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1 ve tissue cells in tooth-supporting tissues (periodontium).
2 ts on the tooth-supporting structures of the periodontium.
3 and temporal aspects of inflammation in the periodontium.
4 minant extracellular matrix component in the periodontium.
5 sulting in the destruction of tissues of the periodontium.
6 etermine autoreactivity to components of the periodontium.
7 ute to a breakdown in the homeostasis of the periodontium.
8 entum, which are important components of the periodontium.
9 capable of differentiating into cells of the periodontium.
10 maintaining the functional integrity of the periodontium.
11 d the diagnosis of sarcoidosis affecting the periodontium.
12 he dental pulp, the deciduous tooth, and the periodontium.
13 virus (HIV) disease and its therapies on the periodontium.
14 of gingival pemphigoid lesions on the human periodontium.
15 crobial-induced inflammatory response in the periodontium.
16 these deleterious effects of smoking on the periodontium.
17 tory pathways involving sex steroids and the periodontium.
18 required for appropriate development of the periodontium.
19 roblasts, and in multinucleated cells in the periodontium.
20 wn much potential in the regeneration of the periodontium.
21 logic evaluation of all lesions found in the periodontium.
22 ntrations (1 to 30 mM) found in the diseased periodontium.
23 poxia, HIF-1 signaling and angiogenin in the periodontium.
24 ther than the deeper, connective tissues and periodontium.
25 ioactivity) to affect cells derived from the periodontium.
26 ation in local inflammatory responses in the periodontium.
27 e the delivery of this agent to the inflamed periodontium.
28 tribute to reparatory events in the inflamed periodontium.
29 ting the maintenance and regeneration of the periodontium.
30 strategies aimed at the regeneration of the periodontium.
31 responses from several cell types within the periodontium.
32 tical for the maintenance and healing of the periodontium.
33 ene expression in cells of importance to the periodontium.
34 xic disturbances in the pulp and surrounding periodontium.
35 f aberrant fibers in the dental follicle and periodontium.
36 the underlying inflammatory imbalance in the periodontium.
37 promoting hyperactive host responses in the periodontium.
38 ntify the main source cells of Ifi204 in the periodontium.
39 ase is the chronic infectious disease of the periodontium.
40 and promoted bone gain in the diseased mouse periodontium.
41 ribution of Gli1(+) MSCs within the inflamed periodontium.
42 o have deleterious effects on adjacent teeth periodontium.
43 x impact on the inflammatory response in the periodontium.
44 es the key feature of interfacial tissues in periodontium.
45 nds, tongue, floor of mouth, oropharynx, and periodontium.
46 rmation of enamel, dentin, cementum, and the periodontium.
47 d AgP and those with gingivitis or a healthy periodontium.
48 the healing and regeneration process of the periodontium.
49 mediators involved in the destruction of the periodontium.
50 a crucial role in the innate defense of the periodontium.
51 enamel formation and the development of the periodontium.
52 the factors involved in the breakdown of the periodontium.
53 a unique immune surveillance role within the periodontium.
54 apy is associated with severe destruction of periodontium.
55 25(OH)D] exerts any beneficial effect on the periodontium.
56 formation and maintenance of the surrounding periodontium.
57 application to achieve reconstruction of the periodontium.
58 to successfully enhance regeneration of the periodontium.
59 ms driving pathogenic events in the infected periodontium.
60 s do not cause permanent damage to a healthy periodontium.
61 lic alveolar bone homeostasis in the healthy periodontium.
62 hysiologic alveolar bone loss in the healthy periodontium.
63 asminogen activation by fibroblasts from the periodontium.
64 he known anabolic actions of thrombin in the periodontium.
65 e clinical and immunologic parameters of the periodontium.
66 that contribute to local inflammation in the periodontium.
67 s, cementoblasts, and fibroblasts within the periodontium.
68 P and 24 individuals with clinically healthy periodontium.
69 nuclear factor-kappaB immunostaining in the periodontium.
70 s specific site and bone cell actions in the periodontium.
71 lated among obese individuals with a healthy periodontium.
72 potential role in the tooth and surrounding periodontium.
