An in-depth look at the pathophysiology and treatment of Osgood-Schlatter Disease - Part A

Part A: Pathophysiology

In 1903, Robert Osgood, a US orthopedic surgeon, and Carl Schlatter a Swiss surgeon, concurrently described the possible pathophysiology of the disease that now bears their names, 'Osgood-Schlatter Disease' (Munisha Mehra Bhatia, 2004). They described it as an avulsion of a small portion of the tibia tuberosity caused by a violent contraction of the quadriceps extensor mechanism (Atsushi Hirano, Toru Fukubayashi, Tomoo Ishii, Naoyuki Ochiai, 2002). Since then many theories have been suggested by others to further explain the etiology of Osgood-Schlatter Disease (OSD), such as, degeneration of the patellar tendon, aseptic necrosis, infection, (Atsushi Hirano et al, 2002), trauma, local alternations of the chondral tissue, mechanical 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 (Antonio Gigante, Claudia Bevilacqua, Massimo G Bonetti & Francesco Greco, 2003). It is now generally accepted that OSD is an avulsion fracture of the growing tibial tubercle (Kazunari Ishida, Ryosuke Kuroda, Keizo Sato, Tetsuhiro Iguchi, Minoru Doita, Masahiro Kurosaka, & Tetsuji Yamamoto, 2005), characterised by pain at the tibial tubercle resulting from repeated stress at the insertion of the patellar tendon due to extensor mechanism abnormalities (William E. Prentice & Michael I. Voight, 2001).

OSD is essentially patellofemoral apophysitis condition (L. Pearce McCarty III, 2005), which is part of a group of disease called osteochondrosis. These are a series of childhood disease involving areas of significant tensile or compromise stress (Sue E. Huether & Kathryn McCance, 2004) effecting the growing epiphysis (Leslie Klenerman, 1994). There are 5 broad diagnostic categories of patellofemoral pathology: acute traumatic, chronic overuse, patellofemoral pain syndrome, degenerative joints disease, and miscellaneous (L. Pearce Mccarty III, 2005). OSD is categorised as a chronic overuse injury (McKesson Health Solutions, 2004), 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, basketball, dance, and gymnastics (Eric j. Wall, 1998). It usually manifest itself in boys around the ages of 10-15, and in girls around 8-13 coinciding with growth spurts and peak height velocity (Munisha Mehra Bhatia, 2004). The condition is usually unilateral (James F. Dunn Jr., 1990), with 25% to 50% of patients developing a bilateral condition (Cliggott Publishing Co, 2001). There is a close relationship between the leg preferentially involved in jumping, and sprinting and it developing OSD (Antonio Gigante et al., 2003). Traditional literature suggest that boys are more prevalent to OSD than girls, but more recent evidence indicates that with more and more girls being involved in sport, there is no longer any significant difference (David M. Peck, 1995).

Diagnosis of OSD is not clinically challenging once symptoms are present and clear, but it is very difficult to diagnose clinically at its onset (William E. Prentice & Michael I. Voight, 2001, Atsushi Hirano et al.2002). In most circumstances patient who have the signs and symptoms, can be diagnosed by family physician, with a physical exam (Josh Bloom & Leslie Mackler, 2004). 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 my require a imaging study (Munisha Mehra Bhatia, 2004,Walter L. Calmbach & Mark Hutchens, 2003, Eric J. Wall, 1998) Diagnosis should focus on how and when the injury developed, in order to be able to best develop treatment and prevention recommendations (John. P. DiDiori, 1999). 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 (William E. Prentice & Michael I. Voight, 2001),
  2. Visible enlargement or prominence of tibial tubercle (Munisha Mehra Bhatia, 2004).
  3. Pain generally occurs during activities involving the legs (especially eccentric contractions of quadriceps) and goes away with rests (Hiroshi Ikeda et al.,1999).
  4. There is no history of the knee giving way, locking out, or catching (Eric j. Wall, 1998).
  5. Pain worsens with activities that require squatting, walking up and down stairs, and forceful contractions of the quadriceps muscle. (Walter L. Calmbach & Mark Hutchens, 2003).
  6. No signs of effusion, meniscal damage, and normal neurovascular examination (Munisha Mehra Bhatia, 2004).
  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 cause referred pain to knee) (Eric J. Wall, 1998)

