Chlorhexidine, a Matrix Metalloproteinase Inhibitor and the Development of Secondary Caries Wall Lesions in a Microcosm Biofilm Model

2018 ◽  
Vol 53 (1) ◽  
pp. 107-117
Author(s):  
Tamires T. Maske ◽  
Nicolien K. Kuper ◽  
Maximiliano S. Cenci ◽  
Marie-Charlotte D.N.J.M. Huysmans

This study investigated the role of a matrix metalloproteinase (MMP) inhibitor (CHX 2%) in the development of secondary caries wall lesions in different interface conditions with small (run 1) and wider gaps (run 2). Dentin discs were restored and pretreated with or without CHX 2%. In run 1, interfaces were made with gaps of 30, 60, or 90 µm. Interfaces with composite placed directly onto the dentin were either bonded (Adper Single Bond 2) or not bonded. In run 2, interfaces were made with gaps of 100 µm, with or without adhesive on the composite side (CLEARFIL SE Bond). Interfaces were either bonded or not bonded, as in run 1. Microcosm biofilms were grown on dentin-composite samples for 14 days. Caries lesion outcomes were analyzed by transversal wavelength-independent microradiography at 3 locations: the outer surface, and the interface wall at a distance of 200 and 500 µm from the gap entrance. Linear regression analyses showed that pretreatment with MMP inhibitor did not influence progression of the wall lesion at any location (p ≥ 0.218). Interfaces with intentional gaps showed positive and significant effect on the wall lesion progression at 200 µm from the gap entrance (p ≤ 0.005). A small trend of increase in wall lesion development was observed at the 200-µm location when bonding was present on the composite side. In conclusion, the dentin pretreatment with CHX 2% was not able to slow down the development of secondary caries wall lesions in small and wide gaps in this biofilm model.

2017 ◽  
Vol 51 (5) ◽  
pp. 475-481 ◽  
Author(s):  
Tamires T. Maske ◽  
Nicolien K. Kuper ◽  
Maximiliano S. Cenci ◽  
Marie-Charlotte D.N.J.M. Huysmans

This in vitro study investigated the development of dentin wall lesions next to resin composite containing very small gap sizes using an in vitro biofilm model, and evaluated whether a relevant threshold for the gap size could be established. Microcosm biofilms were grown for 14 days within small interfacial gaps between dentin-resin composite discs under intermittent cariogenic challenge. The factor under study was gap size: samples were either restored with composite resin without adhesive procedure (no intentional gap; no bonding [NB] group) or with intentional gaps of 30, 60, or 90 µm, or with complete adhesive procedure (no gap; bonding [B] group). Secondary caries wall lesion progression was measured in lesion depth (LD) and mineral loss (ML) using transversal wavelength independent microradiography at 3 locations: outer surface lesion and wall lesions at 200 and 500 µm distance from gap entrance. Results from linear regression analysis showed that the presence of an intentional gap (30, 60, and 90 µm) affected the secondary caries progression at 200 µm from the gap entrance (p ≤ 0.013). The NB group did not show significant wall lesion development (ML and LD, p ≥ 0.529). At 500 µm distance almost no wall caries development was observed. In conclusion, dentin wall lesions developed in minimal gap sizes, and the threshold for secondary wall lesion development was a gap of around 30 µm in this microcosm biofilm model.


2018 ◽  
Vol 71 ◽  
pp. 49-53 ◽  
Author(s):  
T.T. Maske ◽  
N.K. Kuper ◽  
A.C.C. Hollanders ◽  
E.M. Bronkhorst ◽  
M.S. Cenci ◽  
...  

2015 ◽  
Vol 43 (8) ◽  
pp. 1007-1012 ◽  
Author(s):  
Anelise F. Montagner ◽  
Nicolien K. Kuper ◽  
Niek J.M. Opdam ◽  
Ewald M. Bronkhorst ◽  
Maximiliano S. Cenci ◽  
...  

2016 ◽  
Vol 311 (1) ◽  
pp. H183-H189 ◽  
Author(s):  
Xiaohu Fan ◽  
Bryan G. Hughes ◽  
Mohammad A. M. Ali ◽  
Brandon Y. H. Chan ◽  
Katherine Launier ◽  
...  

Cardiomyocyte dedifferentiation may be an important source of proliferating cardiomyocytes facilitating cardiac repair. Cardiomyocyte dedifferentiation and proliferation induced by oncostatin-M (OSM) is characterized by sarcomere degeneration. However, the mechanism underlying sarcomere degeneration remains unclear. We hypothesized that this process may involve matrix metalloproteinase-2 (MMP-2), a key protease localized at the sarcomere in cardiomyocytes. We tested the hypothesis that MMP-2 is involved in the sarcomere degeneration that characterizes cardiomyocyte dedifferentiation. Confocal immunofluorescence and biochemical methods were used to explore the role of MMP-2 in OSM-induced dedifferentiation of neonatal rat ventricular myocytes (NRVM). OSM caused a concentration- and time-dependent loss of sarcomeric α-actinin and troponin-I in NRVM. Upon OSM-treatment, the mature sarcomere transformed to a phenotype resembling a less-developed sarcomere, i.e., loss of sarcomeric proteins and Z-disk transformed into disconnected Z bodies, characteristic of immature myofibrils. OSM dose dependently increased MMP-2 activity. Both the pan-MMP inhibitor GM6001 and the selective MMP-2 inhibitor ARP 100 prevented sarcomere degeneration induced by OSM treatment. OSM also induced NRVM cell cycling and increased methyl-thiazolyl-tetrazolium (MTT) staining, preventable by MMP inhibition. These results suggest that MMP-2 mediates sarcomere degeneration in OSM-induced cardiomyocyte dedifferentiation and thus potentially contributes to cardiomyocyte regeneration.


2017 ◽  
Vol 4 (7) ◽  
pp. 2369 ◽  
Author(s):  
Prakrati Gupta ◽  
Srisha Senthil ◽  
Arjun Srirampur ◽  
Priya Mittal

Importance of matrix metalloproteinase inhibitor like Doxycycline in the management of conjunctival dehiscence following glaucoma drainage device. A 50 years old man developed conjunctival retraction after a glaucoma grainage device with was managed with oral doxycycline. After 4 month of continuous treatment there was complete healing of conjunctival defect. Oral doxycycline is a viable alternative in the conservative management of conjunctival retraction obviating the need for surgical intervention.


2011 ◽  
Vol 45 (4) ◽  
pp. 346-352 ◽  
Author(s):  
H.M. Nassar ◽  
C. González-Cabezas

Renal Failure ◽  
2010 ◽  
Vol 32 (8) ◽  
pp. 941-946 ◽  
Author(s):  
Hari Krishan Aggarwal ◽  
Deepak Jain ◽  
Paulomi Talapatra ◽  
Raj Kumar Yadav ◽  
Tarana Gupta ◽  
...  

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