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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histopathological and ultrastructural studies of 82 skin specimen from 81 cases of Lichen sclerosus et atrophicus (LSA) are reported. Among 64 cases of fully developed LSA, 65 specimens showed atrophy of the epidermis and hydropic degeneration at the basal layer. The collagenous fibers were swollen and homogeneous n the superficial dermis with inflammatory cells infiltrating beneath the areas of collagenous homogenization. There were 4 early cases of LSA in which epithelial thinning with flattening of the rete ridges, lichenoid lymphocytes and some histiocytes in the papillary dermis and along the dermo-epidermal junction were seen. Lichen simplex chronicus superimposed upon LSA lesions was present in 13 cases showing hyperplastic epidermis, all other observations were the same as those described in fully developed LSA. By electron microscopy, the intercellular spaces in the lesions appeared dilated, particularly those near basal cells, and desmosomes were found to be fewer than normal. Some lymphocytes and neutrophilic granulocytes were seen in the epithelial basement membrane, which was thinner than that in normal samples. Collagen fibers of varying diameters were arranged irregularly and with unclear fine structures.
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PMID:[Histopathological and ultrastructural studies of lichen sclerosus et atrophicus of the vulva]. 183 50

Despite an overall thinning of the epidermis and focal areas of cytologic atypia, there was no morphologic evidence that the protective function of this tissue was compromised by age. The characteristic morphologic markers associated with the keratinization process were not altered either in appearance or in amounts. A well-formed stratum corneum was present, suggestive that barrier ability is not compromised in senile skin. Whereas alterations in the aged epidermis are slight, the dermal-epidermal changes are marked and have greater physiologic consequences. The major change is a relatively flat dermal-epidermal junction because of retraction of the epidermal papillae as well as the microprojections of basal cells into the dermis. This flattening results in a more fragile tissue that is less resistant to shearing forces. Retraction of the epidermal downgrowths may also explain the loss in proliferative capacity associated with the aged epidermis. The major alterations in the aged dermis concern the architecture of the collagen and elastin networks. Both fibrous components appear more compact because of a decrease in the voids or spaces between the fibers; the spaces resulted from a loss of ground substance. Collagen bundles appear to unravel, and the individual elastic fibers show signs of elastolysis. The net effect of these fibrous rearrangements and alterations is a dermis that is less stretchable, less resilient, more lax, and prone to wrinkling.
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PMID:Morphology of aged skin. 264 2

Clinical tissue expansion has been quite successful but takes 2 to 3 months. This study compares the effects of a conventional tissue expansion regimen of 6 weeks with an accelerated regimen of 2 weeks in the dog model, which is biomechanically similar to the human. In 22 dogs, the skin expanded 34.4 percent in the 2-week and 35.8 percent in the 6-week protocol, excluding stretch and recruitment. There was thinning of the panniculus carnosus in the 6-week group and otherwise no significant decrease in dermal thickness in either group. The biomechanical properties of elasticity and creep did not differ in expanded skin from both groups, while stress/relaxation mildly decreased from a control value of 53.5 percent to 48.8 percent in the 6-week group (p less than 0.05). Collagen activity was increased in both the 6-week and the 2-week groups (p less than 0.001) over nonexpanded skin, and immunohistochemical staining with a monoclonal procollagen antibody demonstrated collagen synthesis by dermal fibroblasts in both groups. We conclude that rapid tissue expansion did not demonstrate any deleterious effects when compared with a conventional regimen.
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PMID:Physical, biomechanical, histologic, and biochemical effects of rapid versus conventional tissue expansion. 292 4

Pectus excavatum is a common malformation in diseases of elastic tissue (Marfan, Ehlers-Danlos...). When observed apparently alone it may represent a minor form of dystrophy, implying the same risk of a cardiac lesion. Abnormalities of the thoracic skeleton and echocardiographic mitral valve prolapse is a well established association, suggesting a common disorder of connective tissue. However, there is no absolute proof that this is a statistically significant association. Histological connective tissue changes relating these two markers have yet to be found. Clinical and echocardiographic examinations and skin biopsies were performed in 17 patients with pectus excavatum. Mitral valve prolapse was detected in 65% of cases (associated in 1 out of 3 cases with tricuspid valve prolapse). In 53% of cases electron microscopy showed abnormal skin collagen and elastin. Collagen abnormalities were twice as common as those of elastin and could be associated. Mixed changes of thinning of elastin and collagen fibres of irregular calibre were particularly suggestive. Pectus excavatum would therefore seem to be the expression of a minor form of dystrophy of collagen and elastin tissues and a clinical marker of possible mitral valve prolapse.
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PMID:[Mitral valve prolapse and pectus excavatum. Expressions of connective tissue dystrophy?]. 309 Sep 60

