2018
DOI: 10.1080/08869634.2018.1446770
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Immunohistochemical expression of TLR-4 in temporomandibular joint dysfunction

Abstract: Objective Toll-like receptor 4 (TLR-4) is a transmembrane protein involved in the innate immune system and has been implicated in the pathogenesis of temporomandibular joint dysfunction (TMD). The purpose of this study was to histologically examine the level of expression of TLR-4 relative to severity of TMD. Methods Thirty-one human TMJ disc samples were immunostained for TLR-4 and evaluated for intensity of stain. Among the samples, 8 were control samples, 16 were from patients with anterior disc displacemen… Show more

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Cited by 6 publications
(4 citation statements)
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“…18 Several studies mentioned that NFκB is the main inflammatory mediator in rheumatoid arthritis and cancer, cervical cancer, nasopharyngeal carcinoma, periapical lesions and TMJ osteoarthritis. [19][20][21][22][23] Activation of NFκB in the synovial layer also occurred among mice that had synovitis caused by a mechanical stress response due to excessive pressure. 24 NFκB expression was shown to be higher on the 7 th and 14 th days and was at its highest on the 21 st day.…”
Section: Discussionmentioning
confidence: 99%
“…18 Several studies mentioned that NFκB is the main inflammatory mediator in rheumatoid arthritis and cancer, cervical cancer, nasopharyngeal carcinoma, periapical lesions and TMJ osteoarthritis. [19][20][21][22][23] Activation of NFκB in the synovial layer also occurred among mice that had synovitis caused by a mechanical stress response due to excessive pressure. 24 NFκB expression was shown to be higher on the 7 th and 14 th days and was at its highest on the 21 st day.…”
Section: Discussionmentioning
confidence: 99%
“…TLR-4 is known to participate in carcinogenesis, inflammation, and increased levels of TLR-4, TLR-5 and IRF4 were proposed as diagnostic markers of knee osteoarthritis [25] and joint dysfunction [26]. In keratinocytes and epithelium, as well as in other connective tissue cells, in places of chronic and acute inflammation, under the influence of NFkB, the synthesis of HIF1 and VEGF/VEGFR pathway can be activated via the TLR-5-NOX4-ROS signaling pathway [20] [21] The decrease in the level of monocytes in the experimental group may be caused by non-specific reasons, such as an infectious or inflammatory process, autoimmune pathology, prolonged hypoxia.…”
Section: Discussionmentioning
confidence: 99%
“…FGFs are known to be involved in the regulation of proliferation and differentiation of osteoblasts and fibroblasts, in the processes of angiogenesis and tissue regeneration, they activate osteoblast differentiation and inhibit osteoclast differentiation. Individual FGF fractions positively regulate bone growth and density [25] [26]. An increased level of FGF stimulates angiogenesis in the cartilage tissue, so this is one of the possible causes of the formation of defective cartilage.…”
Section: Discussionmentioning
confidence: 99%
“…It can participate in the development of multiple diseases by specifically activating autoimmune responses. [14] Located at 9q32-33, TLR-4 consists of 879 amino acids, and the extracellular domain is made up of the sequence rich in leucines. [15] TLR-4 shares a high homology with IL-1β in the inflammatory reaction.…”
Section: Discussionmentioning
confidence: 99%