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1 eter for monitoring periodontal/peri-implant alveolar bone loss.
2 result in resistance to T. forsythia-induced alveolar bone loss.
3 the regulation of gingival inflammation and alveolar bone loss.
4 ) were used to determine the heritability of alveolar bone loss.
5 A periodontal probe was used to measure alveolar bone loss.
6 betes-associated severe inflammation-induced alveolar bone loss.
7 s that are able to modulate inflammation and alveolar bone loss.
8 healthy children who subsequently developed alveolar bone loss.
9 ate healing following extraction to minimize alveolar bone loss.
10 ease in the oral cavity, which culminates in alveolar bone loss.
11 hree methods yielded efficient evaluation of alveolar bone loss.
12 c strategy for the prevention of progressive alveolar bone loss.
13 el to compare three approaches for assessing alveolar bone loss.
14 esponses promote severe infection-stimulated alveolar bone loss.
15 ate immune system, resulting in inflammatory alveolar bone loss.
16 omponent in the extent of implant-associated alveolar bone loss.
17 esis in the mouse model of infection-induced alveolar bone loss.
18 Radiographic evaluation demonstrated severe alveolar bone loss.
19 lack of interleukin-10 leads to accelerated alveolar bone loss.
20 ain-matched interleukin-10(+/+) controls for alveolar bone loss.
21 ive against subsequent P. gingivalis-induced alveolar bone loss.
22 lammatory periodontal disease, and therefore alveolar bone loss.
23 STAMP-mAb downregulated the ligature-induced alveolar bone loss.
24 AGE, paralleling the observed suppression in alveolar bone loss.
25 bone metabolism and can therefore influence alveolar bone loss.
26 ut not HIV status was the primary factor for alveolar bone loss.
27 one density allowing for a greater amount of alveolar bone loss.
28 ith P. gingivalis (W50) or placebo to induce alveolar bone loss.
29 nt acid phosphatase-positive (TRAP+) OCs and alveolar bone loss.
30 ces LPS-induced periodontal inflammation and alveolar bone loss.
31 efense responses to oral bacteria can induce alveolar bone loss.
32 ostimulatory activity, which is critical for alveolar bone loss.
33 result in irreversible inflammation-mediated alveolar bone loss.
34 t against pathobionts, but also by promoting alveolar bone loss.
35 hich is characterized by inflammation-driven alveolar bone loss.
36 recently to stimulate osteoblasts and reduce alveolar bone loss.
37 emic attack in relation to mean radiographic alveolar bone loss (a measure of periodontitis history)
40 effects of a 2% cholesterol-enriched diet on alveolar bone loss (ABL) and serum levels of pro-oxidant
41 depth (PD), myeloperoxidase (MPO) activity, alveolar bone loss (ABL) for periodontal tissues; histop
42 probing, clinical attachment loss (CAL), and alveolar bone loss (ABL) from radiographs were measured
43 related orphan receptor (ROR) gammat; and 3) alveolar bone loss (ABL) in experimental periodontitis.
44 nt on serum oxidative stress index (OSI) and alveolar bone loss (ABL) in rats with diabetes mellitus
45 tigate effects of strontium ranelate (SR) on alveolar bone loss (ABL) in rats with experimental perio
47 se tolerance development are associated with alveolar bone loss (ABL) in susceptible individuals.
48 es) demonstrated that EP-TIL1 presented less alveolar bone loss (ABL) than EP (P <0.05), whereas EP-T
51 proinflammatory cytokine levels, apoptosis, alveolar bone loss (ABL), lipid metabolism, and diabetic
52 (PD), bleeding on probing, and radiographic alveolar bone loss (ABL), measured on intraoral periapic
57 dysregulation participates in the increased alveolar bone loss after bacterial infection observed in
62 To study the effects of RANKL inhibition on alveolar bone loss, an experimental ligature-induced mod
63 , and osteopontin as potential biomarkers of alveolar bone loss and 2) determine whether the glycemic
64 ed with DTrp(8)-gammaMSH presented decreased alveolar bone loss and a lower degree of neutrophil infi
65 ignificantly decreased RANKL+ Th1-associated alveolar bone loss and coexpression of human gamma inter
66 fective in the stabilization or reduction of alveolar bone loss and collagen degradation in rats.
