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1 f a pathogenic consortium in the etiology of adult periodontitis.
2 sts between oral and peripheral blood PMN in adult periodontitis.
3 ar matrix breakdown, including bone loss, in adult periodontitis.
4 gative oral anaerobe associated with chronic adult periodontitis.
5 c bacterial species strongly associated with adult periodontitis.
6 asures as important environmental factors in adult periodontitis.
7 n implicated as a primary causative agent in adult periodontitis.
8 ant component of prevention and treatment of adult periodontitis.
9 brush and a manual brush in 40 patients with adult periodontitis.
10 e oral anaerobe, is strongly associated with adult periodontitis.
11 has been implicated as an etiologic agent of adult periodontitis.
12 repressed in patients diagnosed with chronic adult periodontitis.
13 e anaerobe, is implicated in the etiology of adult periodontitis.
14 e of the principal organisms associated with adult periodontitis.
15 alis fimbrillin as a mucosal vaccine against adult periodontitis.
16 ated with increased susceptibility to severe adult periodontitis.
17 ved proteases in the pathogenesis of chronic adult periodontitis.
18 ial effect on the microflora associated with adult periodontitis.
19 associated with an increased risk of severe adult periodontitis.
20 valis has been implicated in the etiology of adult periodontitis.
21 or tooth sites occurs as a frequent event in adult periodontitis.
22 ng the susceptibility of Chinese patients to adult periodontitis.
23 ignificantly associated with the severity of adult periodontitis.
24 idered among the etiological agents of human adult periodontitis.
25 re significantly associated with severity of adult periodontitis.
26 that has been implicated in the etiology of adult periodontitis.
27 y of disease status in subjects with chronic adult periodontitis.
28 te anaerobe strongly associated with chronic adult periodontitis.
29 red in 15 patients with moderate to advanced adult periodontitis.
30 suggested to be associated with severity of adult periodontitis.
31 cal probing methods in patients with chronic adult periodontitis.
32 alis in the development of a vaccine against adult periodontitis.
33 attachment level change in untreated chronic adult periodontitis.
34 alis is one of the major causative agents of adult periodontitis.
35 control subjects as well as 31 patients with adult periodontitis.
36 ly to be correlated with low risk for severe adult periodontitis.
37 nted, oral anaerobe strongly associated with adult periodontitis.
38 adjunctive chemotherapy for the treatment of adult periodontitis.
39 improving clinical attachment level (CAL) in adult periodontitis.
40 hat is an important etiologic agent of human adult periodontitis.
41 42 patients with moderately advanced chronic adult periodontitis.
42 is a risk factor for severity of disease in adult periodontitis.
43 he principal pathogens in the development of adult periodontitis.
44 45.5 years) with moderately advanced chronic adult periodontitis.
45 human population and largely responsible for adult periodontitis.
46 nce for a major role of TNF-alpha in chronic adult periodontitis.
47 vival on treatment outcomes in patients with adult periodontitis.
48 l pathogens was assessed in 10 patients with adult periodontitis 1 year following randomized therapy.
50 s for the majority of sites in patients with adult periodontitis; 3) pre-operative probing depth, the
51 s one of the major pathogens associated with adult periodontitis, a major chronic inflammatory diseas
52 ere determined in 32 Caucasian patients with adult periodontitis and 32 orally-healthy matched contro
53 cytes (PMN) was examined in 40 patients with adult periodontitis and 40 orally healthy matched contro
54 The study included 10 patients with advanced adult periodontitis and a minimum of one set of similar
56 tive means of reducing the clinical signs of adult periodontitis and exhibits a benign safety profile
57 subjects diagnosed with generalized moderate adult periodontitis and having at least 2 teeth with > o
58 with localized aggressive periodontitis and adult periodontitis and is the causative agent for other
60 t tissue biopsies from patients with chronic adult periodontitis and patients with healthy periodonta
61 st-localized juvenile periodontitis, 41 with adult periodontitis, and 19 periodontally normal subject
62 who showed a low prevalence and severity of adult periodontitis, and thus allowed us to monitor earl
63 by MTL from 41 patients with a diagnosis of adult periodontitis (AP) and 41 with a diagnosis of recu
65 revious studies have suggested that risk for adult periodontitis (AP) has a genetic (heritable) compo
66 subjects, 2 Aa-infected, slowly progressing adult periodontitis (AP) patients and 2 LJP patients.
68 ted with periodontal health in patients with adult periodontitis (AP) when used as an adjunct to a ma
69 (type 2) control and presence or absence of adult periodontitis (AP): group 1, systemically and peri
71 d methyl mercaptan have been associated with adult periodontitis as well as with healing surgical wou
72 s gingivalis, one of the causative agents of adult periodontitis, attaches and forms biofilms on subs
73 ing leads to improved clinical parameters of adult periodontitis, but has raised questions about pote
74 d the association between social factors and adult periodontitis by comparing self-reported informati
75 s gingivalis, one of the causative agents of adult periodontitis, can invade and survive within host
76 s gingivalis, one of the causative agents of adult periodontitis, develops biofilm microcolonies on s
77 nd alveolar bone resorption are hallmarks of adult periodontitis, elicited in response to oral micro-
78 and subjects with refractory periodontitis, adult periodontitis, human immunodeficiency virus period
85 phyromonas gingivalis, a primary pathogen in adult periodontitis, may establish itself in the oral ca
87 hyromonas gingivalis, the causative agent of adult periodontitis, must maintain nitric oxide (NO) hom
88 = 6); group 4, well-controlled diabetes with adult periodontitis (n = 5); group 5, poorly controlled
90 (n = 6); group 2, systemically healthy with adult periodontitis (n = 7); group 3, well-controlled di
91 the microbial flora associated with chronic adult periodontitis on cytokine induction, lipopolysacch
92 romonas gingivalis, a causative bacterium of adult periodontitis, on human blood coagulation was inve
100 ental biopsies were obtained, 6 from chronic adult periodontitis patients and 6 from healthy voluntee
101 ear cells or whole gingival biopsies from 32 adult periodontitis patients and five healthy individual
102 e analyzed human tissue samples from chronic adult periodontitis patients to assess the levels of spe
103 ent, double-blind, placebo-controlled study, adult periodontitis patients were administered for 6 mon
105 subgingival plaque samples collected from 26 adult periodontitis patients yielded > 98% specificity f
107 les were obtained from patients with chronic adult periodontitis (probing depths ranged from 5 to 9 m
109 95% Confidence interval [CI]) in the chronic adult periodontitis specimens when compared to healthy s
110 ngival tissues and crevicular fluid (GCF) of adult periodontitis subjects in short-term studies.
113 ough herpesviruses have been associated with adult periodontitis, their relationship with juvenile pe
115 ariances and heritability for gingivitis and adult periodontitis using data from twins reared togethe
116 idate the role of these cytokines in chronic adult periodontitis, we tested whether the prevalence of
117 d West Virginia University, 76 subjects with adult periodontitis were entered and randomly assigned t
119 ears, with generalized, moderate to advanced adult periodontitis were recruited and randomized to one
121 rIL-4 may inhibit the persistence of MOs in adult periodontitis, which could then lead to decreased
122 the TNF-alpha 308 genotype in patients with adult periodontitis, with increased production found in
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