Osgood-Schlatter disease

ABSTRACT

Gout is one form of acute inflammation of the connective tissues, caused by the deposition of needleshaped crystals of uric acid which reach saturation levels in the tissues. The most common sites of gouty tophi include the auricle and the great toe, followed by the ankle and wrist joints and tendons, Achilles tendon, and the knee joint. Intraosseous tophi are rare, except around the metatarsophalangeal joint of the great toe, and there have only been sporadic reports of cases in the patella, including the patella partita. We report the first case to our knowledge of a gouty tophus which invaded an ossicle in an unresolved Osgood-Schlatter lesion.

Key words: unresolved Osgood-Schlatter lesion, gout, tophus

INTRODUCTION

Intraosseous tophi are rare in the knee joints.'O There have only been sporadic reports of cases in the patella. 5,6,7 We observed a gouty tophus which invaded an ossicle in an unresolved Osgood-Schlatter lesion.

CASE REPORT

A 28-year-old man, 170 cm. tall arM of 100 kg weight, was examined in our department for a progressively worsening 3-week-old pain of obscure origin in his left knee. He had played basketball actively between the ages of 12 and 17 years. His medical history included Osgood-Schlatter disease of both knees when he was about 15 years old. Pain on exertion of the left patellar tendon had occasionally occurred up to the present. Findings in the left knee on initial examination included swelling, heat, and redness with marked tenderness of the soft tissues around the centre of the tibial tuberosity Knee movement was limited to 0' for extension and 500 for flexion, but there was no evidence of a floating patella or inflammation of the joint. No inflammatory findings were observed in the MTP joint of the great toe and in other joints which are common sites of gouty tophi. The initial plain X-ray film showed an ossicle lying above the centre of the tibial tuberosity, and a multilocular radiolucent lesion was present in the ossicle (Fig. 1). The right knee also showed protrusions and irregularity of the tibial tuberosity, lesions that appeared to have been caused by the old Osgood-Schlatter disease. Patella alta was not observed in either knee. Magnetic resonance imaging (MRI) showed a low-intensity area that was assumed to be ossification in the posterior part of the patellar tendon on TI- and T2-weighted images. This was surrounded by a low-intensity region on the TI-weighted image and a high-intensity region on the T2-weighted image, which appeared to be caused by inflammation of the patellar tendon and the adjacent tissues (Fig. 2). Laboratory tests revealed a high uric acid level of 9.1 mg/dl and high triglyceride level of 420 mg/dl. The C-reactive protein (CRP) was 0.9 mg/dl and mild elevation of liver enzymes and total cholesterol were observed.

From these findings, progression of the unresolved Osgood-Schlatter disease or an attack of gout was suspected. An anti-inflammatory agent was administered, with rest locally, and the symptoms were alleviated. Several weeks later, an operation was performed for both treatment and diagnostic purposes.

The patellar tendon was exposed by a longitudinal incision. The surface of the tendon was covered with a congested synovial membrane. When a longitudinal cut was made in the tendon, a mass thought to be an ossicle, was observed and it was excised. This mass was 20 x 15 x 10 mm. in size, and contained a chalklike muddy substance. On cross-section, the muddy substance appeared to be a mass containing bone fragments. The mass was shown to be a gouty tophus containing a vast number of needle-shaped microscopic crystals.

Histological examination of the congested synovial membrane on the surface of patellar tendon showed infiltration of inflammatory cells, mainly lymphocytes. The ossicle showed amorphous deposits around the bone histologically, as well as infiltration of inflammatory cells including foreign body giant cells (Fig. 3).

Postoperative course

The localized inflammation resolved a few days postoperatively, and rehabilitation was started. By 3 weeks postoperatively, full knee movement had recovered and the patient could walk unaided. Benzbromarone was administered immediately after the operation and the serum uric acid level was normalized after about 2 months. At present (after 15 months), no recurrence of gout has occurred and the clinical outcome is good.

