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(Radiology. 2001;218:848-853.)
© RSNA, 2001


Musculoskeletal Imaging

Tuberculous versus Pyogenic Arthritis: MR Imaging Evaluation1

Sung Hwan Hong, MD, Sung Moon Kim, MD, Joong Mo Ahn, MD, Hye Won Chung, MD, Myung Jin Shin, MD and Heung Sik Kang, MD

1 From the Depts of Radiology and Institute of Radiation Medicine, Seoul National University College of Medicine, 28 Yongon-dong, Chongno-gu, Seoul 110-744, Korea (S.H.H., H.S.K.); Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea (S.M.K., M.J.S.); Samsung Medical Center, Sungkunkwan University School of Medicine, Seoul, Korea (J.M.A.); and Seoul City Boramae Hospital, Korea (H.W.C.). Received Apr 5, 2000; revision requested May 25; revision received July 10; accepted Aug 2. Address correspondence to H.S.K. (e-mail: kanghs@radcom.snu.ac.kr).


    ABSTRACT
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
PURPOSE: To assess magnetic resonance (MR) imaging features in differentiating tuberculous arthritis from pyogenic arthritis.

MATERIALS AND METHODS: Findings in 29 patients with tuberculous arthritis were compared with those of 13 patients with pyogenic arthritis. Bone erosion, marrow signal intensity, synovial lesion signal intensity, boundaries (smooth or irregular) for extraarticular extension of infection, and abscess rim enhancement (thin and smooth or thick and irregular) were analyzed.

RESULTS: Bone erosion was more common in patients with tuberculous arthritis (24 [83%] of 29) than in those with pyogenic arthritis (six [46%] of 13) (P = .026), while subchondral marrow signal intensity abnormality was seen more frequently in patients with pyogenic arthritis (12 [92%] of 13) than in those with tuberculous arthritis (17 [59%] of 29) (P = .036). On T2-weighted images, there was no significant difference between the synovial lesion signal intensities of tuberculous arthritis and pyogenic arthritis. Lesions in 16 (70%) of 23 patients with tuberculous arthritis and two (17%) of 12 patients with pyogenic arthritis had smooth extraarticular boundaries, while those in seven (30%) of 23 patients with tuberculous arthritis and 10 (83%) of 12 patients with pyogenic arthritis had irregular boundaries (P = .005). Tuberculous abscesses (16 [100%] of 16) had thin and smooth rim enhancement, while most pyogenic abscesses (five [71%] of seven) had thick and irregular rims (P = .001).

CONCLUSION: MR imaging of bone abnormalities, extraarticular lesions, and associated abscesses provides useful information in the differentiation of tuberculous arthritis and pyogenic arthritis.

Index terms: Arthritis, septic, 4*.232, 4*.26 • Joints, MR, 4*.121411, 4*.12143 • Tuberculosis, musculoskeletal, 4*.23


    INTRODUCTION
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Infectious arthritis can result in serious disability, so pertinent treatment based on a specific diagnosis is imperative. Making a specific diagnosis is particularly important in the differentiation of tuberculous arthritis and pyogenic arthritis because appropriate therapy is essential to preserve joint function. Insidious onset of disease, substantial osteopenia, minimal sclerosis, and relative preservation of joint space favor the diagnosis of tuberculous arthritis (1), as pyogenic arthritis usually has the more aggressive course (2). However, tuberculosis may have a virulent pattern of destruction (3). Ultimate diagnosis can be made by isolating the causative organism from the synovial fluid or by performing a synovial biopsy (4).

There is now a growing body of literature that shows magnetic resonance (MR) imaging to be a useful imaging modality in the evaluation of musculoskeletal infection (510). However, to our knowledge, no study findings have been published to date on the differentiation of tuberculous arthritis and pyogenic arthritis with the use of this technique. Mycobacterium tuberculosis forms tubercles with central caseating necrosis that shows intermediate signal intensity on T2-weighted images (11). Unlike most bacteria, M tuberculosis does not produce proteolytic enzymes (12). Tuberculosis forms a cold abscess, an abscess type that is not accompanied by prominent inflammation (13). We hypothesized that the MR imaging features of tuberculous arthritis and pyogenic arthritis may allow differentiation of the two. The purpose of our study was to determine these features.