  8. Commonly used diagnostic tests to test for signs and symptoms of OSD are:
  9. Pain elicited with extension of the knee at 90 degrees of flexion, while a resisted straight-leg raise does not. (David M. Peck, 1995)
  10. 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. (Springhouse publishing company, 2005)
  11. Pain can also be reproduced with passive hyperflexion of the knee. (Walter L. Calmbach & Mark Hutchens, 2003)
  12. A positive Ely test, (Gregory S. Kolt & Lynn Snyder-Mackler, 2003)
  13. Point tenderness eliciting pain approximately 2inches under knee cap over tibial tuberosity. (Sheila Globus, 2002)
  14. Full ROM is available at the knee, but tightness in hamstring muscle group is noticeable (Munisha Mehra Bhatia, 2004)

The cause and etiology of OSD is still debated (Atsushi Hirano et. al, 2002), but there is general consensus in literature that it is probably the 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 (R.P. Jakob, S. Von Gumppenberg, and P Engelhardt, 1989), increase external tibial torsion (Antonio Gigante et al., 2003), and possibly an increased Q-angle, observed especially in flat footed and knock-kneed children (Medical Multimedia Group, 2005). Traction-induced, microtrauma to the apophysis, due to chronic overuse (William E. Prentice & Michael I. Voight, 2001, John. P. DiDiori, 1999), skeletal immaturity, quadriceps muscletendon imbalance, hamstring, and calf flexibility restriction (David M. Peck, 1995, McKesson Health Solutions, 2004) All these factors are reported in literature to cause, or predispose growing children to OSD. In a longitudinal study by Atsushi Hirano et al (2002), MRI was used to track and clarify the nature and course of OSD in 285 boys belonging to the junior team of the Japan Professional Soccer Team. They identified and described 5 stages of the disease, each with its distinct characteristics and pathological alterations.

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 progress 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 topartial 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 pediatric sport injuries in children (John. P. DiDiori, 1999) Overuse injuries occur when tissue is repeatedly stressed by repeated submaximal (John. P. DiDiori, 1999) and maximal eccentric loading (L. Pearce McCarty III, 2005). The process starts when repetitive activity fatigues a specific structure such as tendon or 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 the release 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 OSD (John. P. DiDiori, 1999, William E. Prentice & Michael I. Voight, 2001).

Contributing factors to overused injuries with special consideration to OSD can be classified as intrinsic and extrinsic. With children special consideration needs to be given to the immature musculoskeletal systems (John. P. DiDiori, 1999). 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 (John. P. DiDiori, 1999). The development of the tibial apophysis begins as a cartilaginous outgrowth. During this stage the tuberosity tissue has a decreased resistance to mechanical stress (John. P. DiDiori, 1999). Secondary ossification centres appear with a subsequent progression to an epiphyseal phase when the proximal tibial physis closes and the tibial apophysis fuses to the tibia (Graf BK. Fujisaki CK, Reider B, 1991). 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 OSD development), (Kujala UM, Kvist M, Heinonen O, 1985). 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. At the apophysis there is a normal transition between distal fibrocartilage to proximal fibrous tissue. The fibrous tissue is better able to withstand high tensile loads, than weaker cartilage of the secondary ossification centre. Because of the growth characteristics at the tibial tuberosity, microavulsion are more likely to occur due to repeated stress though the area of bone and cartilage at the secondary ossification centre, leading to the terminal stage of OSD as described by Atsushi Hirano et al (2002) (William E. Prentice & Michael I. Voight, 2001, Atsushi Hirano et al., 2002, John. P. DiDiori, 1999). Children's bones are also more porous than adults, and further weakened by the epiphysial plate. This and other factors explained later are evidence explaining why OSD is more prevalent in children who are undergoing a rapid growth spurt (Leslie Klenerman, 1994).

