1.Does Percutaneous Lumbosacral Pedicle Screw Instrumentation Prevent Long-Term Adjacent Segment Disease after Lumbar Fusion?
Stuart CHANGOOR ; Michael Joseph FALOON ; Conor John DUNN ; Nikhil SAHAI ; Kimona ISSA ; Kumar SINHA ; Ki Soo HWANG ; Arash EMAMI
Asian Spine Journal 2021;15(3):301-307
Retrospective cohort study. To assess long-term clinical outcomes of adjacent segment disease (ASD) in patients who underwent lumbar interbody fusion with percutaneous pedicle screw (PS) instrumentation. ASD is a well-known sequela of spinal fusion, and is reported to occur at a rate of 2%–3% per year. There is debate as to whether ASD is a result of the instrumentation and fusion method or is the natural history of the patient’s disease. Minimally invasive percutaneous PS augmentation of lumbar interbody fusion aims to prevent the disruption of posterior soft tissue stabilizers. From 2004–2014, 419 consecutive patients underwent anterior, lateral, or minimally invasive transforaminal lumbar interbody fusion with percutaneous PS placement at a single institution. The mean follow-up was 4.5 years. The primary outcome measure was reoperation due to ASD. Patients were divided into two cohorts: those who underwent revision surgery secondary to ASD and those who did not require further surgery. Radiographic parameters were performed using postoperative radiographs. Patients with a pelvic incidence–lumbar lordosis (PI–LL) mismatch >10° were noted. Revision proportion secondary to ASD was 4.77% (n=20). Mean time to revision surgery was 2.5 years. Revision rate secondary to ASD was 1.1% per year. Patients who developed ASD were younger than those who did not (50.5 vs. 56.9 years, ASD rates in patients who underwent percutaneous PS placement were lower than those previously published after open PS placement, possibly related to greater preservation of the posterior stabilizing elements of the lumbar spine.
2.Does Percutaneous Lumbosacral Pedicle Screw Instrumentation Prevent Long-Term Adjacent Segment Disease after Lumbar Fusion?
Stuart CHANGOOR ; Michael Joseph FALOON ; Conor John DUNN ; Nikhil SAHAI ; Kimona ISSA ; Kumar SINHA ; Ki Soo HWANG ; Arash EMAMI
Asian Spine Journal 2021;15(3):301-307
Retrospective cohort study. To assess long-term clinical outcomes of adjacent segment disease (ASD) in patients who underwent lumbar interbody fusion with percutaneous pedicle screw (PS) instrumentation. ASD is a well-known sequela of spinal fusion, and is reported to occur at a rate of 2%–3% per year. There is debate as to whether ASD is a result of the instrumentation and fusion method or is the natural history of the patient’s disease. Minimally invasive percutaneous PS augmentation of lumbar interbody fusion aims to prevent the disruption of posterior soft tissue stabilizers. From 2004–2014, 419 consecutive patients underwent anterior, lateral, or minimally invasive transforaminal lumbar interbody fusion with percutaneous PS placement at a single institution. The mean follow-up was 4.5 years. The primary outcome measure was reoperation due to ASD. Patients were divided into two cohorts: those who underwent revision surgery secondary to ASD and those who did not require further surgery. Radiographic parameters were performed using postoperative radiographs. Patients with a pelvic incidence–lumbar lordosis (PI–LL) mismatch >10° were noted. Revision proportion secondary to ASD was 4.77% (n=20). Mean time to revision surgery was 2.5 years. Revision rate secondary to ASD was 1.1% per year. Patients who developed ASD were younger than those who did not (50.5 vs. 56.9 years, ASD rates in patients who underwent percutaneous PS placement were lower than those previously published after open PS placement, possibly related to greater preservation of the posterior stabilizing elements of the lumbar spine.
3.Rescue Endoscopic Ultrasound (EUS)-Guided Trucut Biopsy Following Suboptimal EUS-Guided Fine Needle Aspiration for Mediastinal Lesions.
