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Letter to the Editor Concerning: and#8220;The Role of Human Leukocyte Antigen Typing in Libyan Patients with Chronic Periodontitisand#8221; | OMICS International
ISSN: 2332-0877
Journal of Infectious Diseases & Therapy
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Letter to the Editor Concerning: “The Role of Human Leukocyte Antigen Typing in Libyan Patients with Chronic Periodontitis”

Joana Maira Valentini Zacarias*, Luciana Conci Macedo, Jeane Eliete Laguila Visentainer and Ana Maria Sell

Post Graduation Program of Biosciences and Physiopathology, Department of Analysis Clinical and Biomedicine, Maringa State University, Parana, Brazil

*Corresponding Author:
Joana Maira Valentini Zacarias
Post Graduation Program of Biosciences and Physiopathology
Department of Analysis Clinical and Biomedicine
Maringa State University, Parana, Brazil
Tel: 55-44-3011-4864
Fax: 55-44-3011-4833
E-mail: [email protected]

Received Date: April 28, 2016; Accepted Date: May 09, 2016; Published Date: May 13, 2016

Citation: Zacarias JMV, Macedo LC, Visentainer JEL, Sell AM (2016) Letter to the Editor Concerning: “The Role of Human Leukocyte Antigen Typing in Libyan Patients with Chronic Periodontitis”. J Infect Dis Ther 4:279. doi: 10.4172/2332-0877.1000279.

Copyright: © 2016 Zacarias JMV. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Letter To The Editor

According to the article written by Daeki et al. [1] published in this journal, the authors of the manuscript investigated possible relationships between HLA and chronic periodontitis in Libyan patients and concluded that some HLA class I may represent risk factors and one class II allele group and the HLA-DRB5 loci may indicate protective factors for disease. This is an important study because the correlation between genetic marker with oral diseases could be influenced by geographical diversity in populations. However, we have concerns about the HLA and about a citation in the article published by our research group (Probst et al. [2]).

About HLA: The correct nomenclature of HLA alleles is described in http://hla.alleles.org/nomenclature/index.html. The naming of HLA genes and allele sequences and their quality control is the responsibility of the WHO Nomenclature Committee for Factors of the HLA System, which first met in 1968 [3]. Therefore, HLA-A2 for example indicates specificity or serological group and not allele group. The correct naming is HLA-A*02 (besides that, HLA-A*02 is an allele group not an allele). The class II loci of the DR region are naming as DRB1, DRB3, DRB4 and DRB5 (not DRB1, DRB3, DRB4 and DRB5). Furthermore, DRB1 group alleles may be named as DRB1*13 for example (not HLADRB113 or DRB13 as described in table 4 of the manuscript). On the other hand, the HLA-A35, A42 and A27 shown in the table 2, and HLA-B80 shown in the table 3 are not found in the literature as specificity or allele groups (http://hla.alleles.org/alleles/class1.html) [4].

In that manuscript [1] the authors cited twice the article published by Probst et al. [2]. In the introduction it was referred as a number 12 and the authors affirm that the “certain HLA alleles seem to be associated with susceptibility or resistance to periodontitis as published in previous study”. In the discussion it was referred to as a number 17 and according the authors “Probst et al. defined that CP is predominantly in white European origin (80.6%), 12.5% in African and 7.0% in Amerindian population”. In fact, Probst et al. did not study the chronic periodontitis (CP). They studied the HLA polymorphism and evaluated its contribution to the Brazilian populations. In accordance with HLA phenotypic classification, they affirm that the white population from Paraná is predominantly of European origin (80.6%), with a smaller contribution of African (12.5%) and Amerindian (7.0%) genes and the Mulatto population consisting of African (49.5%) and European (41.8%) ancestry, with a smaller but significant contribution of Amerindian (8.7%) ancestry.

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