J Orthop Sci (2004) 9:404–407 DOI 10.1007/s00776-004-0799-y
Acute calcific tendinitis of the gluteus medius: a case report with serial magnetic resonance imaging findings Takashi Sakai1, Yasunori Shimaoka2, Mizuo Sugimoto2, and Toshiaki Koizumi2 1 2
Department of Orthopaedic Surgery, Osaka National Hospital, 2-1-14 Hoenzaka, Chuo-ku, Osaka 540-0006, Japan Department of Orthopaedic Surgery, Ikeda Municipal Hospital, Ikeda, Japan
Abstract A case of calcific tendinitis of the gluteus medius is presented. Calcification was evident in the soft tissue adjacent to the greater trochanter on plain radiographs. On the initial magnetic resonance images (MRI), inflammatory edematous change was detected not only in the gluteus medius but also in the bone marrow of the greater trochanter, corresponding to the painful area. Three months later, calcification disappeared on plain radiographs and the femur showed normal signal intensity on MRI. Initial MRI excluded other diseases’ including infection and bone tumor, and serial MRI confirmed that the change in extraosseous and intraosseous findings were in accordance with self-limiting clinical symptoms. Key words Calcific tendinitis · Gluteus medius · Magnetic resonance imaging
Introduction Calcific tendinitis of the gluteus medius has been sporadically reported.6,10 Clinical symptoms of calcific tendinitis usually diminish spontaneously. We report that calcific tendinitis of the gluteus medius involves self-limiting changes in the extraosseous and intraosseous area on serial radiographs and magnetic resonance images (MRI).
greater trochanter, with decreased range of motion of the right hip due to severe pain. Although he had a temperature of 36.5°C, his leukocyte count was 11 230/µl with 74% neutrophils and a positive left shift, and C-reactive protein level was 3.3 mg/dl. Laboratory studies showed normal calcium and alkaline phosphatase levels and normal liver and renal function. Normal urine acid level denied inflammation by gout. On plain radiographs, there was no fracture, but a soft tissue calcification was seen adjacent to the greater trochanter (Fig. 1a,b). Computed tomography showed calcification and cortical erosive change (Fig. 2a,b). On the initial MRI (Fig. 3a–e), inflammatory edematous change was detected not only in the soft tissues adjacent to the greater trochanter, namely the gluteus medius muscle, but also in the bone marrow, corresponding to the painful area. Septic arthritis of the hip was excluded because there was no effusion in the hip joint. The diagnosis was thought to be calcific tendinitis of the hip
Case report A 69-year-old man presented with constant pain in the right thigh for 2 days. He did not have a history of trauma or unusual activities such as climbing mountains or jogging. He was unable to walk without the assistance of crutches. There was marked tenderness over the a
Offprint requests to: T. Sakai Received: February 12, 2004 / Accepted: April 26, 2004
b Fig. 1. Anteroposterior radiograph (a) and lateral radiograph (b) of the right hip show a soft tissue calcification (arrow) adjacent to the greater trochanter at the third day after the patient felt right thigh pain
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Fig. 4. Anteroposterior radiograph of the right hip shows no calcification beside the greater trochanter 3 months later b Fig. 2. Axial computed tomography (a) and coronal computed tomography (b) show a soft tissue calcification adjacent to the greater trochanter and cortical erosion (arrows)
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e Fig. 3. Magnetic resonance imaging (MRI) was performed 1 week after the patient felt right thigh pain. a Coronal T1weighted MR image (TR, 466; TE, 14) shows a low signal intensity area in the intraosseous lesion and beside the greater trochanter. b Coronal T2-weighted MR image (TR, 4800; TE, 14) shows a high signal intensity area demarcated by a low signal intensity line in the intraosseous lesion and a high signal intensity area in the soft tissue adjacent to the greater trochanter. c Coronal fat saturated T2-weighted MR image (TR, 5000; TE 13.6) shows a high signal intensity area surrounded
by an inhomogeneous high signal intensity area in the intraosseous lesion and a high signal intensity area in the soft tissue adjacent to the greater trochanter. d Axial T1-weighted MR image (TR, 600; TE, 14) shows a low signal intensity area in the intraosseous lesion and beside the greater trochanter. e Axial fat saturated T2-weighted MR image (TR, 4050; TE 96) shows a high signal intensity area surrounded with an inhomogeneous high signal intensity area in the intraosseous lesion and a high signal intensity area in the gluteus medius
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c Fig. 5. Coronal T1-weighted MR image (TR, 466; TE 14) (a), coronal T2-weighted MR image (TR, 4150; TE, 105) (b), and coronal fat saturated T2-weighted MR image (TR, 5000; TE 13) (c) show normal signal intensity in the greater trochanter 3 months later
due to the radiologic findings and MR findings. He was treated conservatively using nonsteroidal antiinflammatory drugs. Ten days later, the severe right thigh pain and tenderness over the greater trochanter diminished spontaneously. He was able to walk alone without any assistance. His leukocyte count and C-reactive protein level returned to within normal limits. Three months later, calcification disappeared on plain radiographs (Fig. 4), and the femur showed normal signal intensity on MRI (Fig. 5a–c). At the 2-year follow-up examination, his clinical symptoms had not reccurred, and no calcification was evident on plain radiographs.
