1992, The British Journal of Radiology, 65, 271-273 SPENCER, R. & LEVY, D. M., 1962. Hydrometrocolpos: report
WILSON, D. A., STACY, T. M. & SMITH, E. I., 1978. Ultrasound
of three cases and review of the literature. Annals of Surgery, 155, 558-571.
diagnosis of hydrocolpos and hydrometrocolpos. Radiology, 128, 451-454.
WESTERHOUT, F. C , HODGMAN, J. E., ANDERSON, G. V. et al,
1964. Congenital hydrocolpos. American Obstetrics & Gynecology, 89, 957-961.
Journal
of
An unusual osteochondral body in association with calcium pyrophosphate dihydrate crystal deposition disease By A. C. Jones, BSc, MRCP, *B. J. Preston, FRCR and M. Doherty, MA, MD, MRCP Rheumatology Unit, City Hospital, Nottingham NG5 1 PB and 'Department of Radiology, University Hospital, Nottingham, Clifton Boulevard, Nottingham NG7 2UH (Received 19 June 1991, accepted 23 July 1991) Keywords: Osteochondral body, Chondrocalcinosis, Knee, Pyrophosphate arthropathy
Chronic pyrophosphate arthropathy is a recognized subset of osteoarthritis (OA) characterized by deposition of calcium pyrophosphate dihydrate (CPPD) crystals (McCarty, 1976). Typically a disease of the elderly, there is symptomatic and radiographic involvement of characteristic sites, including the patellofemoral, radiocarpal and glenohumeral joints (McCarty & Haskin, 1963; Resnick & Resnick, 1983). CPPD deposition in cartilage (chondrocalcinosis) occurs particularly in the articular and the meniscal cartilages of the knee, the symphysis pubis and the triangular ligament of the wrist (McCarty & Haskin, 1963; Resnick & Resnick, 1983). It has been postulated that sporadic pyrophosphate arthropathy may represent a hypertrophic response to joint insult (Doherty et al, 1984), with CPPD crystal formation being a marker of high extracellular pyrophosphate production reflecting increased cellular biosynthetic activity (Caswell etal, 1983). Osteochondral bodies, arising in synovium by enchondral ossification of islands of chondroid metaplasia, are a common accompaniment to OA and may be particularly florid in the subset of pyrophosphate arthropathy (McCarty & Haskin, 1963; Resnick & Resnick, 1983). Such bodies form by a process of layered growth (Milgram, 1977b), and possibly reflect a generalized hyperplastic response {i.e. attempted repair) by joint tissues. We present a patient with CPPD arthropathy who developed an osteochondral body that showed features both of ossification and chondrocalcinosis.
episodes of acute synovitis. CPPD crystals, identified by compensated polarized light microscopy, were repeatedly isolated from the knee synovial fluid. The patient had also experienced episodes of diuretic-induced gout affecting the olecranon bursa and the first metatarsophalangeal, ankle and knee joints (confirmed by identification of monosodium urate crystals). Diuretics had been given for episodes of ischaemic congestive cardiac failure; all symptoms of gout resolved when they were withdrawn. There was no family history of arthropathy. On examination he was obese and had clinical signs of osteoarthritis of the knees with bony deformity and crepitus. Biochemically there was no evidence of predisposing metabolic
Case report An 83-year-old man presented with a 3 year history of symptomatic knee arthropathy associated with multiple Address correspondence to A. C. Jones, Rheumatology Unit, City Hospital, Nottingham NG5 1PB. Vol. 65, No. 771
Figure 1. Lateral radiograph of the osteochondral body demonstrating the dense, possibly trabeculated core.
