scholarly journals Role of Calprotectin as a Biomarker in Periodontal Disease

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Lili Wei ◽  
Mingwen Liu ◽  
Haofei Xiong

Periodontal disease (PD) is a common infectious and inflammatory disease characterised by inflammation of tissues surrounding and supporting the teeth and destruction of the associated alveolar bone, eventually resulting in tooth loss. This disease is caused by periodontopathic bacteria in plaque biofilm and resultant innate and adaptive immune responses in periodontal tissues. Calprotectin (CLP) is a calcium-binding protein of the S-100 protein family and is found to be induced by activated granulocytes, monocytes, and epithelial cells. CLP has been shown to play an important role in numerous inflammatory diseases and disorders. Increasing evidence indicates that CLP is involved in the progression of PD, and its levels may be associated with disease severity and outcome of periodontal treatments. This review will summarise recent studies regarding the presence, regulation, and function of CLP in PD. The findings indicate that CLP may be an effective biomarker for diagnosis and treatment for the PD.

2021 ◽  
Vol 22 (9) ◽  
pp. 4636
Author(s):  
Kexin Jiao ◽  
Laurence J. Walsh ◽  
Sašo Ivanovski ◽  
Pingping Han

Periodontitis is a chronic complex inflammatory disease associated with a destructive host immune response to microbial dysbiosis, leading to irreversible loss of tooth-supporting tissues. Regeneration of functional periodontal soft (periodontal ligament and gingiva) and hard tissue components (cementum and alveolar bone) to replace lost tissues is the ultimate goal of periodontal treatment, but clinically predictable treatments are lacking. Similarly, the identification of biomarkers that can be used to accurately diagnose periodontitis activity is lacking. A relatively novel category of molecules found in oral tissue, circular RNAs (circRNAs) are single-stranded endogenous, long, non-coding RNA molecules, with covalently circular-closed structures without a 5’ cap and a 3’ tail via non-classic backsplicing. Emerging research indicates that circRNAs are tissue and disease-specific expressed and have crucial regulatory functions in various diseases. CircRNAs can function as microRNA or RNA binding sites or can regulate mRNA. In this review, we explore the biogenesis and function of circRNAs in the context of the emerging role of circRNAs in periodontitis pathogenesis and the differentiation of periodontal cells. CircMAP3K11, circCDK8, circCDR1as, circ_0062491, and circ_0095812 are associated with pathological periodontitis tissues. Furthermore, circRNAs are expressed in periodontal cells in a cell-specific manner. They can function as microRNA sponges and can form circRNA–miRNA–mRNA networks during osteogenic differentiation for periodontal-tissue (or dental pulp)-derived progenitor cells.


2020 ◽  
Vol 73 (8) ◽  
pp. 1761-1764
Author(s):  
Maria O. Stetsyk ◽  
Andriy O. Stetsyk ◽  
Natalia I. Zhero ◽  
Eugene Y. Kostenko ◽  
Svetlana B. Kostenko ◽  
...  

The aim: To investigate current trends in the study of oral biofilm and its control. Materials and methods: A research of 32 literature sources has been made and it has been taken into account that some terminological differences in determining objects of study. Conclusions: Detailed analysis of modern domestic and foreign literature argues the necessity of further in-depth study of oral biofilms. Understanding the ethiological factors and mechanisms of the pathogenesis periodontal tissues inflammatory diseases gives the opportunity to treat targetly by destroying complicated sections of the vital activities and oral biofilm microorganisms relationships.


Author(s):  
G. A. Loban ◽  
T. O. Petrushanko ◽  
V. V. Chereda ◽  
M. O. Faustova ◽  
M. M. Ananieva ◽  
...  

