scholarly journals The Role of Myofibroblasts and Mast Cells in Oral Mucosa Repair After Fractional Laser Treatment

2019 ◽  
Vol 8 (1) ◽  
pp. 59-67
Author(s):  
E. S. Sergeeva ◽  
V. V. Gusel'nikova ◽  
L. A. Ermolaeva ◽  
A. V. Belikov ◽  
D. Yu. Fedotov ◽  
...  

The aimof this study was to clarify the features of the reparative process of the rat's oral mucosa in the later periods after fractional laser treatment with an analysis of the possible involvement of mast cells and myofibroblasts in this process.Material and methods.The samples of the oral mucosa of male Wistar rats (n=9) were used as a material for this study. Fractional laser treatment was carried out using stLase (DentalPhotonics, USA) with power P=7–10 W and pulse duration tp=100–200 ms (wavelength 980 nm). Histological sections of the oral mucosa from the control zones (unaffected) and zones treated with laser radiation were stained with hematoxylin and eosin and with Masson’s aniline blue. To identify mast cells, toluidine blue was used. For the detection of blood vessels and myofibroblasts, immunohistochemical reaction to smooth-muscle α-actin was performed.Results.On the 28th day after fractional laser treatment in rat oral mucosa the signs of incomplete repair were present. At this period in laser treated areas within the lamina propria rows of densely adjacent myofibroblasts were found. In the rows of myofibroblasts the mast cells are not visualized, while in the similar areas of the intact mucosa mast cells are present in large numbers.Conclusion.Fractional laser treatment stimulates the prolongation of regeneration process of rat oral mucosa while formation of myofibroblasts occurs in the laser treated zone. During this process mast cells may be involved. The ability to degranulate under laser radiation was shown.

2019 ◽  
Vol 24 (2) ◽  
pp. 20-31
Author(s):  
Solange de Oliveira Braga Franzolin ◽  
Maria Inês Moura Campos Pardini ◽  
Leda A. Francischone ◽  
Elenice Deffune ◽  
Alberto Consolaro

Abstract This study contributes to the understanding of the mechanisms associated with signs and symptoms of tooth eruption, by investigating the presence of mast cells in pericoronal tissues during the intraosseous (Group 1) and submucosal (Group 2) phases of eruption. We compared findings for these two groups with each other and with those for the oral mucosa (Group 3). In each group, 14 specimens were analyzed microscopically after hematoxylin and eosin staining and immunohistochemical analysis of c-Kit and tryptase expression. Results revealed that the number and density of mast cells is different in follicular tissues according to the eruption phase, which may mean that: 1) masticatory trauma of the oral mucosa and dental follicles in the submucosa may explain why reduced enamel epithelium exposes enamel to the cells of the connective tissue; 2) exposure of antigenic enamel proteins might correspond to the release of sequestered antigens, which may lead to the interaction of IgE and a greater number of mast cells in the region; and 3) the consequent degranulation and the local release of mediators, such as histamine, leukotrienes, prostaglandins, proteases, cytokines and growth factors, contribute to the understanding of signs and symptoms associated with tooth eruption.


Author(s):  
Ruth V.W. Dimlich

Mast cells in the dura mater of the rat may play a role in cerebral pathologies including neurogenic inflammation (vasodilation; plasma extravasation) and headache pain . As has been suggested for other tissues, dural mast cells may exhibit a close spatial relationship to nerves. There has been no detailed ultrastructural description of mast cells in this tissue; therefore, the goals of this study were to provide this analysis and to determine the spatial relationship of mast cells to nerves and other components of the dura mater in the rat.Four adult anesthetized male Wistar rats (290-400 g) were fixed by perfusion through the heart with 2% glutaraldehyde and 2.8% paraformaldehyde in a potassium phosphate buffer (pH 7.4) for 30 min. The head of each rat was removed and stored in fixative for a minimum of 24 h at which time the dural coverings were removed and dissected into samples that included the middle meningeal vasculature. Samples were routinely processed and flat embedded in LX 112. Thick (1 um) sections from a minimum of 3 blocks per rat were stained with toluidine blue (0.5% aqueous).


Author(s):  
Thomas T.F. Huang ◽  
Patricia G. Calarco

The stage specific appearance of a retravirus, termed the Intracisternal A particle (IAP) is a normal feature of early preimplantation development. To date, all feral and laboratory strains of Mus musculus and even Asian species such as Mus cervicolor and Mus pahari express the particles during the 2-8 cell stages. IAP form by budding into the endoplasmic reticulum and appear singly or as groups of donut-shaped particles within the cisternae (fig. 1). IAP are also produced in large numbers in several neoplastic cells such as certain plasmacytomas and rhabdomyosarcomas. The role of IAP, either in normal development or in neoplastic behavior, is unknown.


Author(s):  
Tomoko Yamaguchi ◽  
Yumi Ikeda ◽  
Katsuhisa Tashiro ◽  
Yasuyuki Ohkawa ◽  
Kenji Kawabata

1997 ◽  
Vol 77 (03) ◽  
pp. 577-584 ◽  
Author(s):  
Mehrdad Baghestanian ◽  
Roland Hofbauer ◽  
Hans G Kress ◽  
Johann Wojta ◽  
Astrid Fabry ◽  
...  

SummaryRecent data suggest that auricular thrombosis is associated with accumulation of mast cells (MC) in the upper endocardium (where usually no MC reside) and local expression of MGF (mast cell growth factor) (25). In this study, the role of vascular cells, thrombin-activation and MGF, in MC-migration was analyzed. For this purpose, cultured human auricular endocardial cells (HAUEC), umbilical vein endothelial cells (HUVEC) and uterine-(HUTMEC) and skin-derived (HSMEC) microvascular endothelial cells were exposed to thrombin or control medium, and the migration of primary tissue MC (lung, n = 6) and HMC-1 cells (human MC-line) against vascular cells (supernatants) measured. Supernatants (24 h) of unstimulated vascular cells (monolayers of endocardium or endothelium) as well as recombinant (rh) MGF induced a significant migratory response in HMC-1 (control: 3025 ± 344 cells [100 ± 11.4%] vs. MGF, 100 ng/ml: 8806 ± 1019 [291 ± 34%] vs. HAUEC: 9703 ± 1506 [320.8 ± 49.8%] vs. HUTMEC: 8950 ± 1857 [295.9 ± 61.4%] vs. HSMEC: 9965 ± 2018 [329.4 ± 66.7%] vs. HUVEC: 9487 ± 1402 [313.6 ± 46.4%], p <0.05) as well as in primary lung MC. Thrombin-activation (5 U/ml, 12 h) of vascular cells led to an augmentation of the directed migration of MC as well as to a hirudin-sensitive increase in MGF synthesis and release. Moreover, a blocking anti-MGF antibody was found to inhibit MC-migration induced by unstimulated or thrombin-activated vascular cells. Together, these data show that endocardial and other vascular cells can induce migration of human MC. This MC-chemotactic signal of the vasculature is associated with expression and release of MGF, augmentable by thrombin, and may play a role in the pathophysiology of (auricular) thrombosis.


Sign in / Sign up

Export Citation Format

Share Document