67 s fractured molar roots, distorted incisors, alveolar bone loss and compressed temporomandibular join
68 HLA-B27 rats are susceptible to accelerated alveolar bone loss and could serve as an animal model of
69 s HN019 promotes a protective effect against alveolar bone loss and CTALs attributable to EP in rats,
70 Positive correlations were found between alveolar bone loss and density of inflammation (rho = 0.
71 able genetic basis for P. gingivalis-induced alveolar bone loss and open the possibility of exploitin
72 rated that simvastatin inhibited LPS-induced alveolar bone loss and periodontal tissue inflammation i
73 n A. actinomycetemcomitans can induce severe alveolar bone loss and proinflammatory cytokine producti
74 jection of anti-DC-STAMP-mAb also suppressed alveolar bone loss and reduced the total number of multi
75 stomorphometric analyses confirmed increased alveolar bone loss and revealed increased numbers of TRA
77 ice infected with P. gingivalis demonstrated alveolar bone loss and serum anti-P. gingivalis antibody
78 rformed to study the association of AMD with alveolar bone loss and the number of teeth by controllin
79 s study was to evaluate the effect of HFA on alveolar bone loss and the rate of bone formation after
80 ships and multivariate relationships between alveolar bone loss and three sets of variables were eval
83 hat skeletal BMD is related to interproximal alveolar bone loss and, to a lesser extent, to clinical
84 e safe treatment that can be used to prevent alveolar bone loss and/or accelerate bone healing after
85 (i.e., at least one site with > or =3 mm of alveolar bone loss) and a random sample of 66 periodonta
86 indicate an association of this enzyme with alveolar bone loss, and may warrant special attention in
87 ge, sex, smoking, diabetes, body mass index, alveolar bone loss, and number of teeth), having WPSs as
88 gingival bleeding, clinical attachment loss, alveolar bone loss, and presence of subgingival microorg
89 s an important organism involved in inducing alveolar bone loss, and the BspA protein is an important
91 nship between this biochemical parameter and alveolar bone loss around natural teeth and dental impla
92 dental disease which results in irreversible alveolar bone loss around teeth, and subsequent tooth lo
94 on to being associated with the incidence of alveolar bone loss (as demonstrated in previous studies)
95 djusting for confounders, each millimeter of alveolar bone loss at baseline increased the risk of too
96 Using a model involving inflammation-driven alveolar bone loss attributable to infection, we showed
97 severity of periodontitis for premolars with alveolar bone loss based on 3D's or 2D's measurement is
98 All ARIs demonstrated efficacy in preventing alveolar bone loss because of periodontitis in both anim
99 se model, we investigated the progression of alveolar bone loss by gene expression profiling of susce
102 ion with the two species induces synergistic alveolar bone loss, characterized by bone loss which is
103 a reduction of serum inflammatory cytokines, alveolar bone loss, cholesterol, and atherosclerotic les
104 ificant increases in inflammatory cytokines, alveolar bone loss, cholesterol, and atherosclerotic les
105 sequence, there is significant interproximal alveolar bone loss, combined with detachment between the
106 Mixed infection with capsulated Pg augmented alveolar bone loss compared with that of mixed infection
107 teinase 9 (Mmp9) in the gingiva; support and alveolar bone loss; connective tissue attachment; and th
108 he relationship between pairwise kinship and alveolar bone loss data to determine the heritability of
109 ons were found between smoking and extent of alveolar bone loss (distance) (P < 0.001) as well as the
110 fic RANKL-expressing CD4(+) Th cell-mediated alveolar bone loss during the progression of periodontal
112 ed tomography was used to measure volumetric alveolar bone loss, expressed as bone volume fraction (B
113 F-deficient (Tnf(-/-)) mice are resistant to alveolar bone loss following oral infection with P. ging
114 veness of immunization in protecting against alveolar bone loss following P. gingivalis infection was
115 ground and observed a similar enhancement in alveolar bone loss following P. gingivalis infection.
116 eria, and neutralizing TNF in vivo abrogated alveolar bone loss following P. gingivalis infection.
118 CAL), the radiographic pattern and extent of alveolar bone loss, gingival inflammation measured as bl
119 re, and periodontal bone loss was defined as alveolar bone loss >/=3 mm on >/=1 permanent tooth site
120 ttachment loss >/=5 mm (1.19; 1.00 to 1.41), alveolar bone loss >/=40% (1.25; 1.00 to 1.56), and toot
121 nt loss (>/=5 mm), mobility (>/=0.5 mm), and alveolar bone loss (>/=40% of the distance from the ceme
122 l therapy, sites with angular and horizontal alveolar bone loss had additional bone loss of 5.56% and
126 e progression of attachment and radiographic alveolar bone loss in a ligature-induced beagle dog mode
127 is being required for the pathogen to induce alveolar bone loss in a model of periodontitis and revea
128 timulate the host immune response and induce alveolar bone loss in a murine experimental periodontiti
129 specific elevated fatty acid (FA) levels on alveolar bone loss in a Porphyromonas gingivalis-induced
130 associated with HIV infection are related to alveolar bone loss in a sample of subjects screened at a
131 ization, immunoglobulin (Ig) G response, and alveolar bone loss in Aggregatibacter actinomycetemcomit
132 with increased periodontal inflammation and alveolar bone loss in an LPS-induced periodontitis anima
133 s of MMPs, preventing collagen breakdown and alveolar bone loss in animal models of periodontitis.
