Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D03301 (PDL)
658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This article described research aimed at testing the hypothesis that tissue remodeling during orthodontic tooth movement is modulated, at least in part, by factors derived from the nervous and vascular (immune) systems. Specifically, the neurotransmitters SP and VIP and the cytokines IL-1 alpha and IL-1 beta were localized immunohistochemically in paradental tissues of cat canines that had been treated by the application of an 80 g tipping force for 1 hour to 14 days. Increased staining (concentrations) of these agents were found in areas of PDL tension and compression at different time periods. Moreover, administration of SP and IL-1 beta to human PDL fibroblasts in vitro for 1 to 60 minutes resulted in significant increases in the levels of the intracellular "second messenger" cAMP, as well as of PGE2, a plasma membrane-associated fatty acid believed to serve as a local regulator of bone cell activity. Taken together, these results tend to support the hypothesis that neurotransmitters and cytokines play a regulatory role in orthodontic force-induced alveolar bone remodeling. Consequently, determination of the cytokine synthetic activity by leukocytes of orthodontic patients may inform about their alveolar bone remodeling potential.
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PMID:Neurotransmitters, cytokines, and the control of alveolar bone remodeling in orthodontics. 290 Jan 59

The recognition that periodontal regeneration can be achieved has resulted in increased efforts focused on understanding the mechanisms and factors required for restoring periodontal tissues so that clinical outcomes of such therapies are more predictable than those currently being used. In vitro models provide an excellent procedure for providing clues as to the mechanisms that may be required for regeneration of tissues. The investigations here were targeted at determining the ability of enamel matrix derivative (EMD) to influence specific properties of periodontal ligament cells in vitro. Properties of cells examined included migration, attachment, proliferation, biosynthetic activity and mineral nodule formation. Immunoassays were done to determine whether or not EMD retained known polypeptide factors. Results demonstrated that EMD under in vitro conditions formed protein aggregates, thereby providing a unique environment for cell-matrix interaction. Under these conditions, EMD: (a) enhanced proliferation of PDL cells, but not of epithelial cells; (b) increased total protein production by PDL cells; (c) promoted mineral nodule formation of PDL cells, as assayed by von Kossa staining; (d) had no significant effect on migration or attachment and spreading of cells within the limits of the assay systems used here. Next, EMD was screened for possible presence of specific molecules including: GM-CSF, calbindin D, EGF, fibronectin, bFGF, gamma-interferon, IL-1 beta, 2, 3, 6; IGF-1,2; NGF, PDGF, TNF, TGF beta. With immunoassays used, none of these molecules were identified in EMD. These in vitro studies support the concept that EMD can act as a positive matrix for cells at a regenerative site.
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PMID:In vitro studies on periodontal ligament cells and enamel matrix derivative. 931 Aug 73

External apical root resorption (EARR) is a common sequela of orthodontic treatment, although it may also occur in the absence of orthodontic treatment. The degree and severity of EARR associated with orthodontic treatment are multifactorial, involving host and environmental factors. Genetic factors account for at least 50% of the variation in EARR. Variation in the Interleukin 1 beta gene in orthodontically treated individuals accounts for 15% of the variation in EARR. Historical and contemporary evidence implicates injury to the periodontal ligament and supporting structures at the site of root compression following the application of orthodontic force as the earliest event leading to EARR. Decreased IL-1beta production in the case of IL-1B (+3953) allele 1 may result in relatively less catabolic bone modeling (resorption) at the cortical bone interface with the PDL, which may result in prolonged stress concentrated in the root of the tooth, triggering a cascade of fatigue-related events leading to root resorption. One mechanism of action for EARR may be mediated through impairment of alveolar resorption, resulting in prolonged stress and strain of the adjacent tooth root due to dynamic functional loads. Future estimation of susceptibility to EARR will likely require the analysis of a suite of genes, root morphology, skeleto-dental values, and the treatment method to be used-or essentially the amount of tooth movement planned for treatment.
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PMID:GENETIC FACTORS IN EXTERNAL APICAL ROOT RESORPTION AND ORTHODONTIC TREATMENT. 1505 46

There is growing evidence that apoptosis involves the nuclear transcription factor NF-kappaB in conjunction with related genes. However, in the context of mechanical orthodontic forces, force-sensing target genes assigned to pathways of NF-kappaB and apoptosis have not been fully characterised. To contribute to the identification of putative target genes, we used cDNA arrays specific for NF-kappaB and apoptotic pathways and analysed elevated gene expression in primary human periodontal ligament fibroblasts (PDL-F) after a 6 h application of mechanical force. Among several identified genes (including several caspases), interleukin-1 beta (IL-1 beta) and NF-kappaB displayed significantly higher expression on the NF-kappaB array, whereas higher expression was obtained for BCL2-antagonist of cell death (BAD), member 6 of the TNF-receptor superfamily (FAS) and CASP2 and RIPK1 domain-containing adaptor with death domain (CRADD) on the apoptosis array. Based on a defined cut-off level of a more than 1.5-fold higher expression, this significance in elevated gene expression was corroborated by reverse transcription/polymerase chain reaction (RT-PCR). Here, semi-quantitative (sq) PCR revealed a more pronounced elevation of mRNA gene expression in PDL-F after 6 h of stretch, when compared with 12 h. Moreover, the elevation after 6 h as observed by sq-PCR was convergent with quantitative PCR (q-PCR). q-PCR yielded levels of 5.8-fold higher relative gene expression for IL-1 beta and 1.7-fold for NF-kappaB, whereas that computed for BAD indicated a 5.2-fold, for CRADD a 2.1-fold and for FAS a 2.0-fold higher expression. The data obtained from the expression analysis thus indicate a stretch-induced transcriptional elevation of genes assigned to the NF-kappaB and apoptotic pathways. This elevation may render them target candidates for being addressed by mechanical orthodontic forces.
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PMID:Elevated expression of genes assigned to NF-kappaB and apoptotic pathways in human periodontal ligament fibroblasts following mechanical stretch. 1734 Jan 52