PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Elastic Tissue”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 397 records · Page 22Linked to original sources

A clinical, histological, and immunohistochemical comparison of acrodermatitis chronica atrophicans and morphea.

We compared 19 patients with acrodermatitis chronica atrophicans (ACA), a dermatosis caused by Borrelia burgdorferi infection, and 40 patients with morphea, a disease of heterogeneous origin where a borrelia etiology has been suggested in some cases, both clinically and histologically to define the differences between these two dermatoses. Clinically, ACA involves acral body sites with lower temperatures, is seen mostly in elderly persons, and presents as a livid discoloration that is not sharply demarcated. Morphea can be localized in embryonal structures, affects any age and body site, and exhibits extension at the periphery of the lesions. Histologically, ACA shows atrophy of collagen and elastic tissue as well as hypertrophic basophilic elastic tissue; whereas in morphea, sclerosis and polarizing elastic tissue are prominent. Graft-versus-host-like reactions may be present in both dermatoses. Immunohistochemical testing with different lymphocyte markers showed differences only in the expression of HLA-DR antigens. These conditions can be distinguished from each other on a clinical and histological basis in most cases. In 17% of morphea biopsy specimens, however, histological differentiation from ACA was not possible. Moreover, the histological pattern of morphea was not associated with a positive borrelia serology.

Acrodermatitis↗

Wrinkling due to mid-dermal elastolysis: two cases and literature review.

BACKGROUND: Mid-dermal elastolysis is an acquired disorder of elastic tissue clinically characterized by diffuse fine wrinkling, most often of the trunk and arms. Histologically, a clear band of elastolysis is present in the mid-dermis. OBJECTIVE: Although examples of diffuse elastolysis are well known, only a small number of patients with mid-dermal elastolysis have been reported to date. We present two patients with clinical and histological evidence of mid-dermal elastolysis, review the literature, and summarize the salient features of some common disorders of elastic tissue. METHODS: The first patient presented with fine wrinkles and papules over the upper arms, upper chest, and axillae, and demonstrated increased laxity of the eyelids. The second patient had striking wrinkles extending in a band-like pattern on her arms, upper chest, back, and abdomen. Neither one of our patients had a previous history of skin inflammation, urticaria, or any other underlying diseases related to their skin changes. Skin biopsies were taken from lesional and perilesional skin of both patients, and were stained with hematoxylin and eosin, and with elastic tissue stain. In addition, a tissue sample from Patient 1 was fixed for electron-microscopy. RESULTS: Hematoxylin and eosin stains did not demonstrate specific changes or diagnostic patterns. However, elastic tissue stains revealed a band-like loss of elastic tissue in the mid-dermis. Elastic tissue in the remaining superficial and deep dermis stained normally. Electron-microscopy was consistent with these findings and revealed significant loss of elastic tissue limited to the mid-dermis. CONCLUSION: We have presented two cases of mid-dermal elastolysis and reviewed the literature. To date, the pathophysiology of mid-dermal elastolysis had not been elucidated and no definitive therapy exists.

Adult↗

Three-dimensional structures of uterine elastic fibers: scanning electron microscopic studies.

