ライフサイエンスコーパス: alveolar bone loss

1 result in irreversible inflammation-mediated alveolar bone loss.

2 t against pathobionts, but also by promoting alveolar bone loss.

3 recently to stimulate osteoblasts and reduce alveolar bone loss.

4 eter for monitoring periodontal/peri-implant alveolar bone loss.

5 result in resistance to T. forsythia-induced alveolar bone loss.

6 the regulation of gingival inflammation and alveolar bone loss.

7 ) were used to determine the heritability of alveolar bone loss.

8 A periodontal probe was used to measure alveolar bone loss.

9 betes-associated severe inflammation-induced alveolar bone loss.

10 healthy children who subsequently developed alveolar bone loss.

11 ate healing following extraction to minimize alveolar bone loss.

12 ease in the oral cavity, which culminates in alveolar bone loss.

13 hree methods yielded efficient evaluation of alveolar bone loss.

14 c strategy for the prevention of progressive alveolar bone loss.

15 el to compare three approaches for assessing alveolar bone loss.

16 esponses promote severe infection-stimulated alveolar bone loss.

17 ate immune system, resulting in inflammatory alveolar bone loss.

18 omponent in the extent of implant-associated alveolar bone loss.

19 esis in the mouse model of infection-induced alveolar bone loss.

20 Radiographic evaluation demonstrated severe alveolar bone loss.

21 lack of interleukin-10 leads to accelerated alveolar bone loss.

22 ain-matched interleukin-10(+/+) controls for alveolar bone loss.

23 ive against subsequent P. gingivalis-induced alveolar bone loss.

24 lammatory periodontal disease, and therefore alveolar bone loss.

25 AGE, paralleling the observed suppression in 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 crobiota and accelerated naturally occurring alveolar bone loss.

29 mensal microbiota drives naturally occurring alveolar bone loss.

30 ium (JE) downgrowth, bacterial invasion, and alveolar bone loss.

31 d with the number of periodontal pockets and alveolar bone loss.

32 sponses in gingival tissues, and exacerbates alveolar bone loss.

33 e a pathogenic role of STAT3 in inflammatory alveolar bone loss.

34 lls, resulting in striking susceptibility to alveolar bone loss.

35 tory cytokines, leading to periodontitis and alveolar bone loss.

36 crobiota more pathogenic, leading to greater alveolar bone loss.

37 which in turn trigger inflammation and mild alveolar bone loss.

38 STAMP-mAb downregulated the ligature-induced alveolar bone loss.

39 nt acid phosphatase-positive (TRAP+) OCs and alveolar bone loss.

40 hich is characterized by inflammation-driven alveolar bone loss.

41 s that are able to modulate inflammation and alveolar bone loss.

42 bone metabolism and can therefore influence alveolar bone loss.

43 significantly reduced P. gingivalis-induced alveolar bone loss.

44 ith P. gingivalis (W50) or placebo to induce alveolar bone loss.

45 on of PD, both WT and 5xFAD mice experienced alveolar bone loss.

46 e could eventually arrest the RANKL-mediated alveolar bone loss.

47 ces LPS-induced periodontal inflammation and alveolar bone loss.

48 efense responses to oral bacteria can induce alveolar bone loss.

49 ostimulatory activity, which is critical for alveolar bone loss.

50 , severe periodontal defects and significant alveolar bone loss (14%; P < 0.0001) were evident in Ddr

51 emic attack in relation to mean radiographic alveolar bone loss (a measure of periodontitis history)

52 Periodontal status, i.e., alveolar bone loss (ABL) and alveolar bone crest, was ex

53 sulted in local and systemic damage, such as alveolar bone loss (ABL) and kidney damage, and the cons

54 Higher linear alveolar bone loss (ABL) and lower interradicular bone d

55 effects of a 2% cholesterol-enriched diet on alveolar bone loss (ABL) and serum levels of pro-oxidant

56 depth (PD), myeloperoxidase (MPO) activity, alveolar bone loss (ABL) for periodontal tissues; histop

57 probing, clinical attachment loss (CAL), and alveolar bone loss (ABL) from radiographs were measured

58 related orphan receptor (ROR) gammat; and 3) alveolar bone loss (ABL) in experimental periodontitis.

59 nt on serum oxidative stress index (OSI) and alveolar bone loss (ABL) in rats with diabetes mellitus

60 tigate effects of strontium ranelate (SR) on alveolar bone loss (ABL) in rats with experimental perio

61 diet-induced obesity/hyperlipidemia (CAF) on alveolar bone loss (ABL) in rats.

