Role of polymorphism of the interleukin-1B gene and other genetic polymorphisms in the aetiology of root resorption in patients receiving orthodontic treatment

2017 ◽  
Vol 13 (1) ◽  
pp. 36-42
Author(s):  
Marzena Makowska-Kaczmarska ◽  
Anna Okoń ◽  
Elżbieta Olszewska

Aim. The aim of the work was to present the latest directions in the research on gene polymorphisms in the global population and to discuss their potential role in the pathogenesis of root resorption during orthodontic treatment. Material and methods. A review of the literature in Polish and English from the years 1990–2015 was conducted using PubMed/MEDLINE databases and the results of studies kept in the database of the National Centre for Biotechnology Information were used. Key words used: genetics of root resorption, genetic polymorphism, interleukin-1B. Results. 19 articles were analysed. Special attention was placed on the latest studies on the human genome, especially focused on gene polymorphisms in the global population. Summary. Pathogenesis of root resorption during orthodontic treatment is complex. Its background is undoubtedly genetic. Gene polymorphism is important. The role of polymorphism of the interleukin-1B gene and other genes in the interleukin-1 cluster draws special attention. Identification of genetic factors that play an important role in the aetiology of root resorption may in the future help to identify patients susceptible to such complications even before the beginning of orthodontic treatment. Potential possibilities of DNA testing in clinical practice are enormous. The role of individual gene polymorphisms in the pathogenesis of root resorption has not been yet explained in detail and further multicentre studies are necessary. At this stage of studies no reliable markers have been detected in order to predict which patients would develop this complication. (Makowska- Kaczmarska M, Okoń A, Olszewska E. Role of polymorphism of the interleukin-1B gene and other genetic polymorphisms in the aetiology of root resorption in patients receiving orthodontic treatment. Orthod Forum 2017; 13: 36-42).

Placenta ◽  
1996 ◽  
Vol 17 (5-6) ◽  
pp. A48
Author(s):  
L. Paulesu ◽  
R. Romagnoli ◽  
G. Ghiarar

2021 ◽  
Vol 22 (5) ◽  
pp. 2388
Author(s):  
Masaru Yamaguchi ◽  
Shinichi Fukasawa

The aim of this paper is to provide a review on the role of inflammation in orthodontically induced inflammatory root resorption (OIIRR) and accelerating orthodontic tooth movement (AOTM) in orthodontic treatment. Orthodontic tooth movement (OTM) is stimulated by remodeling of the periodontal ligament (PDL) and alveolar bone. These remodeling activities and tooth displacement are involved in the occurrence of an inflammatory process in the periodontium, in response to orthodontic forces. Inflammatory mediators such as prostaglandins (PGs), interleukins (Ils; IL-1, -6, -17), the tumor necrosis factor (TNF)-α superfamily, and receptor activator of nuclear factor (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) are increased in the PDL during OTM. OIIRR is one of the accidental symptoms, and inflammatory mediators have been detected in resorbed roots, PDL, and alveolar bone exposed to heavy orthodontic force. Therefore, these inflammatory mediators are involved with the occurrence of OIIRR during orthodontic tooth movement. On the contrary, regional accelerating phenomenon (RAP) occurs after fractures and surgery such as osteotomies or bone grafting, and bone healing is accelerated by increasing osteoclasts and osteoblasts. Recently, tooth movement after surgical procedures such as corticotomy, corticision, piezocision, and micro-osteoperforation might be accelerated by RAP, which increases the bone metabolism. Therefore, inflammation may be involved in accelerated OTM (AOTM). The knowledge of inflammation during orthodontic treatment could be used in preventing OIIRR and AOTM.


2003 ◽  
Vol 9 (6) ◽  
pp. 535-539 ◽  
Author(s):  
Tineke Hooper-van Veen ◽  
Hans M Schrijver ◽  
Antoon Zwiers ◽  
J Bart A Crusius ◽  
Dirk L Knol ◽  
...  

Multiple sclerosis (MS) is a chronic disease of presumed autoimmune origin with a considerable polygenic influence. We have previously observed that a specific allele combination in genes of the interleukin-1 (IL-1) family influenced the progression rate in MS. We have considerably expanded our patient population (492 MS patients and 228 controls). In the present study, we investigated the role of the IL- 1A - 889, IL-1B - 511, IL-1B+3953 and IL-1RN VNTR gene polymorphisms in MS. In addition, we performed preliminary analyses on longitudinal magnetic resonance imaging (MRI) data. We found no associations between the polymorphisms and susceptibility to MS or clinical features. In addition, we observed no significant effect of the polymorphisms on brain or lesion volumes, Based on our data and those from the literature, one can conclude that there is currently no evidence to support a role for the IL-1 genes in MS.


Cytokine ◽  
2008 ◽  
Vol 43 (2) ◽  
pp. 110-113 ◽  
Author(s):  
Maha Kammoun-Krichen ◽  
Noura Bougacha-Elleuch ◽  
Kaouthar Makni ◽  
Mouna Mnif ◽  
Joumaa Jouida ◽  
...  

2015 ◽  
Vol 25 (1) ◽  
pp. 81-85 ◽  
Author(s):  
Gulhan Akcil ◽  
Ibrahim Dogan ◽  
Mustafa Cengiz ◽  
Evren Doruk Engin ◽  
Mehmet Dogan ◽  
...  

2014 ◽  
Vol 41 (5) ◽  
pp. 945-954 ◽  
Author(s):  
Zvezdana Mladenovic ◽  
Anne-Sophie Saurel ◽  
Francis Berenbaum ◽  
Claire Jacques

Objective.To determine the effect of hyaluronic acid (HA) on proteolytic enzymes and bone remodeling mediators induced by interleukin 1β (IL-1β) and related to cartilage catabolism in murine osteoblasts.Methods.Osteoblasts were obtained from Swiss mice and cultured for 3 weeks. HA-treated osteoblasts were incubated with 100 μg/ml HA during the last week of culture, then stimulated with IL-1β (10 ng/ml) for 24 h. The expression of matrix metalloproteinases 3 and 13 (MMP-3 and MMP-13), ADAMTS-4 and ADAMTS-5, tissue inhibitor of metalloproteinases (TIMP), osteoprotegerin, and receptor activator of nuclear factor-κB ligand (RANKL) was determined by real-time polymerase chain reaction. MMP-3 and MMP-13 release was assessed by Western blot analysis.Results.IL-1β increased the mRNA levels of MMP-3 and MMP-13 and ADAMTS-4 and ADAMTS-5 and release of MMP-3 and MMP-13. Seven days of HA treatment significantly prevented the IL-1β-increased mRNA levels of MMP-3 (−61%, p < 0.01), MMP-13 (−56%, p < 0.01), ADAMTS-4 (−58%, p < 0.05), ADAMTS-5 (−52%, p < 0.01), and RANKL (−49%, p < 0.05), but not TIMP. As well, IL-1β-induced production of MMP-3 and MMP-13 was inhibited, by 27% (p < 0.01) and 40% (p < 0.01), respectively.Conclusion.In an inflammatory context in murine osteoblasts, HA can inhibit the expression of MMP and ADAMTS. Because HA can counteract the production of these mediators in chondrocytes, its beneficial effect in osteoarthritis may be due to its action on cartilage and subchondral bone.


2013 ◽  
Vol 148 (2-3) ◽  
pp. 316-322 ◽  
Author(s):  
Alex Hatzimanolis ◽  
Silia Vitoratou ◽  
Laura Mandelli ◽  
Chrysostomos Vaiopoulos ◽  
Finiki A. Nearchou ◽  
...  

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