    MATERIALS AND METHODS
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
We collected the cases of infectious arthritis with an MR study from three tertiary referral hospitals during 7 years from January 1992 to December 1998. Initially, 53 patients were chosen by searching an MR imaging database for diagnoses of tuberculous arthritis and pyogenic arthritis. Of these patients, nine were excluded because microbiologic examination failed to disclose an etiologic organism. Furthermore, two other patients were excluded because clinical data and imaging features suggested that the joint infection could be secondary to osteomyelitis. The remaining 42 patients with microbiologically or histopathologically proved cases of disease included 29 patients with tuberculous arthritis and 13 patients with pyogenic arthritis.

Involved joints were as follows: for tuberculous arthritis, the hip (n = 5), knee (n = 14), wrist (n = 5), elbow (n = 2), ankle (n = 2), and shoulder (n = 1), and for pyogenic arthritis, the hip (n = 9), knee (n = 3), and ankle (n = 1). Of 29 patients with tuberculous arthritis, 18 were male and 11 were female; their ages ranged from 13 to 73 years (mean, 43 years). Of 13 patients with pyogenic arthritis, seven were male and six were female; their ages ranged from 3 to 89 years (mean, 46 years).

MR imaging had been performed with various MR units. In all patients, spin-echo T1- and T2-weighted images were obtained with gadolinium-enhanced spin-echo T1-weighted images. The following imaging parameters were used: 400–600/10–30 (repetition time msec/echo time msec) for T1-weighted spin-echo imaging and 2,500–4,000/80–108 for T2-weighted spin-echo imaging. The imaging planes were variable in each patient. In all patients, transverse images and at least one appropriate longitudinal (sagittal or coronal) image were obtained.

MR images were assessed by two musculoskeletal radiologists (S.H.H., H.S.K.) who were experienced in musculoskeletal MR imaging. The two radiologists, who were blinded to the cause of the arthritis, reviewed the MR images together and arrived at a consensus. We analyzed diverse MR imaging findings of arthritis in terms of bone erosion, marrow signal intensity abnormality, synovial lesion signal intensity, boundaries (smooth or irregular) of extraarticular extension of infection, and abscess rim enhancement (thin and smooth or thick and irregular).

We recorded the presence of bone abnormalities, which were classified as either bone erosion or marrow signal intensity abnormality. Bone erosion was regarded as a well-demarcated lesion that caused disruption of the normal bone cortical contour. Marrow signal intensity abnormality was defined as poorly demarcated areas, diffuse or patchy hypointense areas (on the T1-weighted image), or as hyperintense areas (on the T2-weighted image) in the subchondral bone marrow.

The signal intensity of synovial abnormalities was qualitatively compared with that of muscle and fluid. On T2-weighted images, signal intensity was classified as low, intermediate, and high, where signal intensity of normal muscle was regarded as low and that of fluid was rated as high. Signal intensity between high and low was designated intermediate. When a lesion demonstrated mixed signal intensities, the intensity of the largest part of the lesion was chosen for classification.

When infection extended beyond the joint, we assessed the characteristics of extraarticular extension and associated abscesses. The boundaries of extraarticular abnormalities were assessed as being smooth or irregular. To evaluate soft-tissue abscesses, we focused on the characteristics of the abscess wall, that is, thick or thin and smooth or irregular.

The findings in tuberculous arthritis and pyogenic arthritis were tabulated and then examined statistically with use of the Fisher exact test. Significance was accepted with a P value of less than .05.


