Relevant bibliographies by topics / Periodontal disease Molecular aspects

Academic literature on the topic 'Periodontal disease Molecular aspects'

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Published: 4 June 2021
Last updated: 1 February 2022

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  2. Dissertations / Theses
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Journal articles on the topic "Periodontal disease Molecular aspects":

1

Tsuchida, Sachio. "Proteome Analysis of Molecular Events in Oral Pathogenesis and Virus: A Review with a Particular Focus on Periodontitis." International Journal of Molecular Sciences 21, no. 15 (July 22, 2020): 5184. http://dx.doi.org/10.3390/ijms21155184.

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Some systemic diseases are unquestionably related to periodontal health, as periodontal disease can be an extension or manifestation of the primary disease process. One example is spontaneous gingival bleeding, resulting from anticoagulant treatment for cardiac diseases. One important aspect of periodontal therapy is the care of patients with poorly controlled disease who require surgery, such as patients with uncontrolled diabetes. We reviewed research on biomarkers and molecular events for various diseases, as well as candidate markers of periodontal disease. Content of this review: (1) Introduction, (2) Periodontal disease, (3) Bacterial and viral pathogens associated with periodontal disease, (4) Stem cells in periodontal tissue, (5) Clinical applications of mass spectrometry using MALDI-TOF-MS and LC-MS/MS-based proteomic analyses, (6) Proteome analysis of molecular events in oral pathogenesis of virus in GCF, saliva, and other oral Components in periodontal disease, (7) Outlook for the future and (8) Conclusions. This review discusses proteome analysis of molecular events in the pathogenesis of oral diseases and viruses, and has a particular focus on periodontitis.
2

Lin, Peiya, Hiromi Niimi, Yujin Ohsugi, Yosuke Tsuchiya, Tsuyoshi Shimohira, Keiji Komatsu, Anhao Liu, et al. "Application of Ligature-Induced Periodontitis in Mice to Explore the Molecular Mechanism of Periodontal Disease." International Journal of Molecular Sciences 22, no. 16 (August 18, 2021): 8900. http://dx.doi.org/10.3390/ijms22168900.

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Periodontitis is an inflammatory disease characterized by the destruction of the periodontium. In the last decade, a new murine model of periodontitis has been widely used to simulate alveolar bone resorption and periodontal soft tissue destruction by ligation. Typically, 3-0 to 9-0 silks are selected for ligation around the molars in mice, and significant bone loss and inflammatory infiltration are observed within a week. The ligature-maintained period can vary according to specific aims. We reviewed the findings on the interaction of systemic diseases with periodontitis, periodontal tissue destruction, the immunological and bacteriological responses, and new treatments. In these studies, the activation of osteoclasts, upregulation of pro-inflammatory factors, and excessive immune response have been considered as major factors in periodontal disruption. Multiple genes identified in periodontal tissues partly reflect the complexity of the pathogenesis of periodontitis. The effects of novel treatment methods on periodontitis have also been evaluated in a ligature-induced periodontitis model in mice. This model cannot completely represent all aspects of periodontitis in humans but is considered an effective method for the exploration of its mechanisms. Through this review, we aimed to provide evidence and enlightenment for future studies planning to use this model.
3

Teng, Y. T. A. "Protective and Destructive Immunity in the Periodontium: Part 2—T-cell-mediated Immunity in the Periodontium." Journal of Dental Research 85, no. 3 (March 2006): 209–19. http://dx.doi.org/10.1177/154405910608500302.

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Based on the results of recent research in the field and Part 1 of this article (in this issue), the present paper will discuss the protective and destructive aspects of the T-cell-mediated adaptive immunity associated with the bacterial virulent factors or antigenic determinants during periodontal pathogenesis. Attention will be focused on: (i) osteoimmunology and periodontal disease; (ii) some molecular techniques developed and applied to identify critical microbial virulence factors or antigens associated with host immunity (with Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis as the model species); and (iii) summarizing the identified virulence factors/antigens associated with periodontal immunity. Thus, further understanding of the molecular mechanisms of the host’s T-cell-mediated immune responses and the critical microbial antigens related to disease pathogenesis will facilitate the development of novel therapeutics or protocols for future periodontal treatments. Abbreviations used in the paper are as follows: A. actinomycetemcomitans ( Aa), Actinobacillus actinomycetemcomitans; Ab, antibody; DC, dendritic cells; mAb, monoclonal antibody; pAb, polyclonal antibody; OC, osteoclast; PAMP, pathogen-associated molecular patterns; P. gingivalis ( Pg), Porphyromonas gingivalis; RANK, receptor activator of NF-κB; RANKL, receptor activator of NF-κB ligand; OPG, osteoprotegerin; TCR, T-cell-receptors; TLR, Toll-like receptors.
4