73 periodontitis from individuals with healthy periodontium.
74 ction of fibrillar support structures of the periodontium.
75 ry between healthy and diseased sites in the periodontium.
76 Thirty-one females with PCOS and healthy periodontium, 30 females with PCOS and gingivitis, and 1
77 nduced diabetic mouse model and examined the periodontium 8 weeks later by histology, molecular and c
78 cells are the first line of defense for the periodontium against bacteria, we also evaluated whether
80 e had more osteoprogenitors recruited to the periodontium, allowing more bone formation to balance th
81 ere was no obvious morphologic change in the periodontium, although slight elevations of AGEs and RAG
83 d that two adjacent mesenchymal tissues, the periodontium and dental pulp, are maintained by distinct
84 umbers of osteoblasts and apoptotic cells in periodontium and diminished expression of osteoblast sig
86 ted effects of smokeless tobacco (ST) on the periodontium and high prevalence of ST use in rural popu
87 ve been shown to enhance inflammation in the periodontium and increase the risk or severity of period
88 and Fusobacterium nucleatum to colonize the periodontium and induce local and systemic inflammatory
89 eriodontal disease and patients with healthy periodontium and investigate the effects of periodontal
90 uronidase (GUS) degrades constituents of the periodontium and is used as a biomarker for periodontiti
92 concentrations of polyamines in the inflamed periodontium and possess a transport system for taking u
93 effectively transduce cells derived from the periodontium and promote biological activity equivalent
96 en restorative margins may interact with the periodontium and/or orthodontic treatment is indicated.
97 xpression of microRNAs (miRNAs) in maxillas (periodontium) and spleens isolated from ApoE(-/-) mice i
99 progressed to include deeper portions of the periodontium, and more of the teeth unaffected at baseli
100 n as problems that might have impacts on the periodontium, and reciprocal effects of periodontal dise
101 at Dmp1 is critical for the integrity of the periodontium, and that deletion may lead to increased su
102 that, even though oral cancers involving the periodontium are a relatively rare occurrence, periodont
105 y was to evaluate the impact of FTF on teeth periodontium, as well as assessing the impact of periodo
107 by ovariectomy in the apposition side of the periodontium but maintains bone formation over all the s
108 Periodontitis not only causes injury to the periodontium, but also damages other tissues such as: ar
109 ways altered by inflammation in the diabetic periodontium by using ligatures to induce periodontitis
110 e were grouped into 36 patients with healthy periodontium (CAD only) and 24 patients with periodontit
111 erant growth of connective tissue within the periodontium can result from hyperactivity of resident f
114 specific effects of cigarette smoking on the periodontium compared to never-smokers; (2) patterns of
117 It is thought that during development of the periodontium, dental follicle cells, when appropriately
118 nucleic acids are abundantly present in the periodontium, derived through release after phagocytic u
119 tin application showed beneficial effects on periodontium during and after induction of experimental
122 (MPO)-mediated carbamylation in the inflamed periodontium during the earliest phases of RA, which may
123 Orthodontic treatment can greatly impact the periodontium, especially in dentitions with a thin perio
124 s through proteolytic remodelling within the periodontium following the application of external force
125 ngivitis (Gg), 30 women with GDM and healthy periodontium (Gh), 28 systemically and periodontally hea
126 mice, although it is reduced in the lateral periodontium (gums) of neonatal Magel2-deficient mice co
127 raditional methods aimed at regenerating the periodontium have limited indications, and their results
129 mpromised, including reduced contribution to periodontium homeostasis and impaired injury response.
131 soft tissue healing and regeneration of the periodontium; however, the mechanisms of this action are
133 study demonstrated that regeneration of the periodontium in gingival recession defects was possible
138 of necrotizing ulcerative infections of the periodontium in the severely immunosuppressed patient.
139 molars, including the apposition side of the periodontium, in which RANKL expression was significantl
140 the occurrence of sarcoidosis affecting the periodontium, including its clinical features, diagnosis
142 t may be the precursor of other cells of the periodontium, including osteoblasts and cementoblasts.