Background. Periodontal tissues inflammatory diseases are widespread among young people. Objective. This study was aimed at elaborating the method to assess risks of periodontal inflammatory diseases and determining its efficacy depending on the state of dental tissues, gum tissues and sex.          Methods. The study included 182 students (93 men, 89 women) aged 19-29: 22 individuals had no lesions of hard dental tissues and no signs of periodontal disease; 51 individuals were found to have DMF index <6; 52 individuals – DMF index ≥6; 57 individuals were diagnosed with chronic catarrhal gingivitis. Primary groups were formed in autumn; re-examination was carried in spring. The research participants were assessed for detection of risks of periodontal inflammatory disease by the method developes by the authors (Patent UA 54041). Results. The study revealed that the risk of development of preiodontitis increases in individuals with high caries and gingivitis intensity. In spring, more individuals suffer from microbial imbalance in in the composition of gingival sulcus fluid and decrease in the mean stability coefficient value that indicates an increased risk of inflammatory periodontal disease development. Women were less likely to experience seasonal dysbiotic changes in the gingival sulcus fluid composition compared with men. Conclusions. The method suggested for assessment of the risk of periodontal inflammatory diseases is of high informativeness. It allows clinicians detecting early pre-nosological signs of oral microbiocenosis imbalance that enhances the effectiveness of early diagnosis of inflammatory periodontal diseases.


Cells ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 537 ◽  
Author(s):  
Jin Liu ◽  
Jianping Ruan ◽  
Michael D. Weir ◽  
Ke Ren ◽  
Abraham Schneider ◽  
...  

Periodontitis is a prevalent infectious disease worldwide, causing the damage of periodontal support tissues, which can eventually lead to tooth loss. The goal of periodontal treatment is to control the infections and reconstruct the structure and function of periodontal tissues including cementum, periodontal ligament (PDL) fibers, and bone. The regeneration of these three types of tissues, including the re-formation of the oriented PDL fibers to be attached firmly to the new cementum and alveolar bone, remains a major challenge. This article represents the first systematic review on the cutting-edge researches on the regeneration of all three types of periodontal tissues and the simultaneous regeneration of the entire bone-PDL-cementum complex, via stem cells, bio-printing, gene therapy, and layered bio-mimetic technologies. This article primarily includes bone regeneration; PDL regeneration; cementum regeneration; endogenous cell-homing and host-mobilized stem cells; 3D bio-printing and generation of the oriented PDL fibers; gene therapy-based approaches for periodontal regeneration; regenerating the bone-PDL-cementum complex via layered materials and cells. These novel developments in stem cell technology and bioactive and bio-mimetic scaffolds are highly promising to substantially enhance the periodontal regeneration including both hard and soft tissues, with applicability to other therapies in the oral and maxillofacial region.


2018 ◽  
pp. 54-59
Author(s):  
N.N. Saveleva ◽  
I.I. Sokolova ◽  
S.I. German ◽  
T.V. Tomilina

The review of the scientific literature is devoted to the topical issues of studying the etiology of periodontal diseases, which are one of the most common and complex pathologies of the maxillofacial region. Analysis of recent studies proves a stable relationship between the development of periodontal diseases and disorders in the immune system, the neurohumoral system, metabolic disorders, genetic predisposition, and so on. The article presents the data obtained in the course of studying the literature on the role of disorders in the functioning of individual organs (gastrointestinal tract, liver, lungs, heart, and urinary system) in the development of chronic periodontal diseases. The article notes that the anatomical and physiological proximity of the periodontal and digestive tract tissues, the generality of innervation and humoral regulation create prerequisites for the involvement of periodontal disease in the pathological process in diseases of the gastrointestinal tract. One of the main etiological factors in the development of inflammatory diseases of the gastrointestinal tract and periodontium is Helicobacter pylori, which is found in the loci of the oral cavity: in the oral and gingival fluid, on the mucous membrane of the tongue and cheeks, and in the periodontal pockets. It is pointed out that the liver also occupies a special place in the development of periodontal diseases, which is explained by the performance of its significant functions for the human body: regulatory, metabolic, antitoxic and other. There is evidence that the pathology of periodontal disease plays a leading role in the structure of dental diseases in patients with chronic obstructive pulmonary diseases, which is clinically manifested by symptoms of generalized periodontitis of the І-ІІ degrees of development and its complications - partial or complete secondary adentia, and with tooth preservation - defects in dental series and violations of occlusion, function, aesthetics. Scientists suggest a general biological mechanism for the development of generalized periodontitis and cardiovascular diseases, linking the development of periodontal diseases in patients with cardiovascular pathology with microcirculatory disorders. The dependence of the severity of inflammatory changes in the periodontal tissues on the disturbances of salt metabolism in urolithiasis is proved. The data obtained indicate that diseases of the internal organs contribute to the structural damage of periodontal tissues and they are a risk factor for periodontal diseases, which necessitate the presence of not only theoretical knowledge and practical skills in dentistry, but also their awareness of the features and clinical manifestations of somatic pathology. An urgent and justified step in the treatment of periodontal diseases is also the involvement in the process of rendering complex dental care to internist doctors capable of quickly and qualitatively assessment the condition of the internal organs and the basic systems of the patient's body.