We report findings that demonstrate for the first time that the structure of the elastic fibers of the uterus and cervix are characteristic to these tissues. Elastic fibers of the uterine corpus and cervix were studied by scanning electron microscopy (SEM). Elastic tissues were prepared from non-pregnant human uteri and pregnant rat uteri by three different methods: extraction from the tissue homogenates, in situ digestion by autoclaving of sliced tissue, and in situ formic acid digestion of sliced tissue. In addition, in situ formic acid digestion of the glutaraldehyde-fixed uterine wall of pregnant rats was done. Under SEM, the uterine elastic fibers revealed two distinct structures--fibrils and thin sheets of elastic membranes. Isolated fibers and membranes ranged in thickness from 0.1 to 0.4 micron which is thinner than aortic elastic lamellae (1-2.5 microns in thickness). These thin sheets of elastic membranes and elastic fibrils probably allow the uterus to maintain its elasticity without exerting excess pressure on the growing fetus. Formic acid digestion of fixed uterine walls of pregnant rats preserved the structural organization of elastic tissues near in vivo conditions. In these tissues, the fibers were arranged in a honeycomb structure made up largely of membranes, although sparse fibrils were present. These elastic, membranous sheets were arranged parallel to the plane of the uterine surface and interconnected with the threads of the membranes or fibrils. In the rat uterine wall, at least 12 parallel layers of elastic sheets were present. In contrast, at low magnification, the elastic tissues in the non-pregnant human uterus had no specific architectural arrangement and exhibited a sponge-like structure. Elastic fibers of the cervix were also made up of membranes and fibrils, and these fibers were organized into fishnet-like structures. These cervical membranes had fenestrations and pits with a diameter of 3-5 microns. In these studies, the concentrations of insoluble elastin in human uteri were found to be 1.38 and 1.32-1.41% of dry-defatted tissues for uterine body and cervix, respectively. The concentrations of total collagen were 38.8 and 64.3-72.4% of dry-defatted tissues for uterine body and cervix, respectively.

Adult↗

Morphometric analysis of the growth of the normal fetal guinea pig lung.

The structural development of the fetal guinea pig lung is described and quantified morphometrically in this report. At 35 days gestation the lung is in the pseudoglandular phase of growth, by 40 days it is in the canalicular phase, and at 50 days the saccular growth phase has begun. At term (67 days), the fetal guinea pig lung appears mature. From the beginning of the canalicular to the end of the saccular phases, the correlation coefficient between lung volume and gestational age is +.98, between internal surface area and gestational age is +.94 and between total number of saccules and gestational age is +.97. Internal surface area (ISA) correlates closely with lung volume (r = +.99) and the correlation coefficient between total number of saccules and lung volume is +.98. At term, lung volume is 4.22 ml. ISA is 0.5 M2, and total number of saccules is 253 million. Parenchymal growth is achieved by increases in both number and size of airspaces in the canalicular phase, primarily by increases in number during the early saccular phase and largely by increases in airspace size near term. The total length of parenchymal elastic tissue increases from 223 M at 45 days gestation to 5,253 M at term. Elastic tissue fibers first appear in the parenchyma of the fetal guinea pig lung during the canalicular phase, when the rate of saccule formation is high. The quantitative increase in elastic tissue correlates closely with the increase in the total number of saccules from day 45 to day 60 of gestation (r = +.99). The rate of elastic tissue growth increases sharply in the late saccular phase, coinciding with the period of greatest saccular expansion. These data suggest an interdependent relationship between saccular growth, i.e., proliferation and expansion, and the development of lung parenchymal elastic tissue.

Animals↗

Colocalization of granuloma annulare and mid-dermal elastolysis.

Mid-dermal elastolysis is an elastic tissue disorder of unknown causation. Various elastic tissue abnormalities have been described in granuloma annulare. To our knowledge, we report the first case illustrating the clinical and histologic colocalization of granuloma annulare and mid-dermal elastolysis.

Adult↗

Papular elastorrhexis: a variant of dermatofibrosis lenticularis disseminata (Buschke-Ollendorff syndrome)?