62 se tolerance development are associated with alveolar bone loss (ABL) in susceptible individuals.

63 Capz prevented alveolar bone loss (ABL) on the external crests and in t

64 es) demonstrated that EP-TIL1 presented less alveolar bone loss (ABL) than EP (P <0.05), whereas EP-T

65 al panoramic radiographs were used to assess alveolar bone loss (ABL) using a Schei ruler.

66 This study examines: 1) alveolar bone loss (ABL), a hallmark of periodontitis, i

67 proinflammatory cytokine levels, apoptosis, alveolar bone loss (ABL), lipid metabolism, and diabetic

68 (PD), bleeding on probing, and radiographic alveolar bone loss (ABL), measured on intraoral periapic

69 f bleeding on probing (BOP) and radiographic alveolar bone loss (ABL).

70 tion between root proximity and the risk for alveolar bone loss (ABL).

71 ed male WT breeding mates, were examined for alveolar bone loss (ABL).

72 ical attachment loss (CAL) and interproximal alveolar bone loss (ABL).

73 s were removed for macroscopic evaluation of alveolar bone loss (ABL).

74 dysregulation participates in the increased alveolar bone loss after bacterial infection observed in

75 s increase susceptibility to and severity of alveolar bone loss after P. gingivalis infection.

76 ion showed over 50% reduction in the risk of alveolar bone loss among non-molars (P = 0.015).

77 tooth loss among molars and minimization of alveolar bone loss among non-molars.

78 Alveolar bone loss among the groups was estimated by mea

79 To study the effects of RANKL inhibition on alveolar bone loss, an experimental ligature-induced mod

80 , and osteopontin as potential biomarkers of alveolar bone loss and 2) determine whether the glycemic

81 ed with DTrp(8)-gammaMSH presented decreased alveolar bone loss and a lower degree of neutrophil infi

82 ignificantly decreased RANKL+ Th1-associated alveolar bone loss and coexpression of human gamma inter

83 fective in the stabilization or reduction of alveolar bone loss and collagen degradation in rats.

84 s fractured molar roots, distorted incisors, alveolar bone loss and compressed temporomandibular join

85 HLA-B27 rats are susceptible to accelerated alveolar bone loss and could serve as an animal model of

86 s HD100 promotes a protective effect against alveolar bone loss and CTAL in rats with EP.

87 s HN019 promotes a protective effect against alveolar bone loss and CTALs attributable to EP in rats,

88 Positive correlations were found between alveolar bone loss and density of inflammation (rho = 0.

89 iorative effect against the ligation-induced alveolar bone loss and effectively inhibits the producti

90 and Sg resulted in a significant increase in alveolar bone loss and gingival IL-17 expression over sh

91 at berberine treatment significantly reduced alveolar bone loss and improved bone metabolism of OVX-p

92 inflammatory disease associated with severe alveolar bone loss and is dominantly induced by lipopoly

93 nomycetemcomitans lipopolysaccharide-induced alveolar bone loss and microcomputed tomography was used

94 able genetic basis for P. gingivalis-induced alveolar bone loss and open the possibility of exploitin

95 rated that simvastatin inhibited LPS-induced alveolar bone loss and periodontal tissue inflammation i

96 First, it reduced alveolar bone loss and preserved bone structure by decre

97 n A. actinomycetemcomitans can induce severe alveolar bone loss and proinflammatory cytokine producti

98 jection of anti-DC-STAMP-mAb also suppressed alveolar bone loss and reduced the total number of multi

99 stomorphometric analyses confirmed increased alveolar bone loss and revealed increased numbers of TRA

100 Alveolar bone loss and root surface lesions developed in

101 ice infected with P. gingivalis demonstrated alveolar bone loss and serum anti-P. gingivalis antibody

102 rformed to study the association of AMD with alveolar bone loss and the number of teeth by controllin

103 s study was to evaluate the effect of HFA on alveolar bone loss and the rate of bone formation after

104 ships and multivariate relationships between alveolar bone loss and three sets of variables were eval

105 classification of disease severity based on alveolar bone loss and tooth loss during follow-up.

106 ient compliance (complete versus erratic) on alveolar bone loss and tooth survival.