    RESULTS
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
The MR findings in patients with tuberculous arthritis and pyogenic arthritis are summarized in the Table. T1-weighted images best depicted bone erosions, which exhibited focal low-signal-intensity lesions in contrast to normal fatty bone marrow (Fig 1). There were significant differences in the frequency of bone erosion between the two kinds of arthritis (24 [83%] of 29 patients with tuberculous arthritis vs six [46%] of 13 patients with pyogenic arthritis; P = .026). Marrow signal intensity abnormality was found more frequently in patients with pyogenic arthritis (12 [92%] of 13) than in those with tuberculous arthritis (17 [59%] of 29) (P = .036) (Figs 1, 2).


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MR Findings of Tuberculous and Pyogenic Arthritis
 


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Figure 1a. Sagittal T1-weighted MR images show bone erosion and marrow signal intensity abnormality. (a) In tuberculous arthritis involving knee joints, image (500/20) shows bone erosions of well-defined hypointense lesions (short arrows) and hypointense marrow (long arrows) in both the femur and tibia. (b) In pyogenic arthritis, image (450/17) shows bone erosions (short arrows) and hypointense marrow (long arrows).

 


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Figure 1b. Sagittal T1-weighted MR images show bone erosion and marrow signal intensity abnormality. (a) In tuberculous arthritis involving knee joints, image (500/20) shows bone erosions of well-defined hypointense lesions (short arrows) and hypointense marrow (long arrows) in both the femur and tibia. (b) In pyogenic arthritis, image (450/17) shows bone erosions (short arrows) and hypointense marrow (long arrows).

 


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Figure 2a. Sagittal T2-weighted MR images of the knee show the signal intensity of synovial abnormalities and increased bone marrow signal intensity (arrows). (a) Image (3,500/90) of tuberculous arthritis shows abnormalities of predominantly intermediate signal intensity (white arrowheads) with small amounts of hyperintense joint fluid (black arrowheads). (b) Image (2,500/80) of pyogenic arthritis shows abnormalities of mixed high and intermediate signal intensity (arrowheads), but the distinction between synovial lesion and joint effusion cannot be made.

 


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Figure 2b. Sagittal T2-weighted MR images of the knee show the signal intensity of synovial abnormalities and increased bone marrow signal intensity (arrows). (a) Image (3,500/90) of tuberculous arthritis shows abnormalities of predominantly intermediate signal intensity (white arrowheads) with small amounts of hyperintense joint fluid (black arrowheads). (b) Image (2,500/80) of pyogenic arthritis shows abnormalities of mixed high and intermediate signal intensity (arrowheads), but the distinction between synovial lesion and joint effusion cannot be made.

 
Variable intermediate- to high-signal-intensity lesions were seen in synovial abnormalities of tuberculous arthritis and pyogenic arthritis on T2-weighted images (Fig 2). In a small number of patients, we could not make a distinction between synovial abnormalities and joint fluid on T2-weighted images. In such patients, we referred to the gadolinium-enhanced images to distinguish between them. In the majority of patients with tuberculous arthritis and pyogenic arthritis, synovial abnormalities were of mixed signal intensity. Images of 24 (83%) of 29 patients with tuberculous arthritis and seven (54%) of 13 patients with pyogenic arthritis showed predominantly intermediate signal intensity, while the rest showed primarily high signal intensity. There was no significant difference in the signal intensities between patients with tuberculous arthritis and those with pyogenic arthritis (P = .066).

On MR images, extraarticular extension of infection was identified in 23 (79%) of 29 patients with tuberculous arthritis and in 12 (92%) of 13 patients with pyogenic arthritis. Extraarticular soft-tissue abnormalities were depicted on T2-weighted images as areas with abnormally high signal intensity in adjacent muscles and connective tissues.

Two patterns of extraarticular infection extension were revealed on gadolinium-enhanced MR images (Fig 3). In the first, the extraarticular lesion had a relatively well-defined smooth margin, which was seen in 16 (70%) of 23 patients with tuberculous arthritis and in two (17%) of 12 patients with pyogenic arthritis. In the second, the extraarticular lesion had an irregular margin and showed an infiltrative spread pattern, which was seen in seven (30%) of 23 patients with tuberculous arthritis and in 10 (83%) of 12 patients with pyogenic arthritis. The extraarticular patterns of tuberculous arthritis and pyogenic arthritis showed a significant difference (P = .005) (Table).



