ライフサイエンスコーパス: periodontal destruction

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1 and offers insight into the role of PGE2 in periodontal destruction.

2 ssociation between poor glycemic control and periodontal destruction.

3 OX-1 and/or COX-2 isoenzymes and may inhibit periodontal destruction.

4 oproteinases (MMPs) that are responsible for periodontal destruction.

5 h appears to have successfully corrected the periodontal destruction.

6 ontal disease groups with moderate or severe periodontal destruction.

7 demonstrated that smoking is associated with periodontal destruction.

8 compared to sites with a history of greater periodontal destruction.

9 nt loss was used to estimate the severity of periodontal destruction.

10 ied by local injection to sites with induced periodontal destruction and compared with similar sites

11 mary, despite their reciprocal relationship, periodontal destruction and diabetes may be independent

12 ngs did not indicate additive interaction of periodontal destruction and diabetes regarding all-cause

13 o mediate multiple functions associated with periodontal destruction and inflammation.

14 interleukin-1 (IL-1), mediators involved in periodontal destruction and keratinocyte proliferation.

15 was to investigate the effect of smoking on periodontal destruction and recession in subjects with m

16 Progression of diabetes-associated periodontal destruction and the roles of advanced glycat

17 s and correlated with clinical parameters of periodontal destruction and with proinflammatory cytokin

18 e diabetic patients in the study, 66% showed periodontal destruction, and 43% of those could be chara

19 alculus, an increased extent and severity of periodontal destruction, and an increased frequency of t

20 the exact pathogenetic mechanisms underlying periodontal destruction are still poorly understood.

21 Periodontal destruction, as measured by CAL, progressed

22 dontal disease, and diabetics can experience periodontal destruction at an earlier age than non-diabe

23 t forms of periodontitis often have advanced periodontal destruction before they are referred for spe

24 Diabetes augments periodontal destruction by reducing the proliferating ca

25 emically modified tetracycline-1, can reduce periodontal destruction by reversing the inhibitory effe

26 nd several studies have analyzed whether the periodontal destruction could have been influenced by sy

27 diseases are defined by the age of onset of periodontal destruction, distribution of lesions, associ

28 Since periodontal destruction exhibits left-right symmetry, ho

29 Since periodontal destruction exhibits left-right symmetry, it

30 The evidence for the role of MMPs in periodontal destruction has accumulated over three and a

31 pment of inflammation and the progression of periodontal destruction in this model.

32 ed decrease in serum IgG2 and an increase in periodontal destruction in white subjects is striking.

33 urpose of this study was to evaluate whether periodontal destruction interacts with diabetes on all-c

34 Periodontal destruction is initiated by bacteria that co

35 of both periodontitis and osteoporosis, and periodontal destruction may be influenced by systemic bo

36 nical stress from mastication contributes to periodontal destruction observed in Bsp(-/-) mice.

37 st, we were unable to detect any increase in periodontal destruction or a significant decrease in ser

38 studies are consistent with the concept that periodontal destruction proceeds in random bursts at spe

39 do not appear at higher risk for more rapid periodontal destruction than women.

40 Stress and depression may be associated with periodontal destruction through behavioral and physiolog

41 Periodontal destruction was assessed via clinical attach

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