BACKGROUND: Buschke-Ollendorff syndrome is an autosomal dominant disorder clinically characterized by the appearance of disseminated white papules and osteopoikilosis. Histologically most cases show normal collagen and increased elastic tissue. Abortive forms of Buschke-Ollendorff syndrome are described, which show characteristic skin involvement, absence of skeletal changes and decreased elastic tissue. Papular elastorrhexis is characterized by nonfollicular, white papules, decreased elastic tissue, no genetic inheritance and no osteopoikilosis. OBJECTIVE: Is papular elastorrhexis a new entity or an abortive form of Buschke-Ollendorff syndrome? METHODS: We examined three members of one family (brother, sister and mother) presenting with nonfollicular, distributed, white papules on the trunk and extremities. Skin biopsies were examined by histological and electron-microscopic methods. RESULTS: The histological and electron-microscopic examinations of skin biopsies showed decreased, fragmented elastic fibers and normal collagen. By X-ray examination, no osteopoikilosis was found. The family presented here supports a genetic background of the disease. CONCLUSION: The clinical appearance with the absence of osteopoikilosis and the histological findings of our cases suggest the diagnosis of papular elastorrhexis. Papular elastorrhexis however was reported to be nonfamilial. Because of the genetic background found here we believe that papular elastorrhexis is an abortive form of Buschke-Ollendorff syndrome. Summarizing our data and reviewing the literature, we suggest that connective tissue nevi with the most prominent alterations in the elastic tissue should be classified under the term elastic tissue nevi.

Adolescent↗

Annular atrophic lichen planus and Sneddon's syndrome.

We report the case of a patient who had 2 rare diseases, annular atrophic lichen planus (AALP) and Sneddon's syndrome (SNS). This patient had also digital nodules with histological abnormalities suggestive of SNS vasculopathy, which have not been reported so far. AALP is the most rare of all varieties of lichen planus since this case is the third reported to date. The association of livedo racemosa and cerebrovascular disease is the hallmark of SNS, the incidence of which is estimated to be 4 cases per year per million inhabitants. In both diseases, an abnormal production of elastic-tissue-degrading enzymes or a constitutional abnormality of the elastic tissue can be postulated, since SNS is characterized by arteriolar changes with deterioration of the internal elastic lamina and AALP by destruction of the dermal elastic tissue.

Adult↗

Ultrastructural changes in arteries proximal to short-term experimental carotid-jugular arteriovenous fistulae in rabbits.

The afferent arteries of 10 carotid-jugular arteriovenous fistulae in rabbits were examined by transmission electron microscopy to determine the early ultrastructural changes in the vicinity of haemodynamically induced tears of the internal elastic lamina. No significant changes appeared to precede the development of the tears but radially orientated partial fractures were observed adjacent to some major tears. The elastic tissue tears became more numerous, extended proximally along the artery and with time involved the innermost medial elastic laminae. Endothelial discontinuities were present over only a few early tears and the small size suggested repair was rapid. Endothelial cells overlying the elastic tissue tears increased in density and thickness. They were adherent to the underlying matrix and eventually to the thickened and multilaminated basal lamina. In the floor of the tears between the edges of the torn internal elastic lamina there were some smooth muscle cells of the synthetic type, degenerative and necrotic muscle cells and areas devoid of matrix with scarce proteoglycan material suggestive of oedema. Sixteen days post-operatively the smooth muscle cells in the floor of the tears were all of the contractile variety with thickened basal laminae overlaid by a relatively normal endothelial layer. There was no suggestion that inflammatory cells were responsible for the elastic tissue tears. The abrupt edges and the adjacent microfractures are consistent with the concept of mechanical failure of the elastic tissue.

Animals↗

Estrogen regulates pulmonary alveolar formation, loss, and regeneration in mice.

Lung tissue elastic recoil and the dimension and number of pulmonary gas-exchange units (alveoli) are major determinants of gas-exchange function. Loss of gas-exchange function accelerates after menopause in the healthy aged and is progressively lost in individuals with chronic obstructive pulmonary disease (COPD). The latter, a disease of midlife and later, though more common in men than in women, is a disease to which women smokers and never smokers may be more susceptible than men; it is characterized by diminished lung tissue elastic recoil and presently irremediable alveolar loss. Ovariectomy in sexually immature rats diminishes the formation of alveoli, and estrogen prevents the diminution. In the present work, we found that estrogen receptor-alpha and estrogen receptor-beta, the only recognized mammalian estrogen receptors, are required for the formation of a full complement of alveoli in female mice. However, only the absence of estrogen receptor-beta diminishes lung elastic tissue recoil. Furthermore, ovariectomy in adult mice results, within 3 wk, in loss of alveoli and of alveolar surface area without a change of lung volume. Estrogen replacement, after alveolar loss, induces alveolar regeneration, reversing the architectural effects of ovariectomy. These studies 1) reveal estrogen receptors regulate alveolar size and number in a nonredundant manner, 2) show estrogen is required for maintenance of already formed alveoli and induces alveolar regeneration after their loss in adult ovariectomized mice, and 3) offer the possibility estrogen can slow alveolar loss and induce alveolar regeneration in women with COPD.