271
Case reports
of interest in this case is that chondrocalcinosis occurred in newly formed cartilage, in the setting of a compromised joint and in an individual predisposed to CPPD crystal formation. It is also of interest that this patient had coexisting urate gout; such predisposition to multiple crystal deposition is well recognized (Dieppe et al, 1988) and supports the importance of common factors that enhance crystal nucleation and growth (Stockman et al, 1980). Although the appearance of this osteochondral body could arise from layered growth (Milgram, 1977b), possibly of a bony nidus (Milgram, 1977a), the central ossification appears too pronounced for such an explanation. Chondroid metaplasia with subsequent enchondral ossification seems a more likely explanation; this process reflecting an aspect of the hypertrophic repair process associated with pyrophosphate arthropathy (Doherty et al, 1984). Although the patient is elderly the osteochondral body contains newly formed fibrocartilage. Chondrocalcinosis, even in those with familial or metabolic predisposition (Hamilton, 1976; McCarty, 1976), is strongly age-related. This observation suggests that fibrocartilage synthesized by chondrocytes within aged joints is qualitatively different from that synthesized in younger tissues. This could arise through age-related changes either in the synthetic cells themselves or in the perichondrocyte environment. Figure 2. Repeat radiograph after 2 years demonstrating the development of a fine outer rim of calcification.
Acknowledgments A. C. Jones is an Arthritis and Rheumatism Council junior clinical research fellow. References
disease (Hamilton, 1976); the only abnormality was mild chronic renal failure (urea 16.3 mmol/1, creatinine 217 /xmol/1). Plain radiographs of his right knee demonstrated a well defined intracapsular body near the head of the fibula (Fig. 1). The densely calcified core appeared to contain trabeculae, and serial films (Fig. 2) demonstrated developing fine calcification of the outer rim, suggestive of chondrocalcinosis. In addition there was bilateral tricompartmental knee OA with faint chondrocalcinosis of the menisci and several other loose bodies. Radiographs of his lumbar spine showed large lateral osteophytes. There were minor OA changes of his first metatarsalphalangeal joints. There was no chondrocalcinosis at other sites.
Discussion The radiographic appearance suggests ossification of the core of the chondrometaplastic island (osteochondral body) with calcification (i.e. chondrocalcinosis) of the superficial, newly formed fibrocartilage rim. Although confirmation of the crystal species responsible for the peripheral chondrocalcinosis would require tissue examination, it is tempting to speculate that it is CPPD, since this is the commonest cause for chondrocalcinosis of fibrocartilage and hyaline cartilage (McCarty et al, 1966). The patient had chondrocalcinosis elsewhere in the same joint and synovial fluid CPPD crystals were repeatedly identified. The principal feature 272
CASWELL, A., GUILLAND-CUMMING, D. F., HEARN, P. R., MCGUIRE, M. K. B. & RUSSELL, R. G. G., 1983.
Pathogenesis of chondrocalcinosis and pseudogout. Metabolism of inorganic pyrophosphate and production of calcium pyrophosphate dihydrate crystals. Annals of the Rheumatic Diseases, 42(S), 27-36. DIEPPE, P., CAMPION, G. & DOHERTY, M., 1988. Mixed crystal
deposition. Rheumatic Disease Clinics of North America, 14, 415-426. DOHERTY, M., DIEPPE, P. & WATT, I., 1984. Low incidence of
calcium pyrosphosphate dihydrate crystal deposition in rheumatoid arthritis, with modification of radiographic features in coexistent disease. Arthritis and Rheumatism, 27, 1002-1009. HAMILTON, E. B. D., 1976. Diseases associated with CPPD deposition disease. Arthritis and Rheumatism, 19, 353-357. MCCARTY, D. J., 1976. Calcium pyrophosphate dihydrate crystal deposition disease—1975. Arthritis and Rheumatism, 19, 275-285. MCCARTY, D. J. & HASKIN, M. E., 1963. The roentgenographic
aspects of pseudogout (articular chondrocalcinosis). American Journal of Roentgenology, Radium Therapy and Nuclear Medicine, 90, 1248-1257. MCCARTY, D. J., HOGAN, J. M., GATTER, R. A. & GROSSMAN,
M., 1966. Studies on pathological calcifications in human cartilage. Journal of Bone and Joint Surgery, 48 (A), 309-324. MILGRAM, J. W., 1977a. The classification of loose bodies in human joints. Clinical Orthopaedics and Related Research, 124, 282-291.
The British Journal of Radiology, March 1992
1992, The British Journal of Radiology, 65, 273-278 1977b. The development of loose bodies in human joints. Clinical Orthopaedics and Related Research, 124, 292-303. RESNICK, C. S. & RESNICK, D., 1983. Crystal deposition disease. Seminars in Arthritis and Rheumatism, 12, 390-403.