Luan, X., X. Zhou, J. Trombetta-eSilva, M. Francis, A. K. Gaharwar, P. Atsawasuwan, and T. G. H. Diekwisch. "MicroRNAs and Periodontal Homeostasis." Journal of Dental Research 96, no. 5 (January 9, 2017): 491–500. http://dx.doi.org/10.1177/0022034516685711.

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MicroRNAs (miRNAs) are a group of small RNAs that control gene expression in all aspects of eukaryotic life, primarily through RNA silencing mechanisms. The purpose of the present review is to introduce key miRNAs involved in periodontal homeostasis, summarize the mechanisms by which they affect downstream genes and tissues, and provide an introduction into the therapeutic potential of periodontal miRNAs. In general, miRNAs function synergistically to fine-tune the regulation of biological processes and to remove expression noise rather than by causing drastic changes in expression levels. In the periodontium, miRNAs play key roles in development and periodontal homeostasis and during the loss of periodontal tissue integrity as a result of periodontal disease. As part of the anabolic phase of periodontal homeostasis and periodontal development, miRNAs direct periodontal fibroblasts toward alveolar bone lineage differentiation and new bone formation through WNT, bone morphogenetic protein, and Notch signaling pathways. miRNAs contribute equally to the catabolic aspect of periodontal homeostasis as they affect osteoclastogenesis and osteoclast function, either by directly promoting osteoclast activity or by inhibiting osteoclast signaling intermediaries or through negative feedback loops. Their small size and ability to target multiple regulatory networks of related sets of genes have predisposed miRNAs to become ideal candidates for drug delivery and tissue regeneration. To address the immense therapeutic potential of miRNAs and their antagomirs, an ever growing number of delivery approaches toward clinical applications have been developed, including nanoparticle carriers and secondary structure interference inhibitor systems. However, only a fraction of the miRNAs involved in periodontal health and disease are known today. It is anticipated that continued research will lead to a more comprehensive understanding of the periodontal miRNA world, and a systematic effort toward harnessing the enormous therapeutic potential of these small molecules will greatly benefit the future of periodontal patient care.
5

Divaris, K. "Searching Deep and Wide: Advances in the Molecular Understanding of Dental Caries and Periodontal Disease." Advances in Dental Research 30, no. 2 (October 21, 2019): 40–44. http://dx.doi.org/10.1177/0022034519877387.

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During the past decades, remarkable progress has been made in the understanding of the molecular basis of the 2 most common oral diseases, dental caries and periodontal disease. Improvements in our knowledge of the diseases’ underlying biology have illuminated previously unrecognized aspects of their pathogenesis. Importantly, the key role of the oral (supragingival and subgingival) microbiome is now well recognized, and both diseases are now best understood as dysbiotic. From a host susceptibility standpoint, some progress has been made in dissecting the “hyperinflammatory” trait and other pathways of susceptibility underlying periodontitis, and novel susceptibility loci have been reported for dental caries. Nevertheless, there is a long road to the translation of these findings and the realization of precision oral health. There is promise and hope that the rapidly increasing capacity of generating multiomics data layers and the aggregation of study samples and cohorts comprising thousands of participants will accelerate the discovery and translation processes. A first key element in this process has been the identification and interrogation of biologically informed disease traits—these “deep” or “precise” traits have the potential of revealing biologically homogeneous disease signatures and genetic susceptibility loci that might present with overlapping or heterogeneous clinical signs. A second key element has been the formation of international consortia with the goals of combining and harmonizing oral health data of thousands of individuals from diverse settings—these “wide” collaborative approaches leverage the power of large sample sizes and are aimed toward the discovery or validation of genetic influences that would otherwise be impossible to detect. Importantly, advancements via these directions require an unprecedented engagement of systems biology and team science models. The article highlights novel insights into the molecular basis of dental caries and chronic periodontitis that have been gained from recent and ongoing studies involving “deep” and “wide” analytical approaches.
6

Teng, Y. T. A. "Protective and Destructive Immunity in the Periodontium: Part 1—Innate and Humoral Immunity and the Periodontium." Journal of Dental Research 85, no. 3 (March 2006): 198–208. http://dx.doi.org/10.1177/154405910608500301.