Animals↗

Mid-dermal elastolysis preceded by acute neutrophilic dermatosis.

BACKGROUND: Mid-dermal elastolysis is a rare idiopathic elastic tissue disorder that is characterized by localized patches of finely wrinkled skin and a "band-like" loss of elastic tissue in the mid-reticular dermis. Lesions may be preceded by erythema and/or urticaria, and histological examination of inflamed lesional skin may demonstrate lymphohistiocytic dermal infiltration. CASE REPORT: We report a case of mid-dermal elastolysis in a 31-year-old woman who developed multiple erythematous and urticarial plaques on the arms and trunk. Histologic examination of a representative lesion revealed a neutrophilic infiltrate and a normal pattern of elastic tissue. Several months later, the erythema and urticaria was noted to have resolved, leaving soft, pendulous plaques with overlying finely wrinkled skin. A follow-up biopsy at this time showed minimal lymphocytic inflammation but almost complete absence of elastic tissue in the mid-reticular dermis. CONCLUSIONS: To our knowledge, acute neutrophilic dermatosis resulting in mid-dermal elastolysis has not been previously described. This observation lends support to an emerging theory that the pathogenesis of mid-dermal elastolysis may be inflammatory.

Administration, Topical↗

Comparative metabolism of copper.

Copper is required in trace amounts for many body functions. The prominent effects of Cu deficiency or Cu toxicosis differs greatly between animal species. Along with iron, Cu is necessary for the transfer of O2 via a cascade of enzymes so that energy may be available for vital body functions without overheating of the tissues through rapid oxidation. As a part of lysyl oxidase, Cu has an obligate function in the maturation of all connective tissue (including elastic tissue and bone) maintaining the form and integrity of all body organs. As a constituent of tyrosinase, Cu is involved in the formation of melanin, thus preventing albinism. Copper also is involved in the myelination of nerve fibers and the production of neutrophils, enkephalins, lipoproteins, and cholesterol. Copper must be properly sequestered to prevent toxicosis. Copper is stored primarily as metallothioneins and as superoxide dismutase and is transported primarily as ceruloplasmin or as low molecular weight proteins, peptides, and amino acids.

Animals↗

Short-term survivors of pediatric heart transplantation: an autopsy study of their pulmonary vascular disease.

