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Synovial Proliferation (synovial + proliferation)

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Medical Sciences71%

Selected Abstracts

Sonography of the shoulder after arthrography (arthrosonography): Preliminary results

JOURNAL OF CLINICAL ULTRASOUND, Issue 1 2002
Hak Soo Lee MD
Abstract Purpose The purpose of this study was to verify whether arthrosonography improves diagnostic accuracy in diseases of the shoulder and provides additional information for therapeutic planning, compared with conventional sonography. Methods We prospectively studied 113 consecutive patients with chronic shoulder pain. Sonography was performed before and after arthrography, with the radiologist blinded to the results of arthrography. When a rotator cuff tear was detected sonographically, its type, location, and size were recorded; we also evaluated any changes in the subacromial-subdeltoid bursa and any abnormalities in the biceps tendon sheath. The diagnostic accuracy of conventional sonography and arthrosonography was compared with that of arthrography for rotator cuff tear. Changes in the subacromial-subdeltoid bursa and biceps tendon sheath seen on conventional sonography were also compared with those seen on arthrosonography. Results The sensitivity and specificity of conventional sonography in the diagnosis of rotator cuff tear were 86% (25/29) and 95% (80/84), respectively; for arthrosonography, the values were 97% (28/29) and 95% (80/84), respectively. The differences in sensitivity and specificity for the 2 sonographic techniques were not statistically significant (p > 0.05). The accuracy in localizing the tear was also not significantly different between the 2 sonographic techniques. Synovial proliferation was more easily detected with arthrosonography than it was with conventional sonography in the subacromial-subdeltoid bursa (p < 0.01) and in the biceps tendon sheath (p < 0.0001). Conclusions Our preliminary results suggest that although arthrosonography was not superior to conventional sonography in the diagnosis of rotator cuff tears, it may provide a better assessment of the size of tears and additional information about synovial proliferation in the subacromial-subdeltoid bursa and the biceps tendon sheath. © 2002 John Wiley & Sons, Inc. J Clin Ultrasound 30:23,32, 2002. [source]

Vascular endothelial growth factor 121 and 165 in the subacromial bursa are involved in shoulder joint contracture in type II diabetics with rotator cuff disease

JOURNAL OF ORTHOPAEDIC RESEARCH, Issue 6 2003
Akiyoshi Handa
Vascular endothelial growth factor (VEGF) is a glycoprotein that plays an important role in neovascularization and increases vascular permeability. We reported that VEGF is involved in motion pain of patients with rotator cuff disease by causing synovial proliferation in the subacromial bursa (SAB). The present study investigates whether VEGF is also involved in the development of shoulder contracture in diabetics with rotator cuff disease. We examined 67 patients with rotator cuff disease, including 36 with complete cuff tears, 20 with incomplete tears, and 11 without apparent tears (subacromial bursitis). The patients were into groups according to the presence or absence of diabetes (14 type II diabetics and 53 non-diabetics). Specimens of the synovium of the SAB were obtained from all patients during surgery. Expression of the VEGF gene in the synovium of the subacromial bursa was evaluated by using the reverse transcriptase polymerase chain reaction. The VEGF protein was localized by immunohistochemistry, and the number of vessels was evaluated based on CD34 immunoreactivity. The results showed that VEGF mRNA was expressed in significantly more diabetics (100%, 14/14) than in non-diabetics (70%, 37/53) (P = 0.0159, Fisher's test). Investigation of VEGF isoform expression revealed VEGF121 in all 14 diabetics and in 37 of the 53 non-diabetics, VEGF 165 in 12 of the 14 diabetics and in 21 of the 53 non-diabetics, and VEGF 189 in 1 of the 14 diabetics and in 2 of the 53 non-diabetics. No VEGF206 was expressed in either group. VEGF protein was localized in both vascular endothelial cells and synovial lining cells. The mean number of VEGF-positive vessels and the vessel area were also significantly greater in the diabetics (p < 0.015, Mann-Whitney U test). Synovial proliferation and shoulder joint contracture were more common in the diabetics (P = 0.0329 and P = 0.073, respectively; Fisher's test). The mean preoperative range of shoulder motion significantly differed in terms of elevation between two groups: 103.8° in diabetics and 124.9° in no diabetics (p = 0.0039 Mann,Whitney U test). In contrast, external rotation did not significantly differ: 44° in diabetics and 49° in non-diabetics (p ° 0.4957, Mann,Whitney U test). These results suggest that VEGF121 and VEGF165 expression in the SAB is responsible for the development of shoulder joint contracture, especially in elevation, among type II diabetic patients with rotator cuff disease. © 2003 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved. [source]