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Based on the results of recent research in the field, the present paper will discuss the protective and destructive aspects of the innate vs. adaptive (humoral and cell-mediated) immunity associated with the bacterial virulent factors or antigenic determinants during periodontal pathogenesis. Attention will be focused on: (i) the Toll-like receptors (TLR), the innate immune repertoire for recognizing the unique molecular patterns of microbial components that trigger innate and adaptive immunity for effective host defenses, in some general non-oral vs. periodontal microbial infections; (ii) T-cell-mediated immunity, Th-cytokines, and osteoclastogenesis in periodontal disease progression; and (iii) some molecular techniques developed and used to identify critical microbial virulence factors or antigens associated with host immunity (using Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis as the model species). Therefore, further understanding of the molecular interactions and mechanisms associated with the host’s innate and adaptive immune responses will facilitate the development of new and innovative therapeutics for future periodontal treatments. Abbreviations used in the paper are as follows: A. actinomycetemcomitans ( Aa), Actinobacillus actinomycetemcomitans; Ab, antibody; DC, dendritic cells; mAb, monoclonal antibody; pAb, polyclonal antibody; PAMP, pathogen-associated molecular patterns; P. gingivalis ( Pg), Porphyromonas gingivalis; and TLR, Toll-like receptors.
7

Dieterle, Martin Philipp, Ayman Husari, Thorsten Steinberg, Xiaoling Wang, Imke Ramminger, and Pascal Tomakidi. "From the Matrix to the Nucleus and Back: Mechanobiology in the Light of Health, Pathologies, and Regeneration of Oral Periodontal Tissues." Biomolecules 11, no. 6 (May 31, 2021): 824. http://dx.doi.org/10.3390/biom11060824.

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Among oral tissues, the periodontium is permanently subjected to mechanical forces resulting from chewing, mastication, or orthodontic appliances. Molecularly, these movements induce a series of subsequent signaling processes, which are embedded in the biological concept of cellular mechanotransduction (MT). Cell and tissue structures, ranging from the extracellular matrix (ECM) to the plasma membrane, the cytosol and the nucleus, are involved in MT. Dysregulation of the diverse, fine-tuned interaction of molecular players responsible for transmitting biophysical environmental information into the cell’s inner milieu can lead to and promote serious diseases, such as periodontitis or oral squamous cell carcinoma (OSCC). Therefore, periodontal integrity and regeneration is highly dependent on the proper integration and regulation of mechanobiological signals in the context of cell behavior. Recent experimental findings have increased the understanding of classical cellular mechanosensing mechanisms by both integrating exogenic factors such as bacterial gingipain proteases and newly discovered cell-inherent functions of mechanoresponsive co-transcriptional regulators such as the Yes-associated protein 1 (YAP1) or the nuclear cytoskeleton. Regarding periodontal MT research, this review offers insights into the current trends and open aspects. Concerning oral regenerative medicine or weakening of periodontal tissue diseases, perspectives on future applications of mechanobiological principles are discussed.
8

Obradović, Vesna. "The role of oxidative stress and antioxidant defence system in periodontitis." Medicinski casopis 54, no. 2 (2020): 75–82. http://dx.doi.org/10.5937/mckg54-24883.

