ライフサイエンスコーパス: alveolar bone

1 of root cementum, periodontal ligament, and alveolar bone).

2 r management of periodontal inflammation and alveolar bone.

3 tion in loads transfer and remodeling of the alveolar bone.

4 tors play in the volumetric reduction of the alveolar bone.

5 llular cementum, and osteoid accumulation in alveolar bone.

6 o solution for the long-term preservation of alveolar bone.

7 nt acid phosphatase (TRAP)-positive cells in alveolar bone.

8 on (HFA) has an osteogenic effect on healthy alveolar bone.

9 zed bone structure was the main character of alveolar bone.

10 mice were subjected to mechanical loading in alveolar bone.

11 n and thus may exhibit a favorable effect on alveolar bone.

12 acial mesenchymal cells that form dentin and alveolar bone.

13 ncluding periodontal ligament, cementum, and alveolar bone.

14 ile also facilitating slow remodeling of the alveolar bone.

15 iated and morphological changes occur in the alveolar bone.

16 each other but maintained similar levels of alveolar bone.

17 includes 2 mineralized tissues, cementum and alveolar bone (AB), both essential for tooth attachment.

18 However, it is not known if HFA can preserve alveolar bone after extraction without negatively affect

19 the periodontal diagnostic acumen regarding alveolar bone alterations influenced by orthodontic toot

20 t dental pulp (dental pulp cells [DPCs]) and alveolar bone (alveolar bone cells [ABCs]) were isolated

21 ts the role of PHOSPHO1 in mineralization of alveolar bone and cellular cementum, further revealing t

22 ficant protective effect was not observed on alveolar bone and collagen tissue in this model.

23 on of antibiotics significantly improved the alveolar bone and PDL damage of the knockdown phenotype,

24 th that will progressively cause the loss of alveolar bone and periodontal ligaments and eventually t

25 disease that degrades connective tissue and alveolar bone and results in tooth loss.

26 is vital for maintenance and regeneration of alveolar bone and supporting structures around teeth and

27 oral microbiota that leads to destruction of alveolar bone and tooth loss.

28 ding the teeth that lead to the breakdown of alveolar bone and tooth loss.

29 o periodontal ligament detachment, extensive alveolar bone and tooth root resorption, and incisor mal

30 s were disturbed in Hyp versus WT long bone, alveolar bone, and cementum, including osteocyte/cemento

31 tial stem cells (PDLSCs) giving rise to PDL, alveolar bone, and cementum.

32 P in the normal development of the calvaria, alveolar bone, and dentin-pulp complex.

33 inging attention to direct effects of HPP on alveolar bone, and offering a new model for testing pote

34 ar cementum, periodontal ligament (PDL), and alveolar bone, are critical for tooth function.

35 Histomorphometric analysis, which included alveolar bone area, alveolar bone level, and attachment

36 mbers of osteoclasts in the CCL2 MP group in alveolar bone area.

37 ory cytokines and reduced IL-17A(+) cells in alveolar bone as compared with vehicle-treated OVX-perio

38 Allograft has been extensively studied for alveolar bone augmentation in Piezocision; however, the

39 ive, flapless alternative to corticotomy for alveolar bone augmentation.

40 olume in the extraction site and surrounding alveolar bone by 44% when compared with static, while fu

41 Teeth are attached to alveolar bone by the periodontal ligament (PDL), which c

42 hanges in bone trabeculation, changes in the alveolar bone can be detected quantitatively.

43 ors related to the resorption of the palatal alveolar bone caused by tooth movement after the maxilla

44 dental pulp cells [DPCs]) and alveolar bone (alveolar bone cells [ABCs]) were isolated and separately

45 Primary alveolar bone cells were exposed to the SASP via in vitr

46 pact of genetic background on comorbidity of alveolar bone change and glucose tolerance after HFD con

47 Interleukin-6 significantly correlated with alveolar bone changes (P <0.05), whereas adipsin showed

48 Alveolar bone changes significantly varied among CC line

49 nd IL-10, serum B-ALP and TRAP-5b levels, or alveolar bone compared with conventional periodontal the

50 ion and junctional epithelium, cementum with alveolar bone crest destruction, but animals pretreated

51 nces between the cemento-enamel junction and alveolar bone crest were evaluated.

52 orptive lesions, osteoid accumulation on the alveolar bone crest, and significant differences in seve

53 location of the microgap with respect to the alveolar bone crest, occlusion, and use of a polished co

54 (MSs) was compared at experimentally-created alveolar bone defects in rats.