107 hat skeletal BMD is related to interproximal alveolar bone loss and, to a lesser extent, to clinical

108 e safe treatment that can be used to prevent alveolar bone loss and/or accelerate bone healing after

109 (i.e., at least one site with > or =3 mm of alveolar bone loss) and a random sample of 66 periodonta

110 evated several years prior to progression of alveolar bone loss, and include antecedent elevations in

111 indicate an association of this enzyme with alveolar bone loss, and may warrant special attention in

112 ge, sex, smoking, diabetes, body mass index, alveolar bone loss, and number of teeth), having WPSs as

113 gingival bleeding, clinical attachment loss, alveolar bone loss, and presence of subgingival microorg

114 s an important organism involved in inducing alveolar bone loss, and the BspA protein is an important

115 Periodontitis, alveolar bone loss, and tooth loss are associated with l

116 nship between this biochemical parameter and alveolar bone loss around natural teeth and dental impla

117 dental disease which results in irreversible alveolar bone loss around teeth, and subsequent tooth lo

118 Desipramine administration reduced alveolar bone loss as histologically observed, and modul

119 ed with not only systemic BMD loss, but with alveolar bone loss as well.

120 on to being associated with the incidence of alveolar bone loss (as demonstrated in previous studies)

121 djusting for confounders, each millimeter of alveolar bone loss at baseline increased the risk of too

122 Using a model involving inflammation-driven alveolar bone loss attributable to infection, we showed

123 severity of periodontitis for premolars with alveolar bone loss based on 3D's or 2D's measurement is

124 All ARIs demonstrated efficacy in preventing alveolar bone loss because of periodontitis in both anim

125 se model, we investigated the progression of alveolar bone loss by gene expression profiling of susce

126 In addition, alveolar bone loss can accurately be quantified using an

127 Alveolar bone loss can be a major clinical concern affec

128 ion with the two species induces synergistic alveolar bone loss, characterized by bone loss which is

129 a reduction of serum inflammatory cytokines, alveolar bone loss, cholesterol, and atherosclerotic les

130 ificant increases in inflammatory cytokines, alveolar bone loss, cholesterol, and atherosclerotic les

131 sequence, there is significant interproximal alveolar bone loss, combined with detachment between the

132 t baseline, 5xFAD mice presented significant alveolar bone loss compared to WT mice.

133 Mixed infection with capsulated Pg augmented alveolar bone loss compared with that of mixed infection

134 teinase 9 (Mmp9) in the gingiva; support and alveolar bone loss; connective tissue attachment; and th

135 he relationship between pairwise kinship and alveolar bone loss data to determine the heritability of

136 Silibinin significantly reduced the alveolar bone loss, decreased the gingival inflammation

137 ons were found between smoking and extent of alveolar bone loss (distance) (P < 0.001) as well as the

138 perimental periodontitis (EP) by attenuating alveolar bone loss due to reduction in inflammatory cyto

139 fic RANKL-expressing CD4(+) Th cell-mediated alveolar bone loss during the progression of periodontal

140 Self-report questions related to alveolar bone loss exhibit excellent convergent validity

141 ed tomography was used to measure volumetric alveolar bone loss, expressed as bone volume fraction (B

142 ts surrounding dental implants, and reverses alveolar bone loss following extraction socket remodelin

143 ed with controls, mut-Stat3 mice had reduced alveolar bone loss following ligature-induced periodonti

144 F-deficient (Tnf(-/-)) mice are resistant to alveolar bone loss following oral infection with P. ging

145 veness of immunization in protecting against alveolar bone loss following P. gingivalis infection was

146 ground and observed a similar enhancement in alveolar bone loss following P. gingivalis infection.

147 eria, and neutralizing TNF in vivo abrogated alveolar bone loss following P. gingivalis infection.

148 e loss data to determine the heritability of alveolar bone loss from periodontal disease.

149 nduced significant oral pathology, including alveolar bone loss, gingival epithelial hyperplasia, inf

150 CAL), the radiographic pattern and extent of alveolar bone loss, gingival inflammation measured as bl

151 ted with type 2 diabetes (T2D) by evaluating alveolar bone loss, glycemic control, inflammation, and

152 re, and periodontal bone loss was defined as alveolar bone loss >/=3 mm on >/=1 permanent tooth site

153 ttachment loss >/=5 mm (1.19; 1.00 to 1.41), alveolar bone loss >/=40% (1.25; 1.00 to 1.56), and toot

154 nt loss (>/=5 mm), mobility (>/=0.5 mm), and alveolar bone loss (>/=40% of the distance from the ceme

155 l therapy, sites with angular and horizontal alveolar bone loss had additional bone loss of 5.56% and

156 protection takes place in infection-induced alveolar bone loss has not been investigated.