Despite an overall thinning of the epidermis and focal areas of cytologic atypia, there was no morphologic evidence that the protective function of this tissue was compromised by age. The characteristic morphologic markers associated with the keratinization process were not altered either in appearance or in amounts. A well-formed stratum corneum was present, suggestive that barrier ability is not compromised in senile skin. Whereas alterations in the aged epidermis are slight, the dermal-epidermal changes are marked and have greater physiologic consequences. The major change is a relatively flat dermal-epidermal junction because of retraction of the epidermal papillae as well as the microprojections of basal cells into the dermis. This flattening results in a more fragile tissue less resistant to shearing forces. Retraction of the epidermal downgrowths may also explain the loss in proliferative capacity associated with the aged epidermis. The major alterations in the aged dermis concern the architecture of the collagen and elastin networks. Both fibrous components appear more compact because of a decrease in the voids or spaces between the fibers; the spaces resulted from a loss of ground substance. Collagen bundles appear to unravel, and the individual elastic fibers show signs of elastolysis. The net effect of these fibrous rearrangements and alterations is a dermis that is less stretchable, less resilient, more lax, and prone to wrinkling.
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PMID:Morphology of aged skin. 352 84

The fine structural organization of the epidermis, dermal/epidermal junction, and dermis from an unexposed site (upper inner arm) of elderly people was compared with the organization of a similar region of young people. Despite an overall thinning of the epidermis and focal areas of cytologic atypia, the characteristic morphological markers associated with the keratinization process are not markedly altered in appearance or amount. A well-formed stratum corneum consisting of flattened, enucleated horny cells enveloped by a thickened membrane, and intracellular spaces filled with electron-dense material provide structural evidence that barrier ability is not compromised in senile skin. The dermal/epidermal changes in aged skin are marked and have significant physiologic implications. The major change is a relatively flat dermal/epidermal junction resulting from the retraction of the epidermal papillae as well as the microprojections of basal cells into the dermis. This flattening results in a more fragile epidermal/dermal interface and, consequently, the epidermis is less resistant to shearing forces. Retraction of the epidermal downgrowths (preferential sites of the putative epidermal stem cell) may also explain the loss in proliferative capacity associated with the aged epidermis. The three-dimensional arrangements of collagen and elastic fibers showed marked alterations with age. Both fibrous components appear more compact because of a decrease in spaces between the fibers. Collagen bundles appear to unravel, and the individual elastic fibers show signs of elastosis. These changes may contribute to the loss of resilience that is one of the salient features of senile skin.
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PMID:Aged skin: a study by light, transmission electron, and scanning electron microscopy. 354 15

Temporal changes in infarct collagen and left ventricular topography during healing after myocardial infarction were studied in 132 dogs with coronary artery ligation: 8 sham dogs and 13 with no infarction (controls) and 111 with infarction (3 at 1 day, 54 at 2 days, 25 at 7 days, 3 at 2 weeks, 9 at 4 weeks and 17 at 6 weeks). Myocardial hydroxyproline (a marker of collagen) was measured by spectrophotometry and pathologic infarct size, arteriographic occluded bed size and topography by computerized planimetry of weighed left ventricular rings. Over 6 weeks, hydroxyproline was unchanged in normal regions (average 4.20 mg/g dry weight) but increased progressively between 7 days and 6 weeks (9.94 versus 55.55 mg/g, p less than 0.001) in infarct zones. Progressive infarct contraction occurred over 6 weeks, with infarct size at 6 weeks being 40% less than at 2 days (9.7 versus 16.3% of the left ventricle, p less than 0.001), although total infarct hydroxyproline was directly related to infarct size at each time period (r = 0.73 to 0.81, p less than or equal to 0.05). Significant (p less than or equal to 0.05) left ventricular topographic changes in infarct hearts compared with control hearts included: 1) increase in cavity area (5.0 versus 3.9 cm2), endocardial circumference (8.8 versus 7.4 cm) and expansion index (infarct/normal endocardial segment length, 1.21 versus 1.02) by 7 days; and 2) decrease in thinning ratio (infarct/normal wall thickness, 0.71 versus 0.98) by 6 weeks. Also, compared with 2 day infarcts, by 6 weeks infarct area was decreased (1.8 versus 3.4 cm2) and the noninfarcted segment length increased (6.9 versus 5.4 cm). Changes in hydroxyproline and topography were similar for anterior (n = 54) and posterior (n = 57) infarcts. Thus, healing in canine infarcts is associated with cavity dilation and infarct expansion within 7 days followed by infarct contraction and thinning by 6 weeks, whereas collagen increases between 7 days and 6 weeks. Collagen deposition in expanded and thinned infarct segments explains the permanent regional shape distortion associated with ventricular aneurysms.
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PMID:Healing after myocardial infarction in the dog: changes in infarct hydroxyproline and topography. 394 Dec 23