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The prevalence of periodontal disease is very high in the adult population. According to research results, as much as 46% of the total population was affected by periodontal disease in the period from 2010 to 2012, which would mean that 64.7 million people had periodontitis, of which 8% had a severe form of this disease. Having in mind the clinical and socioeconomic significance of periodontitis, this review aims to present in a comprehensive way the pathogenetic aspects of periodontitis with a special emphasis on oxidative stress and antioxidant protection mechanisms as possible molecular mechanisms for the development of periodontitis in adults. Oxidation stress is involved in the progression of periodontitis as a chronic inflammatory disease of periodontium, which occurs as a result of imbalance between host response and bacterial infection. At the same time there is a decreased antioxidant activity and salivary gland capacity, which contributes to the further development of this disease. MDA is the most common lipid peroxidation derivative that occurs in periodontitis. All of the mentioned literature data suggest that the elevated MDA values may be due to both local and systemic oxidative stress as a response to inflammatory periodontal disease alone or in combination with other systemic disorders and smoking. The harmful effects of ROS during oxidative stress occur through lipid peroxidation processes and irreversible protein modification to cell apoptosis and programmed cell death. In addition to the two most important signal pathways, caspase pathway and NADPH oxidase-4 pathway, several other signaling pathways mediate in oxidative cell damage: PERK/NRF2 signal path, JNK / mitogen-activating pathway (MAP). When a clinically visible inflammatory process occurs in periodontium, this usually presents a condition that is more or less irreversible. In parodontology, therefore, the idea of introducing biochemical analyzes to diagnose the inflammatory process in parodontium is still open before it can be seen at the clinical level. For this reason, the significance of the role of oxidative stress, the antioxidant protection of the organism and the molecular mechanisms by which damage occurs is an indisputable importance. Assessment and measurement of biomarkers of oxidative stress and antioxidant enzymes can play a central role in monitoring biochemical indicators of parodontium state and even assist with various methods of treatment of periodontal disease.
9

Guimarães, Morgana R., Sabrina Garcia de Aquino, Leila S. Coimbra, Luis C. Spolidorio, Keith L. Kirkwood, and Carlos Rossa. "Curcumin modulates the immune response associated with LPS-induced periodontal disease in rats." Innate Immunity 18, no. 1 (January 17, 2011): 155–63. http://dx.doi.org/10.1177/1753425910392935.

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Curcumin is a plant-derived dietary spice ascribed various biological activities. Curcumin therapeutic applications have been studied in a variety of conditions, but not on periodontal disease. Periodontal disease is a chronic inflammatory condition initiated by an immune response to micro-organisms of the dental biofilm. Experimental periodontal disease was induced in rats by injecting LPS in the gingival tissues on the palatal aspect of upper first molars (30 µg LPS, 3 times/week for 2 weeks). Curcumin was administered to rats daily via oral gavage at 30 and 100 mg/kg body weight. Reverse transcriptase-qPCR and ELISA were used to determine the expression of IL-6, TNF-α and prostaglandin E2 synthase on the gingival tissues. The inflammatory status was evaluated by stereometric and descriptive analysis on hematoxylin/eosin-stained sections, whereas modulation of p38 MAPK and NK-κB signaling was assessed by Western blot. Curcumin effectively inhibited cytokine gene expression at mRNA and protein levels, but NF-κB was inhibited only with the lower dose of curcumin, whereas p38 MAPK activation was not affected. Curcumin produced a significant reduction on the inflammatory infiltrate and increased collagen content and fibroblastic cell numbers. Curcumin potently inhibits innate immune responses associated with periodontal disease, suggesting a therapeutic potential in this chronic inflammatory condition.
10

Ma, W., H. Lyu, M. Pandya, G. Gopinathan, X. Luan, and T. G. H. Diekwisch. "Successful Application of a Galanin-Coated Scaffold for Periodontal Regeneration." Journal of Dental Research 100, no. 10 (July 30, 2021): 1144–52. http://dx.doi.org/10.1177/00220345211028852.

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The nervous system exerts finely tuned control over all aspects of the life of an organism, including pain, sensation, growth, and development. Recent developments in tissue regeneration research have increasingly turned to small molecule peptides to tailor and augment the biological response following tissue loss or injury. In the present study, we have introduced the small molecule peptide galanin (GAL) as a novel scaffold-coating agent for the healing and regeneration of craniofacial tissues. Using immunohistochemistry, we detected GAL and GAL receptors in healthy periodontal tissues and in the proximity of blood vessels, while exposure to our periodontal disease regimen resulted in a downregulation of GAL. In a 3-dimensional bioreactor culture, GAL coating of collagen scaffolds promoted cell proliferation and matrix synthesis. Following subcutaneous implantation, GAL-coated scaffolds were associated with mineralized bone-like tissue deposits, which reacted positively for alizarin red and von Kossa, and demonstrated increased expression and protein levels of RUNX2, OCN, OSX, and iBSP. In contrast, the GAL receptor antagonist galantide blocked the effect of GAL on Runx2 expression and inhibited mineralization in our subcutaneous implantation model. Moreover, GAL coating promoted periodontal regeneration and a rescue of the periodontal defect generated in our periodontitis model mice. Together, these data demonstrate the efficacy of the neuropeptide GAL as a coating material for tissue regeneration. They are also suggestive of a novel role for neurogenic signaling pathways in craniofacial and periodontal regeneration.
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Journal articles Dissertations / Theses Books

Dissertations / Theses on the topic "Periodontal disease Molecular aspects":

1

Gully, Neville. "Studies on the growth and metabolism of Eikenella corrodens /." Title page, summary and table of contents only, 2000. http://web4.library.adelaide.edu.au/theses/09PH/09phg973.pdf.

