ライフサイエンスコーパス: periodontal inflammation

1 iodontal probing depth (a measure of current periodontal inflammation).

2 involvement in myeloid cell functions during periodontal inflammation.

3 ident cells express BAFF and/or APRIL during periodontal inflammation.

4 -CarP levels, which strongly correlated with periodontal inflammation.

5 Intermittent fasting decreased systemic and periodontal inflammation.

6 valis exacerbates tissue hypoxia and worsens periodontal inflammation.

7 lammatory phenotype is crucial for resolving periodontal inflammation.

8 ivary IL-1B (p < 0.001)-a putative marker of periodontal inflammation.

9 s a cumulative outcome result of both MI and periodontal inflammation.

10 cation in governing macrophage responses and periodontal inflammation.

11 and their role has not been characterized in periodontal inflammation.

12 wnstream signaling molecule in the course of periodontal inflammation.

13 onfirming the biological relevance of A20 in periodontal inflammation.

14 pathways and may play a role in restraining periodontal inflammation.

15 naling molecules that trigger and perpetuate periodontal inflammation.

16 thogens in systemic diseases associated with periodontal inflammation.

17 e levels and attachment integrity to prevent periodontal inflammation.

18 efore, LPA may potentially modulate/regulate periodontal inflammation.

19 new potential therapeutic target to control periodontal inflammation.

20 ked by periodontitis-related bacteria and/or periodontal inflammation.

21 ges in the TLR4 expression in neurons during periodontal inflammation.

22 elements that initiate and propagate chronic periodontal inflammation.

23 ts of anti-inflammation and antioxidation on periodontal inflammation.

24 possible role for nucleic acid receptors in periodontal inflammation.

25 c pathways and modified systemic response to periodontal inflammation.

26 receptors might be of benefit in controlling periodontal inflammation.

27 Diabetes impairs the resolution of periodontal inflammation.

28 s, contributing to the destructive nature of periodontal inflammation.

29 n periodontal fibroblasts, in the context of periodontal inflammation.

30 requently observed in tissue exudates during periodontal inflammation (0.05 to 5 ng/ml).

31 Systemic therapy with MT decreases periodontal inflammation and ABL in ligature-induced per

32 ated that MetS was associated with increased periodontal inflammation and alveolar bone loss in an LP

33 hypothesized that MetS enhances LPS-induced periodontal inflammation and alveolar bone loss.

34 potential clinical utility for management of periodontal inflammation and alveolar bone.

35 ted in significant prevention of macroscopic periodontal inflammation and bone loss (75%; P <0.05) co

36 he adoptive transfer of B10 cells alleviated periodontal inflammation and bone loss in experimental p

37 ne the effect of local B10 cell induction on periodontal inflammation and bone loss in ligature-induc

38 In mice, C3 was required for maximal periodontal inflammation and bone loss, and for the sust

39 tion of IL-6 receptor demonstrated to reduce periodontal inflammation and bone loss, and may be consi

40 er, we showed that sFRP5 blocks experimental periodontal inflammation and bone loss, suggesting a pro

41 of NHPs with Cp40 inhibited ligature-induced periodontal inflammation and bone loss, which correlated

42 induction of B10 cell activity could inhibit periodontal inflammation and bone loss.

43 d for periodontitis, with higher measures of periodontal inflammation and breakdown than those on med

44 exists of the potential association between periodontal inflammation and CGRP in chronic migraine.

45 ull-mouthexamination was conducted to assess periodontal inflammation and collection of stimulated sa

46 The results of this study demonstrate that periodontal inflammation and destruction are increased i

47 n T2DM patients were stratified by extent of periodontal inflammation and disease (i.e., generalized

48 ed topical treatment or preventive agent for periodontal inflammation and disease.

49 on the effects of a reduced-calorie diet on periodontal inflammation and disease.

50 sinuates a possible role of the adipokine in periodontal inflammation and glucose level regulation.

51 of COVID-19 pneumonia, resulted in decreased periodontal inflammation and improved periodontal status

52 could have an important role in suppressing periodontal inflammation and maintaining periodontal hea

53 mechanisms of how risk factors might modify periodontal inflammation and may represent novel therape

54 DSS induces periodontal inflammation and oral dysbiosis, independent

55 Periodontal inflammation and oral microbiota have also b

56 riodontal resident cells express BAFF during periodontal inflammation and participate in providing a

57 The reduction in periodontal inflammation and pocket depths may be a resu

58 Periodontal inflammation and self-perceived OSs were poo

59 ed diet could lead to ABL and an increase in periodontal inflammation and serum pro-oxidants.

60 ated in the gingiva during the resolution of periodontal inflammation and suppressed by diabetes.

61 .039), which indicated a correlation between periodontal inflammation and systemic IL-18 levels.

62 that suggests relationships between chronic periodontal inflammation and the development of CHD, esp

63 T2D seems to be governed by the intensity of periodontal inflammation and the role of T2D in this reg

64 sample of patients with stable CVD, current periodontal inflammation and tissue breakdown are associ

65 The aim of this study is to assess whether periodontal inflammation and tissue breakdown are associ

66 Overall, the sample presented high levels of periodontal inflammation and tissue breakdown.

67 Among patients with prediabetes, periodontal inflammation and whole salivary IL-1beta and

68 sent results, ProCT might play a role during periodontal inflammation, and an elevated salivary ProCT

69 evels diminished with increasing severity of periodontal inflammation, and NSPT remarkably improved t

70 is environment are associated with localized periodontal inflammation, and they are also part of an a

71 een history of periodontitis-but not current periodontal inflammation-and incidence of cerebrovascula

72 biological pathways by which TLR9 instigates periodontal inflammation are yet to be identified.

