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      Pre-Cancerous Lesions in the Oral and Maxillofacial Region: A Literature Review with Special Focus on Etiopathogenesis

      review-article
      Author(s): 1 , 2
      Publication date (Print):
      Journal: Iranian Journal of Pathology
      Publisher: Iranian Society of Pathology
      Keywords: Face, Head, Leukoplakia, Mouth, Neoplasm, Precancerous condition, Skin

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          Abstract

          Many types of cancers develop in the oral and maxillofacial region. Squamous cell carcinoma is the most common cancer and constitutes over 90 percent of these tumors. Malignant transformation is a genetic process, which later makes a phenotyping change at the cellular level. Some cancers such as oral squamous cell carcinomas (OSCCs) develop from pre-malignant lesions and conditions. Despite advances in the treatment of OSCC, the 5-year survival rate remains approximately 50% due to inability of early detection of OSCC and precursor lesions. Early detection of oral cancer, especially in the premalignant stage, can decrease mortality and morbidity significantly. This article reviews some clinical, histopathological features and etiopathogenesis of pre-cancerous lesions of the oral cavity and skin of face and lip vermilion. A relevant English literature search in Pubmed, Science Direct, and Google Scholar was performed from 1930 to 2015. Full text of 191 articles met the specific inclusion criteria for this review.

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          The RNA component of telomerase is mutated in autosomal dominant dyskeratosis congenita.

          T Vulliamy, A Marrone, F. Goldman … (2001)
          Dyskeratosis congenita is a progressive bone-marrow failure syndrome that is characterized by abnormal skin pigmentation, leukoplakia and nail dystrophy. X-linked, autosomal recessive and autosomal dominant inheritance have been found in different pedigrees. The X-linked form of the disease is due to mutations in the gene DKC1 in band 2, sub-band 8 of the long arm of the X chromosome (ref. 3). The affected protein, dyskerin, is a nucleolar protein that is found associated with the H/ACA class of small nucleolar RNAs and is involved in pseudo-uridylation of specific residues of ribosomal RNA. Dyskerin is also associated with telomerase RNA (hTR), which contains a H/ACA consensus sequence. Here we map the gene responsible for dyskeratosis congenita in a large pedigree with autosomal dominant inheritance. Affected members of this family have an 821-base-pair deletion on chromosome 3q that removes the 3' 74 bases of hTR. Mutations in hTR were found in two other families with autosomal dominant dyskeratosis congenita.
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            Genetic progression model for head and neck cancer: implications for field cancerization.

            George W. Koch, J Califano, S Piantadosi … (1996)
            A genetic progression model of head and neck squamous cell carcinoma has not yet been elucidated, and the genetic basis for "field cancerization" of the aerodigestive tract has also remained obscure. Eighty-seven lesions of the head and neck, including preinvasive lesions and benign lesions associated with carcinogen exposure, were tested using microsatellite analysis for allelic loss at 10 major chromosomal loci which have been defined previously. The spectrum of chromosomal loss progressively increased at each histopathological step from benign hyperplasia to dysplasia to carcinoma in situ to invasive cancer. Adjacent areas of tissue with different histopathological appearance shared common genetic changes, but the more histopathologically advanced areas exhibited additional genetic alterations. Abnormal mucosal cells surrounding preinvasive and microinvasive lesions shared common genetic alterations with those lesions and thus appear to arise from a single progenitor clone. Based on these findings, the local clinical phenomenon of field cancerization seems to involve the expansion and migration of clonally related preneoplastic cells.
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              Neuronal nicotinic receptors: from structure to pathology.

              C. Gotti, Cara F. Clementi (2004)
              Neuronal nicotinic receptors (NAChRs) form a heterogeneous family of ion channels that are differently expressed in many regions of the central nervous system (CNS) and peripheral nervous system. These different receptor subtypes, which have characteristic pharmacological and biophysical properties, have a pentameric structure consisting of the homomeric or heteromeric combination of 12 different subunits (alpha2-alpha10, beta2-beta4). By responding to the endogenous neurotransmitter acetylcholine, NAChRs contribute to a wide range of brain activities and influence a number of physiological functions. Furthermore, it is becoming evident that the perturbation of cholinergic nicotinic neurotransmission can lead to various diseases involving nAChR dysfunction during development, adulthood and ageing. In recent years, it has been discovered that NAChRs are present in a number of non-neuronal cells where they play a significant functional role and are the pathogenetic targets in several diseases. NAChRs are also the target of natural ligands and toxins including nicotine (Nic), the most widespread drug of abuse. This review will attempt to survey the major achievements reached in the study of the structure and function of NAChRs by examining their regional and cellular localisation and the molecular basis of their functional diversity mainly in pharmacological and biochemical terms. The recent availability of mice with the genetic ablation of single or double nicotinic subunits or point mutations have shed light on the role of nAChRs in major physiological functions, and we will here discuss recent data relating to their behavioural phenotypes. Finally, the role of NAChRs in disease will be considered in some details.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Iran J Pathol
                Journal ID (iso-abbrev): Iran J Pathol
                Journal ID (publisher-id): IJP
                Title: Iranian Journal of Pathology
                Publisher: Iranian Society of Pathology (Tehran, Iran )
                ISSN (Print): 1735-5303
                ISSN (Electronic): 2345-3656
                Publication date (Print): Fall 2016
                Volume: 11
                Issue: 4
                Pages: 303-322
                Affiliations
                [1 ] Dental Research Center, Dept. of Oral Pathology, Dental Faculty, Hamadan University, Hamadan, Iran
                [2 ] School of Medicine, Griffith University, Queensland, Australia
                Author notes
                Corresponding Information: Dr. Soussan Irani, Dental Faculty, Shahid Fahmideh Street,Hamadan, Iran. Telephone: +98813-8354250 Email: sousanirani@gmail.com
                Article
                Publisher ID: ijp-11-303
                PMC ID: 5563928
                PubMed ID: 28855922
                SO-VID: ecc0fb2c-6cb4-4e8e-ac74-a68b8f4b1855
                Copyright © ©Iran J Pathol. All rights reserved.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License, ( http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 3 October 2015
                Date accepted : 4 April 2016
                Categories
                Subject: Review Article

                Keywords: face,head,leukoplakia,mouth,neoplasm,precancerous condition,skin
                Data availability:
                Keywords: face, head, leukoplakia, mouth, neoplasm, precancerous condition, skin

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