A second growth factor that needs consideration is the imbalance between growth and development of long bones, and the adjacent muscle-tendon attachments (John. P. DiDiori, 1999). This imbalance that can occur rapidly during a growth spurt, were bone length can develop faster than muscle-tendon unit (William E. Prentice & Michael I. Voight, 2001) Joint tightness, reduced flexibility (of special relevance are the quadriceps, and hamstring muscle groups which are associated with OSD), muscle imbalance, and knee extensor mechanism dysfunction can develop as a result of the imbalanced between growth and development of the bone and muscle-tendon unit (John P. DiDiori, 1999).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 OSD development (John P. DiDiori, 1999). Knee extensor mechanism dysfunction is very often cited in literature as a main contributing cause for OSD. The extensor mechanism in the knee consists of the quadriceps muscle (rectus femoris), patella, patellar tendon, patella retinacula, and the tibial tuberosity (H. Ware, 1996). The patellar is subjected to great forces from its attachment to the quadriceps rectus femoris muscle (proximally) and the patellar tendon (distally). As previously mentioned, during rapid growth, the tibial tuberosity, especially at the apophysis, is susceptible to strain as a result of repetitive, submaximal stress from the quadriceps muscle. (James F. Dunn Jr., 1990, R.P. Jakob, S. Von Gumppenberg, and P Engelhardt, 1989). 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. However the hamstring muscle insertions are not affected like the quadriceps attachments (David Edell, 2005). 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 (Naoko Aminaka; Phillip A. Gribble 2005), Thus it is critical to restore balance between the quadriceps and hamstring strength, and flexibility ratios. There is debate regarding the correct H/Q (hamstring/quadriceps) ratio with regard to injury prevention, but a ratio 0.6 at a angular velocity of 1.05 rad.s-1 is frequently quoted as the standard for injury prevention and rehabilitation (Rosalind Coombs and Gerard Garbutt, 2002)

In a study by Hiroshi Ikeda, Hisashi Kurosawa, Keishoku Sakuraba, Hauyasu Ohta and SunGon Kim published in the journal of orthopedic surgery (1999) they looked at quadriceps strength, between athletic and non-athletic boys, with and without OSD. 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 OSD. 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 (Hiroshi Ikeda et al., 1999). A further complication to increased uadriceps tightness and eccentric strength in athletic patients with OSD (as a result of sporting practice), is its effect on the position of the patellar, resulting in patella alta (Antonio Gigante et al., 2003). In a study done by R.P. Jakob, S. Von Gumppenberg, and P Engelhardt, in 1989, they investigated patella position with association to OSD. Measuring the position of the patellar using Blackburne and Peels method, they confirmed that the normal patellar index is 0.80. The value increases to 1.01 in boys and 0.91 in girls with OSD sign and symptoms, but it can go up to 1.06 in boys with radiographic evidence of loose ossicles present in the patellar tendon. Elevation of the patella was attributed to tightness of quadriceps. The same findings were not statistically significant in their research for girls. The rational for this was that the boys used and in general had/have better developed or even hypertrophic quadriceps muscles as a result of sporting conditioning, which increases the pulling force on the tibial tuberosity. Their finding suggests that strong overpull of the well developed quadriceps is one of the most important aetiological factors in patella alta associated with OSD. In other studies looking at OSD and patella alta, the patella has been observed to be as much as 2cm higher than normal, resulting from patella tendon elongation or upward pull on the apophysis, attributed again due to quadriceps tightness.

Increased external tibial torsion is another documented intrinsic factor contributing to OSD. Tibial torsion alters in the growing child. At birth children tend to have medial or neutral torsion. As the child begins to grow, external (also know as lateral) tibial torsion develops. By 5 years of age the adult level of external torsion has developed, which is between 0-20degrees. (M.S. Turner, I.S. Smillie, 1981). In a study by Antonio Gigante et al., (2003) they examined the relationship of OSD and torsional abnormalities of the lower limb. They found a close relationship between, increased external tibial torsion, and OSD. In their study they acknowledge that the relationship between tibial torsion and OSD is not "a cause and effect relationship", but rather, in conjunction with other factors, possibly mechanical, that predisposes children to the onset of OSD. Tibial torsion effects the distribution of stress around the knee. The greater the external tibial torsion angle, the greater the shear stress on the tibial tuberosity during extension of the knee. An increase in shear stress to the tibial tuberosity during activities such as running, jumping, landing, may affect the metabolism of the growth plate and tibial apophysis, which can predispose children to OSD (Antonio Gigante et al., 2003). Increased tibial torsion is also linked closely to the Q-angle. Increases in Q-angle could be due to increased external tibial torsion, and femoral anteversion caused by tight hip internal rotators, laterally displaced tibial tubercles, or genu valgum (knocked kneed) (Beckman, M.; Craig, R.; Lehman, R.C, 1989). however, currently there is no medical literature that supports increased Q-angle and OSD. The author was able to find one such source (Medical Multimedia Group, 2005) but it had no references, thus its validity is unknown. None the less, the implications of an increased Q-angle have to be considered, when physically examining patients with OSD, because of its role in force distribution within knee structures. Other intrinsic factors that are associated with overuse injuries and that should be considered with OSD patients are: history of previous injuries, inadequacy of rehabilitation of previous injuries or unaddressed cause of original injury, limb alignment abnormalities, the child's level of conditioning prior to starting sport specific training program, and psychological factors, especially in consideration to their maturity and ability to focus on safety, and conditioning. (John P. DiDiori, 1999). Extrinsic factors that can lead to OSD development are: Changes in training program though variation of duration, frequency, intensity, in order to improve performance, without allowing for adequate rest. Faulty equipment or gear, such as shoes, poor technique, as well as pressure from others, such as coaches parents who promote excessive intensity (John P. DiDiori, 1999, Leslie Klenerman, 1994).