Fibroblasts were cultured on top of or at the bottom of hydrated collagen lattices. Shortly after initially interacting with the collagen lattices, fibroblasts appeared to attach to individual collagen fibrils and in many cases cell processes were found wrapped around clusters of collagen fibrils. Tension generated by cells during spreading resulted in proximal collagen fibrils becoming aligned distal in the plane of spreading and more densely packed. During subsequent culture, the collagen fibrils to the cells underwent a similar reorganization and the lattice thinned to one-tenth of its original thickness. The rate of thinning was similar regardless of whether the cells were originally above or at the bottom of the lattices. The presence of cells distributed throughout the lattice was unnecessary for lattice reorganization to occur. When the lattices were allowed to come off the underlying substratum, compaction of the collagen gels was observed, and the resulting matrix had the typical appearance of dermis as observed by both light and electron microscopy. Collagen fibrils associated with the cell surface often appeared to be under tension and, in regions of close fibril binding, there was a prominent reorganization of submembranous microfilaments. It is suggested that reorganization of the collagen lattice by fibroblasts may depend upon secreted cell factors as well as physical forces generated by the cells.
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PMID:Reorganization of hydrated collagen lattices by human skin fibroblasts. 654 Feb 73

Keratoconus is a corneal disease of unknown cause that involves a progressive thinning and scarring of the corneal connective tissue. We examined normal human and keratoconus corneas, including one healed penetrating keratoplasty specimen. Organ cell cultures of normal and keratoconus corneal specimens were labeled with radioactive proline and analyzed by CM-cellulose chromatography and slab gel electrophoresis to determine collagen biosynthesis. Collagen types I and III were synthesized in similar amounts by normal and keratoconus stromacytes in culture. Specifically purified antibodies were used to determine the distribution of collagen types in tissue sections by immunofluorescence. The distribution of collagen types I, III, and IV in keratoconus was also similar to that in normal corneas, except that scarred regions in keratoconus and at the host-graft juncture were largely type III. Immunofluorescent reaction of the anti-type IV collagen antibodies with Bowman's layer, in particular, and Descemet's membrane in keratoconus specimens indicated extensive destruction. Basement membrane destruction may play an important role in this disease.
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PMID:Detection of specific collagen types in normal and keratoconus corneas. 701 5

A collagen network, composed largely of type I and III fibrillar collagens, is found in the extracellular space of the myocardium. This network has multiple functions which includes a preservation of tissue architecture and chamber geometry. Given its tensile strength, collagen is a major determinant of tissue stiffness. Its disproportionate accumulation, in the form of either a reactive or a reparative fibrosis, further increases stiffness. A degradation of collagen tethers, on the other hand, is an anatomic requisite for a distortion in tissue architecture and a reduction in stiffness that can lead to chamber dilatation, wall thinning, and even rupture of the myocardium. Collagen turnover in the myocardium is dynamic. When synthesis exceeds degradation, an adverse accumulation of collagen appears to distort tissue structure. This is true for either the hypertrophied and/or nonhypertrophied ventricle. Factors that contribute to the appearance of myocardial fibrosis are largely different from those that promote cardiac myocyte growth. Included amongst these fibrogenic factors are effector hormones of the reinin-angiotensin-aldosterone system (RAAS). Studies conducted both in intact animals (relative to dietary sodium intake) and in cultured adult cardiac fibroblasts have pointed toward the association between collagen accumulation and chronic elevations in circulating angiotensin II and aldosterone. A tissue hormonal system involving angiotensin II, endothelins and bradykinin, may likewise regulate fibrogenesis. In this regard, angiotensin converting enzyme is found in connective tissue of the normal heart, including the matrix of heart valves and the adventitia of the intramural coronary arteries, and fibrous tissue that forms following infarction or with chronic RAAS activation. The importance of ACE in the regulation of local angiotensin II and bradykinin levels and their contribution to collagen turnover is a fruitful area of research with important clinical implications. The myocardium also contains a proteolytic system, including collagenase. The characteristics and regulation of matrix metalloproteinases and their tissue inhibitors in various cardiovascular disease states requires further investigation.
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PMID:Collagen network of the myocardium: function, structural remodeling and regulatory mechanisms. 802 11


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