55 20C(fl/fl) mice showed remarkable dentin and alveolar bone defects, while their enamel did not show a

56 le methods to stimulate bone regeneration in alveolar bone defects.

57 pment, widened PDL space, and interradicular alveolar bone defects.

58 ination, periodontal ligament thickness, and alveolar bone density on the pressure side in IM-T1D wer

59 confirmed decreased bone volume fraction and alveolar bone density.

60 ate of mineral apposition and an increase in alveolar bone density.

61 ally treated root canal with periodontal and alveolar bone-derived cells.

62 murine oral cavity and to prevent subsequent alveolar bone destruction and osteoclastogenesis.

63 s did not protect from or exacerbate crestal alveolar bone destruction but were responsible for promo

64 Th17 cells are redundant in contributing to alveolar bone destruction in a murine model of periodont

65 Kdm3C knockout (KO) in mice led to increased alveolar bone destruction upon induction of experimental

66 he pathogenesis of periodontitis with severe alveolar bone destruction.

67 mparable outcomes in terms of maintenance of alveolar bone dimensions, feasibility of implant placeme

68 sease is characterized by destruction of the alveolar bone due to an aberrant host inflammatory respo

69 urgery that involves the teeth or contiguous alveolar bone) during BMA treatment.

70 bable, and 3-dimensionally printed) used for alveolar bone engineering around teeth and implants and

71 In many instances, surrounding alveolar bone extended into the existing resorptive defe

72 etter results on periodontium with regard to alveolar bone findings.

73 tatin (RSV), are known to be associated with alveolar bone formation and periodontal improvements.

74 (recently shown to play key roles in normal alveolar bone formation), significant loss in alveolar b

75 of the key contribution of the PDL in normal alveolar bone formation, the pathologic changes of the O

76 and osteoclast activity, and an increase in alveolar bone formation.

77 Subjective radiographic classifications of alveolar bone have been proposed and correlated with imp

78 eoporotic phenotype might affect the rate of alveolar bone healing following tooth extraction.

79 bone fragility, but how this disease affects alveolar bone healing is not clear.

80 istically significant difference in residual alveolar bone height (P <0.001).

81 first (M1) and second (M2) molars: relative alveolar bone height (RBH), crestal bone width (CBW), bo

82 Both cKO models exhibited reduced alveolar bone height and 4-fold increased numbers of ost

83 matory reaction corresponded to reduction in alveolar bone height and density (r = 0.74; P <0.05; Spe

84 compared with static, while fully preserving alveolar bone height and width long-term.

85 Prior reports that alveolar bone height is significantly less in normal SPF

86 When characterizing ENAM(-/-) mice, alveolar bone height reduction was observed, and it was

87 pocket depth (PPD), tooth mobility (TM), and alveolar bone height.

88 ibution of mucosal Langerhans cells (LCs) to alveolar bone homeostasis in mice following oral coloniz

89 o the normal oral flora, mediating catabolic alveolar bone homeostasis in the healthy periodontium.

90 Meanwhile, in the adjacent alveolar bone, hyperloading activates bone resorption, t

91 ontia, microdontia, tooth root deficiencies, alveolar bone hypoplasia, and a range of skeletal malfor

92 gated the histologic changes of cementum and alveolar bone in a pycnodysostosis patient, caused by no

93 g protein osteopontin (OPN) was increased in alveolar bone in Phospho1(-/-) mice.

94 Destruction of the alveolar bone in the jaws can occur due to periodontitis

95 f the interface between the root surface and alveolar bone in the replantation/transplantation model,

96 increased the expression of IL-33 and ST2 in alveolar bone in vivo and in osteoblastic cells in vitro

97 C) functions and increased bacterial load in alveolar bone in vivo and whether DC inhibition alone pr

98 pl(+/A116T) mice featured alterations in the alveolar bone, including radiolucencies and resorptive l

99 Furthermore, destruction of crestal alveolar bone induced by P. gingivalis colonization occu

100 During periodontitis, tooth-supporting alveolar bone is resorbed when there is an increased exp

101 ament (PDL), which connects the teeth to the alveolar bone, is essential for periodontal tissue homeo

102 d not demonstrate significant differences in alveolar bone level compared to EP (P >0.05).