In most cases OSD 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 (Munisha Mehra Bhatia, 2004). 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. (Munisha Mehra Bhatia, 2004). The typical complications are tibial tuberosity deformity, which is almost inevitable, non-union 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 in literature, as a result of untreated OSD. Softening of cartilage, displaced avulsion fracture of tibial tubercle, usually occurs in athletes without pre-existing OSD, but the most common reported complication is ossicle formation. (James F. Dunn Jr. 1990, Munisha Mehra Bhatia, 2004, Debera Brodwell Jackson, Rebecca B. Saunders, 1993, Kazunari et al. 2005, Eric J. Wall, 1998). Most of these complications arise due to extensor mechanism dysfunction, and thus are treated by restoring normal extensor mechanism function (Freddie H. Fu & David A. Stone, 1994).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 centres may be avulsed superiorly forming an open-shell like separation. (Atsushi Hirano et al, 2002). If the gap formed is small, fibrocartilage can bridge the gap and ossify, with such a situation leading to the healing stage of OSD (Atsushi Hirano et al, 2002, Kazunari et al. 2005). 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 OSD (Atsushi Hirano et al, 2002).

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 (Kazunari et al. 2005). Histological examination of ossicles shows that they are made from a mixture of hyaline cartilage and fibrocatilage and trabecular bone, covered with fibrous connective tissue and synovial membrane. (Atsushi Hirano et al, 2002). One of the main goals of OSD treatment is to reduce the stress at the tibial tubercle and apophysis, and also reduce the tension from the extensor mechanism (Kathryn L. McCance & Sue Heather, 2002, Kazunari et al. 2005). The main approach to doing this is by running a lengthy period of conservative therapy, which consist of rest and stretching exercises (David M. Peck, 1995, Hiroshi Ikeda et al., 1999), if there is no or little response to conservative therapy than the use of crutches for 2-3 weeks can be employed (David M. Peck, 1995). This is particularly important for children in the terminal stage, because surgery is not recommended until the epiphyseal plate closes, as recurvatum deformity may occur due to premature fusion of the tibial tubercle (Munisha Mehra Bhatia, 2004). If ossicles formation occurs, and pain is persistent, surgical removal of these ossifications is the therapy of choice (Engel A, Windhager R, 1987). Ossicle are excisesed longitudinally though the patellar tendon (R.P. Jakob, S. Von Gumppenberg, and P Engelhardt 1989, James F. Dunn Jr., 1999). Alternative surgical procedures used are internal fixation of avulsed tendon portion, and tibial tuberosity thinning (James F. Dunn Jr., 1990, Munisha Mehra Bhatia, 2004, Dr Emma Lackey and Dr Ron Sutton, 2006).

Before surgery all alternative pathologies (previously listed on page 1) should be ruled out, in order to come to a firm diagnosis before a specific plan of treatment can be decided upon (G.S. Dowd, 1996). Imaging studies are not need to diagnose OSD, but rather to rule out other pathologies, and diagnose complications (Munisha Mehra Bhatia, 2004). Radiography is the recommended method for confirmation of diagnosis and complications in most literature, but in the study by Atsushi Hirano et al (2002), they clearly demonstrate that magnetic resonance imaging (MRI), is able to detect OSD earlier and with more detail, making MRI a better diagnostic tool. Other imaging studies that can be used are CT scans which can reveal changes at the patellar tendon insertion, synography can be useful and reliable means of evaluation (mainly in follow-up) of knee pathologies, X-rays, ultrasound can be used to reveal thickening of the patellar tendon and hypoechoic area of the adjacent tissue (Munisha Mehra Bhatia, 2004, D.Barbuti, C Orazi, G. Bergami, 1995, Emma Lackey and Dr Ron Sutton, 2006)

