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00/0 THE JOURNAL OF ORTHOPAEDIC AND SPORTS PHYSICAL THERAPY Copyright 0 1985 by The Orthopaedic and Sports Physical Therapy Sections of the American Physical Therapy Association

Osgood-Schlatter Disease: Review of Literature and Physical Therapy Management


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Osgood-Schlatter disease is a traction apophysitis of the tibial tubercle, the weakest link of the extensor mechanism of the adolescent. Conventional medical treatment includes plaster casting, injections of various anti-inflammatories, and surgical removal of painful ossicles in resistant cases. While not a very common condition, Osgood-Schlatter disease is being seen with increasing frequency in teenage athletes, especially basketball players (Antich, Lombardo, J Orthop Sports Phys Ther 7 : 1-4, 1985.) With a focus on muscular tightness as a possible causative factor, physical therapy evaluation is outlined, followed by techniques for pain control and stretching exercises for the quadriceps and hamstrings. Ice massage is advocated as a way for the athlete to treat postexertional discomfort in the area of the tubercle. The patient and his or her parents must be assured that while residual deformity may remain, disappearance of symptoms coinciding with closure of the apophyseal plate is often the end result.

Osgood-Schlhtter disease is defined as a separation of the tibial tubercle apophysis from the proximal end of the tibia. This lesion may have a history of trauma, or may present without a significant recognizable injury. KatzI4 classifies this entity as a nonarticular osteochondrosis involving the quadriceps muscle/tendon insertion secondary to excessive muscle pull. Citing the same mechanism of increased quadriceps pull on the adolescent tubercle, Smillie28describes OsgoodSchlatter disease as a traction epiphysitis. Dorland's Medical Dictionary gives as a synonym "apophysitis tibialis adolescentium," while Christie4 states that the radiographically evident bone changes make it a disease entity. He adds that poor epiphyseal nourishment during a time of rapid growth can lead to the onset. However, LaZerte and Rapp'sI7 histological studies of nine specimens indicate no evidence of primary aseptic necrosis in any of the tubercles examined. Increased stress on the weak link of the adolescent knee extensor mechanism accounts for the symptoms experienced by those patients with this ~ e s i o n . ' ~An .'~ initial ~~~ injury can be furthered
Department of Physical Therapy, Southwestern Orthopaedic Medical Group, Inc., 501 E. Hardy Street, Suite 200, Inglewood, CA 90301.

by continuing minor t r a ~ m a t a ~ or ' . heterotopic ~~ calcification and ossification in the patellar liga~~~ ment can occur secondary to o ~ e r u s e . " Instances of tibial tubercle fracture have been reported subsequent to violent quadriceps contract i o n . ' ~The ~ ~ imbalance in the cross-sectional area of the quadriceps muscle bulk to the area of insertion7 also creates a great concentration of force on. a small area.

Microscopic examination of bony ossicles removed at surgery indicates that the separation is due to increased tension over a small area of tendon insertion. All nine cases studied by LaZerte and RappI7 demonstrated an anterior cortical bone defect of the tubercle, in addition to increased vascularization of the infrapatellar tendon surrounding the ossicles.

Osgood-Schlatter disease is easily recognized in the adolescent with complaints of pain which is localized to the area of the tibial tubercle. Discomfort is usually generated with running,21 kneeling,2321 ascending or descending stair^,'^^^' and is


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Fig. 1 . A, Lateral view in a 12-year-old male exhibiting separation of the tubercle; 13, ossicle embedded within the infrapatellar tendon at its insertion in a 13-year-old male.