157 uman gingival tissues and its involvement in alveolar bone loss has yet to be explored.

158 ression in the db/db TG mice prevented early alveolar bone loss; however, it did not impact the devel

159 al disease by evaluating the heritability of alveolar bone loss in a captive baboon population.

160 Blockade of RAGE diminished alveolar bone loss in a dose-dependent manner.

161 e progression of attachment and radiographic alveolar bone loss in a ligature-induced beagle dog mode

162 is being required for the pathogen to induce alveolar bone loss in a model of periodontitis and revea

163 bacteria, on the progression of inflammatory alveolar bone loss in a model of periodontitis.

164 cts against Porphyromonas gingivalis-induced alveolar bone loss in a mouse model.

165 timulate the host immune response and induce alveolar bone loss in a murine experimental periodontiti

166 specific elevated fatty acid (FA) levels on alveolar bone loss in a Porphyromonas gingivalis-induced

167 associated with HIV infection are related to alveolar bone loss in a sample of subjects screened at a

168 ization, immunoglobulin (Ig) G response, and alveolar bone loss in Aggregatibacter actinomycetemcomit

169 with increased periodontal inflammation and alveolar bone loss in an LPS-induced periodontitis anima

170 s of MMPs, preventing collagen breakdown and alveolar bone loss in animal models of periodontitis.

171 he following variables were found related to alveolar bone loss in bivariate relationships: age (P <

172 of LCN-2 in T2D-periodontitis mice decreased alveolar bone loss in buccal and palatal surfaces and pr

173 The objective of this study was to compare alveolar bone loss in control (C) and ovariectomized she

174 but abnormal mandibular condyles, as well as alveolar bone loss in Ddr1(-/-) mice versus WT controls

175 Alveolar bone loss in elderly populations is highly prev

176 ttle information concerning the incidence of alveolar bone loss in estrogen-deficient women.

177 d TIL solution (1 mg/kg body weight) reduced alveolar bone loss in experimental periodontitis and the

178 treatment with rTMD1 hindered Pg-LPS-induced alveolar bone loss in experimental periodontitis in mice

179 We hypothesized that SOCS-3 regulates alveolar bone loss in experimental periodontitis.

180 fects the course of chronic inflammation and alveolar bone loss in females.

181 ation was to compare the naturally occurring alveolar bone loss in HLA-B27 and wild type rats.

182 ount in part for the observed suppression of alveolar bone loss in immunized monkeys.

183 suggest that HIV infection is not related to alveolar bone loss in individuals with high-risk behavio

184 The 30-40% greater alveolar bone loss in interleukin-10(-/-) mice was evide

185 .8 mm is a significant local risk factor for alveolar bone loss in mandibular anterior teeth.

186 The results showed alveolar bone loss in mice infected with the T. forsythi

187 lpha and MIP-2 secretion and ameliorated the alveolar bone loss in mice.

188 r disrupted the oral bacteriome and worsened alveolar bone loss in minocycline-treated SPF mice, vali

189 1 phenotype:M2 phenotype ratio and prevented alveolar bone loss in mouse periodontitis models.

190 ene therapy is a promising strategy to treat alveolar bone loss in osteoporosis.

191 Results showed more alveolar bone loss in patients with cardiac disease than

192 d a bone-targeted gene therapy that reverses alveolar bone loss in patients with osteoporosis by targ

193 orrelation between systemic osteoporosis and alveolar bone loss in periodontal disease pathogenesis.

194 proaches have also been applied to measuring alveolar bone loss in periodontitis models, including hi

195 e SOCS-3 as a critical negative regulator of alveolar bone loss in periodontitis.

196 establish a model of aggressive inflammatory alveolar bone loss in rats using LPS derived from the pe

197 9 (MMP-9), interleukin-1beta (IL-1beta), and alveolar bone loss in rats with diabetes.

198 that PROB supplementation 1) reduces AL and alveolar bone loss in rats with LIP and 2) can protect t

199 cytokine expression, osteoclastogenesis, and alveolar bone loss in rats.

200 ting the up-regulated osteoclastogenesis and alveolar bone loss in SPF mice compared with GF mice.

