Expression of Toll‑like receptor 4 on mast cells in gingival tissues of human chronic periodontitis

Huang, Bo; Dai, Qian; Huang, Shiguang

doi:10.3892/mmr.2018.8648

Cited by 10 publications

(8 citation statements)

References 21 publications

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“…Previous analysis of gene expression profiles in tissue samples of achalasia demonstrated that toll‐like receptor 4 and interleukin (IL)‐18 are key players involved in neuronal/muscular and neuronal/immunity processes . Both proteins are significantly associated with mast cells in immunity diseases, further supporting our present findings . Owing to emerging evidence of autoimmunity and inflammation in the pathophysiology of achalasia, we speculated that mast cells play a crucial role in the development of achalasia.…”

Section: Discussionsupporting

confidence: 89%

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Mast cell infiltration associated with loss of interstitial cells of Cajal and neuronal degeneration in achalasia

Liu

Chen

Wang

et al. 2019

Neurogastroenterology Motil

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Background Achalasia is a motility disorder of unknown etiology. Previous studies supported the hypothesis that autoimmune‐mediated inflammatory responses produce inhibitory neuronal degeneration. This study was designed to explore the role of mast cells in achalasia. Methods We collected information from 116 patients with achalasia who underwent peroral endoscopic myotomy between December 2016 and May 2017. Lower esophageal sphincter (LES) muscle biopsy was performed in all patients with achalasia, as well as 20 control subjects. The number of mast cells, interstitial cells of Cajal (ICCs), nNOS‐positive cells, and S‐100‐positive cells in the LES were evaluated by immunohistochemistry. Pathological and clinical data were compared between groups. Key Results Compared with controls, the LES of patients with achalasia had significantly fewer ICCs, nNOS‐positive cells, and S‐100‐positive cells and a higher number of mast cells (all P < 0.001). Furthermore, the increased mast cell infiltration was significantly associated with decreased ICCs, nNOS‐positive cells, and S‐100‐positive cells in patients with achalasia (all P < 0.05). Clinically, the number of strongly positive mast cells was highest in patients with type I achalasia and lowest in those with type III achalasia (P < 0.001). In addition, patients with a history of autoimmune disease or viral infection had greater mast cell infiltration in the LES muscle (P = 0.040). Conclusions & Inferences In patients with achalasia, mast cell infiltration in the LES muscle is increased, in association with loss of ICCs and neuronal degeneration. Mast cells may thereby play a crucial role in the development of achalasia.

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Section: Discussionsupporting

confidence: 89%

“…35 Both proteins are significantly associated with mast cells in immunity diseases, further supporting our present findings. [36][37][38] Owing to emerging evidence of autoimmunity and inflammation in the pathophysiology of achalasia, we speculated that mast cells play a crucial role in the development of achalasia.…”

Section: Discussionmentioning

confidence: 99%

Mast cell infiltration associated with loss of interstitial cells of Cajal and neuronal degeneration in achalasia

Liu

Chen

Wang

et al. 2019

Neurogastroenterology Motil

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“…In contrast, Gemmell et al reported that tryptase + mast cells were deceased in clinical periodontal lesions, suggesting there is not an increase in mast cell migration into diseased tissue 214 . More recently, Huang et al reported higher toll‐like receptor‐4 expression on mast cells within gingival tissues of chronic periodontitis patients, suggesting that mast cell toll‐like receptor‐4 expression may mediate the disease process 323 . Interleukin‐31 324 and interleukin‐33 325 have been investigated in relation to the role of mast cells in experimental periodontal disease models.…”

Section: Osteoimmunology: Interaction Of Immune Cells: Bone Cellsmentioning

confidence: 97%

“…214 More recently, Huang et al reported higher toll-like receptor-4 expression on mast cells within gingival tissues of chronic periodontitis patients, suggesting that mast cell tolllike receptor-4 expression may mediate the disease process. 323 Interleukin-31 324 and interleukin-33 325 have been investigated in relation to the role of mast cells in experimental periodontal disease models. Tada et al reported that P. gingivalis induces the production of interleukin-31 by human mast cells, which downregulated tight junction molecules to promote gingival epithelial barrier permeability.…”

Section: Mast Cellsmentioning

confidence: 99%

Maintaining homeostatic control of periodontal bone tissue

Hathaway‐Schrader

Novince

2021

Periodontology 2000

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Alveolar bone is a unique osseous tissue due to the integration of the teeth and the proximity of dental plaque biofilms. Periodontal health and homeostasis are mediated by a balanced host immune response to polymicrobial oral biofilms. Shifts in the composition and quantity of microbes within dental plaque biofilms can drive a local proinflammatory immune response state in the epithelial and gingival barrier connective tissues. Infiltrating proinflammatory immune cells within the inflamed connective tissue secrete local factors that induce paracrine signaling to subjacent bone cells.Sustained chronic inflammation disrupts "coupled" osteoclast-osteoblast actions, which ultimately result in alveolar bone destruction. This chapter will provide an overview of alveolar bone physiology and will highlight why the oral microbiota is a critical regulator of alveolar bone remodeling. The ecology of subgingival plaque biofilms will be reviewed considering our understanding that periodontitis is a polymicrobial disruption of host homeostasis. The pathogenesis of periodontal bone loss will be explained from both a historical and current perspective, providing the opportunity to revisit the role of fibrosis in alveolar bone destruction. The molecular basis of host-microbe interactions will be discussed in the context of the commensal oral flora in periodontal health and pathogenic shifts in the oral microbiota during periodontal disease states. The role of periodontal innate and adaptive immune cell interactions with bone cells will be reviewed based on our current understanding of osteoimmunological mechanisms influencing alveolar bone remodeling. Lastly, probiotic/prebiotic therapeutic interventions in the oral microbiota will be evaluated as a potential therapy to support alveolar bone homeostasis/ prevent periodontal bone loss.

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“…102 A previous study has indicated an increased expression level of TLR4 on mast cells in periodontal tissues of patients with chronic periodontitis. 103 In OSCC, mast cell density increases and is correlated with poor prognosis. 104 In the healthy periodontium, keratinocytes protect the oral and sulcular epithelium by producing hBDs.…”

Section: The Role Of Inflammatory Cells In Periodontitis and Cancer Developmentmentioning

confidence: 99%

Periodontitis and oral cancer - current concepts of the etiopathogenesis

Irani¹,

Barati²,

Badiei³

2020

Oncol Rev

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Gingival tissues are attacked by oral pathogens which can induce inflammatory reactions. The immune-inflammatory responses play essential roles in the patient susceptibility to periodontal diseases. There is a wealth of evidence indicating a link between chronic inflammation and risk of malignant transformation of the affected oral epithelium. Periodontitis is associated with an increased risk of developing chronic systemic conditions including autoimmune diseases and different types of cancers. Besides, some risk factors such as smoking , alcohol consumption and human papilloma virus have been found to be associated with both periodontitis and oral cancer. This review article aimed to study the current concepts in pathogenesis of chronic periodontitis and oral cancer by reviewing the related articles.

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Expression of Toll‑like receptor 4 on mast cells in gingival tissues of human chronic periodontitis

Cited by 10 publications

References 21 publications

Mast cell infiltration associated with loss of interstitial cells of Cajal and neuronal degeneration in achalasia

Mast cell infiltration associated with loss of interstitial cells of Cajal and neuronal degeneration in achalasia

Maintaining homeostatic control of periodontal bone tissue

Periodontitis and oral cancer - current concepts of the etiopathogenesis

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