134 he following variables were found related to alveolar bone loss in bivariate relationships: age (P <
135 The objective of this study was to compare alveolar bone loss in control (C) and ovariectomized she
137 d TIL solution (1 mg/kg body weight) reduced alveolar bone loss in experimental periodontitis and the
141 suggest that HIV infection is not related to alveolar bone loss in individuals with high-risk behavio
146 orrelation between systemic osteoporosis and alveolar bone loss in periodontal disease pathogenesis.
147 proaches have also been applied to measuring alveolar bone loss in periodontitis models, including hi
149 establish a model of aggressive inflammatory alveolar bone loss in rats using LPS derived from the pe
151 that PROB supplementation 1) reduces AL and alveolar bone loss in rats with LIP and 2) can protect t
153 ting the up-regulated osteoclastogenesis and alveolar bone loss in SPF mice compared with GF mice.
155 nly the ligature model displayed significant alveolar bone loss in the initial period (7 days), which
157 t BAR reduces P. gingivalis colonization and alveolar bone loss in vivo in a murine model of periodon
158 t TLR2 is required for P. gingivalis-induced alveolar bone loss in vivo, and our in vitro work implic
160 ot 500 nmol caused significant inhibition of alveolar bone loss, increase of bone alkaline phosphatas
162 the role of the adaptive immune response in alveolar bone loss induced by oral infection with the hu
164 bone loss which is greater than the additive alveolar bone losses induced by each species alone.
165 y, CXCR2(KO) mice were highly susceptible to alveolar bone loss; interestingly, these mice also sugge
166 ounterparts suggest that naturally occurring alveolar bone loss is a normal component of healthy peri
169 y published data from a mouse model in which alveolar bone loss is induced by oral infection with Por
171 Periodontal disease, especially measured by alveolar bone loss, is a strong and independent predicto
172 ionships between HIV infection and increased alveolar bone loss may be explained by other factors, su
173 nd able to diagnose this condition, as rapid alveolar bone loss may be the first sign of sarcoidosis.
176 consumption was not significantly related to alveolar bone loss nor to any of the subgingival microor
177 antly associated with greater attachment and alveolar bone loss (odds ratio, OR = 1.70, 95% CI = 1.09
178 icate that Porphyromonas gingivalis mediates alveolar bone loss or osteoclast modulation through enga
179 loss (OR = 2.24, 95% CI = 1.15 to 4.38) and alveolar bone loss (OR = 1.91, 95% CI = 1.15 to 3.17) th
180 nd that a HFD markedly increased LPS-induced alveolar bone loss, osteoclastogenesis, and inflammatory
181 treatment was accompanied by lower rates of alveolar bone loss (P <0.05) and maintenance of the amou
182 owngrowth (P <0.05), inflammation (P <0.05), alveolar bone loss (P <0.05), and osteoclast activity (P
184 with AMD had fewer teeth (P <0.001) and more alveolar bone loss (P = 0.004) compared with non-AMD par
186 tus (NIDDM) have greater risk of more severe alveolar bone loss progression over a 2-year period than
188 and Stat6) or resistance (Il15 and Selp) to alveolar bone loss, providing insight into the genetic e
189 argeting oral bacteria protect the host from alveolar bone loss, recent studies show that particular
191 rinses, and systemic metronidazole therapy, alveolar bone loss resulted in tooth mobility necessitat
195 ed with heat-killed Pg displayed significant alveolar bone loss starting from day 15, which continued
196 nd the severity of gingival inflammation and alveolar bone loss (subgroups) without producing antibio
197 (+) cells are resistant to infection-induced alveolar bone loss, Th cells have been implicated in bon
198 eukin-10(-/-) mice had significantly greater alveolar bone loss than interleukin-10(+/+) mice (p = 0.
200 TLR9(-/-) mice exhibited significantly less alveolar bone loss than their wild-type (WT) counterpart
201 ence of inflammation, it was the presence of alveolar bone loss that lead to significantly higher val
202 d clinical measures of inflammation and less alveolar bone loss under severe inflammatory conditions
205 del adjusted for age, smoking, and diabetes, alveolar bone loss was associated with AMD in males with
206 Conversely, P. gingivalis infection-induced alveolar bone loss was attenuated in mice lacking ST2.
207 ion, and osteoclast activity were evaluated; alveolar bone loss was determined by histomorphometry, m
215 Compared to the ligature + placebo group, alveolar bone loss was reduced in the fluoxetine group (
216 ntages of fat (P = nonsignificant); however, alveolar bone loss was significantly greater in animals
219 +/-2.1 mm, furcation involvement, and severe alveolar bone loss were observed in a 41-year-old Caucas
222 onstrated that group EP/EA presented reduced alveolar bone loss when compared to group EP (P <0.05).
223 alis-infected mice significantly exacerbated alveolar bone loss when compared with infection or IL-33
224 )) were protected from P. gingivalis-induced alveolar bone loss, with a reduction in anti-P. gingival
225 ceptible to A. actinomycetemcomitans-induced alveolar bone loss, with different patterns of immune re
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