Rapidly destructive arthropathy of the hip in haemophilia

HAEMOPHILIA, Issue 1 2001
N. Ishiguro
The aetiology of rapidly destructive arthropathy is still being debated. We report a 48-year-old male haemophiliac who exhibited hip arthropathy that was similar to rapidly destructive arthropathy. The hip joint was destroyed 6 months after the onset of symptoms. Results of clinical and laboratory examinations did not show any features of neuropathic, inflammatory or septic arthropathy, except for coagulopathy. Magnetic resonance imaging revealed an expansive joint capsule with synovial proliferation in the affected hip joint. Total hip arthroplasty was carried out successfully with total resection of the synovial tissue and joint capsule. A histological examination revealed bone necrosis, nonspecific inflammation, haemosiderosis and synovial hypertrophy. The recurrent bleeding into the hip joint induced pronounced inflammation with synovial proliferation and acute destruction of bony tissue. [source]

Sonography of the shoulder after arthrography (arthrosonography): Preliminary results

JOURNAL OF CLINICAL ULTRASOUND, Issue 1 2002
Hak Soo Lee MD
Abstract Purpose The purpose of this study was to verify whether arthrosonography improves diagnostic accuracy in diseases of the shoulder and provides additional information for therapeutic planning, compared with conventional sonography. Methods We prospectively studied 113 consecutive patients with chronic shoulder pain. Sonography was performed before and after arthrography, with the radiologist blinded to the results of arthrography. When a rotator cuff tear was detected sonographically, its type, location, and size were recorded; we also evaluated any changes in the subacromial-subdeltoid bursa and any abnormalities in the biceps tendon sheath. The diagnostic accuracy of conventional sonography and arthrosonography was compared with that of arthrography for rotator cuff tear. Changes in the subacromial-subdeltoid bursa and biceps tendon sheath seen on conventional sonography were also compared with those seen on arthrosonography. Results The sensitivity and specificity of conventional sonography in the diagnosis of rotator cuff tear were 86% (25/29) and 95% (80/84), respectively; for arthrosonography, the values were 97% (28/29) and 95% (80/84), respectively. The differences in sensitivity and specificity for the 2 sonographic techniques were not statistically significant (p > 0.05). The accuracy in localizing the tear was also not significantly different between the 2 sonographic techniques. Synovial proliferation was more easily detected with arthrosonography than it was with conventional sonography in the subacromial-subdeltoid bursa (p < 0.01) and in the biceps tendon sheath (p < 0.0001). Conclusions Our preliminary results suggest that although arthrosonography was not superior to conventional sonography in the diagnosis of rotator cuff tears, it may provide a better assessment of the size of tears and additional information about synovial proliferation in the subacromial-subdeltoid bursa and the biceps tendon sheath. © 2002 John Wiley & Sons, Inc. J Clin Ultrasound 30:23,32, 2002. [source]

Vascular endothelial growth factor 121 and 165 in the subacromial bursa are involved in shoulder joint contracture in type II diabetics with rotator cuff disease

JOURNAL OF ORTHOPAEDIC RESEARCH, Issue 6 2003
Akiyoshi Handa
Vascular endothelial growth factor (VEGF) is a glycoprotein that plays an important role in neovascularization and increases vascular permeability. We reported that VEGF is involved in motion pain of patients with rotator cuff disease by causing synovial proliferation in the subacromial bursa (SAB). The present study investigates whether VEGF is also involved in the development of shoulder contracture in diabetics with rotator cuff disease. We examined 67 patients with rotator cuff disease, including 36 with complete cuff tears, 20 with incomplete tears, and 11 without apparent tears (subacromial bursitis). The patients were into groups according to the presence or absence of diabetes (14 type II diabetics and 53 non-diabetics). Specimens of the synovium of the SAB were obtained from all patients during surgery. Expression of the VEGF gene in the synovium of the subacromial bursa was evaluated by using the reverse transcriptase polymerase chain reaction. The VEGF protein was localized by immunohistochemistry, and the number of vessels was evaluated based on CD34 immunoreactivity. The results showed that VEGF mRNA was expressed in significantly more diabetics (100%, 14/14) than in non-diabetics (70%, 37/53) (P = 0.0159, Fisher's test). Investigation of VEGF isoform expression revealed VEGF121 in all 14 diabetics and in 37 of the 53 non-diabetics, VEGF 165 in 12 of the 14 diabetics and in 21 of the 53 non-diabetics, and VEGF 189 in 1 of the 14 diabetics and in 2 of the 53 non-diabetics. No VEGF206 was expressed in either group. VEGF protein was localized in both vascular endothelial cells and synovial lining cells. The mean number of VEGF-positive vessels and the vessel area were also significantly greater in the diabetics (p < 0.015, Mann-Whitney U test). Synovial proliferation and shoulder joint contracture were more common in the diabetics (P = 0.0329 and P = 0.073, respectively; Fisher's test). The mean preoperative range of shoulder motion significantly differed in terms of elevation between two groups: 103.8° in diabetics and 124.9° in no diabetics (p = 0.0039 Mann,Whitney U test). In contrast, external rotation did not significantly differ: 44° in diabetics and 49° in non-diabetics (p ° 0.4957, Mann,Whitney U test). These results suggest that VEGF121 and VEGF165 expression in the SAB is responsible for the development of shoulder joint contracture, especially in elevation, among type II diabetic patients with rotator cuff disease. © 2003 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved. [source]

