An in-depth look at the pathophysiology and treatment of Osgood-Schlatter Disease - Part B
Part B: Risk Factor
OSD is a self limiting condition, and yet can be very disabling and frustrating for any athlete. There are no major risks of developing OSD as given time and rest the condition treats itself. Certain complications listed in Part A can arise, but in most cases these can be prevented with patient adherence, and correct rehabilitation during the early stages of the OSD. (R.P. Jakob, S. Von Gumppenberg, and P Engelhardt 1989). If conservative treatment is not successful, corrective surgery is shown to have a high success rate with full recovery (R.P. Jakob, S. Von Gumppenberg, and P Engelhardt 1989). The risk factor that is most concerning as a result of developing OSD is the limitation it imposes on an athlete. Even though there is a fair bit of research into the pathophysiology of OSD, current treatment is slow and dependant on a lengthy period of time off sport or physical activity, which usually prevents athletes from taking any part in trainings and play (K. Dean Reeves et al., 2006). Activities that increase stress placed on the extensor mechanism have to be suspended or seriously modified, or the risk of complications developing greatly increases, especially ossicles formation (Eric J. Wall, 1998). An absence away from training and play for extended and even short periods of time can have serious consequences on an athlete's performance. In sever symptomatic patients; their return to the sport is even questionable, due to the long lasting symptoms of OSD (K. Dean Reeves et al., 2006). Unfortunately without undertaking current treatment recommendations, the risk of OSD complications are significantly increased, and even the development of longer lasting effects can occur (Munisha Mehra Bhatia, 2004).
Aims of the Exercise Program
From current available literature, OSD treatment is considered successful when the patient can return to sport, training or play. K. Dean Reeves et al. (2006) suggest an alternative definition to a successful treatment: their definition referred to as "true success" is "a return to full power, full effectiveness, and full aggressiveness of play, unrestricted by fear of the injury worsening". In their study proposal they note that "no study now available on Medline suggests anything close to true success with current OSD treatment" (K. Dean Reeves et al. 2006, pg1)
Thus the desired aims of an exercise program are:
- To have true success as a result of treatment
- Return to sport or daily activity as quickly as possible, with no symptoms of OSD
- Prevent further complications of OSD, by treating any predisposing factors.
- Help athlete deal with the stress of injury (psychology)
- Reduce losses in sporting performance
OSD as described in literature and in Part A, can the result from some form of extensor mechanism abnormality, such as, unbalance in muscle and bone development, normally coinciding with a growth spurt, and major trauma to tibial tuberosity, but an exact cause of OSD is still debated (Atsushi Hirano et al. 2002, K. Dean Reeves et al. 2006). With training all possible extensor mechanism abnormalities, if possible, should be tested and treated, if present, in order to reduce the stress placed on the tibial tuberosity and allow return to sport/activity with reduced risk of aggravation and re-injury (Eric Shamus & Jennifer Shamus, 2001). Prior to the commencement of any training during the acute phase, the first order of treatment is rest. The use of NSAID's and cryotherapy to reduced inflammation and swelling is recomended, and reduction or restrict of all activities that cause pain suspended, at least until pain is controlled and alleviated (Steven J. Anderson, 1991, L Pearce Mccarthy III, 2005, John P. DiFiriori, 1999). Usually a period of 4-8 weeks is sufficient, but if pain is persistent than immobilization of the knee is recommended for a further 6-8 weeks (Kathryn L. McCance & Sue E. Huether, 2002). Some patients can continue to experience pain even after a lengthy rest period due to inflammation of patellar tendon (Steven J. Anderson, 1991). Approximately 8 weeks is required from start of physical rehabilitation for revascularization, healing, and ossification of the tibial tubercle to take place (Kathryn L. McCance & Sue E. Huether, 2002).
