ライフサイエンスコーパス: periodontium

1 d the diagnosis of sarcoidosis affecting the periodontium.

2 he dental pulp, the deciduous tooth, and the periodontium.

3 virus (HIV) disease and its therapies on the periodontium.

4 of gingival pemphigoid lesions on the human periodontium.

5 crobial-induced inflammatory response in the periodontium.

6 these deleterious effects of smoking on the periodontium.

7 tory pathways involving sex steroids and the periodontium.

8 required for appropriate development of the periodontium.

9 roblasts, and in multinucleated cells in the periodontium.

10 wn much potential in the regeneration of the periodontium.

11 logic evaluation of all lesions found in the periodontium.

12 ntrations (1 to 30 mM) found in the diseased periodontium.

13 ther than the deeper, connective tissues and periodontium.

14 ioactivity) to affect cells derived from the periodontium.

15 ation in local inflammatory responses in the periodontium.

16 e the delivery of this agent to the inflamed periodontium.

17 tribute to reparatory events in the inflamed periodontium.

18 ting the maintenance and regeneration of the periodontium.

19 enamel formation and the development of the periodontium.

20 strategies aimed at the regeneration of the periodontium.

21 responses from several cell types within the periodontium.

22 tical for the maintenance and healing of the periodontium.

23 ene expression in cells of importance to the periodontium.

24 the factors involved in the breakdown of the periodontium.

25 xic disturbances in the pulp and surrounding periodontium.

26 a unique immune surveillance role within the periodontium.

27 apy is associated with severe destruction of periodontium.

28 25(OH)D] exerts any beneficial effect on the periodontium.

29 application to achieve reconstruction of the periodontium.

30 to successfully enhance regeneration of the periodontium.

31 ms driving pathogenic events in the infected periodontium.

32 d AgP and those with gingivitis or a healthy periodontium.

33 s do not cause permanent damage to a healthy periodontium.

34 lic alveolar bone homeostasis in the healthy periodontium.

35 hysiologic alveolar bone loss in the healthy periodontium.

36 asminogen activation by fibroblasts from the periodontium.

37 he known anabolic actions of thrombin in the periodontium.

38 e clinical and immunologic parameters of the periodontium.

39 that contribute to local inflammation in the periodontium.

40 s, cementoblasts, and fibroblasts within the periodontium.

41 P and 24 individuals with clinically healthy periodontium.

42 mediators involved in the destruction of the periodontium.

43 nuclear factor-kappaB immunostaining in the periodontium.

44 s specific site and bone cell actions in the periodontium.

45 lated among obese individuals with a healthy periodontium.

46 periodontitis from individuals with healthy periodontium.

47 ction of fibrillar support structures of the periodontium.

48 ry between healthy and diseased sites in the periodontium.

49 and temporal aspects of inflammation in the periodontium.

50 a crucial role in the innate defense of the periodontium.

51 minant extracellular matrix component in the periodontium.

52 sulting in the destruction of tissues of the periodontium.

53 etermine autoreactivity to components of the periodontium.

54 ute to a breakdown in the homeostasis of the periodontium.

55 entum, which are important components of the periodontium.

56 capable of differentiating into cells of the periodontium.

57 maintaining the functional integrity of the periodontium.

58 Thirty-one females with PCOS and healthy periodontium, 30 females with PCOS and gingivitis, and 1

59 cells are the first line of defense for the periodontium against bacteria, we also evaluated whether

60 PMNs are important in defending the periodontium against plaque infections.

61 ere was no obvious morphologic change in the periodontium, although slight elevations of AGEs and RAG

62 d that two adjacent mesenchymal tissues, the periodontium and dental pulp, are maintained by distinct

63 umbers of osteoblasts and apoptotic cells in periodontium and diminished expression of osteoblast sig

64 ted effects of smokeless tobacco (ST) on the periodontium and high prevalence of ST use in rural popu

65 and Fusobacterium nucleatum to colonize the periodontium and induce local and systemic inflammatory

66 erative stomatitis involving the surrounding periodontium and palatal mucosa.

67 concentrations of polyamines in the inflamed periodontium and possess a transport system for taking u

68 effectively transduce cells derived from the periodontium and promote biological activity equivalent

69 en restorative margins may interact with the periodontium and/or orthodontic treatment is indicated.

70 xpression of microRNAs (miRNAs) in maxillas (periodontium) and spleens isolated from ApoE(-/-) mice i

71 polymicrobial infections of the root canal, periodontium, and alveolar bone.

72 progressed to include deeper portions of the periodontium, and more of the teeth unaffected at baseli

73 n as problems that might have impacts on the periodontium, and reciprocal effects of periodontal dise

74 at Dmp1 is critical for the integrity of the periodontium, and that deletion may lead to increased su

75 that, even though oral cancers involving the periodontium are a relatively rare occurrence, periodont

76 The connective tissues of the periodontium are extremely well vascularized, which allo

77 nd resulting ankylosis were occurring in the periodontium as well.

78 Cellular and molecular changes of the periodontium associated with a higher prevalence of oral

79 by ovariectomy in the apposition side of the periodontium but maintains bone formation over all the s

80 ways altered by inflammation in the diabetic periodontium by using ligatures to induce periodontitis

81 erant growth of connective tissue within the periodontium can result from hyperactivity of resident f

82 To study wound healing in the periodontium, cells adherent to expanded polytetrafluoro

83 c periodontitis (CP), and clinically healthy periodontium (control group).

84 manifestations of sarcoidosis affecting the periodontium could mimic aggressive periodontitis.

85 It is thought that during development of the periodontium, dental follicle cells, when appropriately

86 nucleic acids are abundantly present in the periodontium, derived through release after phagocytic u

87 tin application showed beneficial effects on periodontium during and after induction of experimental

88 ng the regulatory actions of estrogen on the periodontium during pregnancy.

