ライフサイエンスコーパス: bone loss

1 argeting DC-STAMP could suppress periodontal bone loss.

2 , causes significant cortical and trabecular bone loss.

3 , keratinized mucosa dimension, and marginal bone loss.

4 e protected against 1 wk post-OVX-associated bone loss.

5 +)-dependent mechanisms causing pathological bone loss.

6 e able to modulate inflammation and alveolar bone loss.

7 is safe and also limits unwarranted surgical bone loss.

8 s pulpitis while also displaying periodontal bone loss.

9 with cartilage degeneration and subchondral bone loss.

10 e their ability to prevent treatment-induced bone loss.

11 of implant success and peri-implant marginal bone loss.

12 and observed a 40% reduction in OVX-induced bone loss.

13 an effective countermeasure for muXg induced bone loss.

14 l sites and 37% of distal sites exhibited no bone loss.

15 ecome a therapeutic target for conditions of bone loss.

16 abolism and can therefore influence alveolar bone loss.

17 duction of type CD31(hi)Emcn(hi) vessels and bone loss.

18 roles of androgen and estrogen deficiency in bone loss.

19 inhibiting cancer progression and preventing bone loss.

20 cessive weight gain, immune suppression, and bone loss.

21 eneficial effects against estrogen-deficient bone loss.

22 nflammation, and completely protects against bone loss.

23 ngivalis (W50) or placebo to induce alveolar bone loss.

24 e of gut microbiota in mediating hypogonadal bone loss.

25 process known to be involved in OVX-induced bone loss.

26 from subsequent development of pulpitis and bone loss.

27 L (PTX-CrEL) or saline (control) showed >50% bone loss.

28 downregulated the ligature-induced alveolar bone loss.

29 he efficacy of ZOL in mitigating ART-induced bone loss.

30 in sex steroid deficiency-induced trabecular bone loss.

31 t osteoclast differentiation in inflammatory bone loss.

32 n, decreased bone formation, and significant bone loss.

33 een neuronal TRPV1 signaling and periodontal bone loss.

34 e of alendronate significantly mitigated the bone loss.

35 enescence, but also prevented aging-mediated bone loss.

36 ex steroid deficiency, leading to trabecular bone loss.

37 tern is consistent with an increased rate of bone loss.

38 hosphatase-positive (TRAP+) OCs and alveolar bone loss.

39 a net effect of impaired bone formation and bone loss.

40 IFN-gamma in TcREG-mediated protection from bone loss.

41 network homeostasis and ovariectomy-induced bone loss.

42 is and treatment of diseases associated with bone loss.

43 HIV infection causes bone loss.

44 naling mediates the induction of periodontal bone loss.

45 may be an option to attenuate ART-associated bone loss.

46 d under pressure not only fills the areas of bone loss.

47 cted TLR9(-/-) mice, which were resistant to bone loss.

48 mass and age-related trabecular and cortical bone loss.

49 ne health and the attenuation of age-related bone loss.

50 (TMJs), displaying as subchondral trabecular bone loss.

51 s and contribute to induction of periodontal bone loss.

52 depletion is a major contributing factor to bone loss.

53 cal dimensions, and significant endocortical bone loss.

54 icantly associated with greater peri-implant bone loss.

55 owing ART initiation may explain ART-induced bone loss.

56 stress-mediated arterial calcium accrual and bone loss.

57 c and prosthetic complications, and marginal bone loss.

58 osteoclast differentiation and pathological bone loss.

59 y could inhibit periodontal inflammation and bone loss.

60 defects but also for measuring the amount of bone loss.

61 d with exaggerated disuse-induced cancellous bone loss.

62 e CD4+ T cells additionally induced cortical bone loss.

63 haracterized by inflammation-driven alveolar bone loss.

64 e majorly to the estrogen deficiency-induced bone loss.

65 tis with excessive cartilage destruction and bone loss.

66 cell infiltration, osteoclast activity, and bone loss.

67 nfluence on the pathogenesis of peri-implant bone loss.

68 round impact between comorbidity of t2DM and bone loss.

69 bone resorption, and cortical and trabecular bone loss.

70 tinomycetemcomitans-induced inflammation and bone loss.