103 analysis, which included alveolar bone area, alveolar bone level, and attachment loss, and immunohist

104 Alveolar bone level, serum antibody, and lymphocyte resp

105 eriodontal disease often result in decreased alveolar bone levels and a loss of connective tissue hom

106 10, serum B-ALP and TRAP-5b, and calcium and alveolar bone levels between the groups receiving SRP an

107 id phosphatase 5b (TRAP-5b), and calcium and alveolar bone levels in rats with experimentally induced

108 Alveolar bone levels in the periodontitis group were sig

109 olved, and there was progressive loss of the alveolar bone, likely as a result of increased colonizat

110 miRNAs direct periodontal fibroblasts toward alveolar bone lineage differentiation and new bone forma

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

158 1 phenotype:M2 phenotype ratio and prevented alveolar bone loss in mouse periodontitis models.

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

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

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

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

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

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

165 PT reduced alveolar bone loss in unstressed animals.

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

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

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

169 Alveolar bone loss measurements were made on histologica

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

171 Alveolar bone loss resulting from LPS-induced periodonti

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

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

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

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

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

177 Alveolar bone loss was also evaluated radiographically i

178 Alveolar bone loss was analyzed by micro-computed tomogr

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

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

181 Greater radiographic alveolar bone loss was observed among participants repor

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

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

184 Alveolar bone loss was significantly higher in the PED g

185 Alveolar bone loss was significantly reduced in the liga

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

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

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

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

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

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

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

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

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

195 crobiota and accelerated naturally occurring alveolar bone loss.

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

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

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

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

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

201 bone metabolism and can therefore influence alveolar bone loss.

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

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

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

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

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

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

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

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

210 4-DPCA/hydrogel), to promote regeneration of alveolar bone lost owing to experimental periodontitis.

211 lveolar bone formation), significant loss in alveolar bone mass ( P < 0.01), and a sharp reduction in

212 and ultrastructural changes of cementum and alveolar bone might be affected by CTSK mutation via red

213 Alveolar bone mineral density and alveolar bone volume w

214 Concomitantly, alveolar bone mineral density was significantly lower in

215 Despite alveolar bone mineralization defects, periodontal attach

216 Phospho1(-/-) mice featured disturbances in alveolar bone mineralization, shown by accumulation of u

217 ion of DMP1 in vivo in cellular cementum and alveolar bone of mice treated with a single dose (50 mic

218 of osteoclasts, especially noted around the alveolar bone of molars (buccal side) and incisors.

219 nd PHOSPHO1 protein were expressed by active alveolar bone osteoblasts and cementoblasts during cellu

220 function resulted in an increased number of alveolar bone osteoclasts and increased RANKL expression

221 We hypothesized that alveolar bone osteocytes develop senescence characterist

222 While long bone and alveolar bone osteocytes in Hyp mice overexpressed fibro

223 Alveolar bone osteocytes negatively regulate Gli1+ PDLSC

224 16(Ink4a) mRNA expression were identified in alveolar bone osteocytes with aging.

225 d appeared to be a protective factor against alveolar bone osteonecrosis.

226 orosis that manifest as thinner, more porous alveolar bone, PDL thinning, and slower bone repair.

227 om the enamel, dentin, periodontal ligament, alveolar bone, pulp, and other regions are identified an

228 Linear measurements of alveolar bone (radiographic bone level [rBL]), assessed

229 tructure with surrounding native dentine and alveolar bone, Raman microspectroscopy analysis is used.

230 Mean thickness of alveolar bone ranged from 6.66 to 4.51 mm (standard devi

231 ad all premolar teeth extracted and adjacent alveolar bone reduced.

232 stigate the biological mechanisms underlying alveolar bone regeneration (ABR) and orthodontic tooth m

233 fficiently induces new bone formation in the alveolar bone regeneration model.

234 Part I included the alveolar bone regeneration model.

235 On the other hand, APR promoted alveolar bone regeneration through enhancing osteogenic

236 CR4-dependent accumulation of Treg cells and alveolar bone regeneration, suggesting a novel approach

237 ens and their contribution to destruction of alveolar bone remain unknown.

238 maintaining proper periodontal function and alveolar bone remodeling and point to dental dysfunction

239 Alveolar bone repair was evaluated histomorphometrically

240 In rat alveolar bone repair, meloxicam did not affect VEGF expr

241 oinflammatory cytokines and its influence on alveolar bone resorption (ABR) in rats.

242 in treatment significantly inhibits regional alveolar bone resorption and contributes to periodontal

243 Alveolar bone resorption and gingival collagen fibers we

244 a murine model of periodontitis by measuring alveolar bone resorption and gingival IL-17 expression a

245 On day 14, there were no differences in alveolar bone resorption and gingival RANKL expression b

246 Tooth extraction results in alveolar bone resorption and is accompanied by postopera

247 Boldine, administered orally, inhibited the alveolar bone resorption and modulated the Th17/Treg imb

248 Alveolar bone resorption and myeloperoxidase activity we

249 RP-SG) is indicated to attenuate physiologic alveolar bone resorption as a consequence of tooth extra

250 tion analysis adopting the amount of palatal alveolar bone resorption as a dependent variable demonst

251 tor and TES on the inflammatory response and alveolar bone resorption associated with ligature-induce

252 main effector Caspase-1 in inflammation and alveolar bone resorption associated with periodontitis.