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2

Irani, Dilshad Minocher. "Role of the surface associated material of Eikenella corrodens in bone resorption associated with periodontal disease : a research thesis submitted in fulfilment of the requirements for the degree of Master of Science in Dentistry." Title page, contents and summary only, 1998. http://web4.library.adelaide.edu.au/theses/09DSM/09dsmi65.pdf.

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Mooney, John. "Molecular and cellular aspects of the humoral immune response in periodontal disease and other related conditions." Electronic Thesis or Diss., University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321510.

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Kennedy, Rebekah Storm. "Microbiological and immunological aspects of equine periodontal disease." Electronic Thesis or Diss., University of Glasgow, 2017. http://theses.gla.ac.uk/8064/.

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Periodontal disease is a common and painful condition in the horse. Although awareness of the condition is growing amongst the veterinary profession and horse owners, the presence of the disease is often overlooked and treatment can be difficult. Despite this, there have been few recent studies of the aetiopathogenesis of the condition. Certain species of bacteria may act as periodontal pathogens, stimulating a destructive inflammatory response in periodontal tissues and this has been well recognised as being important to the aetiopathogenesis of the disease in man. However few equine studies on this aspect of the disease have been carried out. The main aims of this study were: - 1) to identify the bacteria associated with a healthy oral cavity and periodontitis in horses using culture dependent and independent methods; 2) to assess the differences in bacterial populations between the healthy and periodontitis groups and identify putative pathogens; 3) to quantify the expression patterns of TLRs 2, 4 and 9, the pro-inflammatory cytokines IL-1β and TNFα, anti-inflammatory cytokine IL-10 and Th1/Th2/Th17 cytokines IL-4, IL-6/ IL-12, IFNɣ/ IL-17, within gingival tissue from each sample group; 4) to use matched data to establish if associations exist between the presence and quantity of bacterial species present and TLR expression and 5) to determine activation of TLRs 2, 4 and 9 by putative pathogens using specific in- vitro TLR assays. Swabs were taken from the gingival sulcus of 42 orally healthy horses and plaque samples were taken from the periodontal pockets of 61 horses with periodontal disease. The location and grade of the lesion was noted and an equine dental chart completed for each case. Bacteria were identified using high throughput 16S rRNA gene sequencing, QPCR, whole genome sequencing and conventional culture followed by 16S gene sequencing. Gingival biopsies were taken from 13 orally healthy horses and 20 horses with periodontitis and gene expression of TLR 2, TLR 4, TLR 9, IL-1β, IL-4, IL-6, IL-10, IL-12, IL-17, TNFα and IFNɣ was measured. THP-1X Blue, MyD88 THP-1X Blue, HEK hTLR 2 Blue and HEK hTLR 4 Blue human cell lines were co-cultured with putative periodontal pathogens and their response measured via level of secreted embryonic alkaline phosphatase. Clinical, microbiological and immunological data underwent cross-matching analysis. Microbial populations showed 89% dissimilarly between oral health and periodontitis with a less diverse population present in diseased equine periodontal pockets. The most discriminative bacteria between health and disease identified at genus level were Fusobacteria and Acinetobacter in health and Pseudomonas and Prevotella in periodontitis. The most abundant genera were Gemella (36.5%), Pseudomonas (14%) and Acinetobacter (8%) in orally healthy samples and Pseudomonas (25%), Prevotella (14%) and Acinetobacter (9.4%) in periodontitis samples. Whole genome sequencing revealed the presence of 75 species of Prevotella in the equine oral cavity and a significantly higher number of reads corresponding to Prevotella bivia, Prevotella dentalis, Prevotella denticola, Prevotella intermedia, Prevotella melaninogenica, Prevotella nigrescens were noted in diseased samples. Significant increases in expression of TLR 4 mRNA, TLR 9 mRNA and, in particular TLR 2, mRNA were noted in diseased equine gingival tissue in addition to increased pro-inflammatory and anti-inflammatory cytokine mRNA expression. Presence of P. intermedia was significantly positively correlated with expression of TLR 2 in equine periodontitis. In addition, the presence of Aggregatibacter actinomycetemcomitans was positively associated with disease severity and expression of TLR 4 mRNA in the horse. Co-culture of periodontal pathogens with human cell lines revealed that the innate immune response to the presence of these bacteria is mainly mediated through TLR 2 activation. The use of both culture dependent and culture independent methods to investigate the equine oral microbiome has provided significant breadth and depth of information on the microbiology of equine periodontal disease. Microbial populations are significantly different as expected and bacteria belonging to the Prevotella genus have been strongly implicated in the aetiopathogenesis of the condition. The innate immune response produced in periodontally diseased equine gingival tissue has been characterised for the first time in the horse.
5

