Association Between HLA-Antigens and Periodontal Disease

Reinholdt, Jesper; Bay, Inger; Svejgaard, A.

doi:10.1177/00220345770560102901

Cited by 69 publications

(43 citation statements)

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“…Most recently, Shapira and colleagues (1994) found that, among non-Ashkenazi lews, HLA antigens A9 and Bl 5 are associated with the generalized form of early-onset periodontal disease but not with the localized form. Earlier studies in other populations also reported an association between HLA-A9 and early-onset periodontal disease (Reinholdt et al, 1977;MarggrafeUl., 1983;KloudaeU/., 1986;AmereUl., 1988); the criteria for case selection suggest that primarily generalized early-onset periodontal disease cases were included in these studies . Shapira and colleagues (1994) conclude that generalized earlyonset periodontal disease and localized early-onset disease are different diseases "under different genetic control".…”

Section: Population Association Studiesmentioning

confidence: 86%

Genetic Influences in Caries and Periodontal Diseases

Hassell

Harris

1995

Critical Reviews in Oral Biology & Medicine

114

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Deciphering the relative roles of heredity and environmental factors ("nature vs. nurture") in the pathogenesis of dental caries and diseases of the periodontium has occupied clinical and basic researchers for decades. Success in the endeavor has come more easily in the case of caries; the complex interactions that occur between host-response mechanisms and putative microbiologic pathogens in periodontal disease have made elucidation of genetic factors in disease susceptibility more difficult. In addition, during the 30-year period between 1958 and 1987, only meager resources were targeted toward the "nature" side of the nature/nurture dipole in periodontology. In this article, we present a brief history of the development of genetic epistemology, then describe the three main research mechanisms by which questions about the hereditary component of diseases in humans can be addressed. A critical discussion of the evidence for a hereditary component in caries susceptibility is next presented, also from a historical perspective. The evolution of knowledge concerning possible genetic ("endogenous", "idiotypic") factors in the pathogenesis of inflammatory periodontal disease is initiated with an analysis of some foreign-language (primarily German) literature that is likely to be unfamiliar to the reader. We identify a turning point at about 1960, when the periodontal research community turned away from genetics in favor of microbiology research. During the past five years, investigators have re-initiated the search for the hereditary component in susceptibility to common adult periodontal disease; this small but growing body of literature is reviewed. Recent applications of in vitro methods for genetic analyses in periodontal research are presented, with an eye toward a future in which persons who are at risk-genetically predisposed-to periodontal disease may be identified and targeted for interventive strategies. Critical is the realization that genes and environment do not act independently of each other; the appearance or magnitude of heritability may differ with various environments.

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Section: Population Association Studiesmentioning

confidence: 86%

Genetic Influences in Caries and Periodontal Diseases

Hassell

Harris

1995

Critical Reviews in Oral Biology & Medicine

114

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“…Since activation of lymphocyte and -blast transformation is controlled by the HLA system in man, association between the HLA system and various diseases, including localized juvenile periodontitis, has been sought. For example, juvenile periodontitis patients have been found to have decreased frequency of HLA-A2 (Kaslick et al, 1975;Kaslick et al, 1980), and increased frequency of HLA-A9, HLA-A28, and HLA-BW15 (Reinholdt et al, 1977). However, Cullinan et al (1980) and Saxen and Koskimies (1984) did not confirm these alterations in HLA frequency.…”

