Browsing by Subject "RANKL"
Now showing items 1-9 of 9
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(Blackwell Munksgaard, 2014)Aim: Destructive periodontitis is associated with a Th1–Th17 immune response and activation of RANKL-induced osteoclasts. In addition, Porphyromonas gingivalis K1 and K2 serotypes induce a strong Th1–Th17 response. This ...
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(Wiley-Blackwell, 2018)BACKGROUND: Aggregatibacter actinomycetemcomitans expresses several virulence factors that may contribute to the pathogenesis of periodontitis. Based on the antigenicity of the O-polysaccharide component of the ...
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(Springer, 2017)The aim of this study is to assess the levels and diagnostic accuracy of a set of bone resorption biomarkers, including TRAP-5, RANKL, and OPG in symptomatic and asymptomatic apical lesions and controls. Apical tissues ...
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(Wiley, 2020)Aim T lymphocytes play a central role during the pathogenesis of periodontitis, and the imbalance between the pathogenic T-helper type 17 (Th17) and protective T-regulatory (Treg) lymphocytes determines the tooth-supporting ...
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(2009)Aim: T regulatory (Treg) cells have been detected in periodontitis lesions, and forkhead box P3 (Foxp3) expression has been negatively correlated to receptor activator of nuclear factor-κ B ligand (RANKL). The aim of this ...
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(Wiley, 2020)Objective This study aimed to determine the expression of distinct matrix metalloproteinases, cytokines, and bone resorptive factors in temporomandibular joint osteoarthritis (TMJ-OA) patients and their association with ...
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(International Society on Aging and Disease, USA, 2021)Cellular senescence is a biological process triggered in response to time-accumulated DNA damage, which prioritizes cell survival over cell function. Particularly, senescent T lymphocytes can be generated prematurely during ...
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(Wiley, 2018-08)It is well accepted that the presence of cytokines belonging to the Th1/Th17/Th22 axis of immuno-inflammatory response in the joint environment, such as IL-1, IL-17 and IL-22, respectively, are associated with pathogenesis ...