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1 ive causative agent of the disease localized aggressive periodontitis.
2 ditary gingival fibromatosis associated with aggressive periodontitis.
3 in patients (>50% smokers) with generalized aggressive periodontitis.
4 dition, the brother also exhibited localized aggressive periodontitis.
5 ly nondiseased subjects and 51 subjects with aggressive periodontitis.
6 be expected to exhibit a more severe form of aggressive periodontitis.
7 th the current classification of chronic and aggressive periodontitis.
8 ssociated with susceptibility to chronic and aggressive periodontitis.
9 in treatment of intrabony defects (IBDs) in aggressive periodontitis.
10 is the main periodontopathogen of localized aggressive periodontitis.
11 cillin and metronidazole in individuals with aggressive periodontitis.
12 nomycetemcomitans is implicated in localized aggressive periodontitis.
13 n the treatment of patients with generalized aggressive periodontitis.
14 IL-17 may play a role in the pathogenesis of aggressive periodontitis.
15 might be detected in sera from patients with aggressive periodontitis.
16 strain, D7S-1, isolated from a patient with aggressive periodontitis.
17 comitans, an organism highly associated with aggressive periodontitis.
18 AgP) and 49 patients with generalized (GAgP) aggressive periodontitis.
19 aque of a patient diagnosed with generalized aggressive periodontitis.
20 ng toxin (Cdt) are associated with localized aggressive periodontitis.
21 periodontal pathogens from individuals with aggressive periodontitis.
22 f African American children with and without aggressive periodontitis.
23 rated implants in a patient with generalized aggressive periodontitis.
24 , especially those who exhibited generalized aggressive periodontitis.
25 dosis affecting the periodontium could mimic aggressive periodontitis.
26 ome may be at the basis of susceptibility to aggressive periodontitis.
28 itans is the causative organism of localized aggressive periodontitis, a rapidly progressing degenera
29 comitans is the etiologic agent of localized aggressive periodontitis, a rapidly progressing oral dis
30 terleukin (IL)-1 influence the risk for both aggressive periodontitis (AgP) and chronic periodontitis
31 ingival plaque samples from individuals with aggressive periodontitis (AgP) and chronic periodontitis
32 dren, 7 to 19 years of age, with and without aggressive periodontitis (AgP) and compared to healthy u
33 patients with chronic periodontitis (CP) or aggressive periodontitis (AgP) and periodontally healthy
34 t planing for the treatment of patients with aggressive periodontitis (AgP) compared to placebo gel.
35 RT) enzyme in chronic periodontitis (CP) and aggressive periodontitis (AgP) compared with healthy ind
37 hile partially inhibiting IL-6 production in aggressive periodontitis (AgP) human gingival fibroblast
38 about the epidemiology and risk factors for aggressive periodontitis (AgP) in Latin American and Bra
41 nocytes, and this is striking in cultures of aggressive periodontitis (AgP) monocytes, where DC numbe
45 l sample of the severe early-onset phenotype aggressive periodontitis (AgP) with the Illumina Immunoc
46 th generalized chronic periodontitis (CP) or aggressive periodontitis (AgP), and periodontally health
47 amples obtained from patients diagnosed with aggressive periodontitis (AgP), chronic periodontitis (C
57 ng a German and Dutch case-control sample of aggressive periodontitis (AgP, 896 cases, 7,104 controls
60 AS data from a German case-control sample of aggressive periodontitis (AgP; 651 cases, 4,001 controls
61 of patients with gingivitis, the group with aggressive periodontitis [AgP], and the group with chron
62 terium is strongly associated with localized aggressive periodontitis and adult periodontitis and is
64 llected 66 GCF samples from 15 patients with aggressive periodontitis and examined both the GCF sampl
65 comitans is a pathogen that causes localized aggressive periodontitis and extraoral infections includ
66 llus that has been associated with localized aggressive periodontitis and infections of the heart, br
67 thogens commonly associated with chronic and aggressive periodontitis and opportunistic pathogens may
69 e investigated whether leukocyte activity in aggressive periodontitis (AP) is increased compared with
70 rs of vascular inflammation in patients with aggressive periodontitis are associated with elevated le
72 ar-old female was diagnosed with generalized aggressive periodontitis based on clinical and radiograp
73 was diagnosed with gingival fibromatosis and aggressive periodontitis based on the clinical and radio
76 isits with a primary diagnosis for acute and aggressive periodontitis, covered by Medicare insurance,
77 s (63 with chronic periodontitis and 27 with aggressive periodontitis) each contributed at least two
79 edentulous patients treated for generalized aggressive periodontitis (GAgP) and in periodontally hea
80 th chronic periodontitis (CP) or generalized aggressive periodontitis (GAgP) and their association wi
81 1 (TIMP-1) gene polymorphisms in generalized aggressive periodontitis (GAgP) and to assess the effect
82 lay a role in the development of generalized aggressive periodontitis (GAgP) are investigated using g
83 f this study is to study whether generalized aggressive periodontitis (GAgP) has similar survival rat
84 h chronic periodontitis (CP) and generalized aggressive periodontitis (GAgP) positive for anti-CL (16
85 h chronic periodontitis (CP) and generalized aggressive periodontitis (GAgP) to test the utility of G
87 ntitis (CP), 14 individuals with generalized aggressive periodontitis (GAgP), 18 individuals with gin
88 onic periodontitis (CP), 20 with generalized aggressive periodontitis (GAgP), 20 with gingivitis, and
89 (GT) samples of 12 patients with generalized aggressive periodontitis (GAgP), 6 patients with localiz
90 odontitis (CP), 12 patients with generalized aggressive periodontitis (GAgP), 6 patients with localiz
91 is a primary etiologic agent of generalized aggressive periodontitis (GAgP), and gingipains, a group
92 es in patients with a history of generalized aggressive periodontitis (GAgP), chronic periodontitis (
93 grouped into control group (CG), generalized aggressive periodontitis (GAgP), or chronic periodontiti
96 ic periodontitis (GChP; n = 30), generalized aggressive periodontitis (GAgP; n = 30), and periodontal
97 seased subjects and 63% of the subjects with aggressive periodontitis harbored multiple clones of E.