Ng, Kwai-sang Sam, and 吳桂生. "Psychological perspectives of periodontal disease." PG_Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B36918210.

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Preber, Hans. "Cigarette smoking and periodontal disease clinical and therapeutic aspects /." Stockholm : Dept. of Periodontology, Karolinska Institutet, 1986. http://books.google.com/books?id=4ulpAAAAMAAJ.

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7

Porter, S. R. "Immunological aspects of rapidly progressive periodontitis." Electronic Thesis or Diss., University of Bristol, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377350.

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8

Sörgjerd, Karin. "Molecular Aspects of Transthyretin Amyloid Disease." Doctoral thesis, comprehensive summary, Linköpings universitet, Biokemi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-12566.

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This thesis was made to get a deeper understanding of how chaperones interact with unstable, aggregation prone, misfolded proteins involved in human disease. Over the last two decades, there has been much focus on misfolding diseases within the fields of biochemistry and molecular biotechnology research. It has become obvious that proteins that misfold (as a consequence of a mutation or outer factors), are the cause of many diseases. Molecular chaperones are proteins that have been defined as agents that help other proteins to fold correctly and to prevent aggregation. Their role in the misfolding disease process has been the subject for this thesis. Transthyretin (TTR) is a protein found in human plasma and in cerebrospinal fluid. It works as a transport protein, transporting thyroxin and holo-retinol binding protein. The structure of TTR consists of four identical subunits connected through hydrogen bonds and hydrophobic interactions. Over 100 point mutations in the TTR gene are associated with amyloidosis often involving peripheral neurodegeneration (familial amyloidotic polyneuropathy (FAP)). Amyloidosis represents a group of diseases leading to extra cellular deposition of fibrillar protein known as amyloid. We used human SH-SY5Y neuroblastoma cells as a model for neurodegeneration. Various conformers of TTR were incubated with the cells for different amounts of time. The experiments showed that early prefibrillar oligomers of TTR induced apoptosis when neuroblastoma cells were exposed to these species whereas mature fibrils were not cytotoxic. We also found increased expression of the molecular chaperone BiP in cells challenged with TTR oligomers. Point mutations destabilize TTR and result in monomers that are unstable and prone to aggregate. TTR D18G is naturally occurring and the most destabilized TTR mutant found to date. It leads to central nervous system (CNS) amyloidosis. The CNS phenotype is rare for TTR amyloid disease. Most proteins associated with amyloid disease are secreted proteins and secreted proteins must pass the quality control check within the endoplasmic reticulum (ER). BiP is a Hsp70 molecular chaperone situated in the ER. BiP is one of the most important components of the quality control system in the cell. We have used TTR D18G as a model for understanding how an extremely aggregation prone protein is handled by BiP. We have shown that BiP can selectively capture TTR D18G during co-expression in both E. coli and during over expression in human 293T cells and collects the mutant in oligomeric states. We have also shown that degradation of TTR D18G in human 293T cells occurs slower in presence of BiP, that BiP is present in amyloid deposition in human brain and mitigates cytotoxicity of TTR D18G oligomers.
Denna avhandling handlar om proteiner. Särskilt de som inte fungerar som de ska utan har blivit vad man kallar ”felveckade”. Anledningen till att proteiner veckas fel beror ofta (men inte alltid) på mutationer i arvsmassan. Felveckade proteiner kan leda till sjukdomar hos människor och djur (man brukar tala om amyloidsjukdomar), ofta av neurologisk karaktär. Exempel på amyloidsjukdomar är polyneuropati, där perifera nervsystemet är drabbat, vilket leder till begränsad rörelseförmåga och senare till förlamning; och Alzheimer´s sjukdom, där centrala nervsystemet är drabbat och leder till begränsad tankeförmåga och minnesförluster. Studierna som presenteras i denna avhandling har gått ut på att få en bättre förståelse för hur felveckade proteiner interagerar med det som vi har naturligt i cellerna och som fungerar som skyddande, hjälpande proteiner, så kallade chaperoner. Transtyretin (TTR) är ett protein som cirkulerar i blodet och transporterar tyroxin (som är ett hormon som bland annat har betydelse för ämnesomsättningen) samt retinol-bindande protein (vitamin A). I TTR genen har man funnit över 100 punktmutationer, vilka har kopplats samman med amyloidsjukdomar, bland annat ”Skellefteåsjukan”. Mutationer i TTR genen leder ofta till att proteinet blir instabilt vilket leder till upplösning av TTR tetrameren till monomerer. Dessa monomerer kan därefter sammanfogas på nytt men denna gång på ett sätt som är farligt för organismen. I denna avhandling har fokus legat på en mutation som kallas TTR D18G, vilken har identifierats i olika delar av världen och leder till en dödlig form av amyloidos i centrala nervsystemet. Det chaperon som vi har studerat benämns BiP och är beläget i en cellkomponent som kallas för det endoplasmatiska retiklet (ER). I ER finns cellens kontrollsystem i vilket det ses till att felveckade proteiner inte släpps ut utan istället bryts ned. Denna avhandling har visat att BiP kan fånga upp TTR D18G inuti celler och där samla mutanten i lösliga partiklar som i detta fall är ofarliga för cellen. Avhandligen har också visat att nedbrytningen av TTR D18G sker mycket långsammare när BiP finns i riklig mängd.
9

