Cellular ultrastructure of the ruptured anterior cruciate ligament: A transmission electron microscopic and immunohistochemical study in 55 cases

Printz, H.; Stofft, E

doi:10.3109/17453679408993722

Cited by 29 publications

(14 citation statements)

References 20 publications

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“…cells have been noted to be intimately related to the crimped collagen fibers and distributed throughout the midsubstance of the anterior cruciate ligament. These cells have also been found in the outer zones of human anterior cruciate ligaments (23). Ovoid cells have been identified in columns (1,21,34), in lacunae (6,34), and in central areas of the human anterior cruciate ligament (23).…”

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confidence: 77%

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Fibroblast distribution in the anteromedial bundle of the human anterior cruciate ligament: The presence of α‐smooth muscle actin‐positive cells

Murray

Spector

1999

Journal Orthopaedic Research

112

105

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The anterior cruciate ligament is a complex tissue composed of structural proteins, proteoglycans, and cells. The histology of the human anterior cruciate ligament is characterized by the specific distribution and density of the fibroblast phenotype as well as by the unique organization of the structural proteins. A notable finding of this study was the identification of three histologically different zones along the anteromedial bundle as it coursed from the femoral to the tibial attachment. Two of the zones, the fusiform and ovoid, were located in the proximal one-quarter of the bundle; the third zone, the spheroid, occupied the distal three quarters of the bundle fascicles. The fusiform cell zone was characterized by a high number density of longitudinally oriented cells with a fusiform-shaped nucleus, longitudinal blood vessels, and high crimp length. The cytoplasm of the cells in this zone appeared to be intimately attached to the extracellular collagen and followed the crimp waveform of the fibers. Fusiform cells were noted to stain positively for the alpha-smooth muscle actin isoform in this region, particularly at areas of crimp disruption. The ovoid cell zone was characterized by a high number density of cells with an ovoid-shaped nucleus, longitudinal vessels, and a high crimp length. In this zone as well, the cytoplasm of the cells appeared to follow the waveform of the adjacent collagen. Ovoid cells were noted to stain positively for the alpha-smooth muscle actin isoform in this region. The spheroid cell zone was characterized by a low density of spheroid cells, few blood vessels, and short crimp length. Cells were noted within and among fascicles, as well as within lacunae. In selected areas, as many as 50% of the cells in this region stained positively for the alpha-smooth muscle actin isoform. This is also the first report of cells expressing the alpha-smooth muscle actin isoform in the intact human anterior cruciate ligament. This specific type of contractile actin, initially identified only in smooth-muscle cells, pericytes, and myofibroblasts, was seen in cells with various morphologies and predominantly in cells located at areas of crimp disruption. Further work is necessary to elucidate the role of the various fibroblast phenotypes in the maintenance of the human anterior cruciate ligament.

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confidence: 77%

“…These cells have also been found in the outer zones of human anterior cruciate ligaments (23). Ovoid cells have been identified in columns (1,21,34), in lacunae (6,34), and in central areas of the human anterior cruciate ligament (23). Periodic acid-Schiff staining has been positive in the ovoid ccll columns, suggesting the presence of glycosaminoglycans (6).…”

mentioning

confidence: 89%

Fibroblast distribution in the anteromedial bundle of the human anterior cruciate ligament: The presence of α‐smooth muscle actin‐positive cells

Murray

Spector

1999

Journal Orthopaedic Research

112

105

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“…In human ruptured ACL tissues, structural alterations of the intraligamentous fibroblasts and disorganization of the tissue repair are reported. 24 Some fibroblasts show signs of cell death, but the reason has remained unclear.…”

Section: Discussionmentioning

confidence: 99%

“…Histological analysis of the chronic-stage ACL remnants has shown that refilling of fibroblasts occurs in the ligaments, but the collagen fibers are in disarray and they seem to be quite different from the normal appearance of ACL tissue. 24 Why are the chronic-phase ACL remnants lacking in the obvious apoptotic changes despite the possible existence of NO around the ligaments? One explanation is that the sensitivity to NO is much different between normal ACL cells and the migrated fibroblasts in the remnants.…”