The Receptors and Role of Angiotensin II in Knee Joint Blood Flow Regulation and Role of Nitric Oxide in Modulation of Their Function

MICROCIRCULATION, Issue 5 2003
H. NAJAFIPOUR
ABSTRACT Objectives: Angiotensin-converting enzyme (ACE) upregulation in the stroma cells of arthritis rheumatoid joints may produce a higher tissue concentration of angiotensin II (angII), which is a vasoconstrictor and mitogen factor that causes local hypoxia and synovial proliferation. No study in the literature has examined the role of angII in joint blood flow (JBF) regulation and the potential effect of ACE inhibitors on JBF. Methods: The study was performed on 20 Dutch white rabbits to examine the JBF response to angII, angII receptor subtypes, and the role of nitric oxide (NO) in angII effects in knee joint blood vessels. Drugs were administered locally through retrograde saphenous artery cannulation. Joint vascular resistance (JVR) was calculated by dividing the arterial blood pressure by the JBF. Results: AngII increased JVR dose dependently. The angII type 1 (AT1) receptor antagonist losartan did not change the basal JVR but completely blocked the effect of angII on JVR. N, -nitro-L-arginin methyl ester (L-NAME) increased JVR by a mean (±SEM) of 25.8 ± 8.7% (p < 0.05) but did not affect the joint vessel response to angII and losartan. Conclusions: AngII receptors are from the AT1 subtype in normal joint blood vessels, but angII plays no significant role in JBF regulation. The basal release of NO plays a role in resting JBF regulation, but NO does not affect the AT1 receptor-mediated vasoconstriction of joint blood vessels. [source]

Sphingosine 1-phosphate/sphingosine 1-phosphate receptor 1 signaling in rheumatoid synovium: Regulation of synovial proliferation and inflammatory gene expression

ARTHRITIS & RHEUMATISM, Issue 3 2006
Masayasu Kitano
Objective Sphingosine 1-phosphate (S1P) is involved in various pathologic conditions and has been implicated as an important mediator of angiogenesis, inflammation, cancer, and autoimmunity. This study was undertaken to examine the role of S1P/S1P1 signaling in the pathogenesis of rheumatoid arthritis (RA). Methods We examined S1P1 messenger RNA (mRNA) and protein levels in RA synoviocytes and MH7A cells by reverse transcriptase,polymerase chain reaction and Western blotting. We also performed S1P1 immunohistochemistry analysis in synovial tissue from 28 RA patients and 18 osteoarthritis (OA) patients. We investigated the effects of S1P on proliferation by WST-1 assay, and its effects on tumor necrosis factor , (TNF,), or interleukin-1, (IL-1,),induced cyclooxygenase 2 (COX-2) expression and prostaglandin E2 (PGE2) production in RA synoviocytes and MH7A cells by Western blotting and enzyme-linked immunosorbent assay, respectively. Finally, we examined whether these effects of S1P were sensitive to pertussis toxin (PTX), an inhibitor of the Gi/Go proteins. Results S1P1 mRNA and protein were detected in RA synoviocytes and MH7A cells. S1P1 was more strongly expressed in synovial lining cells, vascular endothelial cells, and inflammatory mononuclear cells of RA synovium compared with OA synovium. S1P increased the proliferation of RA synoviocytes and MH7A cells. S1P alone significantly enhanced COX-2 expression and PGE2 production. Moreover, S1P enhanced expression of COX-2 and production of PGE2 induced by stimulation with TNF, or IL-1, in RA synoviocytes and MH7A cells. These effects of S1P were inhibited by pretreatment with PTX. Conclusion These findings suggest that S1P signaling via S1P receptors plays an important role in cell proliferation and inflammatory cytokine,induced COX-2 expression and PGE2 production by RA synoviocytes. Thus, regulation of S1P/S1P1 signaling may represent a novel therapeutic target in RA. [source]