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Effect of Posterior Cruciate Ligament Rupture on Biomechanical and Histological Features of Lateral Femoral Condyle

View Article: PubMed Central - PubMed

ABSTRACT

Background: The aim of this study was to investigate bone mineral density (BMD) and the biomechanical and histological effects of posterior cruciate ligament (PCL) rupture on the lateral femoral condyle.

Material/methods: Strain on different parts of the lateral femoral condyle from specimens of normal adult knee joints, including 12 intact PCLs, 6 ruptures of the anterolateral bundle, 6 ruptures of the postmedial bundle, and 12 complete ruptures, was tested when loaded with different loads on the knee at various flexion angles. Lateral femoral condyles were also collected randomly from both the experimental side in which the PCLs were transected and the control side from 4 sets of 12 matched-mode pairs of rabbits at 4, 8, 16, and 24 weeks after surgery, and their BMD and morphological and histological changes were observed.

Results: Partial and complete rupture of the PCL may cause an abnormal load on all parts of the lateral femoral condyle with any axial loading at all positions. Noticeable time-dependent degenerative histological changes of the lateral femoral condyle were observed in the rabbit model of PCL rupture. All of the PCL rupture groups had a higher expression of matrix metalloproteinase-7 (MMP-7) and collagen type II than the control group at all time points (P<0.05), but no significant difference in BMD (P>0.05).

Conclusions: Rupture of the PCL may trigger a coordinated response of lateral femoral condyle degeneration in a time-dependent manner, to which the high level of expression of MMP-7 and collagen type II could contribute.

No MeSH data available.


Related in: MedlinePlus

The images were visualized with macro-observation (first row), HE staining (second row), MMP-7 immunohistochemical staining (third row), and collagen type II immunohistochemical staining (fourth row) in PCL rupture side and the control side of the lateral femoral condyle. (A) the control side: continuous and smooth surface, chondrocytes in columnar shape and regularly ranged, even nuclear size and staining, mild deep staining in cytoplasm, continuous tidemark; weakly MMP-7 positive-staining expressed in superficial layer, few in cytoplasm; even collagen type II expression in ECM, few positive-staining cells, and almost no staining in cytoplasm; (B) 4th week after PCL rupture: smooth and approximately flat surface, chondrocytes regularly arranged, clear tissue layers, even HE staining, and continuous tidemark; MMP-7 positive-staining weakly expressed in surface, matrix, and cytoplasm, full oval-shaped nuclear, partly expressed in cytoplasm; uneven collagen type II positive-staining in matrix, partly expressed in cytoplasm; (C) 8th week after PCL rupture: slight rough surface, chondrocytes arranged disorderly, few gathered in clusters, unclear layers, uneven staining; MMP-7 strongly expressed in superficial layer, positive in matrix and cytoplasm, deeper than 4th week; more collagen type II positive-staining cells; (D) 16th week after PCL rupture: rough surface, chondrocytes arranged disorderly, more clusters, disorderly arrangement tissue layers; MMP-7 strongly expressed in superficial layer, matrix and cytoplasm, matrix partly degraded, cytomorphosis; more collagen type II positive-staining cells; (E) 24th week after PCL rupture: superficial layer fibrosis, cell number decreased obviously, layers disorderly arranged; decreased MMP-7 staining, especially in cytoplasm, matrix degradation, uneven cell size and shape; few collagen type II positive-staining cells.
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f2-medscimonit-22-4369: The images were visualized with macro-observation (first row), HE staining (second row), MMP-7 immunohistochemical staining (third row), and collagen type II immunohistochemical staining (fourth row) in PCL rupture side and the control side of the lateral femoral condyle. (A) the control side: continuous and smooth surface, chondrocytes in columnar shape and regularly ranged, even nuclear size and staining, mild deep staining in cytoplasm, continuous tidemark; weakly MMP-7 positive-staining expressed in superficial layer, few in cytoplasm; even collagen type II expression in ECM, few positive-staining cells, and almost no staining in cytoplasm; (B) 4th week after PCL rupture: smooth and approximately flat surface, chondrocytes regularly arranged, clear tissue layers, even HE staining, and continuous tidemark; MMP-7 positive-staining weakly expressed in surface, matrix, and cytoplasm, full oval-shaped nuclear, partly expressed in cytoplasm; uneven collagen type II positive-staining in matrix, partly expressed in cytoplasm; (C) 8th week after PCL rupture: slight rough surface, chondrocytes arranged disorderly, few gathered in clusters, unclear layers, uneven staining; MMP-7 strongly expressed in superficial layer, positive in matrix and cytoplasm, deeper than 4th week; more collagen type II positive-staining cells; (D) 16th week after PCL rupture: rough surface, chondrocytes arranged disorderly, more clusters, disorderly arrangement tissue layers; MMP-7 strongly expressed in superficial layer, matrix and cytoplasm, matrix partly degraded, cytomorphosis; more collagen type II positive-staining cells; (E) 24th week after PCL rupture: superficial layer fibrosis, cell number decreased obviously, layers disorderly arranged; decreased MMP-7 staining, especially in cytoplasm, matrix degradation, uneven cell size and shape; few collagen type II positive-staining cells.

Mentions: Compared with the control groups, the cartilage of the lateral femoral condyle in the PCL rupture group presented noticeable degenerative characteristics (Table 2). The HE and immunohistochemical staining of the lateral femoral condyle in the PCL rupture groups showed time-dependent abnormities and deterioration in comparison with the control groups, indicating that PCL rupture may act as a progressive degenerative factor of the lateral femoral condyle (Figure 2).