143 ell RNA sequencing (scRNAseq) atlas of human periodontium, including sulcular and junctional keratino
144 tration of leukocytes and neutrophils to the periodontium increased at the site of ligature, which wa
145 ulate the host response to challenges in the periodontium, increasing the expression of periodontal b
150 on of structure and function of the diseased periodontium is often considered an unpredictable task.
152 pression of the subset of semaphorins in the periodontium likely to be most involved with regulating
153 high load of bacterial antigens--such as the periodontium, lung, and gut--may represent the initial s
154 ease is characterized by inflammation of the periodontium manifested by recruitment of neutrophils, w
155 re elevation at sites of inflammation in the periodontium may be a significant environmental regulato
158 both hard and soft tissue components of the periodontium, may be preferable for assessing efficacy o
160 esent report describes active CMV within the periodontium of a 37-year-old patient affected by GBS.
162 hages were demonstrated to be present in the periodontium of old and young mice in equal numbers in c
163 mbers of RANKL+ cells and IL17+ cells in the periodontium of SPF mice demonstrate possible molecular
165 (FTF) elevation could potentially affect the periodontium of the involved teeth; it is not clear if t
168 ts were 21 to 35 years of age with a healthy periodontium or slight gingivitis and were systemically
171 ions in bone, cartilage, enamel, dentin, and periodontium, patient-specific scaffolds, and incorporat
172 the hypotheses that: (1) inflammation of the periodontium (PD(inflammation) ) predicts future CVD ind
174 both infiltrating and resident cells of the periodontium, play a role in physiologic (e.g., tooth er
175 oral inflammation causes destruction of the periodontium, potentially leading to loss of the dentiti
176 film composition in individuals with reduced periodontium (PPC-VI) was similar to health but showed m
180 rmalities, but their roles in regulating the periodontium remain undefined and were the focus of our
181 redictable and complete regeneration of lost periodontium remains an elusive goal, despite advances i
182 he trigeminal ganglion including the lateral periodontium, rostral periodontium, tongue, olfactory ep
183 After this time period, the stability of the periodontium should be evaluated rather than the effects
185 wer degree of neutrophil infiltration in the periodontium than vehicle-treated animals; these actions
186 wed mitigation of microbial dysbiosis in the periodontium that correlated with a reduction in microbi
187 imbalanced host-microbe interactions in the periodontium that culminate in dysbiosis and inflammator
188 ic periodontitis is a chronic disease of the periodontium that elicits a general inflammatory respons
190 ator of inflammatory cell trafficking to the periodontium that protects against bone loss and offers
194 AM20C and Periostin was examined using mouse periodontium tissues by immunohistochemical analysis.
196 elial cells (GEC) are the first cells of the periodontium to encounter known periodontal pathogens, s
198 including the lateral periodontium, rostral periodontium, tongue, olfactory epithelium, whisker pads
199 stemic and local atorvastatin application on periodontium using histomorphometric and immunohistochem
202 ) in mediating diabetic tissue damage to the periodontium was investigated in a novel model of chroni
206 eriodontitis and gingivitis and with healthy periodontium was the purpose of this clinical research.
207 eriodontitis and gingivitis and with healthy periodontium was the purpose of this clinical research.
208 xamine the effects of these compounds on the periodontium, we assayed periodontal ligament (PDL) cell
212 ring from gingival inflammation with reduced periodontium were taken before professional mechanical p
213 t (12-15 y), and aged (>17 y)-with a healthy periodontium were used to characterize gene expression i
214 s with mixed cell populations such as in the periodontium, where similar tissues like bone and cement
216 ared to those from participants with healthy periodontiums, whereas no differences in the expression
217 d in biopsies from participants with healthy periodontiums, whereas TLR2 levels were significantly up
218 blasts (GFs) are essential components of the periodontium, which are responsible for the maintenance
219 ly activated pro-inflammatory factors in the periodontium, which subsequently impact on diabetes, rem
220 erosion of the hard and soft tissues of the periodontium, which, in severe cases, can result in toot
221 flammatory response results in damage to the periodontium while generally failing to control the path
223 astatin application showed better results on periodontium with regard to alveolar bone findings.
224 to find out the early effects of T1DM on the periodontium without any experimentally induced periodon