100 en proposed for the treatment of generalized aggressive periodontitis; however, its effectiveness and
101 ontrols (IL-6 -174 & VDR -1056); chronic and aggressive periodontitis (IL-1A -889); and periodontitis
104 tors may prevent or reduce the prevalence of aggressive periodontitis in this and similar populations
106 test, P < 0.05) in sites from patients with aggressive periodontitis, in sites with pocket depths of
107 c infections, and in patients with localized aggressive periodontitis, its presence is now observed a
108 y responses to infecting agents in localized aggressive periodontitis (LAgP) and weak responses in ge
109 earch indicated that patients with localized aggressive periodontitis (LAgP) had minimal proximal dec
110 in African-American children with localized aggressive periodontitis (LAgP) have been reported previ
111 used to predict susceptibility to localized aggressive periodontitis (LAgP) in an African-American p
116 that in healthy controls (NP) and localized aggressive periodontitis (LAgP) patients (6.8% and 3.2%)
117 globulin G2 (IgG2) are elevated in localized aggressive periodontitis (LAgP) patients, and secretory
118 onocytes in cultures prepared from localized aggressive periodontitis (LagP) patients, and these pati
119 ukocytes (PMNs) from subjects with localized aggressive periodontitis (LAgP) present multiple functio
121 l study of students susceptible to localized aggressive periodontitis (LAgP) was conducted to evaluat
122 iodontitis (GAgP), 6 patients with localized aggressive periodontitis (LAgP), 10 patients with chroni
123 iodontitis (GAgP), 6 patients with localized aggressive periodontitis (LAgP), 6 patients with gingivi
124 issues were probed with serum from localized aggressive periodontitis (LAgP), chronic periodontitis (
125 eutrophils (PMNs) of patients with localized aggressive periodontitis (LAgP), suggesting a genetic ba
128 cter actinomycetemcomitans-induced localized aggressive periodontitis (LAP) in African-American adole
130 ls from individuals diagnosed with localized aggressive periodontitis (LAP) present an in vivo phenot
131 in African American subjects with localized aggressive periodontitis (LAP) who had proximal bone los
132 ne severe form of periodontitis is localized aggressive periodontitis (LAP), a condition to which ind
133 ired PMN chemotaxis is observed in localized aggressive periodontitis (LAP), a familial disorder char
134 ity and is the causative agent for localized aggressive periodontitis (LAP), an aggressive form of pe
140 tans is frequently associated with localized aggressive periodontitis (LAP); however, longitudinal co
142 tin were significantly higher in generalized aggressive periodontitis patients who had elevated anti-
144 s that periodontal pathogens associated with aggressive periodontitis persist in extracrevicular loca
149 GCF were higher in persons with chronic and aggressive periodontitis than in those with gingivitis o
150 GCF were higher in persons with chronic and aggressive periodontitis than in those with gingivitis,
151 al, biofilm-mediated disease are chronic and aggressive periodontitis, the latter being characterized
152 m 45 young adults diagnosed with generalized aggressive periodontitis to study Fc receptors, formyl p
153 of children and young adults with localized aggressive periodontitis treatment (LAgP) affecting prim
154 w of the inflammatory nature and severity of aggressive periodontitis, we hypothesized that IL-17 mig
155 ed by nondiseased subjects and subjects with aggressive periodontitis were 1.3 and 3.0, respectively.
156 ents who had a primary diagnosis of acute or aggressive periodontitis were associated with significan
157 Thirteen patients (36.9+/-7.4 years) with aggressive periodontitis were monitored before and up to
158 wo nondiseased subjects and 11 subjects with aggressive periodontitis were subsequently reexamined af
159 o present a 9-year-old female with localized aggressive periodontitis who had a history of type 1 DM
160 ents a patient with a history of generalized aggressive periodontitis who has been maintained with th
161 addresses antibiotic use during treatment of aggressive periodontitis with emphasis on juvenile disea
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