STOCKMAN, A., DARLINGTON, L. G. & SCOTT, J. T.,
1980.
Frequency of chondrocalinosis of the knees and avascular necrosis of the femoral head in gout: a controlled study. Annals of the Rheumatic Diseases, 39, 7-11.
Three-dimensional imaging of dual isotope data-sets in a case of acute myocardial infarction By Hugo P. Dilhuydy, Blng, *Daniel McNamara, MD, 'Raymond J. Lemieux, MD, Yves Martel, Blng and Jacques A. de Guise, PhD Institut de Genie Biomedical, Ecole Polytechnique de Montreal, Campus de I'Universite de Montreal, Case Postale 6079, succursale "A", Montreal, Que, H3C 3A7, Canada and "Service de Medecine Nucleaire, Hopital du Sacre-Coeur de Montreal, 5400 boul. Gouin ouest, Montreal, Que, H4J 1C5, Canada
{Received 6 December 1990 and in revised form 30 May 1991, accepted 4 September 1991)
Keywords: Myocardial infarction, Thallium 201, Indium 111-antimyosin, Dual isotope, Three-dimensional imaging
A patient with acute myocardial infarction was injected with indium 111 ( ni In)-antimyosin Fab. He then underwent planar imaging before receiving an additional dose of thallium 201 (2O1T1) so as to perform a dual isotope single photon emission computed tomography (SPECT) acquisition. Planar images showed vague myocardial uptake of antimyosin antibody. With tomographic slices, a more defined area of antimyosin uptake was seen but still with a low l u I n signal-to-noise ratio. This area corresponded to a 2O1T1 defect. Two three-dimensional (3D) rendering methods showed a well matched 2O1 T1 3D defect and m I n 3D hot spot and seemed to facilitate the localization of the infarct as well as the evaluation of its importance relative to the remaining viable tissue. This case study illustrates a situation where 3D imaging of dual isotope data-sets could be useful for direct visualization and localization of myocardial infarction.
considered at risk and triple bypass surgery was carried out 20 days after his admission. During the procedure, the surgeon noticed an extensive antero-apical fibrosis. Four months later, the patient returned to work. To evaluate further the location and extent of the infarct, '"In-antimyosin (Amersham Canada Ltd, Oakville) scintigraphy was performed before surgery, 10 days after his admission. Acquisition of an antimyosin scan was obtained 36 h after intravenous administration of 80 MBq (2.2 mCi) of m In-DTPA-antimyosin. Chromatography revealed 93% binding. Both planar and tomographic studies were performed with a medium-energy high-resolution parallel-hole collimator on a SophyCamera (Sopha Medical Inc., Paris, France). Planar images were acquired during 10 min (approximately 500000 counts) using both '"In photopeaks (172 and 247 keV) with a 20% energy window and a 128x128 matrix. Three viewing angles were selected: anterior, left anterior oblique (LAO) 45° and LAO 70° (see Fig. 2). Before tomographic imaging, the patient was injected with 100 MBq (2.7 mCi) of 201Tl. 10 min later, a dual isotope SPECT acquisition was performed with 32 projections for 40 s each (approximately 65 000 201Tl counts
Case report A 61-year-old white male with a past history of occasional chest pain was admitted to the ICU for prolonged chest pain. He had multiple risk factors for coronary disease such as smoking (up to 40 cigarettes per day), essential hypertension, diabetes and a family history of coronary artery disease. Laboratory analysis showed elevated plasma enzyme levels of total creatine kinase (CK) (1289 U/l) and the electrocardiogram showed an infarct in the anterior wall and a possible old inferior wall infarction (see Fig. 1). Five days after his admission coronary angiography revealed severe threevessel disease. The patient recovered well during hospitalization without recurrent chest pain at rest or heart failure. Because of the severe three-vessel disease, the patient was *Address correspondence to R. J. Lemieux, MD, Service de Medecine Nucleaire, Hopital du Sacre-Coeur de Montreal, 5400 Boul. Gouin ouest, Montreal, Que. H4J 1C5, Canada.
Vol. 65, No. 771
Figure 1. 12-lead electrocardiogram obtained on the first day of admission showing acute anterior and possible old inferior infarction.
