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 and their role has not been characterized in periodontal inflammation.

3 onfirming the biological relevance of A20 in periodontal inflammation.

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

5 thogens in systemic diseases associated with periodontal inflammation.

6 e levels and attachment integrity to prevent periodontal inflammation.

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

8 new potential therapeutic target to control periodontal inflammation.

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

10 elements that initiate and propagate chronic periodontal inflammation.

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

12 possible role for nucleic acid receptors in periodontal inflammation.

13 c pathways and modified systemic response to periodontal inflammation.

14 receptors might be of benefit in controlling periodontal inflammation.

15 Diabetes impairs the resolution of periodontal inflammation.

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

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

18 wnstream signaling molecule in the course of periodontal inflammation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 Periodontal inflammation and self-perceived OSs were poo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

57 Reduction of periodontal inflammation either with root planing and sy

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

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

60 Odds of periodontal inflammation in individuals with prediabetes

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

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

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

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

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

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

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

68 Periodontal inflammation may not successfully resolve be

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

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

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

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

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

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

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

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

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

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

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

80 Periodontal inflammation with alveolar bone resorption i