Chang Min CHO ; Mohammad AL-HADDAD ; Julia K LEBLANC ; Stuart SHERMAN ; Lee MCHENRY ; John DEWITT
Gut and Liver 2013;7(2):150-156
BACKGROUND/AIMS: Endoscopic ultrasound-guided fine needle aspiration (EUS-FNA) and Trucut biopsy (TCB) are sensitive techniques for diagnosing mediastinal lesions, but it is unclear how either one or both should be used to obtain a pathologic diagnosis. The objective of our study was to evaluate whether EUS-TCB impacts the diagnosis of mediastinal lesions after the initial on-site review of EUS-FNA specimen suggests a suboptimal result. METHODS: We enrolled consecutive patients with mediastinal lesions who underwent EUS-TCB during the same procedure if the initial EUS-FNA demonstrated an inadequate FNA sample or suggested that histopathology was required for diagnosis. Diagnostic accuracies between procedures were compared as the main outcome. RESULTS: Twenty-seven patients (14 men; median age, 56 years; range, 19 to 82 years) underwent EUS-FNA and EUS-TCB to evaluate a mediastinal lymphadenopathy or mass (n=17), to determine the cancer stage (n=3) or to exclude tumor recurrence or metastasis (n=7). The overall diagnostic accuracies of EUS-FNA and EUS-TCB were 78% and 67%, respectively (p=0.375). The combined diagnostic accuracy of EUS-FNA plus EUS-TCB was 82%. In six patients with nondiagnostic EUS-FNA, EUS-TCB provided a final diagnosis in one patient (17%). CONCLUSIONS: In the current series of patients with mediastinal masses or adenopathy, the administration of EUS-TCB following suboptimal results for the on-site cytology review did not increase the diagnostic yield.
Biopsy
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Biopsy, Fine-Needle
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Endoscopic Ultrasound-Guided Fine Needle Aspiration
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Humans
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Lymphatic Diseases
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Mediastinum
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Neoplasm Metastasis
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Recurrence
4.Collagen-Induced Arthritis and the Potential Role of Autoimmunity to Type II Collagen in Rheumatoid Arthritis.
Xiaowen HE ; John M STUART ; Linda K MYERS ; Andrew H KANG
The Journal of the Korean Rheumatism Association 2002;9(1):1-22
Collagen induced arthritis (CIA)is an animal model that in many ways resembles rheumatoid arthritis (RA). CIA can be induced in susceptible animals by immunization with type II collagen (CII). Like RA,CIA is characterized by intense joint inflammation and destruction.On histological examination,there is synovitis accompanied by erosion of cartilage and subchondral bone. Autoanti-bodies to CII initiate joint inflammation by binding to articular cartilage,forming antigen-antibody complexes locally and activating hemolytic complement. Susceptibility to CIA in mice is linked to the expression of specific class II MHC Molecules,which dictate the T cell determinants on CII,and therefore,the subsets of T cells that can be activated by CII.In addition to activation of B cells reactive to CII,the T cells stimulate monocytes/macrophages.These cells amplify the inflammatory cascade by secretion of proinflammatory monokines, including TNF-alpha and IL-1,leading to the production of other proinflammatory proteins,including matrix metalloproteinases (MMPs).The importance of CIA lies in its possible relationship to arthritis in humans.Progress in understanding CIA has contributed to the development of new therapies for RA.In addition,it has been found that mice with human HLA-DR1,DR4 and HLA-DQ8 transgenes,which have been demonstrated to be the susceptibility markers for RA, confer susceptibility to CIA.These observations coupled with the finding of T cells and B cells reactive with CII in the inflamed joints of RA patients establish the potential role of CII autoimmunity in the pathogenesis of RA.
Animals
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Antigen-Antibody Complex
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Arthritis
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Arthritis, Experimental*
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Arthritis, Rheumatoid*
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Autoimmunity*
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B-Lymphocytes
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Cartilage
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Collagen
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Collagen Type II*
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Complement System Proteins
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Humans
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Immunization
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Inflammation
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Joints
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Matrix Metalloproteinases
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Mice
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Models, Animal
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Monokines
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Synovitis
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T-Lymphocytes
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Tumor Necrosis Factor-alpha
5.ARCO Consensus on the Pathogenesis of Non-traumatic Osteonecrosis of the Femoral Head
Quanjun CUI ; Woo-Lam JO ; Kyung-Hoi KOO ; Edward Y. CHENG ; Wolf DRESCHER ; Stuart B. GOODMAN ; Yong-Chan HA ; Phillippe HERNIGOU ; Lynne C. JONES ; Shin-Yoon KIM ; Kyu Sang LEE ; Mel S. LEE ; Yun Jong LEE ; Michael A. MONT ; Nobuhiko SUGANO ; John TALIAFERRO ; Takuaki YAMAMOTO ; Dewei ZHAO
Journal of Korean Medical Science 2021;36(10):e65-
Osteonecrosis of the femoral head (ONFH) is a devastating disease frequently leading to femoral head collapse and hip arthritis. Specifically, non-traumatic ONFH primarily affects young and middle-aged adults. Although compromised local circulation of the femoral head seems to be pathognomonic for the disease, the pathogenesis is perplexing and continues to be an area of scrutiny and research. Comprehension of the pathogenesis is of crucial importance for developing and guiding treatments for the disease. Therefore, we provide an up-to-date consensus on the pathogenesis of non-traumatic ONFH.
