Septal perforation repair: mucosal regeneration technique

2012 ◽  
Vol 269 (12) ◽  
pp. 2505-2510 ◽  
Author(s):  
Alper Yenigun ◽  
Aysenur Meric ◽  
Aysegul Verim ◽  
Berke Ozucer ◽  
Husamettin Yasar ◽  
...  
2016 ◽  
Vol 155 (4) ◽  
pp. 714-717 ◽  
Author(s):  
Orhan Ozturan ◽  
Alper Yenigun ◽  
Erol Senturk ◽  
Sabri Baki Eren ◽  
Fadlullah Aksoy

2020 ◽  
pp. 194589242096197
Author(s):  
So Jeong Kim ◽  
Soo Yeon Jung ◽  
Min Ji Lee ◽  
Jung Ho Bae ◽  
Han Su Kim

Background Nasal septal perforation is caused by bilateral septal mucosal injuries resulting from nasal trauma and septal surgeries. Previous studies have reported that biocompatible materials may be effective for repairing nasal septal perforations. However, they were primarily used for treatment; no study has investigated their use for prevention of nasal septal perforation. Objective To determine whether porcine tracheal mucosa-derived decellularized patch can prevent the progression of nasal mucosa injuries to septal perforations. Methods Bilateral nasal septal mucosal defects were surgically induced in 36 rabbits. Silastic sheets were applied bilaterally in all rabbits, and decellularized mucosal patch was applied unilaterally (n = 12) or bilaterally (n = 12) at the defect site in the respective experimental groups. Between 1 and 8 weeks postoperatively, the animals were sacrificed, and their nasal septa were completely removed. The excised septa were examined macroscopically and microscopically (histopathological examinations). Moreover, glycosaminoglycan (GAG) estimations of the septa were performed to evaluate mucosal regeneration and mechanical properties. Results Septal perforations occurred in 5 animals in the control group (5/12; 42%), 1 in the unilateral group (1/12; 9%), and in none in the bilateral group. Compared with the control group, the experimental groups showed significantly different mucosal and cartilage regeneration. Conclusion Decellularized porcine tracheal mucosa can prevent mucosal defects from progressing to septal perforation, promote the repair of mucosal defects, and protect the nasal cartilage.


2017 ◽  
Vol 68 (10) ◽  
pp. 2378-2381
Author(s):  
Cristian Budacu ◽  
Mihai Constantin ◽  
Iulia Chiscop ◽  
Carmen Gabriela Stelea ◽  
Raluca Dragomir

Post-operative alveolitis is a topical issue in dental practice, which is also reflected by the etiopathogenic aspects. The conservative principle requires the maintenance of dento-periodontal units in the arch for as long as possible, but there are situations where dental extraction is required. The healing process of the post-surgical wound is complex and involves processes of gingival mucosal regeneration and bone reshaping, involving several local factors: wound size, presence of infection, alveolar vascularization, intraalveolar foreign bodies, and general factors, especially general condition, age and body reactivity. The quality, structure, maintenance, and retraction of the clot are key factors in the formation of connective tissue during the healing of the post-extraction would. At the Oral and Maxillofacial Surgery Clinic of Gala�i, during a 2-year period between January 2015 and December 30, 2016, 2780 patients that required surgery - dental extraction were consulted and diagnosed. We found that among those 2780 patients with dental extractions 105 (3.77%) had post-treatment alveolitis. No post-surgical alveolitis from the case study was complicated by osteomyelitis of the jaws or by suppurations of the superficial or deep compartments of the face. The prophylactic measures in each dental extraction, together with the correct and timely curative treatment, combined with the dentist�s competence and responsibility, can shorten the time of suffering, actively combating the risk factor and accelerating the social reintegration of the patient with post-treatment alveolitis.


2021 ◽  
pp. 019459982199201
Author(s):  
Cullen M. Taylor ◽  
Stephen F. Bansberg ◽  
Michael J. Marino

Objective Reporting patient symptoms due to nasal septal perforation (NSP) has been hindered by the lack of a validated disease-specific symptom score. The purpose of this study was to develop and validate an instrument for assessing patient-reported symptoms related to NSP. Study Design Validation study. Setting A tertiary care center. Methods The Nasal Obstruction Symptom Evaluation (NOSE) scale was used as an initial construct to which 7 nonobstruction questions were added to measure septal perforation symptoms. The proposed NOSE-Perf instrument was distributed to consecutive patients evaluated for NSP, those with nasal obstruction without NSP, and a control group without rhinologic complaints. Questionnaires were redistributed to the subgroup with NSP prior to treatment of the perforation. Results The study instrument was completed by 31 patients with NSP, 17 with only nasal obstruction, and 22 without rhinologic complaint. Internal consistency was high throughout the entire instrument (Cronbach α = 0.935; 95% CI, 0.905-0.954). Test-retest reliability was demonstrated by very strong correlation between questionnaires completed by the same patient at least 1 week apart ( r = 0.898, P < .001). Discriminant validity was confirmed via a receiver operating characteristic ( P < .001, area under the curve = 0.700). The NOSE-Perf scale was able to distinguish among all 3 study groups ( P < .001) and between NSP and nasal obstruction ( P = .024). When used alone, the NOSE scale could not discriminate between NSP and nasal obstruction ( P = .545). Conclusions The NOSE-Perf scale is a validated and reliable clinical assessment tool that can be applied to adult patients with NSP.


2012 ◽  
Vol 60 (5) ◽  
pp. 261-267 ◽  
Author(s):  
Kenichiro Noguchi ◽  
Atsushi Yamaguchi ◽  
Kazuhiro Naito ◽  
Kouichi Yuri ◽  
Hideo Adachi

2016 ◽  
Vol 311 (6) ◽  
pp. C874-C883 ◽  
Author(s):  
Yan Xu ◽  
Jie Chen ◽  
Lan Xiao ◽  
Hee Kyoung Chung ◽  
Yuan Zhang ◽  
...  

The RNA-binding protein HuR is crucial for normal intestinal mucosal regeneration by modulating the stability and translation of target mRNAs, but the exact mechanism underlying HuR trafficking between the cytoplasm and nucleus remains largely unknown. Here we report a novel function of transcription factor JunD in the regulation of HuR subcellular localization through the control of importin-α1 expression in intestinal epithelial cells (IECs). Ectopically expressed JunD specifically inhibited importin-α1 at the transcription level, and this repression is mediated via interaction with CREB-binding site that was located at the proximal region of importin-α1 promoter. Reduction in the levels of importin-α1 by JunD increased cytoplasmic levels of HuR, although it failed to alter whole cell HuR levels. Increased levels of endogenous JunD by depleting cellular polyamines also inhibited importin-α1 expression and increased cytoplasmic HuR levels, whereas JunD silencing rescued importin-α1 expression and enhanced HuR nuclear translocation in polyamine-deficient cells. Moreover, importin-α1 silencing protected IECs against apoptosis, which was prevented by HuR silencing. These results indicate that JunD regulates HuR subcellular distribution by downregulating importin-α1, thus contributing to the maintenance of gut epithelium homeostasis.


2009 ◽  
Vol 141 (3) ◽  
pp. P139-P139
Author(s):  
Andrew J. Lerrick ◽  
Alexis M. Mandli
Keyword(s):  

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