ライフサイエンスコーパス: periodontal pocket

1 lls live and die in the gingival crevice and periodontal pocket.

2 of evading the host response in the inflamed periodontal pocket.

3 hance the maintenance of PMN function in the periodontal pocket.

4 ogens in the inflammatory environment of the periodontal pocket.

5 rochete that inhabits the gingival sulcus or periodontal pocket.

6 hysiologic relevance, i.e., reachable in the periodontal pocket.

7 omposition of the bacterial community in the periodontal pocket.

8 omposition of the bacterial community in the periodontal pocket.

9 ses or other oral bacteria to survive in the periodontal pocket.

10 se bone formation on local delivery into the periodontal pocket.

11 1.55 to 10.76 in women who had at >/=1 5-mm periodontal pocket.

12 plays in tissue destruction occurring in the periodontal pocket.

13 se association with the number of teeth with periodontal pockets.

14 hypothetical data to model the treatment of periodontal pockets.

15 portant thiol source for H(2)S production in periodontal pockets.

16 tself as one of the predominant pathogens in periodontal pockets.

17 profile for the delivery of doxycycline into periodontal pockets.

18 olled-release delivery system (DH) placed in periodontal pockets.

19 aspiration of pathogenic colonizers found in periodontal pockets.

20 s of repair, a common status within inflamed periodontal pockets.

21 topical lidocaine gel instillation into the periodontal pockets.

22 t baseline healed at 6 months recall without periodontal pockets.

23 instrumentation in the treatment of residual periodontal pockets.

24 val inflammation and eventually to deepening periodontal pockets.

25 rs and also with a higher percentage of deep periodontal pockets.

26 therapeutic agents against these species in periodontal pockets.

27 air polishing (SubGPAP) in moderate-to-deep periodontal pockets.

28 has been shown to remove biofilms in shallow periodontal pockets.

29 of alcohol use and the number of teeth with periodontal pockets.

30 odontal pockets and the presence of deepened periodontal pockets.

31 ith periodontitis because of the presence of periodontal pockets.

32 re produced from inflammatory tissues within periodontal pockets.

33 ive periodontal disease (> 10% of sites with periodontal pockets 4+ mm) had an increase of approximat

34 SRP showed PD improvements only in moderate periodontal pockets (4 to 6 mm).

35 increase in availability of thin inserts for periodontal pocket access.

36 obing (p = 0.01) and the presence of shallow periodontal pockets after fasting (p < 0.001), while no

37 In deep periodontal pocket analysis (probing depth [PD] >/= 7 mm

38 ce its ability to survive and persist in the periodontal pocket and may play an important role in inf

39 presence of Porphyromonas gingivalis in the periodontal pocket and the high levels of gingipain acti

40 the oxidative stress-rich environment of the periodontal pocket and to significantly alter the microb

41 ilized by oral spirochetes to survive in the periodontal pocket and transition from a minor to a domi

42 elated to periodontal condition, measured as periodontal pocketing and gingival bleeding in this low-

43 were strongly associated with the number of periodontal pockets and alveolar bone loss.

44 r of the human oral microbiome that inhabits periodontal pockets and contributes to chronic periodont

45 However, change in periodontal pockets and DMFT over time varied according

46 d as the number of teeth with deep (>/=4 mm) periodontal pockets and the number of bleeding sextants

47 se their viability within gingival crevices, periodontal pockets and the oral cavity die by necrosis

48 e the number of teeth with deepened (>=4 mm) periodontal pockets and the presence of deepened periodo

49 etween probing attachment changes in treated periodontal pockets and the prevalence of selected perio

50 span of neutrophils in gingival crevices and periodontal pockets and therefore into the pathogenesis

51 tudents (36 periodontally healthy and 2 with periodontal pockets) and 58 healthy A. actinomycetemcomi

52 dontitis (defined as at least two sites with periodontal pockets), and 82.6% sensitive for at least t

53 Cross-sectionally, risks of tooth loss, periodontal pockets, and dry mouth increased from IMD qu

54 retained root fragments, root-surface decay, periodontal pockets, and problem-motivated dental visits

55 d from clinically healthy gingival crevices, periodontal pockets, and the oral cavity (saliva) were e

56 /g in thermosetting agents) for non-invasive periodontal pocket anesthesia was evaluated.

