Changes in biochemical parameters after anterior cruciate ligament injury

Handa, Hiroshi; Shirakura, Kenji; Kimura, Masashi; Terauchi, Masanori; Shinozaki, Tetsuya; Watanabe, Hiroki; Takagishi, Kenji

doi:10.1007/s00264-005-0023-5

Cited by 106 publications

(155 citation statements)

References 20 publications

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“…The mean concentration of IL-18 we measured in synovial fluid was 1.4 times higher than previously reported for OA synovial fluid, 3.5 times higher than previously reported for normal synovial fluid, but still 2 to 3 times lower than typically seen in rheumatoid arthritis (RA) (18,19). IL-1β is not typically detected in normal synovial fluid (20,21) and is very low (3.91 ± 4.66 pg/mL) or undetectable (22) in OA synovial fluid. Our measured concentrations of synovial fluid IL-1β were similarly low or undetectable despite the use of a high sensitivity assay.…”

Section: Discussioncontrasting

confidence: 43%

Uric acid is a danger signal of increasing risk for osteoarthritis through inflammasome activation

Denoble¹,

Huffman²,

Stäbler³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

232

178

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Uric acid (UA) is known to activate the NLRP3 (Nacht, leucine-rich repeat and pyrin domain containing protein 3) inflammasome. When activated, the NLRP3 (also known as NALP3) inflammasome leads to the production of IL-18 and IL-1β. In this cohort of subjects with knee osteoarthritis (OA), synovial fluid uric acid was strongly correlated with synovial fluid IL-18 and IL-1β. Synovial fluid uric acid and IL-18 were strongly and positively associated with OA severity as measured by both radiograph and bone scintigraphy, and synovial fluid IL-1β was associated with OA severity but only by radiograph. Furthermore, synovial fluid IL-18 was associated with a 3-y change in OA severity, on the basis of the radiograph. We conclude that synovial fluid uric acid is a marker of knee OA severity. The correlation of synovial fluid uric acid with the two cytokines (IL-18 and IL-1β) known to be produced by uric acidactivated inflammasomes and the association of synovial fluid IL-18 with OA progression, lend strong support to the potential involvement of the innate immune system in OA pathology and OA progression.arthritis | inflammation | interleukin-18 | interleukin-1β | tumor necrosis factor alpha U ric acid (UA) is constitutively present in normal cells, increased in concentration when cells are injured, and released from dying cells (1). On the basis of a theory proposed by Matzinger, the products of cell stress and tissue damage may represent "danger signals" that function as endogenous adjuvants recognized by the immune system (2). Matzinger proposed that immunity is controlled by an internal conversation between tissues and the cells of the immune system (3). This proposal introduced a new immunological model of an immune system capable of sensing cellular stress and tissue damage (4). Shi subsequently identified uric acid as one of these principal endogenous danger signals released from injured cells and mediating the immune response to antigens associated with injured cells (1). The molecular mechanism of this innate immune response to uric acid was further shown to be the result of the activation of the NALP3 inflammasome, a cytosolic, multiprotein complex that mediates caspase activation by uric acid crystals, leading to the production of the active forms of IL-1β and IL-18 (5). Recently, Kono et al. demonstrated in an in vivo hepatoxicity mouse model that uric acid is a physiological regulator of the inflammation induced by tissue injury (6). These data form the basis for our hypothesis that synovial fluid uric acid is a factor regulating tissue inflammation, disease severity, and progression in osteoarthritis (OA).Uric acid is best known for its role in gout. When uric acid concentrations exceed the limit of solubility (∼6.8 mg/dL or even lower under conditions of low pH or temperature), crystal formation can ensue, which is capable of activating the NALP3 inflammasome (5) and triggering the acute severe attacks of joint inflammation characteristic of gout (7). Several studies have previously posited an association o...

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Section: Discussioncontrasting

confidence: 43%

Uric acid is a danger signal of increasing risk for osteoarthritis through inflammasome activation

Denoble¹,

Huffman²,

Stäbler³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

232

178

View full text Add to dashboard Cite

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“…One possible explanation is the exposure of this region to the joint cavity with synovial fluid access to the implant. In response to intra-articular injury, increased synovial fluid production of matrix metalloproteinases and inflammatory cytokines such as interleukin-6 and tumor necrosis factor-alpha can create an adverse biological healing environment [45][46][47] . Mechanical factors may also reduce osseointegration in the epiphyseal region.…”

Section: Peri-implantation Ipth Increased Osteoblast and Osteoclastmentioning

confidence: 99%

Intermittent Parathyroid Hormone Enhances Cancellous Osseointegration of a Novel Murine Tibial Implant

Yang

Ricciardi

Dvorzhinskiy

et al. 2015

The Journal of Bone and Joint Surgery

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“…Although no specific genes have been identified, a genetic component may play a part in ACL ruptures. Moreover, IL-6, matrix metalloproteinases (MMP)-1 and MMP-3 in synovial fluid have been evaluated after ligament injury (Higuchi et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Association between matrix metalloproteinase-3 polymorphism and anterior cruciate ligament ruptures

Malila¹,

Yuktanandana²,

Saowaprut³

et al. 2011

Genet. Mol. Res.

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ABSTRACT. Anterior cruciate ligament (ACL) ruptures are considered to be the most severe joint injury in sports. However, the precise etiologies of ACL injuries are not fully understood. Recently, the gene encoding the matrix metalloproteinase-3 (MMP-3, stromelysin-1) was shown to be associated with anterior cruciate ligament ruptures. The 5A/6A polymorphism in the promoter of the MMP-3 gene affects the regulation of MMP-3 gene expression. We examined the association between polymorphism within -1612 of the MMP-3 gene and ACL rupture in an independent population. Eighty-six participants between 20 and 40 years of age with surgically diagnosed ACL ruptures and 100 healthy controls between 18 and 28 years of age without history of ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 10 (4): 4158-4165 (2011) MMP-3 SNP in ACL ruptures 4159 ligament or tendon injuries were recruited for the study. All participants were genotyped for the MMP-3 polymorphism (-1612 5A/6A). Statistical analyses of genotype frequencies between patients and healthy controls were performed by the chi-square test. A significant difference was found between ACL rupture subgroups in terms of genotype association (5A+ (5A/5A, 5A/6A): 37.5% in contact sports vs 20% in non-contact sports; P = 0.02). In allelic association, there were significant differences (6A: 81.2% in contact sports vs 89.1% in non-contact sports, 5A: 18.8% in contact sports vs 10.9% in non-contact sports, P = 0.01). The 5A+ genotype of MMP-3 was represented in ACL ruptures in contact sport participants. We propose that this sequence variant is a specific genetic element that should be included in a multifactorial model to understand the etiologies and risk factors for ACL rupture.

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Changes in biochemical parameters after anterior cruciate ligament injury

Cited by 106 publications

References 20 publications

Uric acid is a danger signal of increasing risk for osteoarthritis through inflammasome activation

Uric acid is a danger signal of increasing risk for osteoarthritis through inflammasome activation

Intermittent Parathyroid Hormone Enhances Cancellous Osseointegration of a Novel Murine Tibial Implant

Association between matrix metalloproteinase-3 polymorphism and anterior cruciate ligament ruptures

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