ライフサイエンスコーパス: hard tissue

1 "soft tissue") to bone (a stiff, structural "hard tissue").

2 them were blue-green colored that indicates hard tissue.

3 uring cell differentiation and production of hard tissues.

4 g stream of water effectively removes dental hard tissues.

5 progression were confirmed for both soft and hard tissues.

6 ival toward optimal preservation of soft and hard tissues.

7 systemic impact on the peri-implant soft and hard tissues.

8 ession presents destruction of both soft and hard tissues.

9 mmatory response in the periodontal soft and hard tissues.

10 There were no harmful effects to soft or hard tissues.

11 reference to Clopton Havers, a 17th Century hard tissue anatomist, and Franz Halberg, a long-time ex

12 Periodontists' knowledge of soft and hard tissue anatomy and their ability to manage soft tis

13 dentin, teleost fish enameloid (enamel-like hard tissue), and tetrapod enamel.

14 Digit fusion involves both soft and hard tissues, and is associated with reduced apoptosis a

15 ntal procedures is the creation of soft- and hard-tissue architecture that is consistent with periodo

16 study reported a minimal loss of mineralized hard tissue around dental implants placed non-submerged

17 sed as an interface or surface for soft- and hard-tissue attachment and integration are commercially

18 t differences regarding the loss of marginal hard tissues between mesial and distal surfaces or the m

19 portant shifts reflected in aspects of human hard tissue biology and the archeological record.

20 Hard tissue biopsies of 7 sites in 6 patients were obtai

21 Hard tissue biopsies were taken from 10 representative c

22 issue by measuring leukocyte recruitment and hard tissues by measuring osteoclastogenesis.

23 s a positive effect on marginal peri-implant hard-tissue changes.

24 sue height over time, and 3) if the marginal hard tissue could be detected on the implant platform at

25 ue height over time, and 3) whether marginal hard-tissue could be detected on the implant platform at

26 BSP is present in cementum, the hard tissue covering the tooth root that anchors periodo

27 Often, in these patients, soft and hard tissue defects result from a variety of causes, suc

28 tential to contribute to excessive soft- and hard-tissue destruction.

29 ole in the biological mechanisms controlling hard tissue development, but the details of molecular re

30 e of diagnostic disagreement, progression of hard tissue diagnoses in the right TMJ occurred in 15.2%

31 Of 794 joints with baseline joint-specific hard tissue diagnoses of DJD, progression was observed i

32 oft tissue diagnoses and 71% of the baseline hard tissue diagnoses remained stable.

33 Baseline hard tissue diagnoses showed no statistical association

34 e soft tissue diagnoses were associated with hard tissue diagnostic changes at follow-up ( P < 0.0001

35 ective compares the preservation of soft and hard tissue dimensional changes after alveolar ridge pre

36 and minimal change of peri-implant soft and hard tissue dimensions.

37 overing, the other a morphologically diverse hard tissue distributed at over 200 sites in the body.

38 involved in initiating the mineralization of hard tissue ECMs.

39 sms is likely to be important for successful hard tissue engineering.

40 ation preclinical model is an ideal tool for hard tissue evaluation by micro-computed tomography, his

41 Other hard tissue findings showed similar clinically superior

42 Other hard tissue findings showed similar clinically superior

43 le that statherin plays in the regulation of hard tissue formation in humans, the surface recognition

44 atrix proteins as well as their control over hard tissue formation.

45 derstanding this process would shed light on hard-tissue formation and guide efforts to develop bioma

46 ling semi-automated segmentation of soft and hard tissue from muCT data.

47 Extracellular matrix proteins regulate hard tissue growth by acting as adhesion sites for cells

48 oactive peptide ligands direct both soft and hard tissue growth in a hierarchically organized manner.

49 hat these proteins play in the regulation of hard tissue growth in humans, the exact mechanism used b

50 sight into the recognition and regulation of hard tissue growth.

51 ons, reproducing a key feature of biological hard-tissue growth and assembly.

52 In addition, these implants had hard tissue healing that extended onto the implant shoul

53 Hard tissue healing was determined histomorphometrically

54 Hard-tissue healing was evaluated by microcomputed tomog

55 oning of the implant, 2) changes of marginal hard tissue height over time, and 3) if the marginal har

56 oning of the implant, 2) changes of marginal hard-tissue height over time, and 3) whether marginal ha

57 Hard tissue improvements resulted in the complete closur

58 Both treatments provided soft and hard tissue improvements when compared to baseline (P <

59 tion involvements, both in terms of soft and hard tissue improvements.

