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1 elopment of a new host modulation therapy in periodontitis.
2 lls on periodontal bone loss in experimental periodontitis.
3 pants had periodontitis, and 9.1% had severe periodontitis.
4 n treatment of IBDs in patients with chronic periodontitis.
5 linical AL, and higher odds of having severe periodontitis.
6 hree-fold increase in the odds of developing periodontitis.
7 riodontal pockets and contributes to chronic periodontitis.
8 nt of intrabony defects (IBDs) in aggressive periodontitis.
9 ease burden and significant association with periodontitis.
10 ater extent in patients without a history of periodontitis.
11 nt was only observed in patients with severe periodontitis.
12 e predictive contribution of ETS exposure to periodontitis.
13 umbers are elevated in patients with chronic periodontitis.
14 e influence of ETS exposure on occurrence of periodontitis.
15 tion of the periodontium that is lost due to periodontitis.
16 0.05), highlighting their potential role in periodontitis.
17 examinations demonstrated the development of periodontitis.
18 ts were divided into two groups: control and periodontitis.
19 tes toward understanding of the pathology of periodontitis.
20 r 71 polymorphisms in 29 candidate genes for periodontitis.
21 ic inquiry in the management of inflammatory periodontitis.
22 y, dentoalveolar bone); and 3) management of periodontitis.
23 ate and adaptive immunity in the etiology of periodontitis.
24 le of CBCT in the management of inflammatory periodontitis.
25 as gingivalis, the main etiological agent of periodontitis.
26 en with moderate, and four with mild chronic periodontitis.
27 s pH changes, may be beneficial for treating periodontitis.
28 ment of patients with generalized aggressive periodontitis.
29 d at the messenger RNA (mRNA) level in human periodontitis.
30 ssified as healthy/mild, moderate, or severe periodontitis.
31 , and negatively with IL-34 in patients with periodontitis.
32 ly to IL-34, in patients with gingivitis and periodontitis.
33 ntioxidant enzymes in rats with experimental periodontitis.
34 stratified by sex for each classification of periodontitis.
35 iologic testing is examined in patients with periodontitis.
36 other risk factors may increase the risk of periodontitis.
37 3) alveolar bone loss (ABL) in experimental periodontitis.
38 ifications play a role in the development of periodontitis.
39 ls), the most severe and early onset form of periodontitis.
40 et-induced overweight/obesity on the risk of periodontitis.
41 ne model of A. actinomycetemcomitans-induced periodontitis.
42 onded to a CRR of 5:4, correlating to severe periodontitis.
43 resulting in the common inflammatory disease periodontitis.
44 samples to identify genetic risk variants of periodontitis.
45 using an established model of polymicrobial periodontitis.
46 ukin (IL)-12 correlates with the severity of periodontitis.
47 ipidemia measures no factors were related to periodontitis.
48 d to a CRR of 1:1, relating to mild-moderate periodontitis.
49 creases the risk of an individual developing periodontitis.
50 plays a central mechanism in pathogenesis of periodontitis.
51 ctive approaches for preventing and treating periodontitis.
52 ar bone loss (ABL) in rats with experimental periodontitis.
53 thers showed t2DM development, regardless of periodontitis.
54 tal cholesterol, and C-reactive protein with periodontitis.
55 could be therapeutic tools for treatment of periodontitis.
56 riodontal bacterial profile in patients with periodontitis.
57 upled receptor X2 (MRGPRX2), is increased in periodontitis.
58 t treatment outcome of patients with chronic periodontitis.
59 determined in 48 patients (29 patients with periodontitis, 12 with gingivitis, and seven healthy pat
60 overweight) and 22% (obesity) higher risk of periodontitis; 12% (overweight) and 27% (obesity) higher
61 risk under no intervention was 33.3% for any periodontitis, 14.3%, for moderate/severe periodontitis,
63 27% (obesity) higher risk of moderate/severe periodontitis; 21% (overweight) and 57% (obesity) higher
65 -deficient (TLR9(-/-)) mice are resistant to periodontitis, a disease characterized by a dysbiotic mi
67 and Dutch case-control sample of aggressive periodontitis (AgP, 896 cases, 7,104 controls), a rare b
68 m a German case-control sample of aggressive periodontitis (AgP; 651 cases, 4,001 controls), the most
72 on data were used to determine prevalence of periodontitis among United States non-smoking adults and
73 of this study are to estimate prevalence of periodontitis among United States non-smoking adults exp
75 from 25 individuals with generalized chronic periodontitis and 25 periodontally healthy individuals u
78 adhesion deficiency type 1 (LAD1) had severe periodontitis and an intractable, deep, nonhealing sacra
79 tio (CRR) of extracted teeth to classify the periodontitis and assign a periodontal/prosthetic progno
80 orrelations that were being observed between periodontitis and cardiovascular disease, rheumatoid art
81 ne whether the genetic background of initial periodontitis and caries could be detected using an acti
82 investigate the association between induced periodontitis and damage caused through its systemic eff
83 h in GCF and serum, increased from health to periodontitis and decreased with non-surgical periodonta
84 study is to evaluate the association between periodontitis and ED by means of periodontal clinical pa
86 review of the potential association between periodontitis and gestational diabetes mellitus (GDM) in
87 Results demonstrated higher prevalence of periodontitis and higher levels of GCF IL-1beta and seru
88 howed sociodemographic disparities regarding periodontitis and highlights the importance of further i
90 ion models estimated the association between periodontitis and NAFLD within strata of serum CRP and s
94 ver alternative therapeutic targets to treat periodontitis and other chronic inflammatory diseases.
