Abstract:We reviewed 31 of 33 consecutive patients with intra-articular fractures of the knee at 6 to 22 years (average 14). Of these, 77% had excellent or good results; the others had various degrees of degenerative osteoarthritis. There was no significant difference between the results after surgical or conservative treatment. Secondary degeneration was not related to cause or type of fracture, but its incidence increased with the patient's age at the time of injury, though not with the length of follow-up. Early mob… Show more
“…Intra-articular fractures and bleeding are associated with OA development 32,33 and repeated bleeds, as seen in hemophilia 34 lead to severe joint damage. It is possible that even a single episode of bleeding in the rabbit joint might contribute to synovial inflammation; fibrin can play a pro-inflammatory role and synovial exposure to blood and hemopoetic cells has been shown to lead to chronic synovitis.…”
Section: Cartilage Degeneration After Bone Injury In a Rabbitmentioning
Osteoarthritis (OA) is a leading cause of disability worldwide. We hypothesized that inflammation following isolated intraarticular bone injury can stimulate post-traumatic OA and developed a rabbit model to test that concept. Sixty female New Zealand White Rabbits were used. Twenty-six experimental animals had two holes drilled into their right femoral-notch, 18 rabbits had sham surgery, and 16 were un-operated controls. Rabbits were euthanized in subgroups at 72 h, 3, 6, 9, and 52 weeks. Knees were assessed grossly and tissues collected. Cartilage and synovium were analyzed with histology and qPCR and subgroups compared statistically. All surgical joints showed gross and histological (modified Mankin score) cartilage damage after surgery, with experimentals worsening with time (p < 0.05). Cartilage qPCR showed fivefold increases in TGFb (p < 0.05) expression at 72 h and 3 weeks with sixfold increases in MMP13 (p < 0.025) expression at 72 h. By 6 weeks, expression of these markers was similar to baseline levels. Synovial membrane thickening with increased cellularity was seen at both 9 and 52 weeks (p < 0.05). Short-term synovial inflammatory marker (IL-1b, IL-Ra, IL-6, and IL-8) expression was three-to fourfold increase in experimentals at 72 h (p < 0.01) returning to baseline levels by 3 weeks. Intra-articular bone injury creates early joint inflammation with some chronic synovial changes and progressive cartilage damage consistent with OA in adult rabbits. This model provides an exciting new avenue to potentially explore some relevant inflammatory drivers of OA without major mechanical variables. ß
“…Intra-articular fractures and bleeding are associated with OA development 32,33 and repeated bleeds, as seen in hemophilia 34 lead to severe joint damage. It is possible that even a single episode of bleeding in the rabbit joint might contribute to synovial inflammation; fibrin can play a pro-inflammatory role and synovial exposure to blood and hemopoetic cells has been shown to lead to chronic synovitis.…”
Section: Cartilage Degeneration After Bone Injury In a Rabbitmentioning
Osteoarthritis (OA) is a leading cause of disability worldwide. We hypothesized that inflammation following isolated intraarticular bone injury can stimulate post-traumatic OA and developed a rabbit model to test that concept. Sixty female New Zealand White Rabbits were used. Twenty-six experimental animals had two holes drilled into their right femoral-notch, 18 rabbits had sham surgery, and 16 were un-operated controls. Rabbits were euthanized in subgroups at 72 h, 3, 6, 9, and 52 weeks. Knees were assessed grossly and tissues collected. Cartilage and synovium were analyzed with histology and qPCR and subgroups compared statistically. All surgical joints showed gross and histological (modified Mankin score) cartilage damage after surgery, with experimentals worsening with time (p < 0.05). Cartilage qPCR showed fivefold increases in TGFb (p < 0.05) expression at 72 h and 3 weeks with sixfold increases in MMP13 (p < 0.025) expression at 72 h. By 6 weeks, expression of these markers was similar to baseline levels. Synovial membrane thickening with increased cellularity was seen at both 9 and 52 weeks (p < 0.05). Short-term synovial inflammatory marker (IL-1b, IL-Ra, IL-6, and IL-8) expression was three-to fourfold increase in experimentals at 72 h (p < 0.01) returning to baseline levels by 3 weeks. Intra-articular bone injury creates early joint inflammation with some chronic synovial changes and progressive cartilage damage consistent with OA in adult rabbits. This model provides an exciting new avenue to potentially explore some relevant inflammatory drivers of OA without major mechanical variables. ß
