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      Noise rich in low frequency components, a new comorbidity for periodontal disease? An experimental study

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          Abstract

          Introduction:

          Exposure to noise rich in low frequency components induces abnormal proliferation of extracellular matrix and collagens. The previous studies have shown alterations in the periodontium of both humans and animals. Our objective was the evaluation of collagens I, IV and V of the periodontium of Wistar rats exposed to noise rich in low frequency components.

          Materials and Methods:

          5 groups (each with 10 animals) were exposed to continuous low frequency noise (LFN). The LFN, from previously recorded white noise, frequency filtered and amplified, was applied in growing periods of 1, 3, 5, 9 and 13 weeks, in order to characterize the alterations with exposure time. A control group of ten animals was kept in silence. These animals were used in groups of 2 as aged-matched controls. After exposure, sections were obtained including teeth, alveolar bone and periodontium and observed after immunollabeling for collagens I, IV and V.

          Results:

          A significant increase in collagen I was observed in exposed groups ( P < 0.001) (Kruskal-Wallis test). Post-hoc comparisons (Mann-Whitney test with Bonferroni correction) showed an increase in collagen I in animals exposed for 3 weeks or more ( P < 0.001). The same test was applied to collagen V where significant differences were found when comparing control and exposed groups ( P ≤ 0.004). The t-test for independent samples was applied to collagen type IV where no significant differences were found ( P = 0.410), when comparing to the control group.

          Discussion:

          As in other organs, we can observe fibrosis and the newly formed collagen is likely to be “nonfunctional”, which could have clinical impact.

          Conclusion:

          Noise may constitute a new comorbidity for periodontal disease.

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          Most cited references28

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          Cell differentiation by mechanical stress.

          Growth factors, hormones, and other regulatory molecules are traditionally required in tissue engineering studies to direct the differentiation of progenitor cells along specific lineages. We demonstrate that mechanical stimulation in vitro, without ligament-selective exogenous growth and differentiation factors, induces the differentiation of mesenchymal progenitor cells from the bone marrow into a ligament cell lineage in preference to alternative paths (i.e., bone or cartilage cell lineages). A bioreactor was designed to permit the controlled application of ligament-like multidimensional mechanical strains (translational and rotational strain) to the undifferentiated cells embedded in a collagen gel. The application of mechanical stress over a period of 21 days up-regulated ligament fibroblast markers, including collagen types I and III and tenascin-C, fostered statistically significant cell alignment and density and resulted in the formation of oriented collagen fibers, all features characteristic of ligament cells. At the same time, no up-regulation of bone or cartilage-specific cell markers was observed.
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            Vibroacoustic disease: biological effects of infrasound and low-frequency noise explained by mechanotransduction cellular signalling.

            At present, infrasound (0-20 Hz) and low-frequency noise (20-500 Hz) (ILFN, 0-500 Hz) are agents of disease that go unchecked. Vibroacoustic disease (VAD) is a whole-body pathology that develops in individuals excessively exposed to ILFN. VAD has been diagnosed within several professional groups employed within the aeronautical industry, and in other heavy industries. However, given the ubiquitous nature of ILFN and the absence of legislation concerning ILFN, VAD is increasingly being diagnosed among members of the general population, including children. VAD is associated with the abnormal growth of extra-cellular matrices (collagen and elastin), in the absence of an inflammatory process. In VAD, the end-product of collagen and elastin growth is reinforcement of structural integrity. This is seen in blood vessels, cardiac structures, trachea, lung, and kidney of both VAD patients and ILFN-exposed animals. VAD is, essentially, a mechanotransduction disease. Inter- and intra-cellular communication is achieved through both biochemical and mechanotranduction signalling. When the structural components of tissue are altered, as is seen in ILFN-exposed specimens, the mechanically mediated signalling is, at best, impaired. Common medical diagnostic tests, such as EKG, EEG, as well as many blood chemistry analyses, are based on the mal-function of biochemical signalling processes. VAD patients typically present normal values for these tests. However, when echocardiography, brain MRI or histological studies are performed, where structural changes can be identified, all consistently show significant changes in VAD patients and ILFN-exposed animals. Frequency-specific effects are not yet known, valid dose-responses have been difficult to identify, and large-scale epidemiological studies are still lacking.
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              A new paradigm in the periodontal disease progression: gingival connective tissue remodeling with simultaneous collagen degradation and fibers thickening.

              Bacterial dental plaque is considered to be the main cause of periodontal diseases, but progression of the disease is also related to the host inflammatory response. The earliest affected tissue is the gingiva, but the specific mechanisms involved in the onset of this condition remain unclear. Frequently, collagen degradation is pointed as the main marker of periodontal disease progression, but the organization of the fibers in the gingival tissue is still unknown. The aim of the present study was to investigate the gingival extracellular matrix in a model of ligature-induced periodontal disease. Analysis of the microbiota indicated a progressive increase in the ratio of Gram-negative/Gram-positive microorganisms. There was no difference in the organization of reticulin fibers next to the epithelial basement membrane, whereas the arrangement of collagen fibers in the gingival connective tissue was significantly affected. Animals with inflammation presented a reduction of 35% in the total area occupied by collagen fibers. However, these fibers were thicker and more densely packed. These alterations involve type I, type III and type VI collagens as determined by immunohistochemistry. The results demonstrated the occurrence of marked reorganization of the gingival extracellular matrix in response to the inflammatory process, indicating a new paradigm in the periodontal disease progression: collagen degradation and fibers thickening, simultaneously.
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                Author and article information

                Journal
                J Indian Soc Periodontol
                J Indian Soc Periodontol
                JISP
                Journal of Indian Society of Periodontology
                Medknow Publications & Media Pvt Ltd (India )
                0972-124X
                0975-1580
                Jul-Aug 2014
                : 18
                : 4
                : 503-507
                Affiliations
                [1] Center for Interdisciplinary Research Egas Moniz, CiiEM, Portugal
                [1 ] Abel Salazar Biomedical Sciences Institute, Portugal
                Author notes
                Address for correspondence: Prof. Pedro Miguel Antunes Oliveira, Center for Interdisciplinary Research Egas Moniz, CiiEM, Campus Universitario, Quinta da Granja, Monte de Caparica, 2829 511 Caparica, Portugal. E-mail: pedromaoliveira@ 123456hotmail.com
                Article
                JISP-18-503
                10.4103/0972-124X.138729
                4158595
                73ae4811-b581-4fd8-b420-ce2d7ea5c342
                Copyright: © Journal of Indian Society of Periodontology

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 27 September 2013
                : 27 January 2014
                Categories
                Original Article

                Dentistry
                fibrosis,low frequency noise,periodontal disease,periodontium
                Dentistry
                fibrosis, low frequency noise, periodontal disease, periodontium

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