57 In this large cohort study, the presence of periodontal pockets as measured by CPITN was positively

58 helial cells may promote colonization of the periodontal pocket, as well as retention of treponeme co

59 nd two or more sites with >/= 6 mm or deeper periodontal pocket, associated with elevated salivary MM

60 least two sites with BOP and two sites with periodontal pockets but a lower relationship for single-

61 g did not affect the rate of repopulation of periodontal pockets by the tested pathogens; 2) thorough

62 subgingival cultivable microflora in shallow periodontal pockets compared to curets and is safe when

63 e likelihood of demonstrating a reduction in periodontal pockets compared to erratic compliers under

64 ge amounts of H2S have been reported in deep periodontal pockets, cystalysin may also function in viv

65 beta was associated with an increase in mean periodontal pocket depth (PPD) and mean clinical attachm

66 The periodontal pocket depth (PPD) was greater around implan

67 th (D), filled teeth (F), missing teeth (M), periodontal pocket depth (PPD), attachment loss (AL), an

68 Gingival and periodontal pocket depth and attachment levels were reco

69 There was no association between periodontal pocket depth and the detection of H. pylori.

70 gingival bleeding, gingival recession level, periodontal pocket depth, and calculus were made by dent

71 ures at both times included number of teeth, periodontal pocket depth, self-rated oral health, and dr

72 arameters at the time of sacrifice including periodontal pocket depths (p = 0.81), recession (p = 0.9

73 e of bleeding on probing (BOP) and increased periodontal pocket depths (PPD) after surgical treatment

74 use was not consistently associated with the periodontal pocket development over a period of 11 years

75 nvestigates whether alcohol use predicts the periodontal pocket development over an 11-year follow-up

76 A one-time use of the 3-CO(2) laser in periodontal pockets did not sterilize or substantially r

77 polishing with sonic debridement in residual periodontal pockets during maintenance therapy.

78 s) are being used to treat residual inflamed periodontal pockets during periodontal maintenance thera

79 Periodontal pockets experience a higher temperature duri

80 alis (Pg), and Prevotella intermedia (Pi) in periodontal pockets following scaling and root planing (

81 on of active oxygen-releasing gel inside the periodontal pocket for 3 min; BM + aPDT (n = 17)-SI foll

82 l (either placebo or test gel) placed in the periodontal pockets for 30 seconds.

83 ibuted to the present study with one to four periodontal pockets for a total of 124 subgingival sampl

84 an inflammatory disease that can lead to the periodontal pocket formation and tooth loss.

85 ical migration of the junctional epithelium, periodontal pocket formation, alveolar bone resorption,

86 prevalence of antibiotic resistance genes in periodontal pockets from German volunteers.

87 ed into bleeding (BP) and non-bleeding (NBP) periodontal pocket groups in CP group.

88 t periodontitis, measured by the presence of periodontal pockets > or = 4 mm, was found in about 30%

89 Fifty-two patients with 4 periodontal pockets > or = 5 mm and bleeding on probing

90 ted had two quadrants with a minimum of four periodontal pockets > or = 5 mm in depth with two sites

91 ely to have a reduction in the percentage of periodontal pockets >3 mm compared to erratic compliers,

92 and approximately 20% of the population had periodontal pocketing (>3 mm).

93 no reduction, reduction in the percentage of periodontal pockets>3 mm versus no reduction, no increas

94 abolic pathway leading to H(2)S formation in periodontal pockets has not been determined.

95 debridement (SD) for root decontamination of periodontal pockets has shown better results in the nons

96 L-6(+) cells) were elevated adjacent to deep periodontal pockets; however, there was no significant e

97 t that local delivery of antimicrobials into periodontal pockets improve periodontal health.

98 Local delivery of antimicrobials into periodontal pockets improves periodontal health.

99 nd subgingival plaque taken from the deepest periodontal pocket in each sextant may yield the most re

100 controlled clinical trial design in 24 deep periodontal pockets in 12 patients with periodontitis.

101 ent study evaluated the clinical response of periodontal pockets in beagle dogs after treatment with

102 bridement (OFD) in the treatment of residual periodontal pockets in non-furcation sites.

103 ximal bone height (IBH) in persistent 6-9 mm periodontal pockets in patients receiving periodontal ma

104 ss of a chitosan brush in improving residual periodontal pockets in patients who had already undergon

105 s increase in tissue cells and especially in periodontal pockets in patients with CP, and the periodo

106 the differences between shallow and residual periodontal pockets in patients with periodontitis (stag

107 the differences between shallow and residual periodontal pockets in patients with periodontitis (Stag

108 mmunologic benefits in the treatment of deep periodontal pockets in single-rooted teeth in patients w

109 , for the beagle dogs with severely infected periodontal pockets in this study, treatment with subgin

110 to the proliferation of P. gingivalis within periodontal pockets in which erythrocytes are abundant.

111 n destruction and bone resorption locally in periodontal pockets, in a double-blind placebo-controlle

112 , promotes the growth of the pathogen in the periodontal pocket, initially by enhancing its survivabi

113 nconsistent association with the presence of periodontal pockets (IRRs varied from 0.5 to 1.2) while

114 sistently associated with the development of periodontal pockets (IRRs varied from 0.6 to 1.0).

