The Ultrastructural Characteristics of Abnormal Collagen Fibrils in Various Organs

Staubesand, J.; Fischer, Niko

doi:10.3109/03008208009152356

Cited by 39 publications

(16 citation statements)

References 12 publications

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“…The combined existence of thicker and thinner fibrils has been reported in some forms of skeletal dysplasias such as osteogenesis im perfecta type IV [13], Therefore the term 'collagen dysplasia', according to Staubesand and Fischer [12] may be used for the idio pathic form of CTS. The irregularity of the collagen fibrils in their cross-sectional out lines, as described by Staubesand and Fischer [ 12], may be interpreted as a prior form of 'collagen dysplasia', whereas we observed the subsequent stage where collagen fibrils have already been separated completely. The exis tence of varying diameters of collagen fibrils in idiopathic CTS leads to the following questions: To which type of collagen do these fibrils belong and where and why do these thick fibrils originate [4]?…”

Section: Discussionsupporting

confidence: 66%

“…So far only little attention has been directed to wards the morphology of the transverse car pal ligament in the idiopathic CTS [1]. Pa tiala et al [7] reported varying light mi croscopical aspects of the transverse carpal ligaments of surgical biopsies, ranging from In an ultrastructural inves tigation Staubesand and Fischer [12] re ported the existence of abnormal collagen fibrils in the transverse carpal ligaments of 9 patients with CTS. These abnormal collagen fibrils, particularly thick ones, showed var ious degrees of irregularity in their cross-sec tional outline, ranging from slight peripheral fraying up to an indented circumference.…”

Section: Discussionmentioning

confidence: 99%

“…In this investigation 7 pa tients with idiopathic CTS were treated with surgical decompression of the median nerve by dissection of the transverse carpal ligament. Samples of these dissected liga ments were examined by means of an elec tron microscope, confirming the existence of abnormal collagen fibrils in CTS as de scribed by Staubesand and Fischer [12]. Morphometric analysis was performed in order to identify and quantify ultrastruc tural details of involved collagen fibrils.…”

Section: Introductionmentioning

confidence: 88%

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Morphometric Analysis of Collagen Fibrils in Idiopathic Carpal Tunnel Syndrome

Stransky

Weis

Neumüller³

et al. 1987

Pathobiology

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Surgical biopsies of dissected transverse carpal ligaments of patients with idiopathic carpal tunnel syndrome were examined with an electron microscope revealing collagen fibrils with varying diameters. Morphometric analysis of transversely cut collagen fibrils was performed on photomicrographs exhibiting fibrils with a small diameter comparable to that in normal tissue as well as fibrils with a large diameter that could not be observed in normal tissue.

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Section: Discussionsupporting

confidence: 66%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 88%

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Morphometric Analysis of Collagen Fibrils in Idiopathic Carpal Tunnel Syndrome

Stransky

Weis

Neumüller³

et al. 1987

Pathobiology

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“…1989;Jones et al. 1994] and fibrillation and dystrophic collagen associ ated with atherosclerosis, experimental saccular aneurysms and arteriovenous shunts [Staubesand and Fischer. 1980;Slehbens and Martin.…”

Section: Hemodynamically Induced Intimal Proliferationmentioning

confidence: 99%

Structural and Architectural Changes during Arterial Development and the Role of Hemodynamics

Stehbens

1996

Cells Tissues Organs

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Hemodynamics is a major determinant in the anatomical and mural architectural development of the arterial tree. Arterial intimal proliferation commences in utero at specific anatomical sites often appearing eccentric in transverse section and precedes more diffuse concentric thickening. Regarded as an inherent structural component of the wall or an adaptive mural response to increasing hemodynamic stresses concomitant with growth, its occurrence in utero and in lower animals, though generally supportive of this view, ignores qualitative changes. Further doubt derives from the retrogressive destructive nature of structural changes in the arterial wall in the young, individual differences and their continued progression after birth and maturation. It is postulated that concomitantly with arterial development the associated degenerative changes are attributable to hemodynamically induced bioengineering fatigue caused by longitudinal stretching and circumferential distensile effects of the pulse waves and by lesser vibrations generated by flow at sites of predilection for compensatory intimal thickening. This intimal proliferation is the compensatory reparative response to loss of tensile strength of mural constituents and of the vessel wall as a whole.

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“…First, it is not merely the quantity of collagen that affects myocardial stiffness but the arrangement of the collagen bundles, which cannot be assessed using this technique. Secondly, it has been shown that the collagen content of the vessel wall and of the perivascular spaces may be markedly increased in experimental hypertension (Staubesand & Fischer, 1980). This connective tissue contributes significantly to the overall collagen content but confers little to mechanical stiffness of the heart and cannot be distinguished from the interstitial collagen by a hydroxyproline assay (Thiedemann et al 1983).…”

Section: mentioning

confidence: 99%

Semiquantitative analysis of collagen types in the hypertrophied left ventricle

2001

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Cardiac fibrosis is a characteristic feature of left ventricular hypertrophy. The aim of this study was to develop a simple and accurate method to analyse collagen accumulation, taking into account the variation in cardiac muscle fibre orientation and nonuniform collagen distribution. This technique was used to determine the amount and types of collagen that accumulate during pressure overload cardiac hypertrophy. These data were correlated with myocyte size, and with the diastolic stress-strain relationship of the intact myocardium. Myocyte size was significantly increased in the hypertrophied hearts, compared with age and sex matched controls (control 363p25 µm# vs experimental 244p12 µm# ; meanp.., P 0n05). No overall collagen accumulation was observed in the hypertrophied hearts, but a significant increase in collagen I was found with a reduction in the amount of collagen III in experimental animals. Since no increase in diastolic stiffness of the hearts was observed, these results indicate that an increase in the overall collagen content of the heart, rather than the upregulation of a specific type, may be necessary to cause diastolic dysfunction.

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The Ultrastructural Characteristics of Abnormal Collagen Fibrils in Various Organs

Cited by 39 publications

References 12 publications

Morphometric Analysis of Collagen Fibrils in Idiopathic Carpal Tunnel Syndrome

Morphometric Analysis of Collagen Fibrils in Idiopathic Carpal Tunnel Syndrome

Structural and Architectural Changes during Arterial Development and the Role of Hemodynamics

Semiquantitative analysis of collagen types in the hypertrophied left ventricle

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