253 lly were sufficient to significantly inhibit alveolar bone resorption associated with the experimenta

254 epletion reduced P. gingivalis infection and alveolar bone resorption by modulating the host immune r

255 aimed to determine whether boldine inhibits alveolar bone resorption by modulating the Th17/Treg imb

256 However, the effect of boldine on alveolar bone resorption during periodontitis has not be

257 ccal bone thickness is a strong predictor of alveolar bone resorption in both groups.

258 ects of systemic melatonin administration on alveolar bone resorption in experimental periodontitis i

259 ion of P. gingivalis plays a key role in the alveolar bone resorption induced during periodontitis, a

260 The alveolar bone resorption is a distinctive feature of per

261 mutant strains of P. gingivalis induced less alveolar bone resorption than the encapsulated W50 wild-

262 Alveolar bone resorption was analyzed using microcompute

263 The amount of palatal alveolar bone resorption was measured and various parame

264 n periodontal ligament (PDL) disintegration, alveolar bone resorption, and ultimately tooth loss.

265 gingivalis encapsulation induces more severe alveolar bone resorption, and whether this bone loss is

266 Hence, its actions on alveolar bone resorption, gingival collagen content and

267 al epithelium, periodontal pocket formation, alveolar bone resorption, osteoclast activation, bacteri

268 esponse plays a key role in bacteria-induced alveolar bone resorption.

269 duced periodontitis in mice, as evidenced by alveolar bone resorption.

270 tory M1 macrophages into gingival tissue and alveolar bone resorption.

271 Boldine inhibited the alveolar bone resorption.

272 pressions on the amber match the hadrosaur's alveolar bone ridges, providing some insight into the ta

273 Alveolar bone samples were obtained from young (6 months

274 ted tomography (micro-CT) was used to assess alveolar bone structure and tissue compositions.

275 ents have fewer teeth, greater CAL, and less alveolar bone support compared with controls after adjus

276 tion, causing destruction of soft tissue and alveolar bone supporting the teeth.

277 nt acid phosphatase-positive cells along the alveolar bone surface was significantly decreased after

278 g the positive or deleterious changes on the alveolar bone surrounding natural teeth undergoing ortho

279 thought to contribute to the destruction of alveolar bone surrounding teeth by influencing osteoclas

280 ition affecting tooth-supporting tissues and alveolar bone that surround the tooth, leading to format

281 he rodent incisor apex, the dental pulp, the alveolar bone, the periodontal ligament, the cementum, a

282 dy is to evaluate the changes in the palatal alveolar bone thickness and find the factors related to

283 Changes in the alveolar bone thickness and height around natural teeth

284 Palatal alveolar bone thickness changes and resorption factors w

285 es of maxillary central incisors and palatal alveolar bone thickness were measured, and the correspon

286 size defects were created in intact proximal alveolar bone to each implant.

287 nt between the responses of human and rodent alveolar bone to osteotomy site preparation.

288 cess, as well as restore and regenerate lost alveolar bone to reserve the natural teeth in diabetics,

289 onsequence, both the PDL and the surrounding alveolar bone undergo atrophy.

290 1(phox) KO mice revealed significant loss of alveolar bone volume and enhanced inflammatory cell infi

291 There were no differences in alveolar bone volume at 1 mo, but at 9 mo, severe period

292 mellitus (t2DM) development and significant alveolar bone volume change (P <0.05), whereas others sh

293 there was no significant correlation between alveolar bone volume changes and increased BW or glucose

294 es were quantified by multiplex immunoassay, alveolar bone volume was quantified by microcomputed tom

295 Alveolar bone mineral density and alveolar bone volume were quantified by three-dimensiona

296 points after osteotomy, the fate of the dead alveolar bone was followed.

297 edic treatment on periodontal tissues (i.e., alveolar bone) were included.

298 progressive destruction of tooth-supporting alveolar bone, which is mainly caused by chronic inflamm

299 Hyp mandibles demonstrated expanded alveolar bone with accumulation of osteoid, and micro-CT

300 allenge, Rac-null mice had increased loss of alveolar bone with patterns of resorption characteristic