Effect of Posterior Cruciate Ligament Rupture on Biomechanical and Histological Features of Lateral Femoral Condyle
The images were visualized with macro-observation (first row), HE staining (second row), MMP-7 immunohistochemical staining (third row), and collagen type II immunohistochemical staining (fourth row) in PCL rupture side and the control side of the lateral femoral condyle. (A) the control side: continuous and smooth surface, chondrocytes in columnar shape and regularly ranged, even nuclear size and staining, mild deep staining in cytoplasm, continuous tidemark; weakly MMP-7 positive-staining expressed in superficial layer, few in cytoplasm; even collagen type II expression in ECM, few positive-staining cells, and almost no staining in cytoplasm; (B) 4th week after PCL rupture: smooth and approximately flat surface, chondrocytes regularly arranged, clear tissue layers, even HE staining, and continuous tidemark; MMP-7 positive-staining weakly expressed in surface, matrix, and cytoplasm, full oval-shaped nuclear, partly expressed in cytoplasm; uneven collagen type II positive-staining in matrix, partly expressed in cytoplasm; (C) 8th week after PCL rupture: slight rough surface, chondrocytes arranged disorderly, few gathered in clusters, unclear layers, uneven staining; MMP-7 strongly expressed in superficial layer, positive in matrix and cytoplasm, deeper than 4th week; more collagen type II positive-staining cells; (D) 16th week after PCL rupture: rough surface, chondrocytes arranged disorderly, more clusters, disorderly arrangement tissue layers; MMP-7 strongly expressed in superficial layer, matrix and cytoplasm, matrix partly degraded, cytomorphosis; more collagen type II positive-staining cells; (E) 24th week after PCL rupture: superficial layer fibrosis, cell number decreased obviously, layers disorderly arranged; decreased MMP-7 staining, especially in cytoplasm, matrix degradation, uneven cell size and shape; few collagen type II positive-staining cells.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC5120644&req=5

f2-medscimonit-22-4369: The images were visualized with macro-observation (first row), HE staining (second row), MMP-7 immunohistochemical staining (third row), and collagen type II immunohistochemical staining (fourth row) in PCL rupture side and the control side of the lateral femoral condyle. (A) the control side: continuous and smooth surface, chondrocytes in columnar shape and regularly ranged, even nuclear size and staining, mild deep staining in cytoplasm, continuous tidemark; weakly MMP-7 positive-staining expressed in superficial layer, few in cytoplasm; even collagen type II expression in ECM, few positive-staining cells, and almost no staining in cytoplasm; (B) 4th week after PCL rupture: smooth and approximately flat surface, chondrocytes regularly arranged, clear tissue layers, even HE staining, and continuous tidemark; MMP-7 positive-staining weakly expressed in surface, matrix, and cytoplasm, full oval-shaped nuclear, partly expressed in cytoplasm; uneven collagen type II positive-staining in matrix, partly expressed in cytoplasm; (C) 8th week after PCL rupture: slight rough surface, chondrocytes arranged disorderly, few gathered in clusters, unclear layers, uneven staining; MMP-7 strongly expressed in superficial layer, positive in matrix and cytoplasm, deeper than 4th week; more collagen type II positive-staining cells; (D) 16th week after PCL rupture: rough surface, chondrocytes arranged disorderly, more clusters, disorderly arrangement tissue layers; MMP-7 strongly expressed in superficial layer, matrix and cytoplasm, matrix partly degraded, cytomorphosis; more collagen type II positive-staining cells; (E) 24th week after PCL rupture: superficial layer fibrosis, cell number decreased obviously, layers disorderly arranged; decreased MMP-7 staining, especially in cytoplasm, matrix degradation, uneven cell size and shape; few collagen type II positive-staining cells.
Mentions: Compared with the control groups, the cartilage of the lateral femoral condyle in the PCL rupture group presented noticeable degenerative characteristics (Table 2). The HE and immunohistochemical staining of the lateral femoral condyle in the PCL rupture groups showed time-dependent abnormities and deterioration in comparison with the control groups, indicating that PCL rupture may act as a progressive degenerative factor of the lateral femoral condyle (Figure 2).

View Article: PubMed Central - PubMed

ABSTRACT

Background: The aim of this study was to investigate bone mineral density (BMD) and the biomechanical and histological effects of posterior cruciate ligament (PCL) rupture on the lateral femoral condyle.

Material/methods: Strain on different parts of the lateral femoral condyle from specimens of normal adult knee joints, including 12 intact PCLs, 6 ruptures of the anterolateral bundle, 6 ruptures of the postmedial bundle, and 12 complete ruptures, was tested when loaded with different loads on the knee at various flexion angles. Lateral femoral condyles were also collected randomly from both the experimental side in which the PCLs were transected and the control side from 4 sets of 12 matched-mode pairs of rabbits at 4, 8, 16, and 24 weeks after surgery, and their BMD and morphological and histological changes were observed.

Results: Partial and complete rupture of the PCL may cause an abnormal load on all parts of the lateral femoral condyle with any axial loading at all positions. Noticeable time-dependent degenerative histological changes of the lateral femoral condyle were observed in the rabbit model of PCL rupture. All of the PCL rupture groups had a higher expression of matrix metalloproteinase-7 (MMP-7) and collagen type II than the control group at all time points (P<0.05), but no significant difference in BMD (P>0.05).

Conclusions: Rupture of the PCL may trigger a coordinated response of lateral femoral condyle degeneration in a time-dependent manner, to which the high level of expression of MMP-7 and collagen type II could contribute.

No MeSH data available.


Related in: MedlinePlus