95 icant changes were still observed for severe periodontitis and progression of AL with increases of 0.
99 e actual relationship between STC levels and periodontitis and to establish causality and directional
103 microbiologic profiles of peri-implantitis, periodontitis, and healthy implants based on studies tha
105 loss is the ultimate negative consequence of periodontitis, and reports of the extent to which differ
106 oduction of antioxidants in individuals with periodontitis, and significantly decreased glutamate met
107 are the main trigger for the development of periodontitis, and some species are known to modulate ne
108 e risk of any periodontitis, moderate/severe periodontitis, and the combination of bleeding on probin
109 and S. sputigena, seem to be associated with periodontitis, and their role in periodontal pathogenesi
111 randomized clinical trial, 80 patients with periodontitis are distributed randomly into two groups.
112 ip of expression of Wnt5a and sFRP5 in human periodontitis (as compared to health) and to determine t
113 ism (SNP) context of a previously identified periodontitis-associated locus is investigated, and its
114 n orthologous were interrogated for putative periodontitis-associated variants using existing GWAS da
115 disease phenotypes and were associated with periodontitis at a genome-wide significance level in the
117 the study was to estimate the prevalence of periodontitis at state and local levels across the Unite
118 needs is evaluated in patients with chronic periodontitis before and after completion of non-surgica
119 n situ growth activities of oral bacteria in periodontitis before and after non-surgical periodontal
123 ant associations of age and smoking with all periodontitis case definitions and of male sex with seve
124 uate differences in outcome by applying five periodontitis case definitions for cross-sectional assoc
126 tle difference in odds ratio across the five periodontitis case definitions; however, the level of si
129 Due to the limited sample size of available periodontitis cohorts and the underlying trait heterogen
132 flammation and disease symptoms in models of periodontitis corresponding to recruitment of endogenous
134 evels in the saliva of patients with chronic periodontitis (CP) and acute coronary syndrome (ACS) and
136 individuals with aggressive (AgP) or chronic periodontitis (CP) and healthy controls (HC), as well as
137 zed aggressive periodontitis (GAgP), chronic periodontitis (CP) and in patients with no history of pe
139 e-wide association studies (GWAS) of chronic periodontitis (CP) have been unsuccessful in discovering
145 o two groups: 1) 24 individuals with chronic periodontitis (CP); and 2) 23 individuals without CP.
146 ree groups: 1) healthy (control); 2) chronic periodontitis (CP); and 3) myocardial infarction (MI).
148 stemic, and socioeconomic data on estimating periodontitis development in a population-based prospect
156 ratrol (RESV) on progression of experimental periodontitis (EP) in the presence of cigarette smoke in
157 action of healthy or teeth with experimental periodontitis (EP) in Wistar-Han rats treated with zoled
158 divided into control, experimentally induced periodontitis (EP), DM, EP-DM, EP and melatonin treatmen
160 eriodontitis was defined according to severe periodontitis, European Workshop of Periodontology (EWP)
161 al prognosis and determining the severity of periodontitis for premolars with alveolar bone loss base
162 There was a 28% increase in the odds of periodontitis for those with any ETS exposure compared w
163 nts with a history of generalized aggressive periodontitis (GAgP), chronic periodontitis (CP) and in
165 osed DM and prediabetes were observed in the periodontitis group (32.7%) than in the control group (1
166 alis levels were significantly higher in the periodontitis group (P <0.05), and Td levels were signif
167 a marked reduction in NG2+ pericytes in the periodontitis group compared with the control group.
170 of NLRP3, ASC, and IL-1beta were detected in periodontitis groups in comparison to the periodontally
171 itis (CP) and in patients with no history of periodontitis (H), using microarray and quantitative rev
173 meter of early ACD, and its association with periodontitis has rarely been investigated to date.