201 cteriome and exacerbated naturally occurring alveolar bone loss in SPF mice.

202 phy analysis showed significant reduction of alveolar bone loss in the CCL2 MP treatment group when c

203 e immune response contributes to physiologic alveolar bone loss in the healthy periodontium.

204 nly the ligature model displayed significant alveolar bone loss in the initial period (7 days), which

205 CT findings revealed significantly increased alveolar bone loss in the Lig group, which was significa

206 the junctional epithelium and increased the alveolar bone loss in the ligature-induced periodontitis

207 PT reduced alveolar bone loss in unstressed animals.

208 t BAR reduces P. gingivalis colonization and alveolar bone loss in vivo in a murine model of periodon

209 t TLR2 is required for P. gingivalis-induced alveolar bone loss in vivo, and our in vitro work implic

210 tored the ability of P. gingivalis to induce alveolar bone loss in vivo.

211 han PAMAM-G3 in reducing proinflammation and alveolar bone loss in vivo.

212 ot 500 nmol caused significant inhibition of alveolar bone loss, increase of bone alkaline phosphatas

213 Simultaneously, alveolar bone loss increased from baseline to the 2- and

214 trated this preventative treatment decreases alveolar bone loss, increases the local ratio of Tregs t

215 the role of the adaptive immune response in alveolar bone loss induced by oral infection with the hu

216 rtin agonism as a viable strategy to control alveolar bone loss induced by oral infection.

217 bone loss which is greater than the additive alveolar bone losses induced by each species alone.

218 Alveolar bone loss, infiltrated inflammatory cells, immu

219 y, CXCR2(KO) mice were highly susceptible to alveolar bone loss; interestingly, these mice also sugge

220 ounterparts suggest that naturally occurring alveolar bone loss is a normal component of healthy peri

221 Alveolar bone loss is a result of an aggressive form of

222 Periodontitis-mediated alveolar bone loss is caused by dysbiotic shifts in the

223 In this population-based health survey, alveolar bone loss is independently associated with AMD

224 y published data from a mouse model in which alveolar bone loss is induced by oral infection with Por

225 Using a murine model in which alveolar bone loss is induced by oral infection with Por

226 outcomes, implying that antimicrobial-driven alveolar bone loss is microbiota dependent.

227 Periodontal disease, especially measured by alveolar bone loss, is a strong and independent predicto

228 ionships between HIV infection and increased alveolar bone loss may be explained by other factors, su

229 nd able to diagnose this condition, as rapid alveolar bone loss may be the first sign of sarcoidosis.

230 In this pilot study, analysis of alveolar bone loss measurements from captive baboons ind

231 Alveolar bone loss measurements were made on histologica

232 Postextraction alveolar bone loss, mostly affecting the buccal plate, o

233 consumption was not significantly related to alveolar bone loss nor to any of the subgingival microor

234 antly associated with greater attachment and alveolar bone loss (odds ratio, OR = 1.70, 95% CI = 1.09

235 rapeutics against PMO prevent the aggravated alveolar bone loss of periodontitis in estrogen-deficien

236 icate that Porphyromonas gingivalis mediates alveolar bone loss or osteoclast modulation through enga

237 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

238 nd that a HFD markedly increased LPS-induced alveolar bone loss, osteoclastogenesis, and inflammatory

239 s vehicle-treated germ-free mice had similar alveolar bone loss outcomes, implying that antimicrobial

240 TCZ was able to attenuate linear alveolar bone loss (p < 0.05) and the loss of the number

241 treatment was accompanied by lower rates of alveolar bone loss (P <0.05) and maintenance of the amou

242 owngrowth (P <0.05), inflammation (P <0.05), alveolar bone loss (P <0.05), and osteoclast activity (P

243 Rats with PD exhibited increased alveolar bone loss (P <0.05), as well as increased level

244 with AMD had fewer teeth (P <0.001) and more alveolar bone loss (P = 0.004) compared with non-AMD par

245 e loss and could serve as an animal model of alveolar bone loss pathogenesis.

246 tus (NIDDM) have greater risk of more severe alveolar bone loss progression over a 2-year period than

247 uggest an NIDDM-associated increased rate of alveolar bone loss progression.

248 and Stat6) or resistance (Il15 and Selp) to alveolar bone loss, providing insight into the genetic e

249 argeting oral bacteria protect the host from alveolar bone loss, recent studies show that particular

250 ntal maintenance intervals on tooth loss and alveolar bone loss, respectively.