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confidence: 96%

1985 Kreshover lecture. Molecular Factors Influencing Neutrophil Defects in Periodontal Disease

et al. 1986

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Major advances in our understanding of the role of the neutrophil in host defense against periodontal organisms have been made through studies of localized juvenile periodontitis (LJP). Several lines of evidence suggest that LJP is an infectious process closely associated with Actinobacillus (Haemophilus) actinomycetemomitans as a causative agent, although other organisms may also participate. The immunologic profile of LJP patients suggests that a cell-associated neutrophil locomotory dysfunction is a key underlying immunodeficiency resulting in increased susceptibility to periodontal infection. In addition, LJP patients often exhibit cervical lymphadenopathy and IgG-hypergammaglobulinemia, and a markedly elevated antibody response to the infecting organism, A. actinomycetemcomitans, is found in the serum and crevicular fluid of most patients. Evaluation of the locomotory properties of LJP neutrophils shows that random migration and chemokinesis are normal; however, about 70% of the LJP patients suffer from a defect in chemotaxis, with their neutrophils responding poorly to bacterial chemotactic factors, synthetic chemotactic peptides, and complement fragments (C5a). Depressed chemotaxis of LJP neutrophils is paralleled by their reduced capacity to bind the synthetic chemotactic peptide N-formylmethionylleucylphenylalanine (FMLP), as well as C5a. Furthermore, there is a reduction in the amount of glycoprotein 110, a neutrophil membrane matrix component and differentiation antigen which is associated with FMLP- and possibly also C5a-mediated chemotaxis. Reduction of C5a and of FMLP ligand binding, decreased expression of GP-110, and reduced neutrophil chemotaxis are consistent with a stem cell maturation error in LJP patients. This is further supported by studies demonstrating increased expression of CR2, the C3d/EBV receptor, on peripheral blood neutrophils of LJP patients. CR2 receptors are normally present on immature human neutrophils but are lost during the maturation process. These alterations in neutrophil surface components and their reduced chemotaxis may result from a genetically determined abnormality. Studies demonstrating the familial nature of both the neutrophil chemotactic disorder and the clinical entity represented by localized juvenile periodontitis point to a strong role for genetic determinants in the disease which affect neutrophil surface receptors.

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“…(1977) had reported a positive association of HLA-A9, A28 and B25 with AP. [22] Klouda et al . (1986) reported a higher frequency of HLA-A9 and HLA-A24 in English Caucasians with AP.…”

Section: Discussionmentioning

confidence: 99%

Aggressive periodontitis: A clinico-hematological appraisal

Kundu

Bandyopadhyay

Nair

et al. 2014

J Indian Soc Periodontol

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Background:Human leukocyte antigens (HLA) have been considered a candidate of genetic risk markers for aggressive periodontitis (AP). AP has also been associated with polymorphonuclear leukocyte (PMN) dysfunction. The role of monocyte subsets in AP has also not been completely explored. Therefore, the present study was undertaken to assess in, AP subjects, the possible association between defective PMN adhesion and β2-integrin expression; defective neutrophil migration and actin polymerization level; the expression of ABO blood group and HLA antigen; and the percentage of CD14+ CD16+ monocytes and CD45RA monocytes. All these parameters have been compared with the subjects of chronic periodontitis (CP) and healthy controls.Materials and Methods:A total of 45 subjects of the age group 20-50 years, free from any known systemic disease, were divided into three groups – Group I - periodontally healthy control (n = 15), Group II - CP (n = 15) and Group III - AP (n = 15). Peripheral blood samples were collected. ABO grouping and HLA typing were performed. β2-integrin expression, actin polymerization level and percentage of CD14+ CD16+ monocytes and CD45RA monocytes were estimated by fluorescence-activated cell sorter analysis.Results:Most of the subjects of AP belonged to the blood group AB, and an increased frequency of HLA-A30, CW1 and DR1 (P < 0.1) and B44 and DQ2 (P < 0.05) were also observed in this group. In the AP group, both average values (β2-integrin and actin level) were significantly less than those of normal subjects (P < 0.001). The mean percentage of CD14+ CD16+ monocytes was found to be maximum in CP, followed by AP, and then in healthy subjects, while the mean percentage of CD45RA was maximum in AP, followed by CP, and then in healthy subjects.Conclusions:With the present state of knowledge from this study, a definite association of ABO blood groups and HLA phenotypes with periodontal diseases is yet to be established. Leukocytic functional defects were found in AP subjects. A statistically significant percentage of CD14+ CD16+ and CD45RA monocytes were found in AP subjects as compared with the normal control and CP groups.

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Association Between HLA-Antigens and Periodontal Disease

Cited by 69 publications

References 3 publications

Genetic Influences in Caries and Periodontal Diseases

Genetic Influences in Caries and Periodontal Diseases

1985 Kreshover lecture. Molecular Factors Influencing Neutrophil Defects in Periodontal Disease

Aggressive periodontitis: A clinico-hematological appraisal

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