71 Higher linear alveolar bone loss (ABL) and lower interradicular bone density we

72 f a 2% cholesterol-enriched diet on alveolar bone loss (ABL) and serum levels of pro-oxidants and ant

73 D), myeloperoxidase (MPO) activity, alveolar bone loss (ABL) for periodontal tissues; histopathologic

74 rphan receptor (ROR) gammat; and 3) alveolar bone loss (ABL) in experimental periodontitis.

75 um oxidative stress index (OSI) and alveolar bone loss (ABL) in rats with diabetes mellitus (DM) and

76 fects of strontium ranelate (SR) on alveolar bone loss (ABL) in rats with experimental periodontitis.

77 ced obesity/hyperlipidemia (CAF) on alveolar bone loss (ABL) in rats.

78 nce development are associated with alveolar bone loss (ABL) in susceptible individuals.

79 This study examines: 1) alveolar bone loss (ABL), a hallmark of periodontitis, in anti-ci

80 mmatory cytokine levels, apoptosis, alveolar bone loss (ABL), lipid metabolism, and diabetic control

81 (20- to 22-month-old) mice with established bone loss, activation of the INK-ATTAC caspase 8 in sene

82 ically, antiretroviral therapy (ART) worsens bone loss although existing data suggest that such loss

83 eopontin as potential biomarkers of alveolar bone loss and 2) determine whether the glycemic status a

84 Trp(8)-gammaMSH presented decreased alveolar bone loss and a lower degree of neutrophil infiltration

85 synergistically promote condylar subchondral bone loss and cartilage degradation; such processes are

86 ndibular first molars to measure periodontal bone loss and collagen content.

87 romotes a protective effect against alveolar bone loss and CTALs attributable to EP in rats, modifyin

88 hectomy simultaneously prevented subchondral bone loss and decreased bone norepinephrine level in all

89 odels, for the rescue of ovariectomy-induced bone loss and ear inflammation.

90 Menopause is associated with bone loss and enhanced visceral adiposity.

91 ed a substantial reduction of age-associated bone loss and fat accumulation in bone marrow.

92 ne mineral density, studies have also linked bone loss and higher fracture risk in men to low estroge

93 equired for osteoclast-mediated inflammatory bone loss and hyper-multinucleation of OCs.

94 irculating estrogen levels, which accelerate bone loss and increase the risk of fracture.

95 experimental rats, together with subchondral bone loss and increased osteoclast activity.

96 Subchondral bone loss and increased subchondral bone norepinephrine

97 creases amount of experimental periodontitis bone loss and inflammation in rats.

98 ion and cells) on experimental periodontitis bone loss and inflammation.

99 otential to become symptomatic, resulting in bone loss and kidney stones.

100 phages showed a significantly lower level of bone loss and less tartrate-resistant acid phosphatase (

101 inflammation and abrogated osteoclastogenic bone loss and myositis, but did not affect in vivo viral

102 agonist (propranolol) suppressed subchondral bone loss and osteoclast hyperfunction while beta-agonis

103 th a neutralizing mAb inhibited IL-7-induced bone loss and osteoclast numbers by reducing Th17 cell n

104 f anti-DC-STAMP-mAb also suppressed alveolar bone loss and reduced the total number of multinucleated

105 ta exist on the impact of virus infection on bone loss and regeneration.

106 that administration of XN markedly inhibited bone loss and resorption by suppressing osteoclast activ

107 ted with P. gingivalis demonstrated alveolar bone loss and serum anti-P. gingivalis antibody titers e

108 lts show that inhibition of CTSK can prevent bone loss and the immune response during the progression

109 as to evaluate the effect of HFA on alveolar bone loss and the rate of bone formation after tooth ext

110 cation of disease severity based on alveolar bone loss and tooth loss during follow-up.

111 ontrol study of PD, verified by radiographic bone loss and with a careful consideration of potential

112 eatment that can be used to prevent alveolar bone loss and/or accelerate bone healing after tooth ext

113 smoking, diabetes, body mass index, alveolar bone loss, and number of teeth), having WPSs associated

114 teeth, teeth lost, periodontal disease with bone loss, and root canal treatments.

