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Joint Injury (joint + injury)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Mandibular kinematics associated with simulated low-velocity rear-end impacts

JOURNAL OF ORAL REHABILITATION, Issue 8 2006
I. A. HERNÁNDEZ
summary, Rear-end-impact motor vehicle accidents may result in cervical and temporomandibular-related pain complaints. Head kimematics in simulated low-impact rear-end impacts have been investigated but mandibular kinematics have not been described. Thirty healthy adult subjects underwent three impacts (4·5 m s,2 expected, 10·0 m s,2 unexpected, and 10·0 m s,2 expected). Onset time and peak magnitude of angular head acceleration, angular mandibular acceleration and angular mandibular displacement were measured. Significant mandibular opening acceleration was not identified with rearward head rotation. The peak magnitude of mandibular closing angular acceleration approximately doubled with increased impact magnitude. No differences in peak angular mandibular acceleration regarding expectation were identified. Gender differences were detected in the fast unexpected impact. The peak time for the angular mandibular acceleration (mandibular closure) was approximately 84,120 ms later than peak rearward angular head acceleration for all impacts. Onset and peak times for angular mandibular acceleration (mandibular closure) were similar to the onset and peak times for forward head acceleration. There was also a positive correlation between the magnitude of the forward angular acceleration of the head and angular acceleration of the mandible for the slow (0·65, P = 0·015) and fast expected (0·844, P = 0·001) impacts. The average angular mandibular angular displacement (mandibular closure) was approximately 6°. The hyperextension hypothesis regarding mechanism of temporomandibular joint injury in low-impact rear-end collisions cannot be supported. [source]

Joint degeneration following closed intraarticular fracture in the mouse knee: A model of posttraumatic arthritis

JOURNAL OF ORTHOPAEDIC RESEARCH, Issue 5 2007
Bridgette D. Furman
Abstract Posttraumatic arthritis is one of the most frequent causes of disability following joint trauma. The objective of this study was to develop a model of a closed articular fracture in the mouse knee joint to quantify the temporal sequence of joint degeneration in a model of posttraumatic arthritis. Closed intraarticular fractures were created in the tibial plateau of adult mice (C57BL/6) using a computer-controlled materials testing system and a custom-built indenter tip. Tibial plateau fractures were classified and imaged over time using high-resolution digital radiography. Animals were sacrificed at 2, 4, 8, and 50 weeks following fracture, and the experimental and contralateral control limbs were harvested for histology and micro-computed tomography (microCT) analysis. By radiographic analysis, tibial plateau fractures closely resembled clinical fractures. More complex and comminuted fractures correlated to significantly higher fracture energies. Histologic analysis demonstrated progressive joint degeneration as measured by a modified Mankin scale, with fibrillation and loss of proteoglycan in the articular cartilage. Subchondral bone thickening was also observed in experimental joints. The induction of a closed intraarticular fracture of the mouse tibial plateau generated a reproducible and clinically relevant joint injury that progressed to osteoarthritis-like changes by histologic and microCT evaluations. The ability to induce joint degeneration without an osteotomy or open arthrotomy provides a valuable new model for studying the natural sequelae of posttraumatic arthritis. Notably, the use of a murine model will facilitate the use of genetically modified animals for the investigation of specific genes implicated in the pathology of posttraumatic arthritis. © 2007 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 25:578,592, 2007 [source]

Mechanical injury potentiates proteoglycan catabolism induced by interleukin-6 with soluble interleukin-6 receptor and tumor necrosis factor , in immature bovine and adult human articular cartilage

ARTHRITIS & RHEUMATISM, Issue 10 2009
Yihong Sui
Objective Traumatic joint injury can damage cartilage and release inflammatory cytokines from adjacent joint tissue. The present study was undertaken to study the combined effects of compression injury, tumor necrosis factor , (TNF,), and interleukin-6 (IL-6) and its soluble receptor (sIL-6R) on immature bovine and adult human knee and ankle cartilage, using an in vitro model, and to test the hypothesis that endogenous IL-6 plays a role in proteoglycan loss caused by a combination of injury and TNF,. Methods Injured or uninjured cartilage disks were incubated with or without TNF, and/or IL-6/sIL-6R. Additional samples were preincubated with an IL-6,blocking antibody Fab fragment and subjected to injury and TNF, treatment. Treatment effects were assessed by histologic analysis, measurement of glycosaminoglycan (GAG) loss, Western blot to determine proteoglycan degradation, zymography, radiolabeling to determine chondrocyte biosynthesis, and Western blot and enzyme-linked immunosorbent assay to determine chondrocyte production of IL-6. Results In bovine cartilage samples, injury combined with TNF, and IL-6/sIL-6R exposure caused the most severe GAG loss. Findings in human knee and ankle cartilage were strikingly similar to those in bovine samples, although in human ankle tissue, the GAG loss was less severe than that observed in human knee tissue. Without exogenous IL-6/sIL-6R, injury plus TNF, exposure up-regulated chondrocyte production of IL-6, but incubation with the IL-6,blocking Fab significantly reduced proteoglycan degradation. Conclusion Our findings indicate that mechanical injury potentiates the catabolic effects of TNF, and IL-6/sIL-6R in causing proteoglycan degradation in human and bovine cartilage. The temporal and spatial evolution of degradation suggests the importance of transport of biomolecules, which may be altered by overload injury. The catabolic effects of injury plus TNF, appeared partly due to endogenous IL-6, since GAG loss was partially abrogated by an IL-6,blocking Fab. [source]

Streptococcus pneumoniae septic arthritis in adults

CLINICAL MICROBIOLOGY AND INFECTION, Issue 12 2004
I. Baraboutis
Abstract Streptococcus pneumoniae septic arthritis is an uncommon infection. The classic clinical picture is that of concomitant pulmonary and/or meningeal and joint infections in the presence of predisposing local and systemic factors. Initial laboratory tests are usually inconclusive, and joint aspiration is required for a definitive diagnosis. Treatment options include antibiotic therapy (usually with penicillin) combined with closed or open joint drainage. Increasing reports of infections involving penicillin-resistant strains are a concern. The prognosis is usually favourable, but early recognition and aggressive management are essential to reduce the likelihood of significant joint injury. [source]