60 ears to represent a new strategy for forming hard tissue in animals.

61 dictably led to the preservation of soft and hard tissue in extraction sites.

62 first time the ultrastructure of the dental hard tissues in an archival case of intrinsically pigmen

63 However, stability of peri-implant soft and hard tissues indicates the need to take measures that mi

64 o far, studies have predominantly focused on hard tissue integration.

65 sis of the biopsied specimen revealed dental hard tissue interspersed in a field of odontogenic epith

66 ingiva do not contribute to the formation of hard tissue, it is theoretically possible that under app

67 Degree of hard tissue loss and type of final prosthetic restoratio

68 sthetic restoration as well as the degree of hard tissue loss on 7-y clinical performance of ETT rest

69 therapeutic modality for severe peri-implant hard tissue loss.

70 n the groups regarding marginal peri-implant hard-tissue loss.

71 of mineral leading to dissolution of dental hard tissues may result in a caries lesion that can be s

72 Intrasurgical hard tissue measurements consisted of the vertical open

73 Analysis of soft and hard tissue measurements demonstrated a statistically si

74 Hard tissue measurements included defect depth, alveolar

75 Hard tissue measurements included height of the alveolar

76 at surgical reentry (9 to 13 months later), hard tissue measurements included: stent to defect base,

77 Hard tissue measurements obtained at surgical reentry we

78 e was surgically re-entered and all soft and hard tissue measurements repeated.

79 Hard tissue measurements were recorded during the initia

80 The following soft and hard tissue measurements were recorded prior to initial

81 Both soft and hard tissue measurements were taken the day of surgery (

82 assembly of matrix proteins is a key step in hard tissue mineralization, developing an understanding

83 human form, information about both soft and hard tissues of our ancestors is needed.

84 ations and suggesting that patterning of the hard tissues of the mandible is instructed by the epithe

85 l for the development and maintenance of the hard tissues of the skeleton.

86 77% of the implants in Group B demonstrated hard tissue on the implant platform.

87 The mineralized hard tissue on the implant shoulder was found in 69% of

88 This study aims to compare hard tissue outcomes of VBA, with and without recombinan

89 Baseline and 6-month reentry soft and hard tissue parameter measurements were made by calibrat

90 d similar favorable improvements in soft and hard tissue parameters in the treatment of human intraos

91 ally significant improvement to the soft and hard tissue parameters measured.

92 t using conservative flap reentry surgeries; hard tissue parameters were also assessed at this time.

93 indicate that there may be an enhancement of hard tissue parameters when enamel matrix derivative is

94 iographic findings were non-contributory for hard tissue pathoses.

95 ar origin of the instructive information for hard tissue patterning of the jaws has been the subject

96 y odontogenesis and later differentiation of hard tissue-producing cells.

97 nt position and loss of marginal mineralized hard tissue (r = 0.15; P >0.05).

98 s in structures that can be used as soft and hard tissue-regenerating materials, biosensors, and ener

99 ization have the potential to be utilized in hard tissue regeneration.

100 on and demonstrate their value for promoting hard tissue regeneration.

101 al-dose doxycycline, also indirectly promote hard-tissue regeneration.

102 recession, probing, clinical attachment) and hard tissue (resorption, defect fill) parameters 6 month

103 The evaluation of the hard tissue response at the 12-month re-entry demonstrat

104 omposites in combination with bonding to the hard tissue result in stress transfer and inward deforma

105 ssociated with microdamage and repair at the hard tissue-soft tissue interface.

106 erative medicine is to restore oral soft and hard tissues through cell, scaffold, and/or signaling ap

107 In Biology, this process enables soft and hard tissues to coexist in the same organism with relati

108 2 mm, without loss of interproximal soft and hard tissue, treated with the CAF procedure and evaluate

109 months, upon flap reflection, no regenerated hard tissue was found.

110 The mean marginal loss of hard tissues was 0.11 +/- 0.30 mm for Group A and 0.08 +

111 The mean marginal loss of hard tissues was 0.11 +/- 0.30 mm.

112 al and radiographic measurements of soft and hard tissues were recorded by means of a stent before an