115 hologic changes of the Ocys in periodontitis bone loss, and the novel link between sclerostin and Wnt

116 Periodontitis, alveolar bone loss, and tooth loss are associated with low BMD.

117 ) implant failures; 2) peri-implant marginal bone loss; and 3) complications.

118 coronal 21%-22% 2D RL and the 26%-28% 3D RSA bone loss apical to the cemento-enamel junction correspo

119 of testosterone and estradiol that initiate bone loss are uncertain.

120 rogen and estrogen deficiency in hypogonadal bone loss are unclear.

121 robing depth, clinical attachment level, and bone loss around teeth increased the occurrence of peri-

122 against PTH-induced cortical and trabecular bone loss as well as from increases in serum CTX (C-term

123 expressed by osteocytes is required for the bone loss as well as the increase in B cell number cause

124 therapeutic agent for the prevention of the bone loss associated with advanced periodontal disease.

125 own potential in preventing and regenerating bone loss associated with experimental periodontitis.

126 Peri-implant marginal bone loss at 5 years was 0.95 +/- 0.84 mm for the NDI gr

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

128 Marginal bone loss (BL) and implant and prosthesis survival rates

129 Radiographic bone loss (BL) was examined using orthopantomograms.

130 Extraction-induced bone loss (BL) was noted on buccal, palatal, and interpr

131 reatment inhibit bone resorption and prevent bone loss but fail to influence bone formation and do no

132 Our findings indicate that CLP causes bone loss by enhancing Itch-mediated osteoclastogenesis,

133 ontributes to physiological and pathological bone loss by integrating the MYC/ERRalpha axis to drive

134 duction by B lymphocytes is required for the bone loss caused by estrogen deficiency.

135 duced by osteocytes is also required for the bone loss caused by estrogen deficiency.

136 te comparable baseline indices of bone mass, bone loss caused by hormonal or RANKL perturbations is s

137 eoblastogenesis and mineralization, reversed bone loss caused by ovariectomy, and increased bone stre

138 om the increase in osteoclast number and the bone loss caused by ovariectomy.

139 systematic review is to compare the crestal bone loss (CBL) around dental implants placed in healed

140 and probing depth [PD] >/=4 mm) and crestal bone loss (CBL) around immediately loaded (IL) and delay

141 ery, linear measures of differential crestal bone loss (CBL) as a function of the categorical initial

142 pted the authors of this study to strive for bone loss close to zero and research variables that caus

143 ed WT mice exhibited significantly increased bone loss compared to that in sham-infected WT mice or P

144 ll transfer demonstrated reduced periodontal bone loss compared to the no-transfer group and the grou

145 ection with capsulated Pg augmented alveolar bone loss compared with that of mixed infection with non

146 f bone loss such as lactating (physiological bone loss condition) and ovariectomized (induction of su

147 alyze the amount of attachment loss, crestal bone loss, connective tissue attachment, and the surface

148 ced periodontitis inhibited inflammation and bone loss, correlating with decreased numbers of osteocl

149 coronal 30%-31% 2D RL and the 41%-42% 3D RSA bone loss corresponded to a CRR of 5:4, correlating to s

150 s was observed among participants reporting "bone loss/deep pockets" (P < 0.001) and "loose teeth" (P

151 mulate bone resorption, and cause trabecular bone loss, demonstrating that the gut microbiota is cent

152 inations of the following keywords: "crestal bone loss"; "dental implant"; "surgery"; "flap"; and "fl

153 mechanisms mediating viral infection-induced bone loss depend on the specific inflammatory condition.

154 This protective effect against bone loss disappeared when only studies with formulation

155 Clec11a-deficient mice exhibited accelerated bone loss during aging, reduced bone strength, and delay

156 he cascade of events that lead to cancellous bone loss during estrogen deficiency.

157 n, whereas all doses of SIM/SIM-mPEG reduced bone loss, especially 1.5 mg SIM/SIM-mPEG (0.68 +/- 0.05

158 ne reconstitution as putative mechanisms for bone loss following ART initiation.

159 in male mice and protected female mice from bone loss following ovariectomy, which induces osteoporo

160 neutralizing TNF in vivo abrogated alveolar bone loss following P. gingivalis infection.

