Presence of natural killer cells in human chronic periapical lesions

Torabinejad, M.

doi:10.1111/j.1365-2591.1993.tb00767.x

Cited by 21 publications

(11 citation statements)

References 13 publications

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“…This number was larger in PGs (median 6.5) than RCs (median 2.5), but the difference was not statistically significant (p = 0.129). Kettering and Torabinejad 24 analyzed 10 periapical lesions and detected CD57 + NK cells by immunohistochemistry in all samples, but their numbers varied widely from one lesion to another. The authors concluded that the presence of these cells in chronic periapical lesions is related to a nonspecific reaction of the immune system to microorganisms present in the root canal system.…”

Section: Cd57mentioning

confidence: 99%

Analysis of CD57+ natural killer cells and CD8+ T lymphocytes in periapical granulomas and radicular cysts

et al. 2017

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The aim of this study was to compare the number of CD57 + natural killer (NK) cells and CD8 + T lymphocytes between periapical granulomas (PGs) and radicular cysts (RCs). Twenty-fives cases of PGs and 25 of RCs were submitted to histological analysis and immunohistochemistry using anti-CD57 and anti-CD8 biomarkers. Positive cells were counted in 10 fields (400× magnification) and the median value was calculated for each case. Statistical tests were used to evaluate differences in the number of CD57+ NK cells and CD8 + T lymphocytes according to type of lesion, intensity of the infiltrate and thickness of the lining epithelium. The number of CD57 + NK cells and CD8 + T lymphocytes was higher in PGs than in RCs (p = 0.129 and p = 0.541, respectively). Comparison of the number of CD57 + NK cells in atrophic and hyperplastic epithelium revealed a larger number of cells in the atrophic epithelium (p = 0.042). A larger number of CD57 + NK cells and CD8 + T lymphocytes were observed in grade III infiltrates compared to grade I/II (p = 0.145 and p = 0.725, respectively). CD8 + T lymphocytes were more prevalent than CD57 + NK cells in most cases when PGs and RCs were analyzed separately or in combination (p < 0.0001). CD57+ NK cells and CD8 + T lymphocytes play a key role in antiviral defense and the presence of these cells supports evidence suggesting the participation of these microorganisms in the pathogenesis of PGs and RCs. The response mediated by CD8 + T lymphocytes was more frequent, indicating greater participation of the adaptive immunity in these chronic lesions.

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Section: Cd57mentioning

confidence: 99%

Analysis of CD57+ natural killer cells and CD8+ T lymphocytes in periapical granulomas and radicular cysts

et al. 2017

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“…Natural killer cells represent a link between the nonspecific and antigen‐specific branches of the immune system. However, they were found to be present in periapical lesions in low percentages, except for one study that used the CD16 cellular differentiation antigen, which is identical with the type III receptor for the Fc portion of IgG (FcγRIII) also expressed on granulocytes and macrophages ( 64, 80, 126). It was found that certain T‐cell functions can be partially compensated for by natural killer cells in intracellular infections affecting severe combined immunodeficient mutant mice.…”

Section: T Lymphocytesmentioning

confidence: 99%

Protective and destructive immune reactions in apical periodontitis

Márton¹,

Kiss

2000

Oral Microbiology and Immunology

212

193

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Apical periodontitis is initiated primarily by the mixed microflora of infected root canals. Continuous flow of bacteria and their products through the apical foramen induces influx, activation and coordinated interaction of immune-inflammatory cells within the periapical area. Successful mobilization of host defense mechanisms prevents abundant extraradicular bacterial invasion. However, anti-infective effector mechanisms are not restricted to killing the invading microorganisms but also destroy normal tissue components and induce bone absorption, resulting ultimately in the loss of the affected teeth. Moreover, autocrine and paracrine loops of stimulation may lead to the perpetuation of the local inflammatory lesion and may also alter the function of remote tissues and organs. This review attempts to summarize current knowledge about the pathogenic mechanism of apical periodontitis, focusing on the formation of a special granulation tissue that effectively fights bacteria originated from the infected pulp chamber and, by exerting this protective function, also contributes to harmful local and distant events. The dynamic equilibrium between defensive and destructive mechanisms may provide a pathobiological basis for better understanding of clinical signs and symptoms of various forms of apical periodontitis lesions and influence treatment strategy and practice.

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“…Melo et al. (2004), Kettering & Torabinejad (1993) and Callestini (1996) suggested the participation of Langerhans cells, natural killer cells (NK cells) and macrophages in the cystic structure of apical lesion breakdown respectively.…”

Section: Discussionmentioning

confidence: 99%