ライフサイエンスコーパス: bone loss

1 h both outcomes (increased probing depth and bone loss).

2 ive adverse side effects such as deleterious bone loss.

3 quantification of neutrophils in the JE and bone loss.

4 idate for inhibiting tumor and tumor-induced bone loss.

5 teoclast numbers, and significant trabecular bone loss.

6 n of osteogenesis and osteoclastogenesis and bone loss.

7 orption and diminished formation may promote bone loss.

8 ing of the skeleton, which leads to dramatic bone loss.

9 dentify several risk factors associated with bone loss.

10 ive countermeasure to weight-loss-associated bone loss.

11 osis, and rapid joint destruction, including bone loss.

12 s associated with delayed tissue healing and bone loss.

13 and accelerated naturally occurring alveolar bone loss.

14 more pathogenic, leading to greater alveolar bone loss.

15 injury (TBI) patients that may contribute to bone loss.

16 olol, a beta2-adrenergic antagonist, rescues bone loss.

17 ss tumor growth as well as metastasis-linked bone loss.

18 c and prosthetic complications, and marginal bone loss.

19 +)-dependent mechanisms causing pathological bone loss.

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

21 eneficial effects against estrogen-deficient bone loss.

22 downregulated the ligature-induced alveolar bone loss.

23 t osteoclast differentiation in inflammatory bone loss.

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

25 eth with radiographic evidence of horizontal bone loss.

26 icantly associated with greater peri-implant bone loss.

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

28 stress-mediated arterial calcium accrual and bone loss.

29 osteoclast differentiation and pathological bone loss.

30 y could inhibit periodontal inflammation and bone loss.

31 ent of diseases characterized by accelerated bone loss.

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

33 d with exaggerated disuse-induced cancellous bone loss.

34 probing, visual inspection, and radiographic bone loss.

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

36 s for bone regeneration and the treatment of bone loss.

37 haracterized by inflammation-driven alveolar bone loss.

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

39 tis with excessive cartilage destruction and bone loss.

40 cell infiltration, osteoclast activity, and bone loss.

41 antly reduced P. gingivalis-induced alveolar bone loss.

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

43 round impact between comorbidity of t2DM and bone loss.

44 bone resorption, and cortical and trabecular bone loss.

45 tinomycetemcomitans-induced inflammation and bone loss.

46 arthritis with joint remodeling and profound bone loss.

47 induced their differentiation and triggered bone loss.

48 tis; thus, further promoting the Th17-driven bone loss.

49 uCT measurements of the in vivo peri-implant bone loss.

50 both WT and 5xFAD mice experienced alveolar bone loss.

51 tion promotes osteoclast differentiation and bone loss.

52 ne during treatment helps to prevent palatal bone loss.

53 recently been shown to regulate inflammatory bone loss.

54 rs, and its blockage significantly increases bone loss.

55 otects the subchondral bone plate from early bone loss.

56 ventually arrest the RANKL-mediated alveolar bone loss.

57 consequently ameliorated ovariectomy-induced bone loss.

58 eogenesis and is associated with accelerated bone loss.

59 ruitment to the bone marrow (BM) that causes bone loss.

60 gn have been demonstrated to reduce marginal bone loss.

61 ns or current medication use associated with bone loss.

62 of mouse Cx3cr1(+) and Cx3cr1(neg) i-OCLs to bone loss.

63 or in combination had beneficial effects on bone loss.

64 ence of an estrogen-independent mechanism of bone loss.

65 repair, and attenuated inflammation-mediated bone loss.

66 periodontal defects and significant alveolar bone loss (14%; P < 0.0001) were evident in Ddr1(-/-) ve

67 uscle aging-like deficit but also trabecular bone loss, a feature of osteoporosis.

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

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

70 Capz prevented alveolar bone loss (ABL) on the external crests and in the interr

71 so expressed on bone forming osteoblasts and bone loss accompanies EPO-stimulated erythropoiesis in m

72 or expression in osteoblasts is required for bone loss accompanying EPO-stimulated erythropoiesis.

73 (20- to 22-month-old) mice with established bone loss, activation of the INK-ATTAC caspase 8 in sene

74 romotes a protective effect against alveolar bone loss and CTAL in rats with EP.

75 effect against the ligation-induced alveolar bone loss and effectively inhibits the production of pro

76 -amiR-shn3 in osteoporotic mice counteracted bone loss and enhanced bone mechanical properties.

