scholarly journals Genetic Susceptibility and Protein Expression of Extracellular Matrix Turnover-Related Genes in Oral Submucous Fibrosis

2020 ◽  
Vol 21 (21) ◽  
pp. 8104
Author(s):  
Ru-Hsiu Cheng ◽  
Yi-Ping Wang ◽  
Julia Yu-Fong Chang ◽  
Yu-Hwa Pan ◽  
Mei-Chi Chang ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Oral Cancer ◽  
Genetic Susceptibility ◽  
Molecular Mechanisms ◽  
Lysyl Oxidase ◽  
Oral Submucous Fibrosis ◽  
Tissue Inhibitors Of Metalloproteinases ◽  
Contributing Factors ◽  
Plasminogen Activator Inhibitor 1 ◽  
Submucous Fibrosis

Betel quid (BQ) chewing increased the risk of oral cancer and oral submucous fibrosis (OSMF), an oral premalignant disorder (OPMD) with malignant transformation potential. BQ components such as areca nut (AN), trauma by coarse AN fiber, catechin, copper, alkaloids, stimulated reactive oxygen species (ROS), inflammation and cytotoxicity are suggested to be the contributing factors. They may induce tissue inflammation, proliferation of fibroblasts and collagen deposition, myofibroblast differentiation and contraction, collagen cross-links and inhibit collagen phagocytosis, finally leading to the development of OSMF and oral cancer. These events are mediated by BQ components-induced changes of extracellular matrix (ECM) turnover via regulation of TGF-β1, plasminogen activator inhibitor-1 (PAI-1), cystatin, lysyl oxidase (LOX) and tissue inhibitors of metalloproteinases (TIMPs) and metalloproteinases (MMPs). Genetic susceptibility is also involved in these disease processes. Further understanding the molecular mechanisms of BQ-induced OSMF and oral cancer can be helpful for future disease prevention and treatment.

scholarly journals Mandibular Canal Widening and Bell’s Palsy: Sequelae of Perineural Invasion in Oral Cancer

2016 ◽  
Vol 2016 ◽  
pp. 1-4
Author(s):  
Gopinath Thilak Parepady Sundar ◽  
Vishwanath Sherigar ◽  
Sameep S. Shetty ◽  
Shree Satya ◽  
Sourabh M. Gohil
Keyword(s):  
Oral Cancer ◽  
Perineural Invasion ◽  
Oral Submucous Fibrosis ◽  
Inferior Alveolar Nerve ◽  
Mandibular Canal ◽  
Distinct Disease ◽  
Nerve Tracts ◽  
Submucous Fibrosis ◽  
Neurological Disturbance ◽  
Shed Light

Perineural invasion is an underrecognized route of metastatic spread along the nerve bundles within the nerve sheath into the surrounding tissues. It hinders the ability to establish local control as tumour cells can traverse along nerve tracts well beyond the extent of any local invasion rendering them inoperable and unresectable. Perineural invasion is a marker of poor prognosis. Oral submucous fibrosis with oral cancer constitutes a clinicopathologically distinct disease. Our case highlights an enigmatic presentation of oral submucous fibrosis and its coexistence with oral cancer presenting with unusual neurological disturbance of the inferior alveolar nerve and facial nerve and diffuse widening of the mandibular canal. The objective of this case report is to enumerate the significance of perineural invasion in determining the course of the disease and necessitate the need for future studies that can shed light on molecular mediators and pathogenesis of perineural spread.

Lysyl oxidases: from enzyme activity to extracellular matrix cross-links

2019 ◽  
Vol 63 (3) ◽  
pp. 349-364 ◽  
Author(s):  
Sylvain D. Vallet ◽  
Sylvie Ricard-Blum
Keyword(s):  
Extracellular Matrix ◽  
Molecular Mechanisms ◽  
Catalytic Domain ◽  
Lysyl Oxidase ◽  
Dimensional Structure ◽  
Cross Linking ◽  
Copper Binding ◽  
Molecular Features ◽  
Ecm Proteins ◽  
Cross Links

Abstract The lysyl oxidase family comprises five members in mammals, lysyl oxidase (LOX) and four lysyl oxidase like proteins (LOXL1-4). They are copper amine oxidases with a highly conserved catalytic domain, a lysine tyrosylquinone cofactor, and a conserved copper-binding site. They catalyze the first step of the covalent cross-linking of the extracellular matrix (ECM) proteins collagens and elastin, which contribute to ECM stiffness and mechanical properties. The role of LOX and LOXL2 in fibrosis, tumorigenesis, and metastasis, including changes in their expression level and their regulation of cell signaling pathways, have been extensively reviewed, and both enzymes have been identified as therapeutic targets. We review here the molecular features and three-dimensional structure/models of LOX and LOXLs, their role in ECM cross-linking, and the regulation of their cross-linking activity by ECM proteins, proteoglycans, and by inhibitors. We also make an overview of the major ECM cross-links, because they are the ultimate molecular readouts of LOX/LOXL activity in tissues. The recent 3D model of LOX, which recapitulates its known structural and biochemical features, will be useful to decipher the molecular mechanisms of LOX interaction with its various substrates, and to design substrate-specific inhibitors, which are potential antifibrotic and antitumor drugs.