Treatment without complications can be divided into three phases: acute, recovery, maintenance. Treatment management is usually conservative, for 6months to a 1 year, until the apophyseal union occurs (William E. Prentice & Michael I. Voight, 2001). During the acute phase of the treatment for OSD, the patient should concentrate on reducing the signs and symptoms of inflammation, and pain (William E. Prentice & Michael I. Voight, 2001). The recommended treatment during the acute phase depends on the severity of the symptoms, and the initial management of the first signs leading to the initial diagnosis of OSD. This has a significant impact on the course of the rehabilitative process during the recovery phase (William E. Prentice & Michael I. Voight, 2001, Eric J. Wall, 1998). The recommended treatment management involves things like: PRICE (prevention, rest, ice, compression, elevate), warming up properly before activity, which not surprisingly is claimed to be the key to prevention, icing for 20min after activity, short term rest or immobilization (2-3wks), activity modification like running slower, avoiding deep knee bending activities, reducing jumping activities, for 2-4months till pain is relieved or subdued, use of orthodics, good quality footware, and an infrapetellar strap during activity are all recommended, (William E. Prentice & Michael I. Voight, 2001, Sheila Globus, 2002, Munisha Mehra Bhatia, 2004, David M. Peck,1995, Steven I. Subotnick, 1977 James F. Dunn Jr. 1990, Dr Emma Lackey and Dr Ron Sutton, 2006), even so these remedies have shown little evidence of improving outcome (K. Dean Reeves, Brad Fullerton, Gaston Topol, and Greg Bancroft, 2006). For acute flare-ups, and relief of inflammation, the use of anti-inflammatory medication, analgesics, and cryotherapy is recommended. If pain is mild, and there is no inflammation, using a heating pad or warm, moist compresses for 15min before activity can help reduce symptoms and pain, as well as 15-20min of icing after activity (L. Pearce Mccarty III, 2005, Robert C. Meisterling, Eric J. Wall, Michael R. Meisterling, 1998). 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, and sporting activities are suspended or severely modified till pain is relieved. The only form of physical therapy allowed is hamstring calf stretching, and hip (as it could be indirectly associated) stretching which can begin immediately (L. Pearce Mccarty III, 2005, David M. Peck,1995).

Long term immobilization (6wks+) is only recommended for extremely severe cases, (especially in children) (William E. Prentice & Michael I. Voight, 2001), usually enforced by using a cast where compliance to conservative treatment is not adhered too (Kathryn L. McCance & Sue Heather, 2002, Eric J. Wall, 1998). Immobilization is however contraindicatory, as it is usually not an alternative for a young athlete and it promotes quadriceps weakness and tightness which further promotes symptoms (Gregory S. Kolt & Lynn Snyder-Mackler, 2003). Cast treatment is furthermore not a very effective treatment tool anyway, as symptoms frequently return once the cast is removed (Eric. J. Wall, 1998). In a preliminary study by Badelon O (1996), a dual hinged knee brace was used, that limited motion between 0-400, his findings showed that using this knee brace allowed athletes to return to sport with immediate cessation of pain (Eric J. Wall, 1998), but further research in needed to determine the efficacy of such treatment. Short term use of NSAID's can be helpful. The use of steroids such as cortisol is a contraindication as it can have degenerative changes to the patellar tendon and subcutaneous tissue, such as dipigmentation of the skin, and atrophy of the tendon (Atsushi Hirano et al., 2002). NSAID's have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not completely understood, but it is thought that they inhibit cyclo-oxygenase activity and prostaglandin synthesis, other mechanism of action may also exist such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions (Munisha Mehra Bhatia, 2004). Some commonly prescribed and recommended NSAID's are Ibuprofen (Motrin, Ibuprin) (Munisha Mehra Bhatia, 2004). Along with the treatment received to alleviate symptoms, patient education and reassurance of no long term disability for the patient is of outermost importance, especially in young promising athletes (Munisha Mehra Bhatia, 2004, Eric J. Wall, MD, 1998)

