ライフサイエンスコーパス: dentinal

1 namel, the dentin-enamel junction, and outer dentinal acellular tubules, and then concentrates in odo

2 , OMZ175, Cnm mediates stringent adhesion to dentinal and root tissues as well as collagen-coated sur

3 Due to the collagenous composition of dentinal and root tissues, we hypothesized that Cnm may

4 ouse trigeminal ganglia, we demonstrate that dentinal application of LPS increases the expression of

5 bitor to reduce collagen degradation in root/dentinal caries can be further explored.

6 cular interest was the disease trajectory of dentinal caries in the permanent teeth in groups defined

7 groups defined by the presence or absence of dentinal caries in the primary teeth.

8 The mechanical removal of dentinal caries traditionally involves the use of tactil

9 3 to 7 y with at least 1 primary molar with dentinal carious lesion were randomized across 3 arms (1

10 A significantly lower number of enamel and dentinal carious lesions was observed for the mutant-inf

11 itu mineralization, and promoting biomimetic dentinal collagen remineralization.

12 this study, the effects of 5% and 10% CP on dentinal collagen structure and chemical properties were

13 emical changes resulting from CP exposure in dentinal collagen using Raman spectroscopy.

14 ions of CP result in a deleterious change in dentinal collagen.

15 s between lamniform sharks and other taxa (a dentinal core of osteodentine instead of a hollow pulp c

16 rength, collagen structure preservation, and dentinal enzyme silencing.

17 With these stimuli dentinal fluid flow could not be recorded in vivo for te

18 Tertiary dentin formation reduces dentinal fluid flow due to occluded tubules or discontin

19 After the dentinal fluid flow measurements, specimens were also ev

20 The thresholds of these units in terms of dentinal fluid flow were in the range 0.3-2.1 nl s(-1) m

21 resent in saliva, mineralized dentin, and/or dentinal fluid may affect the dentin caries process at t

22 rupt influx, because of neural regulation of dentinal fluid movement, but it did not.

23 ion of dental sensory neurons in response to dentinal fluid movements.

24 ther inhibited the release and activation of dentinal gelatinases.

25 Postoperative dentinal hypersensitivity (5.7%) was the most frequent c

26 h the initial enamel or root lesion, through dentinal involvement, to eventual cavitation.

27 net increments of occlusal surfaces and deep dentinal lesions SBCPRs (H = 46.4-56.2).

28 er, exposing the soft underlying collagenous dentinal matrix and allowing further infiltration by the

29 from the CS hydrogel could diffuse into the dentinal matrix and penetrate the dentinal tubules, lead

30 s that were caries-lesion-free (PF) and from dentinal (PD) and enamel (PE) caries lesions.

31 Dentinal repair in the postnatal organism occurs through

32 fects of aging, injury, neural function, and dentinal repair on its influx into vital rat teeth.

33 s and distinctive in the demineralization of dentinal root surfaces for periodontal regeneration and

34 e to dentin following the preparation of the dentinal surface with either an Er:YAG laser (lambda = 2

35 ewer carious lesions in the buccal enamel or dentinal surfaces than the sham-immunized animals (P < 0

36 as also associated with abnormalities in the dentinal tubule system and delayed formation of the thir

37 gth tested perpendicular to the direction of dentinal tubules (undemineralized crown = 140.4 +/- 48.6

38 y and fail to form proper dentin with normal dentinal tubules and activate terminal differentiation,

39 distribution of the AAMPs in relation to the dentinal tubules and collagen network using a minimally

40 mineralization as well as the defects in the dentinal tubules and third molar development.

41 Dspp(P19L) dentin contained dentinal tubules but grew slowly and was softer and less

42 ctive mineralized layer on dentin, occluding dentinal tubules by peptide-guided in situ mineralizatio

43 ed by estimating the number and diameters of dentinal tubules exposed.

44 persensitivity commonly occurs due to opened dentinal tubules for many reasons.

45 In the dentinal tubules from the isthmus, at 100 um in-depth, s

46 In the dentinal tubules from the main root canals, at 100 and 1

47 The occlusion of dentinal tubules has become a rapid and effective method

48 anomalies in the number and organization of dentinal tubules in MT-DLX3 TG mice.

49 In particular, the dentinal tubules in the DGI-II patient were very irregul

50 netration ability of CPNE7 molecules through dentinal tubules in vitro.

51 test the hypothesis that fluid flow through dentinal tubules is part of the mechanism involved in th

52 ectively removed the surface smear layer and dentinal tubules remained partially to totally occluded

53 re based on the physical obliteration of the dentinal tubules to reduce hydraulic conductance.

54 Bacterial reduction in the main canals and dentinal tubules were respectively determined by MTT ass

55 as analogous to reparative dentin: it lacked dentinal tubules, contained cellular debris, and was sig

56 e into the dentinal matrix and penetrate the dentinal tubules, leading to both surface and subsurface

57 of tertiary dentin through shallowly exposed dentinal tubules, which decreases dentin permeability.

58 he dentin surface and extended deeply around dentinal tubules.

59 w tracts that exist in human dentine forming dentinal tubules.

60 consequence of fluid movement within exposed dentinal tubules.

61 resent in the predentin matrix and along the dentinal tubules.

62 ansparent carious dentin containing occluded dentinal tubules.

63 ormation, and a relatively high branching of dentinal tubules.

64 antigens that diffuse into the pulp through dentinal tubules.

65 entin surface with a higher number of opened dentinal tubules.

66 few mature odontoblasts, and sharply reduced dentinal tubules; and (5) a dramatic change in Osx and n

67 tiation into odontoblast-like cells near the dentinal walls.

68 losure of immature permanent teeth with thin dentinal walls.