2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Nicole Rusca ◽  
Silvia Monticelli

MicroRNAs (miRNAs) are regulatory molecules able to influence all aspects of the biology of a cell. They have been associated with diseases such as cancer, viral infections, and autoimmune diseases, and in recent years, they also emerged as important regulators of immune responses. MiR-146a in particular is rapidly gaining importance as a modulator of differentiation and function of cells of the innate as well as adaptive immunity. Given its importance in regulating key cellular functions, it is not surprising that miR-146a expression was also found dysregulated in different types of tumors. In this paper, we summarize recent progress in understanding the role of miR-146a in innate and adaptive immune responses, as well as in disease.


2021 ◽  
Vol 17 (8) ◽  
pp. e1009905
Author(s):  
Carlos Henrique D. Barbosa ◽  
Louis Lantier ◽  
Joseph Reynolds ◽  
Jinyong Wang ◽  
Fabio Re

B1 cells, a subset of B lymphocytes whose developmental origin, phenotype, and function differ from that of conventional B2 cells, are the main source of “natural” IgM but can also respond to infection by rapidly producing pathogen-specific IgM directed against T-independent antigens. Francisella tularensis (Ft) is a Gram-negative bacterium that causes tularemia. Infection with Ft Live Vaccine Strain activates B1 cells for production of IgM directed against the bacterial LPS in a process incompletely understood. Here we show that immunization with purified Ft LPS elicits production of LPS-specific IgM and IgG3 by B1 cells independently of TLR2 or MyD88. Immunization, but not infection, generated peritoneum-resident memory B1 cells that differentiated into LPS-specific antibody secreting cells (ASC) upon secondary challenge. IL-5 was rapidly induced by immunization with Ft LPS and was required for production of LPS-specific IgM. Antibody-mediated depletion of ILC2 indicated that these cells were the source of IL-5 and were required for IgM production. IL-25, an alarmin that strongly activates ILC2, was rapidly secreted in response to immunization or infection and its administration to mice significantly increased IgM production and B1 cell differentiation to ASC. Conversely, mice lacking IL-17RB, the IL-25 receptor, showed impaired IL-5 induction, IgM production, and B1 ASC differentiation in response to immunization. Administration of IL-5 to Il17rb-/- mice rescued these B1 cells-mediated responses. Il17rb-/- mice were more susceptible to infection with Ft LVS and failed to develop immunity upon secondary challenge suggesting that LPS-specific IgM is one of the protective adaptive immune mechanisms against tularemia. Our results indicated that immunization with Ft LPS triggers production of IL-25 that, through stimulation of IL-5 release by ILC2, promotes B1 cells activation and differentiation into IgM secreting cells. By revealing the existence of an IL-25-ILC2-IL-5 axis our results suggest novel strategies to improve vaccination against T-independent bacterial antigens.


2020 ◽  
Vol 319 (1) ◽  
pp. L163-L172
Author(s):  
Bingqing Shi ◽  
Yuqiu Hao ◽  
Wei Li ◽  
Hongna Dong ◽  
Mengting Xu ◽  
...  