6.ARCO Consensus on the Pathogenesis of Non-traumatic Osteonecrosis of the Femoral Head
Quanjun CUI ; Woo-Lam JO ; Kyung-Hoi KOO ; Edward Y. CHENG ; Wolf DRESCHER ; Stuart B. GOODMAN ; Yong-Chan HA ; Phillippe HERNIGOU ; Lynne C. JONES ; Shin-Yoon KIM ; Kyu Sang LEE ; Mel S. LEE ; Yun Jong LEE ; Michael A. MONT ; Nobuhiko SUGANO ; John TALIAFERRO ; Takuaki YAMAMOTO ; Dewei ZHAO
Journal of Korean Medical Science 2021;36(10):e65-
Osteonecrosis of the femoral head (ONFH) is a devastating disease frequently leading to femoral head collapse and hip arthritis. Specifically, non-traumatic ONFH primarily affects young and middle-aged adults. Although compromised local circulation of the femoral head seems to be pathognomonic for the disease, the pathogenesis is perplexing and continues to be an area of scrutiny and research. Comprehension of the pathogenesis is of crucial importance for developing and guiding treatments for the disease. Therefore, we provide an up-to-date consensus on the pathogenesis of non-traumatic ONFH.
7.Variation of sexual dimorphism and asymmetry in disease expression of inflammatory arthritis among laboratory mouse models with different genomic backgrounds
Wei DONG ; Cheng TIAN ; Z. Galvin LI ; David BRAND ; Yanhong CAO ; Xiaoyun LIU ; Jiamin MA ; Andy CHAI ; Linda K. MYERS ; Jian YAN ; Karen HASTY ; John STUART ; Yan JIAO ; Weikuan GU ; Xiaojun CAI
Laboratory Animal Research 2023;39(4):402-410
Sex difference has shown in the arthritis diseases in human population and animal models. We investigate how the sex and symmetry vary among mouse models with different genomic backgrounds. Disease data of sex and limbs accumulated in the past more than two decades from four unique populations of murine arthritis models were analyzed. They are (1) interleukin-1 receptor antagonist (IL-1ra) deficient mice under Balb/c background (Balb/c KO); (2) Mice with collagen II induced arthritis under DBA/1 background; (3) Mice with collagen II induced arthritis under C57BL/6 (B6) background and (4) A F2 generation population created by Balb/c KO X DBA/1 KO.Our data shows that there is a great variation in sexual dimorphism for arthritis incidence and severity of arthritis in mice harboring specific genetic modifications. For a F2 population, the incidence of arthritis was 57.1% in female mice and 75.6% in male mice. There was a difference in severity related to sex in two populations: B6.DR1/ B6.DR4 (P < 0.001) and F2 (P = 0.023) There was no difference Balb/c parental strain or in collagen-induced arthritis (CIA) in DBA/1 mice. Among these populations, the right hindlimbs are significantly higher than the scores for the left hindlimbs in males (P < 0.05). However, when examining disease expression using the collagen induced arthritis model with DBA/1 mice, sex-dimorphism did not reach statistical significance, while left hindlimbs showed a tendency toward greater disease expression over the right. Sexual dimorphism in disease expression in mouse models is strain and genomic background dependent. It sets an alarm that potential variation in sexual dimorphism among different racial and ethnic groups in human populations may exist. It is important to not only include both sexes and but also pay attention to possible variations caused by disease expression and response to treatment in all the studies of arthritis in animal models and human populations.