Possible causes for extensor mechanism abnormalities that require attention are:
Patellar position - The normal patellar position, determined though the method described by Blackburn and Peel, shows a normal patellar index as 0.80 with a standard deviation of 0.11 (P.Jakob, S. Von Gumppenberg, and P Engelhardt 1989). OSD patients, can have an index of around 1.01 in boys, and 0.91 in girls with a standard deviation of 0.16, it is even greater at around 1.06 in patients in the terminal stage of OSD (R.P. Jakob, S. Von Gumppenberg, and P Engelhardt 1989) In OSD patients, the patellar is pulled superiorly due, to decreased flexibility in the quadriceps. This places greater stress on patellar tendon insertion at the tibial tuberosity, during knee extension, and can result in patellar alta even after skeletal maturity if OSD is untreated (R.P. Jakob, S. Von Gumppenberg, and P Engelhardt 1989), Restoring normal petallar position, and function is vital for the treatment and prevention of OSD. For effective treatment, the exact causes of patellar misalignment have to be determined. In OSD patients it can be due to quadriceps inflexibility, hamstring tightness, q-angle abnormality, tibial torsion (R.P. Jakob, S. Von Gumppenberg, and P Engelhardt 1989, Naoko Aminaka; Phillip A. Gribble 2005, Medical multimedia group, 2005)
Tibial torsion - Increased external tibial torsion places greater stress at the tibial tuberosity (normal external tibial torsion is 20deg from 5yr onwards) (M.S. Turner, I.S. Smillie, 1981). Thus external tibial rotation will need to be correct though rehab, and correct exercise prescription.
Hamstring and quadriceps flexibility - OSD is linked with decreased flexibility in the quadriceps and hamstrings. Flexibility will need to be increased in order to reduce the stress of the extensor mechanism on the tibial tuberosity (Hiroshi Ikeda et al., 1999, Timothy Floyd, George D. Picetti III, Richard Schneider, 1989). Training should aim to improve and restore normal pain-free ROM in the knee with passive knee flexion, and active knee extension (with the desired to make contralateral ROM as similar as possible) (Walter L. Calmbach & Mark Hutchens, 2003). With consideration that norm value ROM are depend on the sport or activity the individual participates in (Freddie H. Fu and David A. Stone, 1994). Desired normal values for hamstring/gluteus ROM, tested with active straight leg raise test is 900 deg, or a sit and reach test, with a normal value of -5cm (Deborah Roche, 2005). Normal knee flexion tested with by a prone knee flexion test is 1400 deg (Deborah Roche, 2005), and with the Ely test. The goal of the flexibility is to re-establish a normal H/Q ratio of 0.6, which will help reduce the strain on the tibial tuberosity. Stretching exercises should done passively 3-5 times a week, several times a day, with 15-30sec holds (progressively), as this is believed yield fastest results (William E. Prentice & Michael I. Voight, 2001). Stretches should be done passively so that the patient is able to the control pressure, and stop at the sign of pain or excessive pull on the tibial tubercle.
Gastrocnemius and Soleus flexibility - It is also recommended to have normal ROM in the gastrocnemius and soleus, as these muscles cross the knee joint, and play a roll in knee flexion (McKesson Health Solutions, 2004). Assessing dorsiflexion can determine gastrocnemius and soleus flexibility. Normal dorsiflexion ROM is considered to be between 0-20deg (Deborah Roche, 2005, William E. Prentice & Michael I. Voight, 2001). There is some evidence linking patients with OSD and Sever's disease, which is associated with tight gastrocnemius and soleus muscles (Kujala UM, Kvist M, Heinonen O, 1985, Christopher C. Madden & Morris B. Mellion, 1996). As a preventative measure it is highly recommended to work the calf and soleus flexibility, along side quadriceps and hamstrings, as tightness in these muscles has been associated to OSD patients (Kujala UM, Kvist M, Heinonen O, 1985).
