Advancements in Genetic Engineering
Open Access
ISSN: 2169-0111
+44 1478 350008
ISSN: 2169-0111
+44 1478 350008
Short Communication - (2016) Volume 5, Issue 1
Keywords: Orthodontics; Dental specialty; Malocclusion; Etiology; Genetics
The word orthodontics has evolved from Greek word, “orthos” meaning right or correct, and “dons” meaning tooth. This is the first bonafide dental specialty that concerns with the management and treatment of malocclusion. Malocclusion in strict sense does not represent any disease; rather it is a variation from, what is considered normal/ideal [1]. It was rightly said by Jackson that orthodontics is a “science of infinite variations” [2]. Etiology of malocclusion is multifactorial; having specific causes viz. any disturbances during embryonic period, fetal molding and birth trauma, any childhood fracture of jaw, muscle dysfunction, Acromegaly, hemimandibular hyperplasia and developmental disturbances of dentition [3]. Beside this a strong influence of heredity/gene has been found in the etiology of malocclusion. The famous “hapsburgs jaw” (prognathic mandible), which was classical phenotype of European Royal ancestry is the best known example of genetic influence on malocclusion and later on Dr. Stockard’s and Johnson experiment on crossbreeding dogs also strengthened this hypothesis [4]. Contemporary knowledge among orthodontic arena reveals that several genes are linked with etiology of malocclusion, tooth movement following orthodontic treatment and side-effects following orthodontic therapy. The purpose of this article is to highlight the role of genetics involved in different clinical conditions leading to severe skeletal and dental malformation and hence poses a great impact on orthodontics as discipline.3
Data from the studies conducted by Manfredi, et al. [5] and Savoye, et al. [6] confirms that vertical skeletal malocclusion have more genetic preponderance than sagittal skeletal dysplasias. Apertognathia (skeletal open bite) with dolichofacial pattern was most frequent inherited dentofacial deformity [3]. Harris conducted a cephalometric investigation in skeletal class II division 1 malocclusion that revealed significant reduction in mandibular body length as compared to skeletal class I patients, thus supporting polygenic inheritance [7]. A clinical and cephalometric study conducted by Markovic on 114 class II division 2 patients showed a strong evidence for gene as main etiological factor [8]. The association of vascular endothelial growth factor (VEGF), parathyroid-hormone like hormone (PTHLH), Indian hedgehog homolog(IHH) and insulin-like growth factor-1(IGF-1) have been found to cause class III malocclusion (mandibular prognathism ) [9]. Recent study conducted by Guan, et al. on Chinese family has shown that ADAMTS1 gene is associated with familial mandibular prognathism [10]. These entire data do confirms the involvement of genes in the causation of skeletal malocclusion.
In cliedocranial dysplasia, associated gene is RUNX2, presented as hyperdontia and multiple impacted supernumerary teeth [11]. Animal studies have shown that complete lack of RUNX2 gene resulted in the failure of teeth and bone development, whereas mutation in RUNX2 led to arrested tooth development [12]. Cleft lip and palate, several genes have been highlighted viz. 17q12 (RARA), 7p13-15, 2p13 (TGFA), 6p21.3-21.1, 1q22.3-41 (IRF6), 2q35-36, 7q22-qter and 12q24-qter [13]. Crouzon syndrome that has been evidenced to have maxillary hypoplasia, results from mutations in the fibroblast growth factor receptor 2 gene (FGFR2) [14], odonto-onchyo-dermal dysplasia (a rare form of ectodermal dysplasia), causative gene is WNT10A [15]. Duplication of chromosome segment 16p13.3 have been reported as cause for non-syndromic Pierre Robin sequence [16], that is characterized with cleft palate, glossoptossis and micrognathia. Association of SOX-9 gene, PTHrP and IHH with orthodontic tooth movement [17], MSX1 and PAX9 genes with hypodontia [18], MSX1, PAX9, AXIN 2 with oligodontia [19], CBFA 1 (RUNX2), TRAF6 and FGFR 1-3 with some of syndromes associated with tooth eruption failure [20]. External apical root resorption, an unwanted sequel of orthodontic treatment believed to have association of decreased level of IL-1β production in the case of IL-1B (+3953) allele 1 [21] and tight linkage of TNFRSF 11A gene loci [22].
Malocclusion is the result of various combinations and permutation of genetic as well as environmental influences. Although there is tremendous advancement in the science of genetics, but the underlined cause of malocclusion is still unclear. Refinements in the knowledge of genetics in the field orthodontics will pave the way for genetic correction of some traits of malocclusions through human genome project. Future advancements in genomic medicine will help us in the identification of disease causing mutations and zig-zag puzzled network of molecular interaction.