161 roups showed a slight amount of peri-implant bone loss from baseline to 5 years.

162 loss >/=5 mm (1.19; 1.00 to 1.41), alveolar bone loss >/=40% (1.25; 1.00 to 1.56), and tooth mobilit

163 y was a protective factor against developing bone loss >5 mm.

164 >/=5 mm), mobility (>/=0.5 mm), and alveolar bone loss (>/=40% of the distance from the cementoenamel

165 on takes place in infection-induced alveolar bone loss has not been investigated.

166 d CIS + UAC produced more severe subchondral bone loss, higher bone norepinephrine level, and decreas

167 of remaining teeth, percentage of teeth with bone loss, implant function time, implant surface, and p

168 acological inhibition of ERRalpha attenuated bone loss in a mouse model of osteoporosis.

169 elevated fatty acid (FA) levels on alveolar bone loss in a Porphyromonas gingivalis-induced model of

170 unrecognized role for IL-33 in exacerbating bone loss in a RANKL-dependent manner in the context of

171 cts on bone formation to prevent OVX-induced bone loss in adult female rats.

172 cts on bone formation to prevent OVX-induced bone loss in adult female rats.-Chen, J.-R., Lazarenko,

173 Severe gonadal steroid deficiency induces bone loss in adult men; however, the specific roles of a

174 to determine their roles in inflammation and bone loss in an animal model.

175 Furthermore, Ezh2 inhibition also alleviated bone loss in an estrogen-deficient mammalian model for o

176 found that Trpv1(-/-) mice developed severe bone loss in an experimental model of periodontitis.

177 reased periodontal inflammation and alveolar bone loss in an LPS-induced periodontitis animal model.

178 vered with a bone-targeting system prevented bone loss in an osteoporotic animal model.

179 periodontitis resulted in significantly less bone loss in B cell-deficient mice compared with wild-ty

180 SCs ameliorate inflammation-induced systemic bone loss in CIA mice by reducing osteoclast precursors

181 genesis, and protects mice from pathological bone loss in disease models.

182 rthermore, the attenuated skeletal aging and bone loss in DLX3 (Q178R) transgenic mice not only recon

183 rm and also correct cognitive impairment and bone loss in DMD model mice.

184 ells alleviated periodontal inflammation and bone loss in experimental periodontitis in mice.

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

186 ts of TLR-activated B10 cells on periodontal bone loss in experimental periodontitis.

187 als that treatment with denosumab to prevent bone loss in first-year kidney transplant recipients was

188 ts enhancing osteoclastogenesis, which drive bone loss in health.

189 mice to determine if absence of MAT reduced bone loss in hindlimb-unloaded (HU) mice.

190 ow cells of Itch-/- mice in vitro nor induce bone loss in Itch-/- mice.

191 ll induction on periodontal inflammation and bone loss in ligature-induced experimental periodontitis

192 RvE1 treatment prevented bone loss in ligature-induced periodontitis.

193 nist, capsaicin, suppressed ligature-induced bone loss in mice with fewer tartrate-resistant acid pho

194 versed cartilage degradation and subchondral bone loss in mice with OA of the TMJ.

195 ripheral effect intact, prevents Flx-induced bone loss in mice.

196 nhibition of ERRalpha attenuated OVX-induced bone loss in mice.

197 s may highlight new treatment approaches for bone loss in osteoporosis.

198 ight into the molecular mechanisms mediating bone loss in ovariectomized (OVX) mice, a model of human

199 -resorptive therapy could be used to prevent bone loss in patients taking antidepressants, such as CL

200 ution of periodontal bacteria to periodontal bone loss in patients with MetS remains unclear.

201 as a critical negative regulator of alveolar bone loss in periodontitis.

202 reduced inflammation, oxidative stress, and bone loss in rats with EP and GIOP, with participation o

203 ity to protect mice from bone resorption and bone loss in response to high-dose receptor activator of

204 tory pathways that are critical for inducing bone loss in sex steroid-deficient mice.

205 T cells may further contribute to trabecular bone loss in some patients with advanced AIDS, in whom C

206 cates that astronauts experience significant bone loss in space.