73 a potent inhibitor of P. gingivalis-elicited periodontal inflammation, arresting and/or preventing ti

74 tin treatment would result in a reduction in periodontal inflammation as assessed by (18)F-fluorodeox

75 erences were greater in patients with higher periodontal inflammation at baseline (mean -0.74 [95% CI

76 n a significant reduction in the macroscopic periodontal inflammation, attachment, and bone loss (10.

77 compared clinical and radiologic markers of periodontal inflammation between water-pipe smokers (WPs

78 ly affecting periodontal tissues, leading to periodontal inflammation, bone breakdown, and loss of th

79 Confirming the role of SETD1 in p65-mediated periodontal inflammation, BOT-64 reduced the number of S

80 djusted models, CIS was associated with high periodontal inflammation burden (odds ratio [OR], 95% co

81 crucial cooperation between C5aR and TLR2 in periodontal inflammation but also provide proof-of-conce

82 the clinical manifestation of plaque-induced periodontal inflammation by analyzing the association be

83 al of ligatures, which induces resolution of periodontal inflammation, clopidogrel had a significant

84 Furthermore, the changes in periodontal inflammation correlated with changes in caro

85 Periodontal inflammation disrupts PDLF function, which m

86 s literature investigating active lesions of periodontal inflammation during gingivitis.

87 ay an important role both in the presence of periodontal inflammation during pregnancy and subsequent

88 Reduction of periodontal inflammation either with root planing and sy

89 These findings suggest that periodontal inflammation, especially in early RA, may co

90 Here, we report that periodontal inflammation exacerbates gut inflammation in

91 ociation between patient-related factors and periodontal inflammation expressed as BOP%.

92 ociation between patient-related factors and periodontal inflammation expressed by BOP%.

93 romonas gingivalis is strongly implicated in periodontal inflammation, gingival tissue destruction, a

94 Luteolin attenuated periodontal inflammation in both L-50 and L-100 groups.

95 on of periodontal infection and reduction of periodontal inflammation in diabetic patients resulted i

96 zes periodontal health; however, severity of periodontal inflammation in gutka chewers with and witho

97 Odds of periodontal inflammation in individuals with prediabetes

98 weeks, there was a significant reduction in periodontal inflammation in patients randomized to atorv

99 have examined local biochemical measures of periodontal inflammation in patients with type 2 diabete

100 expected therapeutic targets for alleviating periodontal inflammation in people with T2D.

101 CTD interacting factor 1 (PCIF1) attenuates periodontal inflammation in whole-body and myeloid linea

102 yromonas gingivalis, as the biofilm ages and periodontal inflammation increases.

103 t of SOCS3 expression in CD11c(+) DCs during periodontal inflammation-induced osteoclastogenesis and

104 nt of periodontal infection and reduction of periodontal inflammation is associated with a reduction

105 Periodontal inflammation is associated with increased ci

106 Periodontal inflammation is clearly related to the prese

107 n patients with prediabetes, the severity of periodontal inflammation is governed by hyperglycemia wh

108 Among controls, periodontal inflammation is worse among smokers than nev

109 Periodontal inflammation may not successfully resolve be

110 locally administered to adult patients with periodontal inflammation.MethodsThirty-two patients with

111 eased risk for periodontal disease, although periodontal inflammation might, in turn, exacerbate the

112 ue integrity, and enhanced osteogenesis in a periodontal inflammation model in vivo.

113 flammatory diet significantly contributes to periodontal inflammation, modulating inflammatory biomar

114 A proposal is made that periodontal inflammation not only stimulates osteoclasto

115 of this study was to assess the influence of periodontal inflammation on oral HIV transmission using

116 f this study is to investigate the effect of periodontal inflammation on oxidative stress in patients

117 tudy was to explore the influence of chronic periodontal inflammation on tissue periostin levels.

118 Periodontal inflammation, particularly in early RA, was

119 cant (P <0.01) positive associations between periodontal inflammation (PD, CAL, PI, GI) and levels of

120 Here we address the effect of periodontal inflammation (PI) on tumor progression, meta

121 These findings support the idea that periodontal inflammation promotes metastasis of breast c

122 e biological pathways in which A20 mitigates periodontal inflammation remain elusive.

123 nce they start to accumulate, a "two-source" periodontal inflammation results from both bacteria-trig

124 High-dose atorvastatin reduces periodontal inflammation, suggesting a newly recognized

125 betes were significantly more likely to have periodontal inflammation than individuals without predia

126 ms of virulence potential and induce chronic periodontal inflammation that leads to alveolar bone res

127 treatments with a C5aR antagonist inhibited periodontal inflammation through downregulation of TNF,

128 ium, Porphyromonas gingivalis, and restrains periodontal inflammation through its effect on NF-kappaB

129 Among controls, periodontal inflammation was worse, and whole salivary I

130 Aging may induce periodontal inflammation, which interferes with the acti

131 Periodontal inflammation with alveolar bone resorption i

132 vated protein kinase phosphatase to regulate periodontal inflammation yielding new possibilities for