Discussion Calcific tendinitis around the hip has been sporadically reported.1–7,9,10 Pain or tenderness around the affected area is usually so extreme that range of motion is severely limited. Fever, local edema, and elevated levels of acute-phase reactants may be present. The syndrome is usually monophasic in nature. According to the literature, there are two types based on occurrence: acute and chronic disease. In acute calcific tendinitis, most acute attacks last less than 2 weeks,2,3,5,9 and calcification usually disappears on plain radiographs in 4 weeks to 8 months.2,5,7 Although it is usually a self-limiting condition, mild or moderate pain lasts for 2 to 24 months in chronic disease.6,9,10 Kandemir et al. have recommended endoscopic treatment for chronic cases.6 Calcium hydroxyapatite crystal deposition is a multifactorial disease.4 In the natural history of calcific tendinitis, the final step is characterized by resorption of the calcium deposits, leading to relief of the persistent severe pain. In the calcium deposit resorption area, phagocytosing multinucleated osteoclasts exist and an acidic environment is essential for the resorption of mineral deposition.8 In our patient, bone marrow
edema of the greater trochanter and calcium deposition were the cause of severe pain. Bone marrow edema may be the more important cause, because patients who are asymptomatic in spite of radiologic calcification around the hip have been reported.9 Calcific tendinitis is diagnosed based upon clinical suspicion and typical radiographic findings of calcific deposits in the corresponding tendon. In our patient, a calcification adjacent to the greater trochanter existed in the gluteus medius. Although we initially suspected septic arthritis of the hip, it was excluded because there was no effusion in the hip joint and because his white blood cell count and C-reactive protein level returned to within normal limits without antibiotics. Initial MRI can be an extremely useful tool to not only rule out other diseases, including infection, fractures, or bone tumor,10 but also to illustrate the degree of intense inflammation involved in this condition. Kraemer et al. have reported increased signal intensity of soft tissue and marrow in the region of the femur on single T2weighted MR images.7 In our patient, inflammatory edematous findings were detected not only in the gluteus medius but also in the bone marrow of the greater trochanter, corresponding to the painful area. Calcification on plain radiographs and inflammatory changes on MRI had disappeared 3 months after onset. Serial MRI revealed that the changes in the extraosseous and intraosseous findings were in accordance with selflimiting clinical symptoms. References 1. Berney JW. Calcifying peritendinitis of the gluteus maximus tendon. Radiology 1972;102:517–8. 2. Chow HY, Recht MP, Schils J, et al. Acute calcific tendinitis of the hip. Case report with magnetic resonance imaging findings. Arthritis Rheum 1997;40:974–7. 3. Fam AG, Pritzker KPH, Stein JL, et al. Apatite-associated arthropathy: a clinical study of 14 cases and of 2 patients with calcific bursitis. J Rheumatol 1979;6:461–71.
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4. Holt PD, Keats TE. Calcific tendinitis: a review of the usual and unusual. Skeletal Radiol 1993;22:1–9. 5. Jones GB. Acute episodes with calcification around the hip joint. J Bone Joint Surg [Br] 1955;37:448–52. 6. Kandemir U, Bharam S, Philippon MJ, et al. Endoscopic treatment of calcific tendinitis of gluteus medius and minimus. Arthroscopy 2003;19:1–4. 7. Kraemer EJ, El-Khoury GY. Atypical calcific tendinitis with cortical erosions. Skeletal Radiol 2000;29:690–6.
8. Nakase T, Takeuchi E, Sugamoto K, et al. Involvement of multinucleated giant cells synthesizing cathepsin K in calcified tendinitis of the rotator cuff tendons. Rheumatology 2000;39:1074–7. 9. Wepfer JF, Reed JG, Cullen GM, et al. Calcific tendinitis of the gluteus maximus tendon (gluteus maximus tendinitis). Skeletal Radiol 1983;9:198–200. 10. Yang I, Hayes CW, Biermann JS. Calcific tendinitis of the gluteus medius tendon with bone marrow edema mimicking metastatic disease. Skeletal Radiol 2002;31:359–61.