174 monas gingivalis, a major etiologic agent of periodontitis, has been reported to induce the expansion
176 treated with dental implants with different periodontitis histories and the possible influence of th
177 ion with compliance level; however, positive periodontitis history and more years in function were si
179 ted greater compliance than patients without periodontitis history during the two longer follow-up ti
182 phisms of MMP3 and VDR are linked to initial periodontitis in Finnish adolescents, and the aMMP-8 cha
187 <0.05) were recorded by diagnosis of chronic periodontitis in the a* coordinate when comparing treatm
188 ribe the prevalence, severity, and extent of periodontitis in the adult population of circumpolar com
189 mful) association between FRC use and severe periodontitis in the entire sample (odds ratio [OR]: 1.7
192 d bone loss in ligature-induced experimental periodontitis in vivo Purified spleen B cells from C57BL
193 ication, predictive value for development of periodontitis in young adults might be increased by comb
194 chairside test can eventually detect initial periodontitis in young patients with predisposing geneti
195 ural teeth [19 healthy, 12 gingivitis, eight periodontitis] in 15 systemically healthy patients were
196 ith anti-inflammatory properties, to inhibit periodontitis induction via a thermogelling and pH-respo
197 sFRP5 in mice subjected to ligature-induced periodontitis inhibited inflammation and bone loss, corr
208 he aim of this study is to determine whether periodontitis is related to the amyloid beta (Abeta) loa
210 n is upregulated in the gingival tissue with periodontitis, its pathophysiological roles in periodont
212 suggests that DHA + aspirin therapy improves periodontitis largely by modulating host inflammatory re
213 minant disorder characterized by early-onset periodontitis leading to premature loss of teeth, joint
214 sham rats; 3) rats submitted to experimental periodontitis (LPS); and 4) rats submitted to experiment
216 role of bridging species in pathogenesis of periodontitis may be greater than previously suspected i
217 Associations of risk factors/indicators with periodontitis may depend on the included case criterion.
219 1 was also observed in a murine experimental periodontitis model induced by P. gingivalis-soaked liga
220 for race or sex, whereas prevalence of total periodontitis (moderate and severe) among women of simil
222 sease" and two inquired about "self-assessed periodontitis." Multiple logistic regression models were
223 tested in a mouse model of ligature-induced periodontitis ( n = 6-7/group) where Pasteurella pneumot
224 vitis (n = 21) and some of the patients with periodontitis (n = 11) were subjected to non-surgical pe
225 viduals (n = 2) and individuals with chronic periodontitis (n = 2) was done via immunohistochemistry.
228 status was examined in patients with severe periodontitis (n = 49) and healthy controls (n = 39), an
233 Current evidence indicates the effects of periodontitis on diabetes as well as mortality, for whic
234 1:1 was inadequate to assess the severity of periodontitis on the basis of the 2D RL and 3D RSA measu
236 spase-3, 6.8-fold; Xiap: 2.5-fold in chronic periodontitis) (P < 0.05), highlighting their potential
237 y is to investigate whether neutrophils from periodontitis patients are able to produce Eosinophil Ca
240 human gingival tissue specimens from chronic periodontitis patients, further confirming the biologica
241 eatment, and in subgingival dental plaque of periodontitis patients, indicating that eDNA is a common
243 nnabis (FRC) (marijuana and hashish) use and periodontitis prevalence among adults in the United Stat
249 grating multiple datasets to assess risk for periodontitis progression and tooth loss in dental patie
250 d association between obesity and subsequent periodontitis progression in a longitudinal database.
251 fect of baseline central adiposity on future periodontitis progression is conditional on proinflammat
254 Eighty patients with chronic or aggressive periodontitis received periodontal treatment supplemente
257 yromonas gingivalis, a keystone pathogen for periodontitis, revealed reduced neutrophils in TLR9(-/-)
261 leukin (IL)-1 gene variants, known to affect periodontitis severity, influence the previously reporte
262 se of statins on adult patients with chronic periodontitis shows a positive effect on their periodont
265 nse to the possibility of under-reporting of periodontitis, the Centers for Disease Control updated p
268 les harvested from human healthy and chronic periodontitis tissues (Apaf-1, 19.2-fold; caspase-9, 14.
269 peri-implantitis versus healthy implants or periodontitis using conventional microbiologic technique
270 re but highly severe and early-onset form of periodontitis, validated the associations in a German sa
273 estionnaire items with respect to predicting periodontitis was better for severe compared with modera
277 me was statistically significant when severe periodontitis was diagnosed at baseline (2.32%, 95% conf
279 as subgingivally delivered when experimental periodontitis was induced in vivo, and therapeutic effec
288 gin to understand the role of P. stomatis in periodontitis, we studied its interactions with human ne
289 mplantitis compared with healthy implants or periodontitis were considered eligible for inclusion.
290 Fifty-five adults with moderate-to-severe periodontitis were enrolled in a randomized, 3-month dou
292 eighty-four patients with moderate-to-severe periodontitis were randomly allocated to one of four tre
293 Twenty-six patients (52 sites) with chronic periodontitis were treated either with autologous PRF wi
294 proteinase (MMP)-8, a biomarker candidate of periodontitis, were determined in 48 patients (29 patien
295 1) Clinical situation: In patients with periodontitis, what (if any) clinical situations/conditi
298 results link the systemic effects of induced periodontitis with changes in hepatic tissues such as mi
299 be used to inhibit induction of experimental periodontitis with favorable handling and inflammation-r
300 has been associated with the pathogenesis of periodontitis with severe alveolar bone destruction.
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