273
WILSON, D. A., STACY, T. M. & SMITH, E. I., 1978. Ultrasound
of three cases and review of the literature. Annals of Surgery, 155, 558-571.
diagnosis of hydrocolpos and hydrometrocolpos. Radiology, 128, 451-454.
WESTERHOUT, F. C , HODGMAN, J. E., ANDERSON, G. V. et al,
1964. Congenital hydrocolpos. American Obstetrics & Gynecology, 89, 957-961.
Journal
of
An unusual osteochondral body in association with calcium pyrophosphate dihydrate crystal deposition disease By A. C. Jones, BSc, MRCP, *B. J. Preston, FRCR and M. Doherty, MA, MD, MRCP Rheumatology Unit, City Hospital, Nottingham NG5 1 PB and 'Department of Radiology, University Hospital, Nottingham, Clifton Boulevard, Nottingham NG7 2UH (Received 19 June 1991, accepted 23 July 1991) Keywords: Osteochondral body, Chondrocalcinosis, Knee, Pyrophosphate arthropathy
Chronic pyrophosphate arthropathy is a recognized subset of osteoarthritis (OA) characterized by deposition of calcium pyrophosphate dihydrate (CPPD) crystals (McCarty, 1976). Typically a disease of the elderly, there is symptomatic and radiographic involvement of characteristic sites, including the patellofemoral, radiocarpal and glenohumeral joints (McCarty & Haskin, 1963; Resnick & Resnick, 1983). CPPD deposition in cartilage (chondrocalcinosis) occurs particularly in the articular and the meniscal cartilages of the knee, the symphysis pubis and the triangular ligament of the wrist (McCarty & Haskin, 1963; Resnick & Resnick, 1983). It has been postulated that sporadic pyrophosphate arthropathy may represent a hypertrophic response to joint insult (Doherty et al, 1984), with CPPD crystal formation being a marker of high extracellular pyrophosphate production reflecting increased cellular biosynthetic activity (Caswell etal, 1983). Osteochondral bodies, arising in synovium by enchondral ossification of islands of chondroid metaplasia, are a common accompaniment to OA and may be particularly florid in the subset of pyrophosphate arthropathy (McCarty & Haskin, 1963; Resnick & Resnick, 1983). Such bodies form by a process of layered growth (Milgram, 1977b), and possibly reflect a generalized hyperplastic response {i.e. attempted repair) by joint tissues. We present a patient with CPPD arthropathy who developed an osteochondral body that showed features both of ossification and chondrocalcinosis.
episodes of acute synovitis. CPPD crystals, identified by compensated polarized light microscopy, were repeatedly isolated from the knee synovial fluid. The patient had also experienced episodes of diuretic-induced gout affecting the olecranon bursa and the first metatarsophalangeal, ankle and knee joints (confirmed by identification of monosodium urate crystals). Diuretics had been given for episodes of ischaemic congestive cardiac failure; all symptoms of gout resolved when they were withdrawn. There was no family history of arthropathy. On examination he was obese and had clinical signs of osteoarthritis of the knees with bony deformity and crepitus. Biochemically there was no evidence of predisposing metabolic
Case report An 83-year-old man presented with a 3 year history of symptomatic knee arthropathy associated with multiple Address correspondence to A. C. Jones, Rheumatology Unit, City Hospital, Nottingham NG5 1PB. Vol. 65, No. 771
Figure 1. Lateral radiograph of the osteochondral body demonstrating the dense, possibly trabeculated core.