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

78 sulted in a significant increase in alveolar bone loss and gingival IL-17 expression over sham-infect

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

80 ent of Pg/Sg infected mice with BNPs reduced bone loss and IL-17 expression almost to the levels of s

81 ine treatment significantly reduced alveolar bone loss and improved bone metabolism of OVX-periodonti

82 However, these surgeries cause bone loss and increase fracture risk through poorly unde

83 bition may help to explain the phenomenon of bone loss and increased adipogenesis in some patients du

84 sociated with increased risk of peri-implant bone loss and increased implant failure rate.

85 trast, a calorie-restricted (CR) diet causes bone loss and induces BMAT in both mice and humans.

86 i-ketonic curcumin, has been shown to reduce bone loss and inflammatory mediators in experimental per

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

88 comitans lipopolysaccharide-induced alveolar bone loss and microcomputed tomography was used to deter

89 aceflight is known to induce severe systemic bone loss and muscle atrophy of astronauts due to the ci

90 ), whereas excess activity can contribute to bone loss and osteoporosis(10).

91 The association between systemic bone loss and periodontitis remains unresolved; and the

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

93 which deregulate bone turnover and result in bone loss and skeletal-related events.

94 emoral bone of male SCID mice caused massive bone loss and stimulation of mouse osteoclast-promoting

95 Bone loss and the number of osteoclasts were measured th

96 ntifying senescent cells as major drivers of bone loss and the p38MAPK-MK2 axis as a putative therape

97 eceptor significantly increased radiographic bone loss and tissue levels of IL-1alpha (P <0.05), IL-1

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

99 ne mass of aged mice, attenuates age-related bone loss, and accelerates bone regeneration of aged rod

100 f estrogen deficiency-aggravated periodontal bone loss, and berberine represents a promising adjuvant

101 veral years prior to progression of alveolar bone loss, and include antecedent elevations in previous

102 e and may lead to increased bone resorption, bone loss, and increased falls and fractures.

103 disease (IBD) leads to lack of bone accrual, bone loss, and increased fractures.

104 hat some types of exercise prevent falls and bone loss, and meta-analyses support the anti-fracture e

105 rrent PARP inhibitors on bone metastasis and bone loss, and suggest cotreatment with CCL3, beta-caten

106 post-transplant central skeleton trabecular bone loss, and zoledronate does not induce ABD.

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

108 level characteristics with probing depth and bone loss around dental implants METHODS: A total of 642

109 ernal screw length/diameter) on the marginal bone loss around implants with peri-implantitis.

110 ss termed metallosis, can be responsible for bone loss around some dental implants.

111 ooth extractions, gum bleeding, loose teeth, bone loss around teeth, and gum disease-cross-sectionall

112 feel that biofilm is solely responsible for bone loss around the devices.

113 Desipramine administration reduced alveolar bone loss as histologically observed, and modulated key

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

115 atin's therapeutic efficacy in tumor-induced bone loss, as well as VOC-based diagnosis of tumor progr

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

117 om zoledronate); HR-pQCT detected trabecular bone loss at the peripheral skeleton, which zoledronate

118 experienced lower cortical and endocortical bone loss at the radius than did the Alk-D and Neut-D gr

119 is was primarily influenced by the amount of bone loss at the time of treatment.

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

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

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

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

124 -driven estrogen loss is postulated to drive bone loss, but significant data suggests the existence o

125 Mechanical stimulations can prevent bone loss, but their effects on the tumor-invaded bone o

126 Estrogens protect against bone loss by decreasing osteoclast number through direct

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

128 ply that Col6a2 deficiency causes trabecular bone loss by enhancing osteoclast differentiation throug

129 rm our understanding of chemotherapy-induced bone loss by identifying senescent cells as major driver

130 esize that berberine ameliorates periodontal bone loss by improving the intestinal barriers by regula

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

132 ms fed the low protein diet showed extensive bone loss by the end of lactation, followed by full skel

133 We have previously shown that bone loss can be prevented by mechanical loading, but th

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

135 implant soft tissue inflammation and crestal bone loss (CBL) are higher around adjacent implants plac

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

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

138 fied gingival and plaque indices and crestal bone loss (CBL) were measured.

139 robing depth (PD) were evaluated and crestal bone loss (CBL) were measured.

140 robing [BOP], probing depth (PD) and crestal bone loss [CBL]) are worse in cigarette-smokers (CS) and

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

142 e, 5xFAD mice presented significant alveolar bone loss compared to WT mice.

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

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

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

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

147 l periodontitis (EP) by attenuating alveolar bone loss due to reduction in inflammatory cytokines, be

148 tation on peripheral cortical and trabecular bone loss during pregnancy and bone gain postpartum.

149 cient calcium intake could increase maternal bone loss during pregnancy and reduce bone recovery post

150 s been reported to protect from pathological bone loss during rheumatoid arthritis and osteoporosis,

151 nding dental implants, and reverses alveolar bone loss following extraction socket remodeling.