Section: Discussionmentioning

confidence: 99%

Upregulated expression of inducible nitric oxide synthase plays a key role in early apoptosis after anterior cruciate ligament injury

et al. 2006

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The reason that the anterior cruciate ligament (ACL) has a very poor healing potential after injury is not well understood. In this study, we investigated the role of nitric oxide (NO) in the apoptotic cell death of ACL cells using a rabbit model and in vitro cell culture. The apoptosis of ACL cells in vivo was analyzed by TUNEL assay and electron microscopy. NO synthase (NOS) expression was observed by immunohistochemical analysis. ACL cells were cultured and the susceptibility to NO-induced apoptosis was tested. Inducible NOS (iNOS) expression after treatment with cytokines was examined by immunohistochemical and RT-PCR analyses. Mitogen-activated protein kinase (MAPK) inhibitors were used for the analysis of downstream signals. A significant number of apoptotic cells were observed on days 1 to 3 after injury; the apoptotic rate returned to the control level by day 7. Upregulation of iNOS in the ACL remnant was observed at day 1. Intraarticular injection of NOS inhibitor suppressed the apoptotic rate. Isolated ACL cells showed much higher susceptibility to NO-induced apoptosis than did medial collateral ligament cells. IL-1b stimulated ACL cells to upregulate iNOS mRNA and increase NO production. p38 MAPK inhibitor decreased NO-induced apoptosis. Rapid iNOS induction after injury contributes to the high apoptotic rate of ACL cells, and this may partly account for the poor healing capacity of this ligament. iNOS and NO production is suggested to be stimulated by IL-1b, and NO activates the p38 MAPK pathway and triggers an apoptotic signal in ACL cells. ß

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“…The recent study by Spindler et al 29 described the lack of expression of matrix metalloproteinase 1 and matrix metalloproteinase 2 mRNA with an in situ hybridization technique in a ruptured anterior cruciate ligament. These findings conflict with the our results.…”

Section: Discussionmentioning

confidence: 99%

The expression of matrix metalloproteinases and inhibitors in acute rupture of the anterior cruciate ligament

Ishiguro

Shimizu

Ito

et al. 2000

Modern Rheumatology

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Rapid degeneration of the anterior cruciate ligament (ACL) may occur after ligament rupture, making primary repair of the anterior cruciate ligament difficult. Nine completely ruptured anterior cruciate ligaments were collected by arthroscopic surgery performed within 6 months of injury. The authors studied the localization of matrix metalloproteinases and tissue inhibitors of matrix metalloproteinases in ruptured anterior cruciate ligament using immunohistochemistry, and measured messenger ribonucleic acid expression using the reverse transcriptase polymerase chain reaction. Cells in residual ligament tissue seemed to contain matrix metalloproteinases 1 and 3 and tissue inhibitors of matrix metalloproteinases 1 and 2. Promatrix metalloproteinase-9 positive cells were observed in the perivascular area. Promatrix metalloproteinase-2 positive cells frequently were seen between irregular collagen bundles in stumps of ruptured ligaments. Tissue inhibitors of matrix metalloproteinase-2 positive cells commonly were observed in ruptured ligaments. Matrix metalloproteinase-1 and matrix metalloproteinase-3 messenger ribonucleic acid were highly expressed compared with matrix metalloproteinase-2 messenger ribonucleic acid. Tissue inhibitor of matrix metalloproteinase-2 messenger ribonucleic acid was highly expressed compared with tissue inhibitor of matrix metalloproteinase 1. The authors could not identify whether these intrinsic reactions mediated by anterior cruciate ligament cells were the causes of rapid degradation or the results of the degradation process. Various amounts of matrix metalloproteinase and inhibitor production of intrinsic ligament cells were observed in the ruptured anterior cruciate ligament. The biological reaction reported in this study may suggest that pronounced metabolism is undertaken in ruptured ACL cells, and provide N. Ishiguro ( ) · T. Shimizu · T. Ito · T.

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Cellular ultrastructure of the ruptured anterior cruciate ligament: A transmission electron microscopic and immunohistochemical study in 55 cases

Cited by 29 publications

References 20 publications

Fibroblast distribution in the anteromedial bundle of the human anterior cruciate ligament: The presence of α‐smooth muscle actin‐positive cells

Fibroblast distribution in the anteromedial bundle of the human anterior cruciate ligament: The presence of α‐smooth muscle actin‐positive cells

Upregulated expression of inducible nitric oxide synthase plays a key role in early apoptosis after anterior cruciate ligament injury

The expression of matrix metalloproteinases and inhibitors in acute rupture of the anterior cruciate ligament

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