Consumption of areca quid, cigarettes, and alcohol related to the comorbidity of oral submucous fibrosis and oral cancer

2007 ◽  
Vol 104 (5) ◽  
pp. 647-652 ◽  
Author(s):  
Pei-Shan Ho ◽  
Yi-Hsin Yang ◽  
Tien-Yu Shieh ◽  
I.-Yueh Huang ◽  
Yun-Kwan Chen ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Oral Submucous Fibrosis ◽  
Submucous Fibrosis

scholarly journals Cross-Cheek Dumbbell-Shaped Radial Forearm Flap for Simultaneous Correction of Oral Cancer and Submucous Fibrosis

2016 ◽  
Vol 9 (2) ◽  
pp. 162-165 ◽  
Author(s):  
Shreya Bhattacharya ◽  
Sivakumar Vidhyadharan ◽  
Krishnakumar Thankappan ◽  
Subramania Iyer
Keyword(s):  
Oral Cancer ◽  
Buccal Mucosa ◽  
Oral Submucous Fibrosis ◽  
The Other ◽  
Simultaneous Occurrence ◽  
Cancer Resection ◽  
Novel Technique ◽  
Radial Forearm ◽  
Submucous Fibrosis ◽  
Interincisor Distance

Simultaneous occurrence of oral submucous fibrosis along with carcinoma of the buccal mucosa is common. We report a novel technique of a single dumbbell-shaped, cross-cheek radial forearm free flap to repair bilateral defects caused by oral cancer resection on one side and the release of fibrosis on the other side in two patients. The dumbbell-shaped flap provided tissue for both the buccal mucosa defects and central released soft palate preventing fibrosis and reapproximation. The interincisor distance improved in both the patients.

scholarly journals Study of the Role of Salivary Lactate Dehydrogenase in Habitual Tobacco Chewers, Oral Submucous Fibrosis and Oral Cancer as a Biomarker

2019 ◽  
Vol 20 (8) ◽  
pp. 970-973 ◽  
Author(s):  
Sanjay G Thete ◽  
Tejashree Mantri ◽  
Vijayalaxmi Male ◽  
Renu Yadav ◽  
Ishita Grover ◽  
...  
Keyword(s):  
Lactate Dehydrogenase ◽  
Oral Cancer ◽  
Oral Submucous Fibrosis ◽  
Submucous Fibrosis

scholarly journals LOXL2—A New Target in Antifibrogenic Therapy?

2019 ◽  
Vol 20 (7) ◽  
pp. 1634 ◽  
Author(s):  
Angela Puente ◽  
Jose Fortea ◽  
Joaquin Cabezas ◽  
Maria Arias Loste ◽  
Paula Iruzubieta ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Liver Fibrosis ◽  
Animal Studies ◽  
Molecular Mechanisms ◽  
Lysyl Oxidase ◽  
Portal Pressure ◽  
Induce Cell Cycle Arrest ◽  
Cell Functions ◽  
Extracellular Matrix Components ◽  
Matrix Components

The concept of liver fibrosis and cirrhosis being static and therefore irreversible is outdated. Indeed, both human and animal studies have shown that fibrogenesis is a dynamic and potentially reversible process that can be modulated either by stopping its progression and/or by promoting its resolution. Therefore, the study of the molecular mechanisms involved in the pathogenesis of liver fibrosis is critical for the development of future antifibrotic therapies. The fibrogenesis process, common to all forms of liver injury, is characterized by the increased deposition of extracellular matrix components (EMCs), including collagen, proteoglycans, and glycoproteins (laminin and fibronectin 2). These changes in the composition of the extracellular matrix components alter their interaction with cell adhesion molecules, influencing the modulation of cell functions (growth, migration, and gene expression). Hepatic stellate cells and Kupffer cells (liver macrophages) are the key fibrogenic effectors. The antifibrogenic mechanism starts with the activation of Ly6Chigh macrophages, which can differentiate into macrophages with antifibrogenic action. The research of biochemical changes affecting fibrosis irreversibility has identified lysyl oxidase-like 2 (LOXL2), an enzyme that promotes the network of collagen fibers of the extracellular matrix. LOXL2 inhibition can decrease cell numbers, proliferation, colony formations, and cell growth, and it can induce cell cycle arrest and increase apoptosis. The development of a new humanized IgG4 monoclonal antibody against LOXL2 could open the window of a new antifibrogenic treatment. The current therapeutic target in patients with liver cirrhosis should focus (after the eradication of the causal agent) on the development of new antifibrogenic drugs. The development of these drugs must meet three premises: Patient safety, in non-cirrhotic phases, down-staging or at least stabilization and slowing the progression to cirrhosis must be achieved; whereas in the cirrhotic stage, the objective should be to reduce fibrosis and portal pressure.

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