Unlike other members of the tumor necrosis factor (TNF)-α-induced protein 8 (TNFAIP8/TIPE) family that play a carcinogenic role and regulate apoptosis, TNFAIP8-like 2 (TIPE2) can not only maintain immune homeostasis but also regulate inflammation. TIPE2 mainly restrains the activation of T cell receptor (TCR) and Toll-like receptors (TLR), regulating its downstream signaling pathways, thereby regulating inflammation. Interestingly, TIPE2 is abnormally expressed in many inflammatory diseases and may promote or inhibit inflammation in different diseases. This review summarizes the molecular target and cellular function of TIPE2 in immune cells and inflammatory diseases and the underlying mechanism by which TIPE2 regulates inflammation. The function and mechanism of TIPE2 in asthma is also explained in detail. TIPE2 is abnormally expressed in asthma and participates in the pathogenesis of different phenotypes of asthma through regulating multiple inflammatory cells’ activity and function. Considering the indispensable role of TIPE2 in asthma, TIPE2 may be an effective therapeutic target in asthma. However, the available data are insufficient to provide a full understanding of the complex role of TIPE2 in human asthma. Further study is still necessary to explore the possible mechanism and functions of TIPE2 in different asthma phenotypes.


2018 ◽  
Vol 86 (7) ◽  
Author(s):  
Ingar Olsen ◽  
Frank C. Nichols

ABSTRACTThe keystone periodontal pathogenPorphyromonas gingivalisproduces phosphorylated dihydroceramide lipids (sphingolipids) such as phosphoethanolamine dihydroceramide (PE DHC) and phosphoglycerol dihydroceramide (PG DHC) lipids. Phosphorylated DHCs (PDHCs) fromP. gingivaliscan affect a number of mammalian cellular functions, such as potentiation of prostaglandin secretion from gingival fibroblasts, promotion of RANKL-induced osteoclastogenesis, promotion of apoptosis, and enhancement of autoimmunity. InP. gingivalis, these lipids affect anchoring of surface polysaccharides, resistance to oxidative stress, and presentation of surface polysaccharides (anionic polysaccharides and K-antigen capsule). In addition to phosphorylated dihydroceramide lipids, serine dipeptide lipids ofP. gingivalisare implicated in alveolar bone loss in chronic periodontitis through interference with osteoblast differentiation and function and promotion of osteoclast activity. As a prerequisite for designation as bacterial virulence factors, bacterial sphingolipids and serine dipeptide lipids are recovered in gingival/periodontal tissues, tooth calculus, human blood, vascular tissues, and brain. In addition toP. gingivalis, other bacteria of the generaBacteroides,Parabacteroides,Porphyromonas,Tannerella, andPrevotellaproduce sphingolipids and serine dipeptide lipids. The contribution of PDHCs and serine dipeptide lipids to the pathogenesis of periodontal and extraoral diseases may be an underappreciated area in microbe-host interaction and should be more intensively investigated.


2016 ◽  
Vol 397 (12) ◽  
pp. 1315-1333 ◽  
Author(s):  
Isabel Meininger ◽  
Daniel Krappmann

Abstract The CARMA1-BCL10-MALT1 (CBM) signalosome triggers canonical NF-κB signaling and lymphocyte activation upon antigen-receptor stimulation. Genetic studies in mice and the analysis of human immune pathologies unveiled a critical role of the CBM complex in adaptive immune responses. Great progress has been made in elucidating the fundamental mechanisms that dictate CBM assembly and disassembly. By bridging proximal antigen-receptor signaling to downstream signaling pathways, the CBM complex exerts a crucial scaffolding function. Moreover, the MALT1 subunit confers a unique proteolytic activity that is key for lymphocyte activation. Deregulated ‘chronic’ CBM signaling drives constitutive NF-κB signaling and MALT1 activation, which contribute to the development of autoimmune and inflammatory diseases as well as lymphomagenesis. Thus, the processes that govern CBM activation and function are promising targets for the treatment of immune disorders. Here, we summarize the current knowledge on the functions and mechanisms of CBM signaling in lymphocytes and how CBM deregulations contribute to aberrant signaling in malignant lymphomas.


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