An alternative treatment which is to be investigated in a proposed study by K. Dean Reeves et al. (2006) is the use prolotherapy to treat OSD prior to cartilage separation. Prolotherapy is the injection of a growth factor or growth factors, or substance that stimulates the production of growth factors, which stimulation the production of normal cells or tissue (K. Dean Reeves et al. 2003). The science behind this treatment is that cartilage (chondrocyte) and tendon (fibroblasts) cells begin to repair themselves when exposed to specific complex proteins called growth factors (GFs) (K. Dean Reeves et al. 2006). The growth factors for cartilage and tendon are very similar (K. Dean Reeves et al. 2006). GFs that stimulate both chondrocytes and fibroblasts, include platelet-derived growth factor (PDGF), transforming growth factor beta (TGF-b), basic fibroblast growth factor (bFGF), insulin-like growth factor (IGF), and connective tissue growth factor (CTGF) (K. Dean Reeves et al. 2006). During the acute and proliferation stages of injury the body produces multiple growth factors at the same time, which is particularly important since each of these growth factors has a different function, but at the same time they work together as a team in tissue repair (K. Dean Reeves et al. 2006). The GF's that effect chondrocyte and fibroblast cell are specific to that particular kind of cell and do not affect bone, which has its own set of specialized proteins. Thus increased production of chondrocyte and fibroblast GFs will not cause bone spurs or other abnormal structures to grow. (K. Dean Reeves et al. 2006).

It has been demonstrated that by exposing chondrocyte and fibroblast cells to high glucose concentrations (0.5%) in test tubes, cells are stimulated to produce all growth factors previously listed. (K. Dean Reeves et al. 2006) Glucose concentration levels needed such stimulation of the cells is however far too high for oral administration, thus dextrose is believed to be an equally beneficial alternative (K. Dean Reeves et al. 2006). Clinical practice has demonstrated that higher dextrose concentration can safely be injected, because of a dilution effect in the blood, while also keeping the blood glucose level elevated for several hours while local cells absorb the extra dextrose (K. Dean Reeves et al. 2006) Dextrose does not affect the inflammatory process up to a 10% concentration injection (K. Dean Reeves et al. 2006). In the proposed study by K. Dean Reeves et al. (2006) they plan to inject dextrose with concentrations up to 10% in the tibial tuberosity and patellar tendon at 5cm intervals at a 5cm depth, to increase the GF production. Up to now prolotherapy treatment in humans has been successful in demonstrating safe and symptomatic relief from sever arthritis in large and small joints, and the ability to tighten loose ACL ligaments, chronic adductor or abdominal strain, and osteitis pubis. (K. Dean Reeves et al. 2006). Results from the study are awaited, thus the benefits of such a treatment are unknown, but the research sounds exciting, and potentially effective.

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, or restore normal daily function as soon as possible and as safely as possible (McKesson Health Solutions, 2004). Hamstring and quadriceps stretching and hamstring strength are the main objectives. (William E. Prentice & Michael I. Voight, 2001) 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 (William E. Prentice & Michael I. Voight, 2001). 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 (Gregory S. Kolt & Lynn Snyder-Mackler, 2003). Exercises should be pain-free, involving isometrics or low load high repetition knee extension exercises (William E. Prentice & Michael I. Voight, 2001). Stretches must target the quadriceps muscle belly not the tibial tubercle, two joint stretching exercises should be incorporated once adequate flexibility is achieved. (William E. Prentice & Michael I. Voight, 2001) Overzealous stretching can lead to complication rather than benefits and should be discouraged. (William E. Prentice & Michael I. Voight, 2001). 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. (Viktoras Gerulis, Romas Kalesinskas, Sigitas Pranckevicius, Paulius Bergeris, 2004).

If conservative therapy is initiated during the normal, early and progressive stages of the course of OSD, there is a 90% chance of an early recovery and progression to maintenance phase of treatment and healing stage. (Atsushi Hirano et al. 2002). From the study by Atsushi Hirano et al (2002) mentioned earlier, it takes on average 3.8weeks to return to modified training if treatment start 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. (Atsushi Hirano et al. 2002). In other literature the most often reported prognosis is 6-24months till return to sport (Munisha Mehra Bhatia, 2004). However it must be remembered that "everyone recovers from injury at a different rate" (McKesson Health Solutions, 2004), and these recovery times are averages, and should only be used a guidelines.

The progression to the maintenance phase is usually through the recommendation by a general physician, otherapists, 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. (Munisha Mehra Bhatia, 2004). 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:

  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. Your child is able to jog straight ahead without limping.
  5. Your child is able to sprint straight ahead without limping.
  6. Your child is able to do 45-degree cuts.
  7. Your child is able to do 90-degree cuts.
  8. Your child is able to do 20-yard figure-of-eight runs.
  9. Your child is able to do 10-yard figure-of-eight runs.
  10. Your child is able to jump on both legs without pain and jump on the injured leg without pain

(McKesson Health Solutions, 2004).

If pain returns it is recommended that patient take a further 6months, continuing conservative therapy, and rehabilitation program (Dr Emma Lackey and Dr Ron Sutton, 2006).

By Valentin-Angelo T. Uzunov.