BACKGROUND: The most common indications for heart transplantation in children are congenital heart disease and cardiomyopathy. Intracardiac lesions that vary widely in morphology may have a similar impact on pulmonary vascular morphology; for example, any lesion that increases left-sided intracardiac pressure will affect pulmonary venous pressure and morphology and, if long-standing, may affect pulmonary arteries also. METHODS: The lungs of eight children who died 2 days to 7 months after receiving a heart transplant at ages 8 days to 4 years were examined at autopsy with particular regard to the pulmonary arteries and veins. Arteries were evaluated for medial thickness, intimal proliferation, and peripheral extension of muscle; veins for medial thickness and mural elastic tissue configuration; and lymphatics for degree of dilation. RESULTS: The main pulmonary arteries of the children with congenital heart disease showed an abnormal elastic tissue pattern, similar to the pattern of the aorta, indicating that pulmonary arterial hypertension was present in these children at birth. In contrast, the pulmonary trunk of a child who had myocarditis beginning at age 2 years had a normal pulmonary elastic tissue pattern, consistent with normal neonatal pulmonary pressure. Five children with morphologic evidence of early pulmonary arterial hypertension had a left-to-right atrial shunt before the operation and elevated pulmonary artery pressure immediately after transplantation. The pulmonary arteries of all five patients had medial hypertrophy or peripheral extension of muscle; the most advanced pathologic condition occurred in the arteries of the oldest child, who was 5 months of age, at the time of transplantation who died 2 days after the operation with pulmonary arterial hypertension. In the lungs of all eight patients, pulmonary veins showed medial hypertrophy and excess elastic tissue fibers (arterialization), consistent with venous hypertension. The most impressive venous changes in the lungs of the children with hypoplastic left heart syndrome occurred in the two children who had the smallest left ventricles (4 x 6 mm and 8 x 8 mm), and in another child with hypoplastic and anomalous extrapulmonary pulmonary veins. The most impressive lymphangiectasis occurred in the lungs of the child with hypoplastic left heart syndrome who was oldest at the time of transplantation and in the lungs of a child with obstructed venous drainage. CONCLUSIONS: Pulmonary vasculopathy in children who require heart transplantation because of congenital heart disease or long-standing congestive heart failure may involve arteries, veins, and lymphatics. Among the eight patients in this autopsy study of children who died less than a year after heart transplantation, arterial vasculopathy associated with congenital heart disease appeared more pronounced in the five who survived less than 30 days compared with the two longer survivors. The lack of morphologic progression in short-term survivors of pulmonary arterial vasculopathy after heart transplantation correlates with clinical follow-up of long-term survivors who do not have problematic pulmonary arterial hypertension. Pulmonary venous vasculopathy is determined by the degree of pretransplantation left-sided obstruction caused by congenital or acquired disease and may be more persistent morphologically than arterial vasculopathy. This morphologic study of the pulmonary vasculature of short-term survivors of heart transplantation supports the concept that palliative surgical procedures may benefit children awaiting heart transplantation, especially infants with hypoplastic left heart syndrome for whom suitable donors are scarce.

Cardiomyopathies↗

Venous morphology predicts class of chronic venous insufficiency.

OBJECTIVES: this study aimed to determine specific morphological differences in long saphenous veins from patients with various grades of chronic venous insufficiency. DESIGN: comparable veins from a control group were compared with patients with either primary varicose veins or those with associated skin changes including venous ulcers. MATERIALS: below-knee segments of saphenous vein were examined from a total of 64 patients. METHODS: veins were examined for elastic-tissue disruption and endothelial-cell changes and comparisons made between clinical groups. RESULTS: elastic-tissue disruption, as measured by fragmentation of the elastic lamina and the percentage of the intimal-medial boundary containing elastin, increased with increasing severity of venous disease. Moreover, endothelial cells became more densely packed, as measured by endothelial cell and endothelial-cell nuclei density, with increasing severity of disease. Other measures such as the density of multinucleated "giant" endothelial cells and the number of nuclei per "giant" cell did not correlate with venous disease, however. CONCLUSIONS: this study demonstrates that several morphological characteristics of superficial saphenous veins correlate with severity of venous disease. In particular, the alterations to the structure of elastic tissue within these veins appears indicative of the progressive nature of chronic venous insufficiency.

Aged↗

Elastic protein-based materials in tissue reconstruction.

In natural tissues, cells form multiple attachment sites to their extracellular matrix. By means of those attachments, cells deform as the tissue deforms in response to the natural mechanical stresses and strains that the tissue must sustain during function. These mechanical forces are the energy input that instruct the cells to produce the extracellular matrix sufficient to sustain those forces. Thus, an ideal artificial material should have both the attachment sites for the natural cells and a compliance that matches the natural tissue. Elastic protein-based polymers have been designed to provide both cell attachment sites and to exhibit the required elastic modulus of the tissue to be replaced. Thus, this introduces the potential to design a temporary functional scaffolding that will be remodeled, while functioning, into a natural tissue. A feasibility study applies this concept to the problem of urinary bladder reconstruction in terms of the filling and emptying of a simulated bladder comprised of an elastic protein-based matrix containing cell attachment sites with human urothelial cells growing out onto the dynamic matrix. Furthermore, the elastic protein-based materials themselves have been designed to perform the set of energy conversions that occur in living organisms and, in particular, to convert mechanical energy into chemical energy with the result of chemical signals of the sort that could provide the stimuli to turn on the genes for producing the required extracellular proteins.