271
Case reports
of interest in this case is that chondrocalcinosis occurred in newly formed cartilage, in the setting of a compromised joint and in an individual predisposed to CPPD crystal formation. It is also of interest that this patient had coexisting urate gout; such predisposition to multiple crystal deposition is well recognized (Dieppe et al, 1988) and supports the importance of common factors that enhance crystal nucleation and growth (Stockman et al, 1980). Although the appearance of this osteochondral body could arise from layered growth (Milgram, 1977b), possibly of a bony nidus (Milgram, 1977a), the central ossification appears too pronounced for such an explanation. Chondroid metaplasia with subsequent enchondral ossification seems a more likely explanation; this process reflecting an aspect of the hypertrophic repair process associated with pyrophosphate arthropathy (Doherty et al, 1984). Although the patient is elderly the osteochondral body contains newly formed fibrocartilage. Chondrocalcinosis, even in those with familial or metabolic predisposition (Hamilton, 1976; McCarty, 1976), is strongly age-related. This observation suggests that fibrocartilage synthesized by chondrocytes within aged joints is qualitatively different from that synthesized in younger tissues. This could arise through age-related changes either in the synthetic cells themselves or in the perichondrocyte environment. Figure 2. Repeat radiograph after 2 years demonstrating the development of a fine outer rim of calcification.
Acknowledgments A. C. Jones is an Arthritis and Rheumatism Council junior clinical research fellow. References
disease (Hamilton, 1976); the only abnormality was mild chronic renal failure (urea 16.3 mmol/1, creatinine 217 /xmol/1). Plain radiographs of his right knee demonstrated a well defined intracapsular body near the head of the fibula (Fig. 1). The densely calcified core appeared to contain trabeculae, and serial films (Fig. 2) demonstrated developing fine calcification of the outer rim, suggestive of chondrocalcinosis. In addition there was bilateral tricompartmental knee OA with faint chondrocalcinosis of the menisci and several other loose bodies. Radiographs of his lumbar spine showed large lateral osteophytes. There were minor OA changes of his first metatarsalphalangeal joints. There was no chondrocalcinosis at other sites.
Discussion The radiographic appearance suggests ossification of the core of the chondrometaplastic island (osteochondral body) with calcification (i.e. chondrocalcinosis) of the superficial, newly formed fibrocartilage rim. Although confirmation of the crystal species responsible for the peripheral chondrocalcinosis would require tissue examination, it is tempting to speculate that it is CPPD, since this is the commonest cause for chondrocalcinosis of fibrocartilage and hyaline cartilage (McCarty et al, 1966). The patient had chondrocalcinosis elsewhere in the same joint and synovial fluid CPPD crystals were repeatedly identified. The principal feature 272
CASWELL, A., GUILLAND-CUMMING, D. F., HEARN, P. R., MCGUIRE, M. K. B. & RUSSELL, R. G. G., 1983.
Pathogenesis of chondrocalcinosis and pseudogout. Metabolism of inorganic pyrophosphate and production of calcium pyrophosphate dihydrate crystals. Annals of the Rheumatic Diseases, 42(S), 27-36. DIEPPE, P., CAMPION, G. & DOHERTY, M., 1988. Mixed crystal
deposition. Rheumatic Disease Clinics of North America, 14, 415-426. DOHERTY, M., DIEPPE, P. & WATT, I., 1984. Low incidence of
calcium pyrosphosphate dihydrate crystal deposition in rheumatoid arthritis, with modification of radiographic features in coexistent disease. Arthritis and Rheumatism, 27, 1002-1009. HAMILTON, E. B. D., 1976. Diseases associated with CPPD deposition disease. Arthritis and Rheumatism, 19, 353-357. MCCARTY, D. J., 1976. Calcium pyrophosphate dihydrate crystal deposition disease—1975. Arthritis and Rheumatism, 19, 275-285. MCCARTY, D. J. & HASKIN, M. E., 1963. The roentgenographic
aspects of pseudogout (articular chondrocalcinosis). American Journal of Roentgenology, Radium Therapy and Nuclear Medicine, 90, 1248-1257. MCCARTY, D. J., HOGAN, J. M., GATTER, R. A. & GROSSMAN,
M., 1966. Studies on pathological calcifications in human cartilage. Journal of Bone and Joint Surgery, 48 (A), 309-324. MILGRAM, J. W., 1977a. The classification of loose bodies in human joints. Clinical Orthopaedics and Related Research, 124, 282-291.
The British Journal of Radiology, March 1992
1992, The British Journal of Radiology, 65, 273-278 1977b. The development of loose bodies in human joints. Clinical Orthopaedics and Related Research, 124, 292-303. RESNICK, C. S. & RESNICK, D., 1983. Crystal deposition disease. Seminars in Arthritis and Rheumatism, 12, 390-403.