89 of the regulatory actions of estrogen on the periodontium during pregnancy.

90 ngivitis (Gg), 30 women with GDM and healthy periodontium (Gh), 28 systemically and periodontally hea

91 raditional methods aimed at regenerating the periodontium have limited indications, and their results

92 soft tissue healing and regeneration of the periodontium; however, the mechanisms of this action are

93 study demonstrated that regeneration of the periodontium in gingival recession defects was possible

94 n the resorption and apposition sides of the periodontium in ovariectomized rats.

95 in expression to ensure the integrity of the periodontium in response to occlusal load.

96 Nrf2(-/-) mice had more severe loss of periodontium in response to periodontitis-inducing subgi

97 st response to the biofilm that destroys the periodontium in the pathogenesis of the disease.

98 of necrotizing ulcerative infections of the periodontium in the severely immunosuppressed patient.

99 molars, including the apposition side of the periodontium, in which RANKL expression was significantl

100 the occurrence of sarcoidosis affecting the periodontium, including its clinical features, diagnosis

101 Other cells of the periodontium, including oral epithelial cells (OECs), ex

102 t may be the precursor of other cells of the periodontium, including osteoblasts and cementoblasts.

103 ulate the host response to challenges in the periodontium, increasing the expression of periodontal b

104 of the tooth on the healing potential of the periodontium is controversial.

105 smoking induces its negative effects on the periodontium is not clear.

106 on of structure and function of the diseased periodontium is often considered an unpredictable task.

107 pression of the subset of semaphorins in the periodontium likely to be most involved with regulating

108 high load of bacterial antigens--such as the periodontium, lung, and gut--may represent the initial s

109 ease is characterized by inflammation of the periodontium manifested by recruitment of neutrophils, w

110 re elevation at sites of inflammation in the periodontium may be a significant environmental regulato

111 sting literature suggesting that the healthy periodontium may be in a parainflammatory state.

112 The periodontium may serve as a reservoir for CMV and a sour

113 both hard and soft tissue components of the periodontium, may be preferable for assessing efficacy o

114 In the periodontium, miRNAs play key roles in development and p

115 esent report describes active CMV within the periodontium of a 37-year-old patient affected by GBS.

116 her TNF levels and osteoclast numbers in the periodontium of aged versus young mice.

117 mbers of RANKL+ cells and IL17+ cells in the periodontium of SPF mice demonstrate possible molecular

118 th PCOS and with either a clinically healthy periodontium or gingivitis.

119 yndrome (PCOS) and either clinically healthy periodontium or gingivitis.

120 ts were 21 to 35 years of age with a healthy periodontium or slight gingivitis and were systemically

121 orrelate with the detrimental changes to the periodontium over time.

122 ions in bone, cartilage, enamel, dentin, and periodontium, patient-specific scaffolds, and incorporat

123 In a healthy periodontium PDL cells exhibit an osteoblast-like phenot

124 both infiltrating and resident cells of the periodontium, play a role in physiologic (e.g., tooth er

125 ded to test whether viral replication in the periodontium precedes the GBS symptoms.

126 technical complexity, patient morbidity, and periodontium preservation.

127 rmalities, but their roles in regulating the periodontium remain undefined and were the focus of our

128 redictable and complete regeneration of lost periodontium remains an elusive goal, despite advances i

129 After this time period, the stability of the periodontium should be evaluated rather than the effects

130 biologic properties of important proteins in periodontium, such as collagens.

131 wer degree of neutrophil infiltration in the periodontium than vehicle-treated animals; these actions

132 ic periodontitis is a chronic disease of the periodontium that elicits a general inflammatory respons

133 SCs) are responsible for regeneration of the periodontium that is lost due to periodontitis.

134 l trauma (OT) is an injury of the supportive periodontium that results in bone loss.

135 ng tooth to grow and the soft tissues of the periodontium to develop.

136 elial cells (GEC) are the first cells of the periodontium to encounter known periodontal pathogens, s

137 givalis W50 (P. gingivalis) in the maxillary periodontium to induce periodontitis.

138 stemic and local atorvastatin application on periodontium using histomorphometric and immunohistochem

139 The periodontium was analyzed by macroscopy, histometry, his

140 Periodontium was analyzed by macroscopy, microtomography

141 ) in mediating diabetic tissue damage to the periodontium was investigated in a novel model of chroni

142 e time of surgery, CEPs were found where the periodontium was most affected.

143 Autoreactivity to components of the periodontium was observed in CP and LAgP.

144 xamine the effects of these compounds on the periodontium, we assayed periodontal ligament (PDL) cell

145 Dynamic changes of the periodontium were evaluated by microcomputed tomography,

146 tastasizing in the oral mucosa, gingiva, and periodontium were included.

147 -two sites in 3 mini-swine pigs with healthy periodontium were selected.

148 s with mixed cell populations such as in the periodontium, where similar tissues like bone and cement

149 Upon injury, MSCs migrate to the periodontium, where they contribute to regeneration.

150 ared to those from participants with healthy periodontiums, whereas no differences in the expression

151 d in biopsies from participants with healthy periodontiums, whereas TLR2 levels were significantly up

152 ly activated pro-inflammatory factors in the periodontium, which subsequently impact on diabetes, rem

153 erosion of the hard and soft tissues of the periodontium, which, in severe cases, can result in toot

154 flammatory response results in damage to the periodontium while generally failing to control the path

155 riodontitis compared to animals with healthy periodontium (while maintaining normoglycemia).

156 astatin application showed better results on periodontium with regard to alveolar bone findings.