Animals↗

The role of actinically provoked systemic elastolysis in polymyalgic vascular disease. A study based on serum fluorescence and haptoglobin.

This study of cutaneous elastic tissue and serum fluorescence supports the hypothesis that widespread destruction and resorption of elastic tissue (elastolysis) occurs in the temporal arteritis/polymyalgia rheumatica syndrome. A systemic elastolysis of this nature may be provoked by actinic (radiant) damage to the "exposed" elastic tissues in the skin and superficial arteries, the archetype of such injury being seen in temporal arteritis. Scattered giant cells are the usual agents of elastolysis but tuberculoid ("sarcoid") infiltrates often take over in the later stages. In acute polymyalgia, the phenomenon probably becomes diffuse and humoral. Elastolysis may be a direct pathogenetic link between polymyalgia and other vascular diseases such as idiopathic aneurysm and atherosclerosis.

Blood Protein Electrophoresis↗

Cellular expression of tropoelastin mRNA splice variants.

The primary transcript of tropoelastin is alternatively spliced into multiple mRNAs. The pattern and frequency of exon splicing is developmentally regulated, but the cellular profile of isoform expression within and among elastic tissues is not known. We used splice-variant specific antisense oligomeric deoxyribonucleotide probes in an in situ hybridization assay to assess the distribution of cells undergoing specific alternative splicing of tropoelastin pre-mRNA in developing bovine elastic tissues. Antisense oligomers were synthesized to exon sequences that are not alternatively spliced (exon 36) and to sequences that become abutted after high frequency (exon 33) and low frequency (exons 13 and 14) alternative splicing. The specificity of these probes for tropoelastin splice variants was verified by Southern hybridization to tropoelastin cDNAs with known exon deletions, and their specificity for tropoelastin mRNA was demonstrated by Northern hybridization. In situ hybridization with [35S]-labeled oligomers on sections of bovine lobar pulmonary artery and other elastic tissues showed that all elastogenic cells produce multiple forms of tropoelastin mRNA. These observations suggest that the production of tropoelastin isoforms is common to all cells within an elastin tissue and that this multiplicity may not be involved in regional differences in elastic tissue architecture.

Animals↗

The effects of beta-aminopropionitrile on the growing rat lung.

beta-Aminopropionitrile (beta APN), 500 ng/g body weight was injected intraperitoneally into male rats every 2 days between 2 and 28 days after birth. The lungs were examined structurally and functionally and compared with the lungs of control animals given injections of saline and 28-day-old normal male rats which were not given injections. Lungs volumes, both distended with air at 30 cm H2O and with formalin at 25 cm H2O, were increased in beta APN-treated animals. The architecture of the lung was altered so that there was a large increase in the "core," or air internal to the alveoli of the walls of alveolar ducts and sacs. Animals given injections of beta APN had 40--56% fewer alveoli than those given saline injections and normal animals. Experimental animals had larger alveoli. The lungs or beta APN- treated animals were hypercompliant, and their pressure-volume curves were shifted upward and to the left. There were morphologic changes in collagen and elastic tissue, which were more apparent in the elastic tissue. Since beta APN interferes with the synthesis of elastin and collagen, it appears that alterations in the collagen--elastin network reduces alveolar multiplication in the postnatal period. Control animals given saline had abnormal lungs when compared with normal animals. Their alveoli were larger, and they had fewer alveoli per unit volume. Thus the lung may be sensitive to relatively minor insults in the postnatal period.

Aminopropionitrile↗