207 Addition of lactose led to attenuation of bone loss in the capsulated mixed infection and to inten

208 ed mixed infection and to intensification of bone loss in the non-capsulated mixed infection.

209 GSK126 attenuated bone loss in the ovariectomy mouse model of postmenopaus

210 ty and an overall TMJ subchondral trabecular bone loss in the UAC-treated rats.

211 -ECD therapeutically abrogated RANKL-induced bone loss in three mouse models of osteoporosis.

212 ed that beta2-AR signal-mediated subchondral bone loss in TMJ osteoarthritisis associated with increa

213 We also showed that IL-7-induced bone loss in vivo is associated with Th17 cell expansion

214 vprs in vivo in a model of lactation-induced bone loss in which Oxt levels are high.

215 number of periosteal osteoclasts and immense bone loss in wild type mice but not in Tlr2-deficient mi

216 beneficial effect against estrogen-deficient bone loss in women.

217 howed that hPTH-infusion induced significant bone loss in WT mice.

218 These results suggest that OVX-induced bone loss, in part, is a result of increased osteoblasti

219 These results suggest that OVX-induced bone loss, in part, is a result of increased osteoblasti

220 levels after menopause can lead to systemic bone loss, including loss of oral bone and alveolar cres

221 ism as a viable strategy to control alveolar bone loss induced by oral infection.

222 Alveolar bone loss is a result of an aggressive form of periodont

223 Bone loss is mitigated by bone protective therapies, but

224 ART-induced bone loss is most intense within the first 48 weeks of t

225 48 weeks of ART, the period when ART-induced bone loss is most pronounced.

226 ressed MYC in physiological and pathological bone loss is not known.

227 A link between inflammatory disease and bone loss is now recognized.

228 retroviral therapy (ART) are associated with bone loss leading to increased fracture rate among HIV-i

229 we conclude that beneficial effects against bone loss may be enhanced for isoflavone aglycones.

230 attachment loss (AL) were measured; marginal bone loss (MBL) around all teeth was measured on digital

231 y is to evaluate survival rates and marginal bone loss (MBL) around implants placed in sites treated

232 les have been shown to affect early marginal bone loss (MBL).

233 c evidence relating osteoporosis to marginal bone loss (MBL).

234 etic complications; 3) peri-implant marginal bone loss (MBL); 4) esthetic and periodontal parameters;

235 clinical attachment loss [AL], and marginal bone loss [MBL]) and numbers of missing teeth (MT) were

236 clinical attachment loss [AL], and marginal bone loss [MBL]) were measured.

237 Postextraction alveolar bone loss, mostly affecting the buccal plate, occurs des

238 In ovariectomized-induced bone loss mouse model and RANKL-injection-induced bone r

239 s in immunodeficient mice mimics ART-induced bone loss observed in humans.

240 Bone loss occurs in human immunodeficiency virus (HIV) i

241 Peri-implantitis was defined as radiographic bone loss of > 2 mm, probing depth (PD) >/=5 mm with ble

242 Peri-implantitis was defined as radiographic bone loss of >2 mm, probing pocket depth (PD) >/=5 mm wi

243 Ligature alone caused a mean bone loss of 1.01 +/- 0.06 mm from the cemento-enamel ju

244 duced osteoblast-specific gene expression in bone, loss of osteoblasts, and reduced serum markers of

245 oss, could minimize the potential effects of bone loss on periodontal tissues.

246 steoporosis and do not improve prediction of bone loss or fracture within an individual.

247 h normal PDL architecture and no evidence of bone loss over time.

248 tes showed significantly reduced periodontal bone loss (P <0.05) and inflammatory infiltration (P <0.

249 t was accompanied by lower rates of alveolar bone loss (P <0.05) and maintenance of the amount of gin

250 The widespread nature of peri-implant bone loss poses difficulties in the management of biolog

251 stic effects of vitamin D3 and vitamin K2 on bone loss prevention have been reported.