DISCUSSION

Osgood-Schlatter disease is a well-known form of apophysitis that occurs during the growth period, resulting in pain and the development of protrusions on the tibial tuberosity. The main therapy is conservative treatment because symptoms often disappear spontaneously after closure of the epiphyseal line. However, there are patients in whom free bone fragments form after the growth period, and various types of impairment can persist. Mital et al.1 reported such a case in 1980, which they referred to as ,so-called unresolved Osgood-Schlatter lesion'. Sporadic reports of such cases have appeared since then.' In the present patient, the possible causes of the ossicle in the patellar tendon included trauma, a cleavage fracture, Osgood-Schlatter disease, enthesopathy, chronic inflammation, or a sesamoid bone. The lesion appeared to be an ossicle caused by an unresolved Osgood-Schlatter lesion because of the medical history, the irregular tibial tuberosity, and the classical findings of Osgood-Schlatter disease on X-ray films.

Generally, a gouty tophus appears to develop near a body surface suffering from mechanical stimulation.4,11 In this patient, an ossicle in the patellar tendon remained near the body surface and suffered the pulling strain of the quadriceps as a result of the unresolved Osgood-Schlatter lesion. Inflammatory change around the attachment of the patellar tendon caused by repeated stimulation may exaggerate development of a gouty tophus.

Conservative treatment is the mainstay for gout and surgery is rarely indicated, but operating can be reasonable in the following circumstances:'

(1) when functional disorders occur,

(2) when a fistula or infection occurs,

(3) when pain is not alleviated,

(4) when the gouty tophus compresses a nerve,

(5) for cosmetic problems,

(6) when a reduction of the uric acid pool may improve systemic uric acid metabolism, (7) to prevent fracture because of a gouty tophus in a bone, and

(8) to prevent tendon rupture by a gouty tophus in a tendon.2

In the present patient, there was a risk of rupture if the gouty tophus in the patellar tendon had been left alone and an operation was indicated both for treatment and diagnostic purposes.

REFERENCES

1. Binazzi R, Felli L, Vaccari V. Surgical treatment of unresolved Osgood-Sch latter lesion. Clin Orthop 1993, 289:202-4.

2. Hankin FM, Mayhew DE,Coapman RA. Gouty infiltration of a flexor tendon simulating rupture. Clin Orthop 1985,194:1725

3. Mital MA, Matza RA, Cohen). The so-called unresolved Osgood-Sch latter lesion. J Bone joint Surg 1980, 62-A:732-9. 4. Nishioka N, Mikanagi K. Clinical features of 4,000 gouty subjects in Japan. Adv Exp Med Biol 1980, 122:47-54.

5. Ohta M, OhashiT, Otomo K. A case report of multiple gouty tophi, associated with patella partita. Rinshouseikeigeka 1994, 29:731-4.

6. Reber P, Crevoisier X, Noesberger B. Unusual localisation of tophaceous gout: A report of four cases and review of the literature. Arch Orthop Trauma Surg 1996, 115:297-9.

7. Recht MP, Seragini F, Kramer J. Isolated or dominant lesions of the patella in gout: A report of seven patients. Skeletal Radii 1994, 23:113-6.

8. Resnick D. The radiographic manifestations of gouty arthritis. Crit Rev Diagn Imaging 1977, 9:265-335.

9. Straub LIZ, Smith JW, Carpenter GK. The surgery of gout in the upper extremity. J Bone Joint Surg 1961, 43-A:731-52. 10. Tomita Y. Hasegawa M, Sasaki H. A case of gout associated with patella partita. Rinshouseikeigeka 1993, 28:1163-5.

Kou Katou, Yoshihiro Tomita, Yasumitsu Higuchi, Hisatsugu Takagita and Atsumasa Uchida Department of Orthopaedic Surgery, Mie University School of Medicine, Mie, Japan.

Address correspondence and reprint requests to: Dr Kou Katou, Department of Orthopaedic Surgery, Mie University School of Medicine, 2-174 Edobashi Tsu-City, Mie 514-8507, Japan.

Copyright Western Pacific Orthopaedic Association Dec 1998
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