STOCKMAN, A., DARLINGTON, L. G. & SCOTT, J. T.,
1980.
Frequency of chondrocalinosis of the knees and avascular necrosis of the femoral head in gout: a controlled study. Annals of the Rheumatic Diseases, 39, 7-11.
Three-dimensional imaging of dual isotope data-sets in a case of acute myocardial infarction By Hugo P. Dilhuydy, Blng, *Daniel McNamara, MD, 'Raymond J. Lemieux, MD, Yves Martel, Blng and Jacques A. de Guise, PhD Institut de Genie Biomedical, Ecole Polytechnique de Montreal, Campus de I'Universite de Montreal, Case Postale 6079, succursale "A", Montreal, Que, H3C 3A7, Canada and "Service de Medecine Nucleaire, Hopital du Sacre-Coeur de Montreal, 5400 boul. Gouin ouest, Montreal, Que, H4J 1C5, Canada
{Received 6 December 1990 and in revised form 30 May 1991, accepted 4 September 1991)
Keywords: Myocardial infarction, Thallium 201, Indium 111-antimyosin, Dual isotope, Three-dimensional imaging
A patient with acute myocardial infarction was injected with indium 111 ( ni In)-antimyosin Fab. He then underwent planar imaging before receiving an additional dose of thallium 201 (2O1T1) so as to perform a dual isotope single photon emission computed tomography (SPECT) acquisition. Planar images showed vague myocardial uptake of antimyosin antibody. With tomographic slices, a more defined area of antimyosin uptake was seen but still with a low l u I n signal-to-noise ratio. This area corresponded to a 2O1T1 defect. Two three-dimensional (3D) rendering methods showed a well matched 2O1 T1 3D defect and m I n 3D hot spot and seemed to facilitate the localization of the infarct as well as the evaluation of its importance relative to the remaining viable tissue. This case study illustrates a situation where 3D imaging of dual isotope data-sets could be useful for direct visualization and localization of myocardial infarction.
considered at risk and triple bypass surgery was carried out 20 days after his admission. During the procedure, the surgeon noticed an extensive antero-apical fibrosis. Four months later, the patient returned to work. To evaluate further the location and extent of the infarct, '"In-antimyosin (Amersham Canada Ltd, Oakville) scintigraphy was performed before surgery, 10 days after his admission. Acquisition of an antimyosin scan was obtained 36 h after intravenous administration of 80 MBq (2.2 mCi) of m In-DTPA-antimyosin. Chromatography revealed 93% binding. Both planar and tomographic studies were performed with a medium-energy high-resolution parallel-hole collimator on a SophyCamera (Sopha Medical Inc., Paris, France). Planar images were acquired during 10 min (approximately 500000 counts) using both '"In photopeaks (172 and 247 keV) with a 20% energy window and a 128x128 matrix. Three viewing angles were selected: anterior, left anterior oblique (LAO) 45° and LAO 70° (see Fig. 2). Before tomographic imaging, the patient was injected with 100 MBq (2.7 mCi) of 201Tl. 10 min later, a dual isotope SPECT acquisition was performed with 32 projections for 40 s each (approximately 65 000 201Tl counts
Case report A 61-year-old white male with a past history of occasional chest pain was admitted to the ICU for prolonged chest pain. He had multiple risk factors for coronary disease such as smoking (up to 40 cigarettes per day), essential hypertension, diabetes and a family history of coronary artery disease. Laboratory analysis showed elevated plasma enzyme levels of total creatine kinase (CK) (1289 U/l) and the electrocardiogram showed an infarct in the anterior wall and a possible old inferior wall infarction (see Fig. 1). Five days after his admission coronary angiography revealed severe threevessel disease. The patient recovered well during hospitalization without recurrent chest pain at rest or heart failure. Because of the severe three-vessel disease, the patient was *Address correspondence to R. J. Lemieux, MD, Service de Medecine Nucleaire, Hopital du Sacre-Coeur de Montreal, 5400 Boul. Gouin ouest, Montreal, Que. H4J 1C5, Canada.
Vol. 65, No. 771
Figure 1. 12-lead electrocardiogram obtained on the first day of admission showing acute anterior and possible old inferior infarction.
273