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Figure 3a. Gadolinium-enhanced coronal T1-weighted MR images of the hip show the boundaries of extraarticular abnormalities. (a) Image (600/30) shows smooth boundaries in tuberculous arthritis (arrows). (b) Image (500/15) shows irregular borders (arrows) and extraarticular spread of pyogenic arthritis, with a feathery appearance, into adjacent muscles.

 


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Figure 3b. Gadolinium-enhanced coronal T1-weighted MR images of the hip show the boundaries of extraarticular abnormalities. (a) Image (600/30) shows smooth boundaries in tuberculous arthritis (arrows). (b) Image (500/15) shows irregular borders (arrows) and extraarticular spread of pyogenic arthritis, with a feathery appearance, into adjacent muscles.

 
Two kinds of soft-tissue abnormalities were observed after administration of a gadolinium-based contrast agent: (a) diffuse enhancement of an abnormal area, which was indicative of synovitis, myositis, and cellulitis, and (b) rim enhancement with central nonenhancement, which suggested an abscess. Abscesses were divided into two groups on the basis of their rim shapes (Fig 4). In group 1, the rim was thin and smooth internally and had a sharply defined outer margin. All 16 of 16 tuberculous abscesses were included in this group, while only two (29%) of seven pyogenic abscesses revealed this type of rim. The remaining five (71%) pyogenic abscesses were classified as group 2, which had thick and nodular rims and ill-defined external margins. There was a significant difference in the rim shapes of abscesses between the tuberculous arthritis and pyogenic arthritis groups (P = .001).



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Figure 4a. Gadolinium-enhanced transverse T1-weighted MR images show abscesses associated with hip joint infection. (a) Image (600/15) shows that tuberculous abscesses (arrows) in the right thigh have thin, smooth, enhancing rims. (b) Image (500/16) shows a pyogenic abscess (open arrows) adjacent to the right hip joint with a thick irregularly enhanced rim. Poorly defined, enhanced soft-tissue extension (solid arrows) is also seen extending from the coexistent left hip joint infection. A large area of enhancement (arrowheads) in the left buttock suggests cellulitis.

 


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Figure 4b. Gadolinium-enhanced transverse T1-weighted MR images show abscesses associated with hip joint infection. (a) Image (600/15) shows that tuberculous abscesses (arrows) in the right thigh have thin, smooth, enhancing rims. (b) Image (500/16) shows a pyogenic abscess (open arrows) adjacent to the right hip joint with a thick irregularly enhanced rim. Poorly defined, enhanced soft-tissue extension (solid arrows) is also seen extending from the coexistent left hip joint infection. A large area of enhancement (arrowheads) in the left buttock suggests cellulitis.

 

    DISCUSSION
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Initially, we expected that patients with tuberculous arthritis might have fewer bone erosions than those with pyogenic arthritis due to the lack of proteolytic enzyme; however, in patients with tuberculous arthritis, bone erosions were revealed more frequently than in those with pyogenic arthritis. In general, the progression of joint space loss is more prominent with pyogenic arthritis than it is with tuberculous arthritis because proteolytic enzyme production accelerates articular cartilage destruction.

Plasmin, a proteolytic enzyme, may contribute to articular cartilage destruction in pyogenic arthritis but not in tuberculous arthritis because M tuberculosis does not produce a plasminogen activator like the kinases of staphylococci and streptococci do (14). In tuberculous arthritis, the pannus of granulation tissue erodes and destroys cartilage and, eventually, bone (1). This process is not evenly distributed; rather, focal areas of cartilaginous destruction may be intermixed with areas of relatively normal-appearing chondral elements. Consequently, chondral and subchondral bone erosions may be apparent at a stage when the joint space is well preserved (15). We believe that this mode of bone erosion could explain the greater incidence of bone erosions in patients with tuberculous arthritis compared with that of patients with pyogenic arthritis, regardless of the rapidity of joint space loss.