patella alta in their series of 185 knees utilizing relieved with rest.l4 Weakness of the quadriceps2' and Peel method of measuring and pain on resisted knee e ~ t e n s i o n ~ are ~ ~ ~ the ~ ~ Blackburne ' common signs, as is an enlarged t ~ b e r c l e . ~ . ~ 'patellar position. The mean index of knees with Osgood-Schlatterdisease was 0.99, as compared D'Ambrosia and MacDonald6report reproduction 73 normal knees with a mean of 0.84. to of pain with passive knee flexion, which Jakob et Differential diagnosis of this entity includes osa1.12attribute to a hypertrophiedquadriceps group teogenic sarcoma of the proximal tibia2' and osexhibiting decreased flexibility. teomyelitis of the tubercle secondary to contuRadiographic examination is considered nec~ i o n D'Ambrosia . ~ and MacDonald6 emphasize essary in confirming this diagnosis in the adolesthe need to perform a thorough examination on cent with knee pain. In more severe cases, sepadults with previous histories of Osgood-Schlatter aration and fragmentation of the apophysis may disease and report arteriovenous fistula as the be seen32as well as irregular ossification of the cause of knee pain in one individual. t ~ b e r c l e ' ~(Fig. . ~ ' 1). In milder cases without radiographic bony changes, soft tissue swelling, esCONVENTIONAL MEDICAL TREATMENT pecially of the infrapatellar fat pads2' may be the only evidence of this disease. Mital and Matza2' A wide range of treatment philosophy exists, check for a decreased "sharpness" in the angle with some belief that no treatment is needed other formed by the tibial apophysis and the infrapatellar than for pain relief.3.'4Improvement occurs spontendon. Patella infera, as defined by the Insalltaneously in 1-2 years with or without treatment, Salvati patellar height-to-patellar tendon ratio, the only sequela being residual deformity of was seen in a group of 20 patients with OsgoodLimitation of activity is the tibial t ~ b e r c l e . ~ Schlatter disease (mean = 1.21 0.15).'6 This r e c ~ m m e n d e d ~ ~ ~ ' with ~ ~ ~ Willne?' . ~ ~ , ~ ' . more ~' position was determined to be significantly lower specifically restricting running and stairs for 12 (P < 0.05) than a group of 80 normals (mean = weeks, and walking barefoot before the age of 1. O O k 0.11). Conversely, Jakob et a1.12 reported 15. Attributing the problem to lower extremity

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malalignment involving marked foot pronation and genu valgum, he advised decreasing the use of loafers and sneakers, and prescribed "Oxford shoes with a firm inner shank and 3116 inch inner heel wedges." Complete relief of symptoms in 65 of 78 patients is reported in 6 weeks, with the remainder becoming pain free in 12 weeks.31 Bowers2 recommends use of salicylates and local ice application, as needed, to control pain. Conservative treatment to decrease quadriceps and l . ~restriction ~ of motension on the t u b e r c ~ e ~ tion via immobilization from 6 to 8 weeks22to 3 however, ' feels months2' is suggested. ~ i c h e l i , ~ that casting is not indicated in the presence of a tight, weak quadriceps group. Injection of the tubercle with hydrocortisone15 or with lidocaine HCI combined with hydrocort i ~ o n e , ~de~amethasone,~~ ' triamcino~one,~ or methy~prednisolone,~~ may be employed if restriction of activities and immobilization are not successful. Kelly15utilized up to three hydrocortisone injections and reported 52 to 72 patients having relief after one injection. Eight and 9 more were improved after two and three injections, respectively, while 3 of the 72 did not respond to injection. Levine and ashy yap'^ advocate use of an infrapatellar strap during activities to decrease the pull of the quadriceps against the tibial tubercle and report improvement in 92% of patients treated (Table 1). Quadriceps stretching into knee flexion with hip extension is used to stretch the muscle group and decrease tension on the apophysis. While Katz14 states that "rarely is the pain severe enough to require plaster-cast immobilization," 12/~of Mital and Matza's groupz2underwent surgical removal of painful ossicles with instantaneous relief of symptoms.

is not known. Subcutaneous atrophy in 8 of 70 knees injected with methylprednisolone was seen in addition to striae formation in the skin overlying the tubercle.26Patellar tendon avulsions are possible sequellae to Osgood-Schlatter disease and from 14'' to 26%" of those seen with this fracture reported previous histories of Osgood-Schlatter disease.

Premature closure of the anterior tibial epiphysis resulting in genu recurvatum has been rep~rted.'~,~ Conflicting ~,~' reports of patella alta'2~2',30 and patella infera16 exist, while the causal or effectual relationship with this disease
Improvement with infrapatellar stap* Definite improvement Some improvement No improvement From Levine and Kashyap.lg 79.1% 12.5% 8.3%

