. 57, 13th IEEE Symposium on Computer-Based Medical Systems (CBMS‟00), 64. Levine J, Kashyap S (1981). A new conservative treatment of Osgood-Schlatter disease. Clin Orthop. 1981; 158:126-128.