115 Instillation of lidocaine gel into the periodontal pocket is a preferred alternative to injecti

116 athione, a readily available thiol source in periodontal pockets, is a suitable substrate for H(2)S p

117 acterium to the oxidative environment of the periodontal pocket may impact its pathogenicity, an unde

118 The hypothesis of this study is that periodontal pockets may be associated with elevated bloo

119 P. gingivalis colonization of the periodontal pockets may increase visfatin secretion.

120 GCF was collected from two periodontal pockets (mean +/- SD: 5.1 +/- 1.0 mm) at bas

121 onsurgical re-treatment of residual pockets (periodontal pockets not healed) after initial therapy an

122 The microorganism was isolated from a periodontal pocket of a patient with periodontal disease

123 ted with pain in the upper left quadrant and periodontal pocketing of at least 6 mm in each of the fo

124 Twenty patients exhibited no periodontal pockets of > or = 5 mm, other than the study

125 est gel was administered by syringe into the periodontal pockets of 18 systemically healthy adult vol

126 Twenty-two patients revealed multiple periodontal pockets of 5 mm or more and numerous pathoge

127 re capable of establishing themselves in the periodontal pockets of nonimmunocompromised individuals

128 The periodontal pockets of one quadrant in each patient were

129 the most abundant bacteria identified in the periodontal pockets of periodontitis patients.

130 Oral H. pylori was detected from periodontal pockets of various depths and the dorsum of

131 gn endodontic-periodontic lesion with a 7-mm periodontal pocket on tooth #15 in a 40-year-old, non-sm

132 Diode laser therapy was applied to periodontal pockets on days 1, 3, and 7 after SRP.

133 25(OH)D level and teeth with deep (>/=4 mm) periodontal pockets or bleeding sextants.

134 ithin diseased gingiva adjacent to 4 to 6 mm periodontal pockets (P <0.001) and were not correlated w

135 n higher proportions in deep than in shallow periodontal pockets (P = 0.02).

136 NSRI reduced periodontal pockets persisting after initial cause-relat

137 Treatment of residual periodontal pockets (PPD = 5 to 7 mm) with a chitosan br

138 neutrophils were harvested from prespecified periodontal pockets, purified, stained, and examined by

139 temic azithromycin (AZM) in combination with periodontal pocket reduction surgery in the treatment of

140 valis in the inflammatory environment of the periodontal pocket requires an ability to overcome oxida

141 in the inflammatory microenvironment of the periodontal pocket requires an ability to overcome oxida

142 e 2 DM and CP, local delivery of 1% ALN into periodontal pockets resulted in a significant increase i

143 ment loss, probing depths, and percentage of periodontal pocket sites > or =5 mm were measured.

144 Blood vessel features in periodontal pocket soft tissues may be significant in th

145 s that the local delivery of 1% ALN into the periodontal pocket stimulated a significant increase in

146 tudy show that local delivery of MF into the periodontal pocket stimulated significant increase in th

147 t that permits irradiation directly into the periodontal pocket/sulcus.

148 cquire systemic access through the ulcerated periodontal pocket surface; conclusive evidence supporti

149 ving subgingival biofilm in moderate-to-deep periodontal pockets than SRP.

150 major metabolic end product detected in deep periodontal pockets that is produced by resident periodo

151 serts may have advantages in negotiating the periodontal pocket, the relatively narrow structure may

152 However, in diseased periodontal pockets, treponemes thrive and become a domi

153 a matching placebo gel was applied into the periodontal pocket using a blunt applicator.

154 somewhat lower proportion of teeth with deep periodontal pockets was found in higher serum 25(OH)D qu

155 The presence of periodontal pockets was positively associated with highe

156 Patients who presented with residual periodontal pockets were enrolled.

157 The periodontal pockets were exposed to a KTP laser with the

158 ingival biofilm specimens from inflamed deep periodontal pockets were removed before treatment from 4

159 hemorrhagic gingiva adjacent to a > or =3 mm periodontal pocket) were studied.

160 djacent to a < or =3 mm, 4 to 6 mm, or >6 mm periodontal pocket) were studied.

161 emorrhagic gingiva adjacent to a > or = 3 mm periodontal pocket) were studied.

162 plex with respect to the gingival sulcus and periodontal pockets (where the very different defensive

163 ophils are recruited in large numbers to the periodontal pocket, where they play a crucial role in th

164 ationale that indicates that the presence of periodontal pockets which can harbor pathogenic microorg

165 In summary, in the environment of periodontal pockets, which are bathed in gingival crevic

166 levels had a significantly higher number of periodontal pockets with >=4 mm (P < 0.001).

167 Periodontal pockets with a mean probing depth of 5.5 +/-

168 removing most of the subgingival biofilm in periodontal pockets with an APD < or =3 mm.

169 with periodontitis may still have persistent periodontal pockets with bleeding on probing, indicating

170 ts with periodontitis can exhibit persistent periodontal pockets with bleeding representative of infl

171 In periodontal pockets with PD of >/=5.4 mm, a single subgi

172 were randomly assigned to receive SubGPAP in periodontal pockets with probing depths of 4 to 9 mm, Su

173 subgingival debridement efficacy of GPAP in periodontal pockets with various depths.