In assessing the patient's knee pain, location (unilateral or bilateral) of pain and its duration is documented. Whether it is painful during brief physical activity, or following prolonged activity, indicates severity. Answers to questions regarding presence or absence of pain while walking, running, ascending and descending stairs, and kneeling should be documented for later comparison. Examining the patient's gait pattern while walking, the therapist looks for an antalgic limp or other compensatory mechanism to protect the knee from pain. Special attention should be focused on whether or not the individual flexes the involved knee during loading response or attempts to maintain full extension, thereby reducing the need for quadriceps activity. Confirmation of the diagnosis is the first task of the attending therapist. With the patient supine with both knees flexed to 90, inspection of the tubercles is performed. By looking from the side, a silhouette image of one knee against the other reveals enlargement of the apophysis, if present (Fig. 2). Palpation of the tubercle is then performed and tenderness is assessed as none, slight, mild, moderate, or marked (Table 2). Due to the prevalence of Osgood-Schlatter disease during the early adolescent years, at a time when musculoskeletal pain may be secondary to the inability of muscles to elongate at the same rate as bony growth, tightness of knee musculature must be checked. With the patient still supine, hamstring length is assessed by the examiner's flexing the hip while maintaining the knee in full extension. Comparison between involved and uninvolved limbs in unilateral problems, or comparison to normal values in the cases of bilateral involvement, aids the therapist in deciding whether or not muscular tightness plays a role in the conditon. Knee flexion range of motion, taking into account rectus femoris tightness, is performed with the patient prone (Fig. 3). The knee is passively


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Fig. 4. Hamstring stretching is performed with a 10-sec static stretch. Note limited flexibility in this patient with posterior pelvic rotation (tight lumbodorsal fascia), inability to keep knee straight (tight hamstrings), and outward rotation of foot (tight hip external rotators).

Fig. 2. Silhouette appearance of knees flexed to 90 reveals mild enlargement of left tibia1 tubercle.

Assessment of tenderness on palpation Slight Mild Moderate Marked Only complains of pain after questioning Voluntarily reports pain on palpation Withdraws knee from examiner's hand; may indicate pain verbally Withdraws knee and attempts to grab examiner's hand

flexed by the examiner until either the end of range or pain is encountered. If this stretch begins to hurt, the patient must be questioned as to the location of the pain, as this will influence treatment. If pain from this prone stretching is felt in the area of the infrapatellar tendon or tubercle area, stretching the quadriceps is contraindicated, as the pain is caused by further pulling away of the apophysis. If the strain is felt up in the muscle belly or at the proximal attachment of the muscle, quadriceps stretching will be performed as part of the treatment. The results of muscle tightness tests along with the location of pain with stretching are recorded. Manual muscle testing of the knee extensors and flexors can be performed with the patient sitting on the end of the plinth with presence or absence of pain noted. Muscle tone is assessed in the long sitting position as the patient performs a quadriceps set. Quadriceps atrophy should be checked in the form of girth measurements.

Fig. 3. Assessment of passive knee flexion range of motion including evaluation of rectus femoris tightness.

Of primary concern to the therapist treating Osgood-Schlatter disease is relief of pain in the area of the tubercle. lontophoresis is the modality of choice, and a trial period of not more than three treatments should be undertaken.'. l o Use of an anti-inflammatory medication and local anesthetic helps decrease swelling and pain. We feel the benefits of iontophoresis are: 1) Inhibition of pain from the electrical current used; 2) method of administering medication without injecting the tendon/muscle junction, thus avoiding the possibility of associated tendon damage;

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Fig. 5. A, Quadriceps stretch position for individuals with extreme tightne*; B, advanced quadriceps stretch position which increases rectus femoris stretch across the anterior hip.

are injected into the positive electrode. Treatment time is for 20 minutes at up to 5.0 ma. Proper post-treatment application of lotion to both electrode sites minimizes the hazard of skin irritation. Following three treatments with iontophoresis performed every other day, tenderness to palpation is reassessed, and the patient's subjective change in conditions is recorded. The next phase of treatment addresses tight .~~ musculature if found on initial e v a l ~ a t i o n Heating with hot packs to the anterior and posterior thigh is followed by quadriceps and/or hamstring stretching. Hamstrings are stretched over the side of a plinth (Fig. 4) with the involved knee in full extension and the foot pointing upward (neutral hip rotation). A static stretch of 10 sec is used with the patient instructed to slide his hands down his anterior leg until he feels a stretch either in the posterior thigh or at the hamstrings insertion. Quadriceps stretching is performed with the patient lying prone, pulling his foot up toward his buttocks. Strain should be felt in the muscle belly, and not at the tenoperiosteal junction. For cases of extreme tightness, a belt may be needed around the dorsal foot (Fig. 5A), whereas patients with less quadricep tightness can be sidelying with the involved leg up, allowing for a greater rectus femoris stretch with passive hip extension (Fig. 56). Strengthening of the involved limb quadriceps is performed in cases of atrophy secondary to disuse. Isometric quadricep sets, straight leg raises, and short arc quadricep exercises are standard, and are performed only if they are pain free. Exercise concludes with a 5-minute ice massage to the area of the tubercle.

Fig. 6. Residual deformity in a 28-year-old male with neither pain nor functional limitations of the left knee.