152 vel demonstrated significantly less marginal bone loss for implants placed using the early placement

153 ate risk indicators associated with marginal bone loss from a retrospective open cohort study of 4,59

154 Ankle loading ameliorates bone loss from breast cancer-associated bone metastasis.

155 nt data to make a diagnosis based on 3 mm of bone loss from the expected level of bone.

156 eased inflammatory phenotype and more severe bone loss, further verifying the critical function of A2

157 dels to assess glenohumeral anatomy, glenoid bone loss (GBL), and their impact on treatment selection

158 ch there is a furcal lesion with periodontal bone loss; Group I (intermediate) in which the border of

159 icacy of ankle loading for metastasis-linked bone loss has not been investigated.

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

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

162 L) is an antiresorptive drug used to prevent bone loss in a variety of conditions, acting mainly thro

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

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

165 artilage progenitor populations and promotes bone loss in antigen-induced arthritis.

166 up and the luteolin administration decreased bone loss in both groups.

167 e direct support for theories of generalized bone loss in chondrichthyans.

168 mal mandibular condyles, as well as alveolar bone loss in Ddr1(-/-) mice versus WT controls at 9 mo.

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

170 Morphometric analysis revealed greater bone loss in DM+PLAC and DM+INS in comparison to the oth

171 vious studies, DXA showed no post-transplant bone loss in either group; we instead observed an increa

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

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

174 course of chronic inflammation and alveolar bone loss in females.

175 Cancellous bone loss in femur in both genotypes was associated with

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

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

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

179 ing the effect of calcium supplementation on bone loss in lactating women have been small, with incon

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

181 disrupts normal bone remodeling and leads to bone loss in many skeletal diseases, including inflammat

182 gated the capacity of the DP diet to prevent bone loss in mice following exposure to simulated spacef

183 w that parathyroid hormone (PTH) only caused bone loss in mice whose microbiota was enriched by the T

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

185 plum powder (DP) prevented radiation-induced bone loss in mice.

186 oxide (compound E197) prevented pathological bone loss in mice.

187 pe:M2 phenotype ratio and prevented alveolar bone loss in mouse periodontitis models.

188 probiotic bacteria has been shown to prevent bone loss in multiple models of osteoporosis.

189 r osteoporosis, as deletion of shn3 prevents bone loss in osteoporotic mice and short-term inhibition

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

191 tamin D (1,25(OH)2D), osteoclastogenesis and bone loss in response to the high calcium demand associa

192 amined whether gut microbiome contributes to bone loss in SCD mice.

193 cytokines, impaired osteoblast function, and bone loss in SCD mice.

194 orrected the enhanced osteoclastogenesis and bone loss in Slc7a5-deficient mice.

195 kg body weight) blocked tooth injury-induced bone loss in Smoc2(-/-) mutants, reducing matrix metallo

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

197 Bisphosphonates may prevent or treat bone loss in such patients, but there is concern that th

198 sis showed significant reduction of alveolar bone loss in the CCL2 MP treatment group when compared w

199 rocess that allows osteoclast activation and bone loss in the context of osteocyte death.

200 y and efficacy of zoledronate for preventing bone loss in the first year after kidney transplant, we

201 gs revealed significantly increased alveolar bone loss in the Lig group, which was significantly prev

202 tional epithelium and increased the alveolar bone loss in the ligature-induced periodontitis model.

203 7a5 in mice led to osteoclast activation and bone loss in vivo, and Slc7a5 deficiency increased osteo

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

205 , suggesting that leptin is not required for bone loss induced by unweighting.

206 d disorder clinically defined by periodontal bone loss, inflammation of the specialized tissues that

207 Bone loss is a frequent but not universal complication o

208 e alveolar bone resorption, and whether this bone loss is associated with a T-helper (Th)1 and Th17-p

209 ption induced during periodontitis, and this bone loss is associated with a Th1- and Th17-pattern of

210 This accelerated rate of bone loss is associated with significantly reduced bone

211 We find that bone loss is more pronounced in females than in males an

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

213 retroviral therapy (ART) are associated with bone loss leading to increased fracture rate among perso

214 retroviral therapy (ART) are associated with bone loss leading to increased fracture rate among perso

215 on over bone formation is the root cause for bone loss leading to osteoporotic fractures.

216 obiota composition that prevent, or reverse, bone loss may be achieved by nutritional supplements wit

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

218 osis, and rapid joint destruction (including bone loss) may be observed in patients who received IACS

219 on gentle probing, and radiographic marginal bone loss (MBL) >=3 mm.

220 f implant failure was influenced by marginal bone loss (MBL) at T1 and not surgical modality.