“…In addition sufficient cartilage nourishment is provided with stable fixation and early ROM [11]. Volpin et al reported that early motion might help prevent development of osteoarthritis [14].…”
The purpose of this study was to evaluate factors that affect initiation of early postoperative range of motion (ROM) rehabilitation and to investigate whether the postoperative ROM and clinical outcomes were affected by initiation of early ROM, immobilization and other factors. We conducted a retrospective analysis of tibial plateau fractures treated using stable internal fixation between December 2003 and June 2007. The resulting degree of flexion and Rasmussen Clinical and Radiographic Scores were evaluated. Thirty-nine patients were included, and 23 patients underwent a lateral submeniscal arthrotomy for evaluation of joint surface reduction, with 6 lateral meniscus lesions identified via arthrotomy. Three lateral collateral ligament lesions, 3 medial collateral ligament lesions and 1 anterior cruciate ligament lesion were found. Meniscus and ligament lesions significantly and negatively affected the initiation of knee joint ROM. Early ROM was achieved in 26 cases and 13 patients underwent immobilization for 4 weeks. At the final evaluation, the early ROM group had 130.42˚ ± 5.50˚ of flexion, compared with 122.92˚ ± 5.28˚ in the immobilization group. Moreover, the final Rasmussen score was 25.69 ± 2.92 in the early motion group, compared with 22.61 ± 3.5 in the immobilization group. There was no difference between radiographic scores of the groups. Although the initiation of early ROM improved the clinical results, soft tissue lesions influenced initiation of early knee joint motion. Therefore, meniscus and ligament injuries should be considered as prognostic factors in similar cases.
“…the knee increases 3-4-fold after the age of 50 years (2), suggesting that age-related cartilage changes render the tissue incapable of adequately maintaining the extracellular matrix.…”
Objective. Articular chondrocyte senescence is responsible, at least in part, for the increased incidence of osteoarthritis (OA) with increased age. Recently, it was suggested that caveolin 1, a 21-24-kd membrane protein, participates in premature cellular senescence. Caveolin 1 is the principal structural component of caveolae, vesicular invaginations of the plasma membrane. This study was undertaken to investigate whether the catabolic factors oxidative stress and interleukin-1 (IL-1) induce features of premature senescence of articular chondrocytes through up-regulation of caveolin 1 expression.Methods. Caveolin 1 expression was investigated in human OA cartilage by real-time polymerase chain reaction and in rat OA cartilage by immunohistologic analysis. We studied whether IL-1 and H 2 O 2 induce caveolin 1 expression in OA chondrocytes and analyzed the relationship between cellular senescent phenotypes and caveolin 1 expression in human chondrocytes.Results. In human and rat OA articular cartilage, caveolin 1 positivity was associated with cartilage degeneration. Both IL-1 and H 2 O 2 up-regulated caveolin 1 messenger RNA and protein levels, and both treatments induced marked expression of senescent phenotypes: altered cellular morphology, cell growth arrest, telomere erosion, and specific senescence-associated -galactosidase activity. Caveolin 1 overexpression induced p38 MAPK activation and impaired the ability of chondrocytes to produce type II collagen and aggrecan. Articular cartilage stability depends on the biosynthetic activities of chondrocytes, which counteract normal degradation of matrix macromolecules. Aging and the degeneration of articular cartilage in osteoarthritis (OA) are distinct processes; however, the incidence and prevalence of synovial joint degeneration increase dramatically in middle age (1) and the risk of posttraumatic OA following intraarticular fracture of
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