251 rinses, and systemic metronidazole therapy, alveolar bone loss resulted in tooth mobility necessitat

252 Alveolar bone loss resulting from LPS-induced periodonti

253 The current concepts in alveolar bone loss resulting from osteoporosis and its i

254 le evidence suggests that, in most patients, alveolar bone loss results from interactions of a highly

255 etic mice, it reduced osteoclast numbers and alveolar bone loss significantly due to APR's inhibition

256 d presents commonly as progressive and rapid alveolar bone loss similar to periodontitis.

257 ed with heat-killed Pg displayed significant alveolar bone loss starting from day 15, which continued

258 nd the severity of gingival inflammation and alveolar bone loss (subgroups) without producing antibio

259 (+) cells are resistant to infection-induced alveolar bone loss, Th cells have been implicated in bon

260 eukin-10(-/-) mice had significantly greater alveolar bone loss than interleukin-10(+/+) mice (p = 0.

261 with DIO had a significantly higher level of alveolar bone loss than the lean controls.

262 TLR9(-/-) mice exhibited significantly less alveolar bone loss than their wild-type (WT) counterpart

263 Ifi204-deficient mice> exhibited >20% higher alveolar bone loss than wild-type (WT) (P < 0.05), while

264 ence of inflammation, it was the presence of alveolar bone loss that lead to significantly higher val

265 ate periodontitis pathogenesis by inhibiting alveolar bone loss through directly blocking osteoclast

266 flammation, gingival tissue destruction, and alveolar bone loss through sustained exacerbation of the

267 ntal destruction was determined by measuring alveolar bone loss under a stereomicroscope.

268 d clinical measures of inflammation and less alveolar bone loss under severe inflammatory conditions

269 Alveolar bone loss was alleviated in JQ1-treated mice be

270 Alveolar bone loss was also evaluated radiographically i

271 Alveolar bone loss was analyzed by micro-computed tomogr

272 del adjusted for age, smoking, and diabetes, alveolar bone loss was associated with AMD in males with

273 Conversely, P. gingivalis infection-induced alveolar bone loss was attenuated in mice lacking ST2.

274 ion, and osteoclast activity were evaluated; alveolar bone loss was determined by histomorphometry, m

275 Alveolar bone loss was determined by macroscopic and his

276 After 4 wk of treatment, alveolar bone loss was determined by micro-computed tomo

277 Ligature-induced alveolar bone loss was diminished in chemR23tg mice.

278 Alveolar bone loss was evaluated morphometrically under

279 The alveolar bone loss was evaluated using microcomputed tom

280 Alveolar bone loss was greater in vehicle-treated SPF ve

281 At 8 weeks, linear and volumetric alveolar bone loss was measured by micro-computed tomogr

282 periodontal parameters remained stable, and alveolar bone loss was not observed.

283 Greater radiographic alveolar bone loss was observed among participants repor

284 The highest alveolar bone loss was observed in the periodontitis gro

285 Compared to the ligature + placebo group, alveolar bone loss was reduced in the fluoxetine group (

286 ntages of fat (P = nonsignificant); however, alveolar bone loss was significantly greater in animals

287 Alveolar bone loss was significantly greater in groups 2

288 Alveolar bone loss was significantly higher in the PED g

289 Alveolar bone loss was significantly reduced in the liga

290 +/-2.1 mm, furcation involvement, and severe alveolar bone loss were observed in a 41-year-old Caucas

291 Measurements of alveolar bone loss were performed on 390 dry baboon skul

292 The root/enamel ratios (to estimate alveolar bone loss) were analyzed with repeated measures

293 onstrated that group EP/EA presented reduced alveolar bone loss when compared to group EP (P <0.05).

294 Group EP-HN019 presented significantly less alveolar bone loss when compared with Group EP in histom

295 alis-infected mice significantly exacerbated alveolar bone loss when compared with infection or IL-33

296 The MSPEP group exhibited reduced alveolar bone loss when compared with the MSPE group, as

297 PEP and MSPEP groups showed lower levels of alveolar bone loss when compared with the PE and MSPE gr

298 )) were protected from P. gingivalis-induced alveolar bone loss, with a reduction in anti-P. gingival

299 ceptible to A. actinomycetemcomitans-induced alveolar bone loss, with different patterns of immune re

300 Treatment with simvastatin improved alveolar bone loss within all of the parameters studied,