252 ATV decreased bone loss, reduced MPO, TNF-alpha, IL-1beta, IL-6, and I

253 clerostin antibody prevented myeloma-induced bone loss, reduced osteolytic bone lesions, and increase

254 ONFH-induced symptoms such as osteonecrosis, bone loss, reduction in vessel perfusion, and excessive

255 ted to elevate bone angiogenesis and prevent bone loss-related diseases.

256 nergic signaling as a therapeutic target for bone loss-related inflammatory conditions.

257 anisms linking virus-induced inflammation to bone loss remain unclear.

258 Although we know that major glenoid bone loss requires surgical intervention, none of the st

259 Osteoporosis is characterised by trabecular bone loss resulting from increased osteoclast activation

260 Alveolar bone loss resulting from LPS-induced periodontitis was s

261 Bone loss results from an imbalance in remodeling, the p

262 established periodontitis with RvE1 reversed bone loss, reversed inflammatory gene expression, and re

263 n levels of Runx2 and Fbw7alpha in models of bone loss such as lactating (physiological bone loss con

264 ks experimental periodontal inflammation and bone loss, suggesting a promising platform for the devel

265 fundamental mechanism to prevent age-related bone loss suggests a novel treatment strategy not only f

266 ) mice exhibited significantly less alveolar bone loss than their wild-type (WT) counterparts.

267 sult in serious clinical outcomes, including bone loss that may weaken skeletal or periodontal streng

268 nical dentistry is the significant and rapid bone loss that occurs after tooth extraction.

269 well as on algorithms with validated glenoid bone loss threshold values for therapeutic decision-maki

270 te a role for senescent cells in age-related bone loss through multiple approaches.

271 Cimetidine decreases bone loss through reduction of osteoclast number and ind

272 ered at ART initiation prevented ART-induced bone loss through the first 48 weeks of ART, the period

273 l lesions (i.e., decreased attachment level, bone loss, tooth mobility/migration, altered periodontal

274 ise as novel osteoporosis and disuse-induced bone loss treatments by directly modulating the mechanos

275 L), which, in turn, promotes the periodontal bone loss via upregulation of osteoclastogenesis.

276 OVX-induced bone loss was associated with increased osteoblastic cel

277 Increased bone loss was demonstrated in P. gingivalis-infected SOC

278 Periodontal bone loss was induced in 16-wk-old myeloid-specific SOCS

279 was highly expressed at weaning, a time when bone loss was noted to recover.

280 Greater radiographic alveolar bone loss was observed among participants reporting "bon

281 periodontitis compared with wild-type mice, bone loss was only marginally higher compared with Akita

282 Morphometric analysis of bone loss was performed.

283 CLP-induced bone loss was prevented by Zoledronic acid.

284 Periodontal bone loss was significantly decreased and the gingival e

285 fat (P = nonsignificant); however, alveolar bone loss was significantly greater in animals that were

286 The CsA-induced attenuation of periodontal bone loss was strongly correlated positively with the ex

287 nvestigate the effect of the LTB4 pathway in bone loss, we performed osteoclast differentiation assay

288 otective effects of SPI diets on OVX-induced bone loss were associated with down-regulation of the ca

289 cted mice significantly exacerbated alveolar bone loss when compared with infection or IL-33 treatmen

290 mal but statistically significant, with more bone loss when membrane was used (P = 0.05).

291 In addition, neutral PTX-NPs prevented bone loss, whereas animals treated with the rapid-releas

292 enous WNT16 results specifically in cortical bone loss, whereas overexpression of WNT16 surprisingly

293 effects on the prevention of postmenopausal bone loss, which is possibly related to the specific iso

294 MM1.S myeloma cells demonstrated significant bone loss, which was associated with a decrease in fract

295 tablish a causal role for senescent cells in bone loss with aging, and demonstrate that targeting the

296 ase in joint inflammation, joint damage, and bone loss with improvement in joint function and mobilit

297 ns of CsA-induced attenuation of periodontal bone loss with the expressions of gelatinases (i.e., mat

298 rotected from P. gingivalis-induced alveolar bone loss, with a reduction in anti-P. gingivalis serum

299 cient to protect ovariectomized mice against bone loss without disrupting hematopoietic homeostasis.

300 nt mean bone resorption of 2.96 mm increased bone loss, yielding a cumulative implant success rate of