In our study, patients with pyogenic arthritis had a significantly larger percentage of marrow signal intensity abnormalities than did patients with tuberculous arthritis. In the subchondral bone of an infected joint, diffuse bone marrow signal change intensity is a reflection of either osteomyelitis or bone marrow edema (3,16,17). In agreement with our observed incidence of marrow signal intensity abnormality in patients with pyogenic arthritis (12 [92%] of 13), Lee et al (18) reported high rates (eight [89%] of nine) of marrow signal intensity change in patients with a septic hip. Meanwhile, Huang et al (19) suggested that tuberculous spondylitis has a lesser extent of marrow edema than that observed in pyogenic spondylitis. We assumed that these marrow signal intensity changes might be associated with the virulence of the organism. Our results suggest that the presence of bone erosion and absence of marrow signal intensity abnormality favor a diagnosis of tuberculous arthritis rather than pyogenic arthritis.

In our study, most synovial abnormalities in tuberculous arthritis and pyogenic arthritis showed mixed high and intermediate signal intensity rather than pure signal intensity (Fig 2). In our experience, these abnormalities of mixed signal intensity consist of both hypertrophied synovial membrane and joint effusion, but we could not clearly differentiate between the synovial abnormalities and joint effusion in many cases. Gadolinium-enhanced images were used to distinguish between them; however, we could not accurately delineate the extent of synovial abnormalities on T2-weighted images. Suh et al (11) reported that tuberculous arthritis invariably shows intermediate signal intensity in synovial abnormalities on T2-weighted images. In their experimental study, these synovial abnormalities with intermediate signal intensity corresponded to hemorrhage, inflammatory debris, fibrosis, and caseous necrosis. In our study, the overall abnormalities (synovial abnormalities with joint effusion) of tuberculous arthritis were of a predominantly intermediate signal intensity; however, there were no significant differences in the signal characteristics between tuberculous arthritis and pyogenic arthritis. Thus, the signal intensity of synovial abnormalities has a limited value in the distinction between tuberculous arthritis and pyogenic arthritis.

We analyzed the features of extraarticular abnormalities on gadolinium-enhanced images because gadolinium-enhanced images delineate true infection boundaries (20). Contrast enhancement is particularly useful for distinguishing between abscesses and the surrounding myositis (21). In the absence of an abscess, the margins of the infiltrate are ill-defined (6). Extraarticular lesions in tuberculous arthritis usually consist of abscesses and tend to have smooth boundaries (Fig 3a). In contrast, a large number of lesions with pyogenic arthritis showed irregular boundaries of extraarticular extension with or without abscesses (Fig 3b).

On the other hand, a number of tuberculous arthritis lesions revealed irregularly shaped margins, and some pyogenic arthritis lesions had smooth margins. The margins of infectious lesions may be variable and depend not only on the virulence of the organism but also on the phase of the infection and the individual’s immune state. We believe that the average phase of tuberculous arthritis was later than that of pyogenic arthritis because tuberculous arthritis usually has a chronic, slowly progressive course (4). Thus, the patterns of extraarticular extension may be a supplementary rather than a reliable means of distinguishing between tuberculous arthritis and pyogenic arthritis.

Our results suggest that MR imaging of the abscess wall provides the most useful information in the differentiation of tuberculous arthritis and pyogenic arthritis. Several investigators (5,6,2123) have assessed the clinical utility of MR imaging in the diagnosis of soft-tissue abscess; however, to our knowledge, no investigation of abscess wall characterization has been undertaken.

The morphologic characteristics of an abscess alter with time, and the abscess may expand as a result of the progressive necrosis of surrounding cells. In time, it may become walled off by connective tissue that serves as a barrier, which limits further spread (24). In an experimental study by Kang et al (25), MR imaging showed poorly defined abscess walls with active inflammation until 1 week after the inoculation of Escherichia coli into rabbit thigh; thereafter, the abscess wall smoothed gradually as inflammatory reactions subsided and fibrosis progressed. In our study, MR imaging showed well-defined tuberculous abscesses, which usually had thin and smooth walls. In contrast, pyogenic abscesses had thick and irregular walls. We believe that both the minimal inflammation of tuberculous abscess and chronic insidious course of tuberculous arthritis are related to those smooth walls.