221 robing depth (PD) were recorded and marginal bone loss (MBL) were assessed using standardized digital

222 I = -0.34 to 1.14 mm, P = 0.28) for marginal bone loss (MBL).

223 clinical attachment loss (AL), and marginal-bone-loss (MBL) were assessed.

224 ers (clinical attachment loss [AL], marginal bone loss [MBL], plaque index [PI], and bleeding on prob

225 Alveolar bone loss measurements were made on histological and mic

226 lized as a therapeutic agent that can target bone loss mediated by excessive osteoclastic bone resorp

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

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

229 eoclastogenesis, which may explain the rapid bone loss observed with high dosages of GC treatment.

230 Significant marginal bone loss occurred in the early post-diagnosis period of

231 ategies to combat the concomitant muscle and bone loss occurring in people afflicted with disuse atro

232 Lactation-induced bone loss occurs due to high calcium requirements for fe

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

234 Excessive bone loss occurs in inflammatory disorders such as perio

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

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

237 against PMO prevent the aggravated alveolar bone loss of periodontitis in estrogen-deficient women.

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

239 PF-based approaches on peri-implant marginal bone loss or preservation is inconclusive.

240 test groups showed a significant increase in bone loss over time (P < 0.05).

241 onate delivery led to increased peri-implant bone loss over time after immediate implant insertion.

242 ntly restricted ligature-induced periodontal bone loss (P <0 .01) and suppressed the levels of proinf

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

244 y primarily affects bone cells, leading to a bone loss phenotype of KO mice, independent from renal f

245 lthood, D673V homozygotes develop an evident bone-loss phenotype and show impaired osteogenesis.

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

247 rade of SUP are associated with peri-implant bone loss, probing depth, and defect morphology in patie

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

249 Finally, significant bone loss reduction was observed with ARN-NPs compared w

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

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

252 motherapy, long-term comorbidities including bone loss remain a significant problem.

253 mechanisms by which osteocytes contribute to bone loss remain elusive.

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

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

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

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

258 , it reduced osteoclast numbers and alveolar bone loss significantly due to APR's inhibition on osteo

259 s may lead to treatments for therapy-induced bone loss, significantly increasing quality of life for

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

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

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

263 pe (SASP) contribute to chemotherapy-induced bone loss that can be rescued by depleting senescent cel

264 Senescence drives chemotherapy-induced bone loss that is rescued by p38MAPK or MK2 inhibitors.

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

266 rectomy (VSG) caused trabecular and cortical bone loss that was independent of sex, body weight, and

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

268 zoledronic acid (ZOL) prevented ART-induced bone loss through 48 weeks of therapy and here investiga

269 dontitis pathogenesis by inhibiting alveolar bone loss through directly blocking osteoclast formation

270 n, gingival tissue destruction, and alveolar bone loss through sustained exacerbation of the host res

271 Lactation induces bone loss to provide sufficient calcium in the milk, a p

272 ion, hyperosteoclastogenesis, and trabecular bone loss, uncovering a pathological mechanism underlyin

273 ruction was determined by measuring alveolar bone loss under a stereomicroscope.

274 In T1D, major osteoclastogenic activity and bone loss versus other groups were confirmed by a greate

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

276 G2 rats had greater bone loss volume, increased number, and thickness and de

277 The radiographic mean marginal bone loss was 1.52 +/- 1.33 mm (Tb to T1) and 0.58 +/- 0

278 Alveolar bone loss was analyzed by micro-computed tomography and

279 This decreased bone loss was associated with a dismissed RANKL expressi

280 This decreased bone loss was associated with a proresolutive phenotype

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

282 Periodontal bone loss was measured via histological and microcompute

283 tal parameters remained stable, and alveolar bone loss was not observed.

284 The highest alveolar bone loss was observed in the periodontitis group and th

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

286 Periodontal bone loss was significantly decreased and the gingival e

287 Alveolar bone loss was significantly reduced in the ligature + de

288 Epithelial downgrowth and bone loss was similar.

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

290 eding On Probing, Plaque Index) and marginal bone loss were also recorded.

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

292 ing, suppuration, plaque index, and marginal bone loss were recorded.

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

294 mmation, osteoclastogenesis, and periodontal bone loss when transferred to normal germ-free hosts.

295 es released from implants cause inflammatory bone loss, which is a key factor in aseptic loosening, t

296 ons, altered biomechanics, and age-dependent bone loss, which leads to SLC26A2-related spondylolysis.

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

298 to the microbiota contribute to pathological bone loss, while changes in microbiota composition that

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

300 Although not a primary mechanism for bone loss with VSG, G-CSF plays an intermediary role for