Boström, Lennart. "Tobacco smoking and periodontal disease : some clinical, microbiological and immunological aspects /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4456-3/.

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Hanley, Shirley Anne. "Molecular characterisation of an immunodominant 55kDa surface antigen of Porphyromonas gingivalis W50." Electronic Thesis or Diss., Queen Mary, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312824.

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Books on the topic "Periodontal disease Molecular aspects":

1

Bartold, P. Mark. Biology of the periodontal connective tissues. Chicago: Quintessence Pub. Co., 1998.

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2

European, Symposium on the Borderland Between Caries and Periodontal Disease (4th 1990 Geneva Switzerland). Application of molecular science to caries and periodontal disease: 4th European Symposium of Borderland Between Caries and Periodontal Disease, Geneva, Switzerland, 25-26 January, 1990. Oxford: Pergamon, 1990.

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3

Saleh, Mazen T. Molecular aspects of infectious disease. New York: Nova Science Publishers, 2011.

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4

Preber, Hans. Cigarette smoking and periodontal disease: Clinical and therapeutical aspects. [S.l: s.n.], 1986.

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5

Dumitrescu, Alexandrina L. Genetic Variants in Periodontal Health and Disease. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2010.

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Gokhale, David Anand. Molecular genetic aspects of Hodgkin's disease. Manchester: University of Manchester, 1996.

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Parker, Jane, ed. Molecular Aspects of Plant Disease Resistance. Oxford, UK: Wiley-Blackwell, 2008. http://dx.doi.org/10.1002/9781444301441.

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Galton, David J. Molecular genetics of common metabolic disease. London: Edward Arnold, 1985.

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Galton, David J. Molecular genetics of common metabolic disease. New York: Wiley, 1985.

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Dhalla, Naranjan S. Molecular defects in cardiovascular disease. Edited by Ošt̕ádal Bohuslav. New York: Springer, 2011.

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Book chapters on the topic "Periodontal disease Molecular aspects":

1

Braun-Falco, Markus, Henry J. Mankin, Sharon L. Wenger, Markus Braun-Falco, Stephan DiSean Kendall, Gerard C. Blobe, Christoph K. Weber, et al. "Periodontal Diseases." In Encyclopedia of Molecular Mechanisms of Disease, 1620–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_1396.