When infection was confined to a joint without extraarticular spread, MR imaging provided limited information to distinguish tuberculous arthritis from pyogenic arthritis. Furthermore, in cases of arthritis involving the relatively small joints, such as the wrist or ankle, tuberculous arthritis was hardly distinguishable from pyogenic arthritis. Because of the relatively small joint cavity and narrow potential extraarticular spaces, both tuberculous arthritis and pyogenic arthritis showed irregular patterns of extraarticular spread. Abscess formations around these small joints were not common.

There are some limitations to our study. First, a bias may derive from the heterogeneity of MR imaging performed with variable MR units. Second, MR imaging findings, such as extraarticular spread of infection, were not pathologically confirmed in all patients. Third, the MR imaging findings of infectious arthritis depend on several factors, such as the kind of joint involved, resistance to pathogenetic organisms, time to diagnosis, and type of organism involved. Fourth, the phase of infection, in particular, influences disease extent and the histopathologic features of the arthritis (26), but it was difficult to ascertain the exact disease onset in all patients. Fifth, some kinds of treatment prior to MR examination may cause another bias, but the history of treatment was vague in a large number of patients.

In conclusion, MR images in the case of infectious arthritis are nonspecific, but we were able to identify some features that supported discrimination between tuberculous arthritis and pyogenic arthritis. The signal intensity characteristics of synovial abnormalities, however, were not useful in this context. The presence of bone erosion and absence of subchondral marrow signal intensity abnormality favor a diagnosis of tuberculous arthritis rather than of pyogenic arthritis. When an extraarticular lesion of infection shows smooth margins, tuberculous arthritis is more likely than pyogenic arthritis to be the diagnosis. In contrast, thick and irregularly enhanced abscess rims were highly indicative of pyogenic arthritis.


    FOOTNOTES
 
4*. indicates unspecified joint involvement Back

Author contributions: Guarantors of integrity of entire study, S.H.H., H.S.K.; study concepts and design, S.H.H., H.S.K.; definition of intellectual content, S.H.H., S.M.K., J.M.A., H.S.K.; literature research, S.H.H.; clinical studies, S.H.H.; data acquisition, S.H.H., S.M.K., J.M.A.; data analysis, S.H.H., H.S.K.; statistical analysis, S.H.H.; manuscript preparation, S.H.H., H.W.C., M.J.S.; manuscript editing, S.H.H., H.S.K.; manuscript review, all authors; manuscript final version approval, H.S.K.


