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1 increase the host susceptibility to oral and periodontal infection.
2 , such as those in chronic P.gingivalis (PG) periodontal infection.
3 meters as healthy or mild or moderate/severe periodontal infection.
4 d clinical measures and serologic markers of periodontal infection.
5 nal gingival swelling that mimicked an acute periodontal infection.
6 for understanding the role of these cells in periodontal infection.
7 control of patients with DMt2 by eliminating periodontal infection.
8 ate the mechanisms of NKT cell activation in periodontal infections.
9 ory responses in atheromatous lesions due to periodontal infections.
10 ated with inflammatory conditions related to periodontal infections.
11 c bacteremia, which occurs frequently during periodontal infections.
12 ip of inflammation to obesity, diabetes, and periodontal infections.
13 genic factor linking obesity to diabetes and periodontal infections.
14 al epithelial cells are essential aspects of periodontal infections.
15 understanding of the role of F. nucleatum in periodontal infections.
16 eful antimicrobial agents in therapy against periodontal infections.
18 e suggests that inflammation associated with periodontal infections affects both the immediate oral e
20 does not prove, a causal association between periodontal infection and atherosclerotic cardiovascular
21 does not prove a causal association between periodontal infection and cardiovascular disease and sug
22 critically needed to counter the sources of periodontal infection and inflammation that are accelera
23 ly explore and describe familial patterns of periodontal infection and other aspects of periodontal d
24 has the potential for the early detection of periodontal infection and progression to identify incipi
27 ty at Buffalo, Buffalo, New York, i.e., the "Periodontal Infection and Risk for Myocardial Infarction
28 ntial causative role of chronic T. denticola periodontal infection and vascular atherosclerosis in vi
29 tablished the plausibility of a link between periodontal infections and atherogenesis, and have ident
30 th of time of loading; history of implant or periodontal infections; and whether implants replaced si
32 nce from epidemiologic studies suggests that periodontal infections are independently associated with
33 erlying host defense impairment coupled with periodontal infection by HCMV and A. actinomycetemcomita
35 lammatory burden was measured as 1) clinical periodontal infection categorized as no periodontal dise
38 determine whether the prevalence of maternal periodontal infection could be associated with preterm l
42 al peptides (AMPs) as therapeutic agents for periodontal infections has great advantages, such as bro
43 anisms which are markers of past and current periodontal infection have been correlated with cognitiv
46 at the increased oxidative stress induced by periodontal infection in rats can be ameliorated by bone
50 ntal medicine is a term used to describe how periodontal infection/inflammation may impact extraoral
52 ration of host defence cells are symptoms of periodontal infection, iron products released from blood
55 controls to establish an association between periodontal infection markers and rheumatic activity.
56 c kidney disease (CKD), we hypothesized that periodontal infection may affect the systemic inflammato
60 iodontal pathogen; however, association with periodontal infections of other Campylobacter species, e
62 available regarding the effects of long-term periodontal infection on diabetes mellitus (DM) control.
64 moderate or reduce the inhibitory effects of periodontal infection on the expression of type I and ty
66 re we test the hypothesis that Gram-negative periodontal infection promotes pathological platelet act
69 e subjects might represent a contribution of periodontal infections to systemic inflammation in relat
71 To investigate the lymphatic function after periodontal infection, we used K14-VEGF receptor 3-Ig (K
73 form of early-onset periodontitis linked to periodontal infection with uncontrolled inflammation and