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Dumitrescu, Alexandrina L., and Masashi Tanaka. "Particular Aspects of Periodontal Disease Pathogenesis." In Etiology and Pathogenesis of Periodontal Disease, 77–124. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-03010-9_3.

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Dumitrescu, Alexandrina L. "Aspects of the Research Methodology for Periodontal Disease Assessment in Epidemiological Surveys." In Understanding Periodontal Research, 575–643. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-28923-1_19.

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Goodeve, Anne. "von Willebrand Disease: Molecular Aspects." In Textbook of Hemophilia, 278–85. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444318555.ch42.

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Hampshire, Daniel, and Anne Goodeve. "von Willebrand Disease: Molecular Aspects." In Textbook of Hemophilia, 353–61. Oxford, UK: John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118398258.ch48.

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Kapetanaki, Maria G., Ana L. Mora, and Mauricio Rojas. "Aging Mesenchymal Stem Cells in Lung Disease." In Molecular Aspects of Aging, 159–71. Hoboken, NJ: John Wiley & Sons, Inc, 2014. http://dx.doi.org/10.1002/9781118396292.ch12.

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Boyer, Laurent, Jorge Boczkowski, and Serge Adnot. "COPD as a Disease of Premature Aging." In Molecular Aspects of Aging, 173–83. Hoboken, NJ: John Wiley & Sons, Inc, 2014. http://dx.doi.org/10.1002/9781118396292.ch13.

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Maslanka, Susan E. "Botulism as a Disease of Humans." In Molecular Aspects of Botulinum Neurotoxin, 259–89. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-9454-6_12.

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Balding, Elba, Katherine Ververis, and Tom C. Karagiannis. "Molecular Aspects of the Warburg Effect." In Molecular mechanisms and physiology of disease, 371–82. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0706-9_13.

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Knopman, David. "Clinical Aspects of Alzheimer's Disease." In Neurodegeneration: The Molecular Pathology of Dementia and Movement Disorders, 37–50. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444341256.ch8.

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Conference papers on the topic "Periodontal disease Molecular aspects":

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De Luca, Amalia, Christina M. Warboys, Narges Amini, Pedro Ferreira, Peter Gatehouse, David Firmin, Justin Mason, Spencer Sherwin, and Paul C. Evans. "Image-Based Computational Hemodynamics and Microarray Analysis of the Porcine Aortic Arch Reveals a Correlation Between Shear Stress and Endothelial Cell Apoptosis." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80948.

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Abstract:
Atherosclerosis is a focal disease that occurs predominantly at regions of the arterial tree that are exposed to disturbed blood flow, which generates low, oscillatory wall shear stress (WSS) at the lumen. WSS controls the spatial distribution of lesions by influencing numerous aspects of endothelial cell (EC) physiology, including inflammatory activation and viability. Of particular note, ECs in low shear, lesion-prone regions are characterized by increased apoptosis and turnover rates1 thus providing a potential explanation for the distinct spatial localization of lesion formation. Although the molecular mechanisms underlying the effects of WSS on EC physiology are poorly understood, they are known to involve transcriptional changes.
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Hill, F. G. H., C. W. Williams, S. M. Enayat, and P. J. Darbyshire. "ASYMPTOMATIC vWD VARIANT WITH ABSENT RISTOCETIN ACTIVITY BUT PRESERVED BOTROCETIN ACTIVITY AND A DAUGHTER WITH TYPE III (HOMOZYGOUS) vWD." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644109.

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Abstract:
The propositus, female aged 1 year, was investigated because of severe bruising. Bleeding time (BT) was in excess of 20 mins, VIIIC <0.01 u/ml and vWF Ag and ristocetin cofactor absent. Family studies showed:-Multimeric analysis was not possible on the propositus, but was normal in the plasma of all other family members. The father of the propositus, however, had an abnormal multimer pattern on lysed platelets, in that the faint low molecular weight doublet is absent and a dense band in the position of the lower band of the doublet with anodal and cathodal trailing.The maternal grandmother and mother appear to have asynpto-matic type I vWD and the father possibly has asymptomatic type I together with an alteration in the biologically vWF site with loss of the ristocetin site. This abnormality is not seen in his parents and his daughter possibly has type III vWD. The propositus' father although having some similarities to the patient of Howard et al., is different in other aspects.1. Howard MA, Salem HH. et al. (1982) Variant von Willebrand's disease Type B - Revisited. Blood, 60: 1420-1428.

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