    REFERENCES
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. Yao DC, Sartoris DJ. Musculoskeletal tuberculosis. Radiol Clin North Am 1995; 33:679-689.[Medline]
  2. Araki Y, Tsukaguchi I, Shino K, Nakamura H. Tuberculous arthritis of the knee: MR findings (letter). AJR Am J Roentgenol 1993; 160:664.
  3. Forrester DM, Feske WI. Imaging of infectious arthritis. Semin Roentgenol 1996; 31:239-249.[Medline]
  4. Smith JW, Piercy EA. Infectious arthritis. Clin Infect Dis 1995; 20:225-230.[Medline]
  5. Munk PL, Vellet AD, Hilborn MD, Crues JV, III, Helms CA, Poon PY. Musculoskeletal infection: findings on magnetic resonance imaging. Can Assoc Radiol J 1994; 45:355-362.[Medline]
  6. Tang JSH, Gold RH, Bassett LW, Seeger LL. Musculoskeletal infection of the extremities: evaluation with MR imaging. Radiology 1988; 166:205-209.[Abstract/Free Full Text]
  7. Beltran J, Noto AM, McGhee RB, Freedy RM, McCalla MS. Infections of the musculoskeletal system: high-field-strength MR imaging. Radiology 1987; 164:449-454.[Abstract/Free Full Text]
  8. Gylys-Morin VM. MR imaging of pediatric musculoskeletal inflammatory and infectious disorders. Magn Reson Imaging Clin N Am 1998; 6:537-559.[Medline]
  9. Towers JD. The use of intravenous contrast in MRI of extremity infection. Semin Ultrasound CT MR 1997; 18:269-275.[Medline]
  10. Fleckenstein JL, Burns DK, Murphy FK, Jayson HT, Bonte FJ. Differential diagnosis of bacterial myositis in AIDS: evaluation with MR imaging. Radiology 1991; 179:653-658.[Abstract/Free Full Text]
  11. Suh JS, Lee JD, Cho JH, Kim MJ, Han DY, Cho NH. MR imaging of tuberculous arthritis: clinical and experimental studies. J Magn Reson Imaging 1996; 1:185-189.
  12. Davidson PT, Horowitz I. Skeletal tuberculosis: a review with patient presentations and discussion. Am J Med 1970; 48:77-84.[Medline]
  13. Kang HS, Yeon KM. Differentiation between tuberculous and pyogenic spondylitis: MR imaging characteristics of paraspinal mass. J Korean Radiol Soc 1996; 34:825-830.
  14. Akeson WH, Amiel D, Gershuni DH. Articular cartilage physiology and metabolism. In: Resnick D, eds. Diagnosis of bone and joint disorders. 3rd ed. Philadelphia, Pa: Saunders, 1995; 785-787.
  15. Resnick D, Niwayama G. Osteomyelitis, septic arthritis, and soft tissue infection: organisms. In: Resnick D, eds. Diagnosis of bone and joint disorders. 3rd ed. Philadelphia, Pa: Saunders, 1995; 2461-2485.
  16. Deely DM, Schweitzer ME. MR imaging of bone marrow disorders. Radiol Clin North Am 1997; 35:193-212.[Medline]
  17. Brower AC. Septic arthritis. Radiol Clin North Am 1996; 34:293-309.[Medline]
  18. Lee SK, Suh KJ, Kim YW, et al. Septic arthritis versus transient synovitis at MR imaging: preliminary assessment with signal intensity alterations in bone marrow. Radiology 1999; 211:459-465.[Abstract/Free Full Text]
  19. Huang YC, Shih TT, Huang KM, Su CT. Infectious spondylitis: MRI characteristics. J Formos Med Assoc 1996; 95:458-463.[Medline]
  20. Dangman BC, Hoffer FA, Rand FF, O’Rourke EJ. Osteomyelitis in children: gadolinium-enhanced MR imaging. Radiology 1992; 182:743-747.[Abstract/Free Full Text]
  21. Hopkins KL, Li KC, Bergman G. Gadolinium-DTPA-enhanced magnetic resonance imaging of musculoskeletal infectious processes. Skeletal Radiol 1995; 24:325-330.[Medline]
  22. Wall SD, Fisher MR, Amparo EG, Hricak H, Higgins CB. Magnetic resonance imaging in the evaluation of abscesses. AJR Am J Roentgenol 1985; 144:1217-1221.[Abstract/Free Full Text]
  23. Gordon BA, Martinez S, Collins AJ. Pyomyositis: characteristics at CT and MR imaging. Radiology 1995; 197:279-286.[Abstract/Free Full Text]
  24. Cotran RS, Kumar V, Robbins SL. Morphologic patterns in acute and chronic inflammation. In: Cotran RS, Kumar V, Robbins SL, eds. Robbins pathologic basis of disease. 4th ed. Philadelphia, Pa: Saunders, 1989; 68-69.
  25. Kang HS, Chung YK, Jang JJ. Experimental abscess in the thigh of rabbit: magnetic resonance imaging and pathologic correlation. J Korean Radiol Soc 1996; 35:595-604.
  26. Bremell T, Abdelnour A, Tarkowski A. Histopathological and serological progression of experimental Staphylococcus aureus arthritis. Infect Immun 1992; 60:2976-2985.[Abstract/Free Full Text]



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