Quadriceps atrophy and weakness - Quadriceps weakness is not a major concern in most patients, rather they tend to have excellent recruitment and hypertrophy, due conditioning from sport participation. However in chronic cases quadriceps weakness and atrophy can result due to lack of use, and rest. In which cases quadriceps strength has to be developed, along side hamstring flexibility (William E. Prentice & Michael I. Voight, 2001). This is best achieved with sometrics or low load high repetition knee extension exercises (William E. Prentice & Michael I. Voight, 2001)
Q-angle - At the current moment there is no clinical literature that links OSD in patients with an increased Q-angle, but the effects of an increased Q-angle on external tibial torsion (an established factor for OSD predisposition) is well documented is. Leg alignment (ie.genu valgum), and gait abnormalities (i.e.over pronation) are often associated with increased Q-angle, which is often a result of excessive femoral anteversion secondary to tight internal hip rotators (Michael T Cibulka and Julie Threlkeld-Watkins, 2005). Hip abnormalities increase stress on the knee (Marlene A. Prost, 2002). The suggested normal external/internal ratios are 2:1, 60:30 degrees (G.E. Peterson, M. Murray-Weir, L Root, M. Lenhoff, L. Daly, C. Wagner), or 1:1, 45:45deg (Deborah Roche, 2005). The IT band and the tensor fascia latae should be assessed also to determine weakness and inflexibility, which will also contribute to changes in Q-angle (Naoko Aminaka, 2005). IT band tightness can be evaluated with an Ober's test, with normal values being at least a leg drop of 100 below horizontal, and strengthening may also be required (Deborah Roche, 2005) It should be pointed out that to the authors knowledge, there is not research indicating IT band and tensor fascia latae tightness and OSD. However it has been show to effect patella function, which is linked with OSD (L Pearce Mccarthy III, 2005). Once again these values are not sport specific, but general values for the sporting population, with the purpose of providing normal knee biomechanics. The normal Q-angle in males is 11-17deg and 14-20deg in females, through strength and flexibility training, these values should be aimed for.
The effects OSD has on lifestyle can vary, but the patient population group with OSD, whose lifestyle is affected the most is, young athletes (K. Dean Reeves et al. 2006). For a young athlete, it is often very hard to restrict their activity and rest, even if they have pain (Dorathy R. Marlow, Barbara A. Redding, 1988).The lifestyle consequences of OSD in the short term can be very detrimental to sport performance, skill learning, and conditioning (K. Dean Reeves et al. 2006). Long term effects are chronic anterior knee pain, at least mild limitations of activity, chronic discomfort with kneeling, loss of confidence and status among peers and coaches, and lower function on scale of ADLs (K. Dean Reeves et al. 2006). Few reports have been published on the effects OSD has on athletes beyond adolescence. In one study the results indicate that subjects with history of OSD scored significantly lower than control subjects on the Knee Outcome Survey, and Sports Activity Scale (Michael D. Ross, Douglas Villard, 2003). For athletes the sheer time off training and sport participation that is required by modern treatment can be seriously damaging to the careers or lead to participation drop out (K. Dean Reeves et al. 2006). Unless new treatments are developed there is no choice but to either bare the pain and risk complication, or take time off. Some literature advocates that the "best treatment is to ignore symptoms" (Leslie Klenerman, 1994: p695),"If the child wishes to be active they will aggravate their symptoms but come to no harm" (Leslie Klenerman, 1994: p695). This is however most definitely not recommended by majority of literature. "Thus because there is yet no treatment available that enhances or speeds up tissue recovery, limiting activity until healing is usually part of the OSD treatment" (K. Dean Reeves et al. 2006:pg 3). As a result of the disuse loss in muscle strength and muscle atrophy will most likely result.
The sheer psychological development that undergoes during the years OSD is prevalent, makes it a major adverse factor on psychological health in youth (K. Dean Reeves et al. 2006). With activity and exercise restrictions, even the general benefits of exercise, such as, improved self-esteem, leadership skills, self-discipline, development of general fitness and motor skills acquisition, and peer socialisation can become hindered during peak physical and psychological development (John P. DiFiori, 1999). The best a doctor or health ally can do, is to educate and reassure the parents, athletes and coaches that the condition is self limiting, help the patient with making lifestyle alterations until healing has occurred, provide emotional support, and possibly refer children to an good orthopedic surgeon to allow for early treatment and to possibly avoid long interruptions in sporting activities (Springhouse publishing company, 2005, Leslie Klenerman, 1994, John. P. DiDiori, 1999, Munisha Mehra Bhatia, 2004).
By Valentin-Angelo T. Uzunov.