3) localization of treatment required for the size of this particular lesion. The active pad of the PhoresoP (Motion Control, Salt Lake City, UT) unit is positioned over the tubercle of the knee which is supported in about 30' of flexion. The sides of the adhesive pad are then taped down to the skin for better contact and to prevent leakage. One cc of dexamethasone-sodium-phosphate and 1 cc of lidocaine HCI

The symptoms, diagnosis, and conventional forms of treatment for Osgood-Schlatter disease are reviewed. Physical therapy evaluation must concentrate on assessment of tight musculature (quadriceps, hamstrings, calf) as a possible cause of this entity. Treatment concentrates on: I ) decreasing the pain, 2) improving flexibility, and 3) return to function. Perhaps the most important part of rehabilitation is education of the adolescent and his parents, with a reassurance that his condition is temporary and related to the time in his growth when his epiphyseal plates are the weak link of his musculoskeletal system. Activities should be pain limited with instruction in continuation of a



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home program with ice massage following. Explanation that a prominent tubercle may be present ~ .but that pain with activity indefinitely ( ~ i 6), should cease following the teenage years, may prevent later concerns regarding continued presence of an enlarged tubercle.
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The authors would like to thank the other members of the Physical Therapy Research Committee of the Southwestern Orthopaedic Medical Group, Inc. for their suggestions and review of the manuscript in its preparation for publication: Matthew C. Morrissey, MS, PT; Celeste Criswell Randall. MS. PT; and Roxie Westbrwk, PT. The guidance and assistance of Ms. Elizabeth Stone is gratefully appreciated.

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13. Jeffreys TE: Genu recurvatum after Osgood-Schlatter's disease: Report of a case. J Bone Joint Surg (Br) 47:298-299,1965 14. Katz JF: Nonarticular osteochondroses. Clin Orthop 158:70-76. 1981 15. Kelly JM: Osgood-Schlatter's disease: A review of 108 cases. J Irish Med Assoc 64:630-635,1971 16. Lancourt JE. Christini JA: Patella alta and patella infera: Their etiological role in patellar dislocation, chondromalacia, and apophysitis of the tibial tubercle. J Bone Joint Surg (Am) 57:11121115,1975 17. La Zerte GD, Rapp IH: Pathogenesis of Osgwd-Schlatter's disease. Am J Pathol34:803-811,1958 18. Levi JH, Coleman CR: Fractures of the tibial tubercle. Am J Sports Med 4:253-263,1976 19. Levine J, Kashyap S: A new conservative treatment of OsgoodSchlatter's disease. Clin Orthop 158:126-128, 1981 20. Micheli LJ: Overuse injuries in children's sports: The growth factor. Orthp Clin North Am 14:337-360,1983 21. Mital MA, Matza RA: Osgood-Schlatterdisease: The painful puzzler. Phys Sportsmed 560-73, 1977 22. Mital MA, Matza RA, Cohen J: The so-called unresolved OsgoodSchlatter lesion. J Bone Joint Surg (Am) 62:732-739, 1980 23. Ogden JA, Southwick WO: Osgood-Schlatter's disease and tibial tubercle development. Clin Orthop 116:180-189,1976 24. Osgood RB: Lesions of the tibial tubercle occurring during adolescence. Boston Med Surg J 148:114-116,1903 25. Reichmaster J: Injectionof the deep infrapatellar bursa for OsgoodSchlatter's disease. Clin Proc Child Hosp DC 3521-24, 1961 26. Rostron PKM, Calver RF: Subcutaneous atrophy following methylprednisolone injection in Osgood-Schlatter epiphysitis. J Bone Joint Surg (Am) 61:627-628, 1979 27. Scotti DM, Sadhu VK, Heimberg F, O'Hara AE: Osgood-Schlatter's disease, an emphasis on soft tissue changes in roentgendiagnosis. Skeletal Radiol 4:21-25, 1979 28. Smillie IS: Injuries to the Knee Joint, Ed. 5. Edinburgh: Churchill Livingstone. 1978 29. Smillie IS: Diseases of the Knee Joint, Ed. 2. Edinburgh: Churchill F Livingstone, 1980 30. Stirling RI: Implications of Osgood-Schlatter'sdisease (abstract). J Bone Joint Surg (Br) 34:149-150, 1952 31. Willner P: Osgood-Schlatter'sdisease: Etiologyand treatment. Clin Orthop 62:178,1969 32. Woolfrey BF, Chandler EF: Manifestations of Osgood-Schlatter's disease in late teen age and early adulthood. J Bone Joint Surg (Am) 42:327-332.1960